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Are nosebleeds unique to humans?

Are nosebleeds unique to humans?


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Are there other species that get nosebleeds? If so, do they occur for the same reasons that humans get nosebleeds? How would an animal stop a nosebleed?


Cats, dogs and other animals can suffer from epistaxis. The causes differ depending on the animal.

foreign things in the nose, abscess, cancerous growth, snake bite, some poisonings and diseases especially in the trachea and lungs and anthrax. Sometimes excessive sneezing or coughing can result in nose bleeding as well. All animals are susceptible to get nose bleeding.

They would need to see their vet or owner to get it treated.

https://www.thevillager.com.na/articles/7474/Dealing-With-an-Animal-Bleeding-From-the-Nose/


Nose bleeding (or epistaxis, as Graham rightly termed it) is common to many species, such as dogs, cats, pigs, and many other animals. As for the causes, like Graham pointed out, it really varies from species to species.

To take dogs for an example, the leading causes of spontaneous nose bleeding are leishmaniasis (a tropical / subtropical disease transmitted by sandflies) and other bacterial infections, such as CME (canine monocytic ehrlichiosis, a disease spread by ticks).

As you can imagine, minor trauma to the nasal region can also cause nose bleeding, not just in dogs, but in many other animal kinds.

That said, I feel sorry for the elephant who gets a nose bleed.


Sources:

  • A retrospective study of 61 cases of spontaneous canine epistaxis, . Mylonakis, M. N. Saridomichelakis, V. Lazaridis, L. S. Leontides, P. Kostoulas, A. F. Koutinas, 2007
  • Leishmaniasis, Wikipedia
  • Monocytic ehrlichiosis in dogs, Procajło A1, Skupień EM, Bladowski M, Lew S.
  • A Porcine Epistaxis Model: Hemostatic Effects of Octylcyanoacrylate, Adam J. Singer, MD, Steve A. McClain, MD, Arnold Katz, MD, 2004

Once the human genome was sequenced in 2001, the hunt was on for the genes that make each of us unique. But scientists at the European Molecular Biology Laboratory (EMBL) in Heidelberg, Germany, and Yale and Stanford Universities in the USA, have found that we differ from each other mainly because of differences not in our genes, but in how they’re regulated – turned on or off, for instance. In a study published today in Science, they are the first to compare entire human genomes and determine which changes in the stretches of DNA that lie between genes make gene regulation vary from one person to the next. Their findings hail a new way of thinking about ourselves and our diseases.

The technological advances of the past decade have been so great that scientists can now obtain the genetic sequences – or genomes – of several people in a fraction of the time and for a fraction of the cost it took to determine that first human genome. Moreover, these advances now enable researchers to understand how genes are regulated in humans.

A group of scientists led by Jan Korbel at EMBL and Michael Snyder initially at Yale and now in Stanford were the first to compare individually sequenced human genomes to look for what caused differences in gene regulation amongst ten different people. They focused on non-coding regions – stretches of DNA that lie between genes and, unlike genes, don’t hold the instructions for producing proteins. These DNA sequences, which may vary from person to person, can act as anchors to which regulatory proteins, known as transcription factors, attach themselves to switch genes on or off.

Korbel, Snyder, and colleagues found that up to a quarter of all human genes are regulated differently in different people, more than there are genetic variations in genes themselves. The scientists found that many of these differences in how regulatory proteins act are due to changes in the DNA sequences they bind to. In some cases, such changes can be a difference in a single letter of the genetic code, while in others a large section of DNA may be altered. But surprisingly, they discovered even more variations could not be so easily explained. They reasoned that some of these seemingly inexplicable differences might arise if regulatory proteins didn’t act alone, but interacted with each other.

“We developed a new approach which enabled us to identify cases where a protein’s ability to turn a gene on or off can be affected by interactions with another protein anchored to a nearby area of the genome,” Korbel explains. “With it, we can begin to understand where such interactions happen, without having to study every single regulatory protein out there.”

The scientists found that even if different people have identical copies of a gene – for instance ORMDL3, a gene known to be involved in asthma in children – the way their cells regulate that gene can vary from person to person.

“Our findings may help change the way we think of ourselves, and of diseases”, Snyder concludes: “as well as looking for disease genes, we could start looking at how genes are regulated, and how individual variations in gene regulation could affect patients’ reactions.”

Finally, Korbel, Snyder and colleagues compared the information on humans with that from a chimpanzee, and found that with respect to gene regulation there seems to be almost as much variation between humans as between us and our primate cousins – a small margin in which may lie important clues both to how we evolved and to what makes us humans different from one another.

In a study published online in Nature yesterday, researchers led by Snyder in the USA and Lars Steinmetz at EMBL in Heidelberg have found that similar differences in gene regulation also occur in an organism which is much farther from us in the evolutionary tree: baker’s yeast.


Sunlight Exposure and nasal bleeding

ever since I was a child, I've always suffered from nose-bleeds after being exposed to sunlight for long periods of time (1 hour+).
Neither the temperature or humidity level of the day plays a role in this, as my nose only bleeds when I've been exposed to bright sunlight.
I also sneeze allot in bright sunlight.

This has been happening as far back as I can remember, I even had nasal spray prescribed to me because the physicians thought it was caused by allergens. Only, the nosebleeds happened at all times of the year - before, during, and after allergy season.

My question, then, is as follows:

Why (or how) does sunlight cause nosebleeds (regardless of temperature or humidity levels)?

P.S: The last nosebleed happened this morning I spent several hours in the sun yesterdday - the temperature was in the mid-to-upper 70's F.
and it's been relatively humid here in the Appalachian Mountains.

I hope you can provide an answer to my query, as I've been wondering what's wrong with me since I was 10 years of age. Still wonder now.
My husband and I joke that I have an allergy to sunlight.

interesting and speaking as a clinician and a scientist I can't think of an obvious mechanism whereby exposure of your nostrils to sunlight could trigger nose bleeds which will be due to small vessels on the nasal mucosa. Clearly a fair number of doctors over the eyes have considered this each time you have mentioned it and presumably no-one has come up with any bright ideas.

The allergy idea occurred to me and I too might have tried a steroid nasal spray just to see if it had an effect but clearly your doctors have thought of that already!

Assuming this is limited to the nose (ie you don't bleed elsewhere) and you have no other associated symptoms, I suspect this will be with you for the rest of your life and will not be adequately explained.

This may or may not be relevant, but my younger sister had chronic nose bleeds. There was no clear cause, but there did seem to be a link between aspirin use (a blood thinner) and the bleeds. The suggestion was that the mucosal blood vessels were in some manner thin-walled or perhaps too close to the surface, and the combination of blood thinners with extra pressure (like energetic sneezing/swelling) compromised them and caused the bleeding.

thanks and yes asprin or non-steroidals increase the risk of bleeding in the body. Its the relationship to sunlight that has me stumped!


Gero scientists found a way to break the limit of human longevity

The research team of Gero, a Singapore-based biotech company in collaboration with Roswell Park Comprehensive Cancer Center in Buffalo NY, announces a publication in Nature Communications, a journal of Nature portfolio, presenting the results of the study on associations between aging and the loss of the ability to recover from stresses.

Recently, we have witnessed the first promising examples of biological age reversal by experimental interventions. Indeed, many biological clock types properly predict more years of life for those who choose healthy lifestyles or quit unhealthy ones, such as smoking. What has been still unknown is how quickly biological age is changing over time for the same individual. And especially, how one would distinguish between the transient fluctuations and the genuine bioage change trend.

The emergence of big biomedical data involving multiple measurements from the same subjects brings about a whole range of novel opportunities and practical tools to understand and quantify the aging process in humans. A team of experts in biology and biophysics presented results of a detailed analysis of dynamic properties of the fluctuations of physiological indices along individual aging trajectories.

Healthy human subjects turned out to be very resilient, whereas the loss of resilience turned out to be related to chronic diseases and elevated all-cause mortality risks. The rate of recovery to the equilibrium baseline level after stresses was found to deteriorate with age. Accordingly, the time needed to recover was getting longer and longer. Being around 2 weeks for 40 y.o. healthy adults the recovery time stretched to 6 weeks for 80 y.o. on average in the population. This finding was confirmed in two different datasets based on two different kinds of biological measurements - blood test parameters on one hand and physical activity levels recorded by wearable devices on the other hand.

"Calculation of resilience based on physical activity data streams has been implemented in GeroSense iPhone app and made available for the research community via web-based API." - commented the first author of the study, Tim Pyrkov, head of the mHealth project at Gero.

If the trend holds at later ages, the extrapolation shows a complete loss of human body resilience, that is the ability to recover, at some age around 120-150 y.o. The reduced resilience was observed even in individuals not suffering from major chronic disease and led to the increase in the range of the fluctuations of physiological indices. As we age, more and more time is required to recover after a perturbation, and on average we spend less and less time close to the optimal physiological state.

The predicted loss of resilience even in the healthiest, most successfully aging individuals, might explain why we do not see an evidential increase of the maximum lifespan, while the average lifespan was steadily growing during the past decades. The divergent fluctuations of physiological indices may mean that no intervention that does not affect the decline in resilience may effectively increase the maximum lifespan and hence may only lead to an incremental increase in human longevity.

Aging in humans is a complex and multi-stage process. It would, therefore, be difficult to compress the aging process into a single number, such as biological age. Gero's work shows that longitudinal studies open a whole new window on the aging process and produce independent biomarkers of human aging, suitable for applications in geroscience and future clinical trials of anti-aging interventions.

"Aging in humans exhibits universal features common to complex systems operating on the brink of disintegration. This work is a demonstration of how concepts borrowed from physical sciences can be used in biology to probe different aspects of senescence and frailty to produce strong interventions against aging.", - says Peter Fedichev, co-founder and CEO of Gero.

Accordingly, no strong life extension is possible by preventing or curing diseases without interception of the aging process, the root cause of the underlying loss of resilience. We do not foresee any laws of nature prohibiting such an intervention. Therefore, the aging model presented in this work may guide the development of life-extending therapies with the strongest possible effects on healthspan.

"This work by the Gero team shows that longitudinal studies provide novel possibilities for understanding the aging process and systematic identification of biomarkers of human aging in large biomedical data. The research will help to understand the limits of longevity and future anti-aging interventions. What's even more important, the study may help to bridge the rising gap between the health- and life-span, which continues to widen in most developing countries." - says Brian Kennedy, Distinguished Professor of Biochemistry and Physiology at National University Singapore.

"This work, in my opinion, is a conceptual breakthrough because it determines and separates the roles of fundamental factors in human longevity - the aging, defined as progressive loss of resilience, and age-related diseases, as "executors of death" following the loss of resilience. It explains why even most effective prevention and treatment of age-related diseases could only improve the average but not the maximal lifespan unless true antiaging therapies have been developed" - says prof. Andrei Gudkov, PhD, Sr. Vice President and Chair of Department of Cell Stress Biology at Roswell Park Comprehensive Cancer Center, a co-author of this work and a co-founder of Genome Protection, Inc., a biotech company that is focused on the development of antiaging therapies/.

"The investigation shows that recovery rate is an important signature of aging that can guide the development of drugs to slow the process and extend healthspan." - commented David Sinclair, Harvard Medical School professor of genetics.

"The research from Gero surprisingly comes to a similar quantification of human resilience - a proposed biomarker of ageing - based on two very different kinds of data: blood test parameters on one hand and physical activity levels recorded by wearable devices on the other hand. I'm very excited to see how Person-generated Health Data, including data from commercial wearables, can help create individual, longitudinal profiles of health that will be instrumental to shed light on lifetime-scale health phenomena, such as ageing." - commented Luca Foschini, Co-founder & Chief Data Scientist at Evidation Health.

The authors characterized the dynamics of physiological parameters on time scales of human lifespan by a minimum set of two parameters. The first is an instant value, often referred to as the biological age, and is exemplified in this work by the Dynamic Organism State Index (DOSI). The quantity is associated with stresses, lifestyles and chronic diseases and can be computed from a standard blood test.

The other parameter - the resilience - is new and reflects the dynamic properties of the organism state fluctuations: it informs how quickly the DOSI value gets back to the norm in response to stresses.

Age-related changes in physiological parameters start from birth. However, various parameters change in different ways at different stages of life, see, e.g., a previous work by the same authors published in Aging US in 2018).

The data from the Nature Communications work shows that there is a good differentiation between the growth phase (mostly complete by the age of 30 and following the universal growth theory by Geoffrey West and aging. At 40+ years, aging manifests itself as a slow (linear, sub-exponential) deviation of physiological indices from their reference values.

How often should one measure biological age?

Physiological parameters are naturally subject to fluctuations around some equilibrium level. Glucose levels rise and drop after having a meal, the number of sleeping hours is slightly different each day. Yet, one can collect a longitudinal dataset, that is a series of such measurements for the same person, and observe that the average levels are different between individuals. Resilience also requires repeated measurements, since one needs to know exactly when recovery was achieved to calculate the resilience.

Importantly, resilience also provides a convenient guide on how often repeated measurements should be taken. As a rule of thumb, the period of observation required for the robust bioage determination should comprise multiple stress and recovery events. For the most healthy individuals such an observation period would amount to several months and should increase with age. During that time, a robust bioage determination would require several data points per recovery time, that is ideally one measurement in a few days.

Wearable technology comes into play

In 2021, the only practical way to achieve a high (once-per-day or better) sampling rate is to use mobile/wearable sensor data.

In another paper, the authors have focused on wearable/mobile sensor data. They have built "wearable DOSI", which they called GeroSense and reported its validation tests in Pyrkov et al. Aging (Albany NY) 13.6 (2021): 7900. GeroSense can be used to compute resilience. Population study shows that the number of individuals showing signs of the loss of resilience increases exponentially with age and doubles every 8 years at a rate matching that of the Gompertz mortality law (the observation by B. Gompertz from 1827, who observed for the first time that the all-cause mortality rate doubles every 8 years).

Gero is a data-driven biotech company applying modern AI/ML tools to big longitudinal biomedical data to understand aging and major diseases.

Gero AI/ML models are originating from the physics of complex dynamic systems. We have presented our unique approach in Frontiers in Genetics (Fedichev 2018, Frontiers in genetics 9:483). We combine the potential of deep neural networks with the physical models to study human health as a dynamic process. In conjunction with high-quality genetics data, we produce quantitative explanatory models of (aka theory of) aging and complex diseases, as well as actional drug target hypotheses.

Gero conducts high-quality research in collaborations with Harvard Medical School, Massachusetts Institute of Technology, University of Edinburgh, National University of Singapore, Moscow Institute of Physics and Technology, and Roswell Park Comprehensive Cancer Center. The company is a regular contributor to peer-reviewed journals.

Gero has developed a unique framework "GeroSense" for continuous day-to-day monitoring of biological age based on data streams of mobile and wearable sensors. "GeroSense" provides biological age monitoring in our free iPhone app.

Gero encourages using "GeroSense" via web API for monitoring of anti-aging and pro-longevity effects of therapies as well as lifestyle choices, physical activities, diets, food supplements, recommended by health/fitness and wellness apps (see https:/ / techcrunch. com/ 2021/ 05/ 07/ longevity-startup-gero-ai-has-a-mobile-api-for-quantifying-health-changes/ ).

Gero is funded by AI champions, including AIMATTER founders (recently acquired by Google). In 2019 and 2021, Gero was also named one of the leading companies in artificial intelligence in life extension along with Google and IBM.

About Roswell Park Comprehensive Cancer Center

Roswell Park Comprehensive Cancer Center is a community united by the drive to eliminate cancer's grip on humanity by unlocking its secrets through personalized approaches and unleashing the healing power of hope. Founded by Dr. Roswell Park in 1898, it is the only National Cancer Institute-designated comprehensive cancer center in Upstate New York. Learn more at http://www. roswellpark. org, or contact us at 1-800-ROSWELL (1-800-767-9355) or [email protected]

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.


Contents

Several bones and cartilages make up the bony-cartilaginous framework of the nose, and the internal structure. [1] The nose is also made up of types of soft tissue such as skin, epithelia, mucous membrane, muscles, nerves, and blood vessels. In the skin there are sebaceous glands, and in the mucous membrane there are nasal glands. [2] The bones and cartilages provide strong protection for the internal structures of the nose. There are several muscles that are involved in movements of the nose. The arrangement of the cartilages allows flexibility through muscle control to enable airflow to be modified. [2]

Bones Edit

The bony structure of the nose is provided by the maxilla, frontal bone, and a number of smaller bones. [3]

The topmost bony part of the nose is formed by the nasal part of the frontal bone, which lies between the brow ridges, [3] and ends in a serrated nasal notch. [4] A left and a right nasal bone join with the nasal part of the frontal bone at either side and these at the side with the small lacrimal bones and the frontal process of each maxilla. [3] The internal roof of the nasal cavity is composed of the horizontal, perforated cribriform plate of the ethmoid bone through which pass sensory fibres of the olfactory nerve. Below and behind the cribriform plate, sloping down at an angle, is the face of the sphenoid bone.

The wall separating the two cavities of the nose, the nasal septum, is made up of bone inside and cartilage closer to the tip of the nose. [3] The bony part is formed by the perpendicular plate of the ethmoid bone at the top, and the vomer bone below. [3] The floor of the nose is made up of the incisive bone and the horizontal plates of the palatine bones, and this makes up the hard palate of the roof of the mouth. The two horizontal plates join together at the midline and form the posterior nasal spine that gives attachment to the musculus uvulae in the uvula.

The two maxilla bones join at the base of the nose at the lower nasal midline between the nostrils, and at the top of the philtrum to form the anterior nasal spine. This thin projection of bone holds the cartilaginous center of the nose. [5] [6] It is also an important cephalometric landmark. [7]

Cartilages Edit

The nasal cartilages are the septal, lateral, major alar, and minor alar cartilages. [8] The major and minor cartilages are also known as the greater and lesser alar cartilages. There is a narrow strip of cartilage called the vomeronasal cartilage that lies between the vomer and the septal cartilage. [9]

The septal nasal cartilage, extends from the nasal bones in the midline, to the bony part of the septum in the midline, posteriorly. It then passes along the floor of the nasal cavity. [10] The septum is quadrangular–the upper half is attached to the two lateral nasal cartilages which are fused to the dorsal septum in the midline. The septum is laterally attached, with loose ligaments, to the bony margin of the anterior nasal aperture, while the inferior ends of the lateral cartilages are free (unattached). The three or four minor alar cartilages are adjacent to the lateral cartilages, held in the connective tissue membrane, that connects the lateral cartilages to the frontal process of the maxilla.

The nasal bones in the upper part of the nose are joined together by the midline internasal suture. They join with the septal cartilage at a junction known as the rhinion. The rhinion is the midpoint of the internasal suture at the join with the cartilage, and from the rhinion to the apex, or tip, the framework is of cartilage.

The major alar cartilages are thin, U-shaped plates of cartilage on each side of the nose that form the lateral and medial walls of the vestibule, known as the medial and lateral crura. The medial crura are attached to the septal cartilage, forming fleshy parts at the front of the nostrils on each side of the septum, called the medial crural footpods. The medial crura meet at the midline below the end of the septum to form the columella [11] and lobule. The lobule contains the tip of the nose and its base contains the nostrils. [3] At the peaks of the folds of the medial crura, they form the alar domes the tip-defining points of the nose, separated by a notch. [3] They then fold outwards, above and to the side of the nostrils forming the lateral crura. [12] [2] The major alar cartilages are freely moveable and can respond to muscles to either open or constrict the nostrils. [13]

There is a reinforcing structure known as the nasal scroll that resists internal collapse from airflow pressure generated by normal breathing. This structure is formed by the junction between the lateral and major cartilages. Their edges interlock by one scrolling upwards and one scrolling inwards. [12] [14]

Muscles Edit

The muscles of the nose are a subgroup of the facial muscles. They are involved in respiration and facial expression. The muscles of the nose include the procerus, nasalis, depressor septi nasi, levator labii superioris alaeque nasi, and the orbicularis oris of the mouth. As are all of the facial muscles, the muscles of the nose are innervated by the facial nerve and its branches. [3] Although each muscle is independent, the muscles of the nose form a continuous layer with connections between all the components of the muscles and ligaments, in the nasal part of a superficial muscular aponeurotic system (SMAS). [3] [15] The SMAS is continuous from the nasofrontal process to the nasal tip. It divides at level of the nasal valve into superficial and deep layers, each layer having medial and lateral components. [15]

The procerus muscle produces wrinkling over the bridge of the nose, and is active in concentration and frowning. It is a prime target for Botox procedures in the forehead to remove the lines between the eyes. [3]

The nasalis muscle consists of two main parts: a transverse part called the compressor naris, and an alar part termed the dilator naris. The compressor naris muscle compresses the nostrils and may completely close them. The alar part, the dilator naris mainly consists of the dilator naris posterior, and a much smaller dilator naris anterior, and this muscle flares the nostrils. The dilator naris helps to form the upper ridge of the philtrum. [3] The anterior, and the posterior dilator naris, (the alar part of the nasalis muscle), give support to the nasal valves. [3]

The depressor septi nasi may sometimes be absent or rudimentary. The depressor septi pulls the columella, the septum, and the tip of the nose downwards. At the start of inspiration this muscle tenses the nasal septum and with the dilator naris widens the nostrils. [3]

The levator labii superioris alaeque nasi divides into a medial and a lateral slip. The medial slip blends into the perichondrium of the major alar cartilage and its overlying skin. The lateral slip blends at the side of the upper lip with the levator labii superioris, and with the orbicularis oris. The lateral slip raises the upper lip and deepens and increases the curve above the nasolabial furrow. The medial slip pulls the lateral crus upwards and modifies the curve of the furrow around the alae, and dilates the nostrils. [3]

Soft tissue Edit

The skin of the nose varies in thickness along its length. [3] From the glabella to the bridge (the nasofrontal angle) the skin is thick, fairly flexible, and mobile. It tapers to the bridge where it is thinnest and least flexible as it is closest to the underlying bone. From the bridge until the tip of the nose the skin is thin. The tip is covered in skin that is as thick as the top section, and has many large sebaceous glands. [3] [13] The thickness of the skin varies but is still separated from the underlying bones and cartilage by four layers – a superficial fatty layer a fibromuscular layer continued from the SMAS a deep fatty layer, and the periosteum. [3]

Other areas of soft tissue are found where there is no support from cartilage these include an area around the sides of the septum – the paraseptal area –, an area around the lateral cartilages, an area at the top of the nostril, and an area in the alae. [3]

External nose Edit

The nasal root is the top of the nose that attaches the nose to the forehead. [13] The nasal root is above the bridge and below the glabella, forming an indentation known as the nasion at the frontonasal suture where the frontal bone meets the nasal bones. [16] The nasal dorsum also known as the nasal ridge is the border between the root and the tip of the nose which in profile can be variously shaped. [17] The ala of the nose (ala nasi, "wing of the nose" plural alae) is the lower lateral surface of the external nose, shaped by the alar cartilage and covered in dense connective tissue. [1] The alae flare out to form a rounded eminence around the nostril. [17] Sexual dimorphism is evident in the larger nose of the male. This is due to the increased testosterone that thickens the brow ridge and the bridge of the nose making it wider. [18]

Nasal cavity Edit

The nasal cavity is the large internal space of the nose, and is in two parts – the nasal vestibule and the nasal cavity proper. [2] The nasal vestibule is the frontmost part of the nasal cavity, enclosed by cartilages. The vestibule is lined with skin, hair follicles, and a large number of sebaceous glands. [1] [2] A mucous ridge known as the limen nasi separates the vestibule from the rest of the nasal cavity and marks the change from the skin of the vestibule to the respiratory epithelium of the rest of the nasal cavity. [2] This area is also known as a mucocutaneous junction and has a dense microvasculature. [19]

The nasal cavity is divided into two cavities by the nasal septum, and each is accessed by an external nostril. [13] [1] The division into two cavities enables the functioning of the nasal cycle that slows down the conditioning process of the inhaled air. [20] At the back of the nasal cavity there are two openings, called choanae (also posterior nostrils), that give entrance to the nasopharynx, and rest of the respiratory tract. [1]

On the outer wall of each cavity are three shell-like bones called conchae, arranged as superior, middle and inferior nasal conchae. Below each concha is a corresponding superior, middle, and inferior nasal meatus, or passage. [1] Sometimes when the superior concha is narrow, a fourth supreme nasal concha is present situated above and sharing the space with the superior concha. [21] The term concha refers to the actual bone when covered by soft tissue and mucosa, and functioning, a concha is termed a turbinate. [3] Excessive moisture as tears collected in the lacrimal sac travel down the nasolacrimal ducts where they drain into the inferior meatus in the nasal cavity. [22]

Most of the nasal cavity and paranasal sinuses is lined with respiratory epithelium as nasal mucosa. In the roof of each cavity is an area of specialised olfactory epithelium. This region is about 5 square cm, covering the superior concha, the cribriform plate, and the nasal septum. [23]

There is a nasal valve area that is the narrowest part of the nasal passage. An external valve exists in the larger ala part of the vestibule. An internal nasal valve typically referred to as the nasal valve, is a slit-like segment between part of the upper lateral cartilage and the septum in the middle third of the cavity. [24] [25] The valves regulate the airflow and resistance. Air breathed in is forced to pass through the narrow internal nasal valve, and then expands as it moves into the nasal cavity. The sudden change in the speed and pressure of the airflow creates turbulence that allows optimum contact with the respiratory epithelium for the necessary warming, moisturising, and filtering. The turbulence also allows movement of the air to pass over the olfactory epithelium and transfer odour information. [3] The angle of the valve between the septum and the sidewall needs to be sufficient for unobstructed airflow, [26] and this is normally between 10 and 15 degrees. [3]

The borders of each nasal cavity are a roof, floor, medial wall (the septum), and lateral wall. [2] [3] The middle part of the roof of the nasal cavity is composed of the horizontal, perforated cribriform plate of the ethmoid bone, through which pass sensory fibres of the olfactory nerve into the cranial cavity. [2]

Paranasal sinuses Edit

The mucosa that lines the nasal cavity extends into its chambers, the paranasal sinuses. [13] The nasal cavity and the paranasal sinuses are referred to as the sinonasal tract or sinonasal region, and its anatomy is recognised as being unique and complex. [27] [28] Four paired paranasal sinuses – the frontal sinus, the sphenoid sinus, the ethmoid sinus and the maxillary sinus drain into regions of the nasal cavity. The sinuses are air-filled extensions of the nasal cavity into the cranial bones. [13] The frontal sinuses are located in the frontal bone the sphenoidal sinuses in the sphenoid bone the maxillary sinuses in the maxilla and the ethmoidal sinuses in the ethmoid bone. [2] [13]

A narrow opening called a sinus ostium from each of the paranasal sinuses allows drainage into the nasal cavity. The maxillary sinus is the largest of the sinuses and drains into the middle meatus. Most of the ostia open into the middle meatus and the anterior ethmoid, that together are termed the ostiomeatal complex. [29] Adults have a high concentration of cilia in the ostia. The cilia in the sinuses beat towards the openings into the nasal cavity. The increased numbers of cilia and the narrowness of the sinus openings allow for an increased time for moisturising, and warming. [29]

Nose shape Edit

The shape of the nose varies widely due to differences in the nasal bone shapes and formation of the bridge of the nose. Some nose shapes were classified for surgeries by Eden Warwick in Nasology 1848:

Class II. The Grecian nose.

Class III. The African nose.

Class VI. The celestial nose.

Paul Topinard developed the nasal index as a method of classifying ethnic groups. The index is based on the ratio of the breadth of the nose to its height. [30] The nasal dimensions are also used to classify nasal morphology into five types: Hyperleptorrhine is a very long, narrow nose with a nasal index of 40 to 55. [31] Leptorrhine describes a long, narrow nose with an index of 55–70. [31] Mesorrhine is a medium nose with an index of 70–85. Platyrrhine is a short, broad nose with an index of 85–99·9. The fifth type is the hyperplatyrrhine having an index of more than 100. [31]

Some deformities of the nose are named, such as the pug nose and the saddle nose. The pug nose is characterised by excess tissue from the apex that is out of proportion to the rest of the nose. A low and underdeveloped nasal bridge may also be evident. [32] A saddle nose deformity involving the collapse of the bridge of the nose is mostly associated with trauma to the nose but can be caused by other conditions including leprosy. [33] [34]

Werner syndrome, a condition that causes the appearance of premature aging, causes a "bird-like" appearance due to pinching of the nose. [35]

Down syndrome commonly presents a small nose with a flattened nasal bridge. This can be due to the absence of one or both nasal bones, shortened nasal bones, or nasal bones that have not fused in the midline. [36] [37]

Supply Edit

The blood supply to the nose is provided by branches of the ophthalmic, maxillary, and facial arteries – branches of the carotid arteries. Branches of these arteries anastomose to form plexuses in and under the nasal mucosa. [3] In the septal region Kiesselbach's plexus is a common site of nosebleeds.

Branches of the ophthalmic artery – the anterior and posterior ethmoidal arteries supply the roof, upper bony septum, and ethmoidal and frontal sinuses. The anterior ethmoidal artery also helps to supply the lower septal cartilage. [3] Another branch is the dorsal nasal artery a terminal branch that supplies the skin of the alae and dorsum.

Branches of the maxillary artery include the greater palatine artery the sphenopalatine artery and its branches – the posterior lateral nasal arteries and posterior septal nasal branches the pharyngeal branch and the infraorbital artery and its branches – the superior anterior and posterior alveolar arteries.

The sphenopalatine artery and the ethmoid arteries supply the outer walls of the nasal cavity. There is additional supply from a branch of the facial artery – the superior labial artery. The sphenopalantine artery is the artery primarily responsible for supplying the nasal mucosa. [3]

The skin of the alae is supplied by the septal and lateral nasal branches of the facial artery. [3] The skin of the outer parts of the alae and the dorsum of the nose are supplied by the dorsal nasal artery a branch of the ophthalmic artery, and the infraorbital branch of the maxillary arteries. [3]

Drainage Edit

Veins of the nose include the angular vein that drains the side of the nose, receiving lateral nasal veins from the alae. The angular vein joins with the superior labial vein. Some small veins from the dorsum of the nose drain to the nasal arch of the frontal vein at the root of the nose.

In the posterior region of the cavity, specifically in the posterior part of the inferior meatus is a venous plexus known as Woodruff's plexus. [38] This plexus is made up of large thin-walled veins with little soft tissue such as muscle or fiber. The mucosa of the plexus is thin with very few structures. [39]

From different areas of the nose superficial lymphatic vessels run with the veins, and deep lymphatic vessels travel with the arteries. [40] Lymph drains from the anterior half of the nasal cavity, including both the medial and lateral walls, [2] to join that of the external nasal skin to drain into the submandibular lymph nodes. [2] [3] The rest of the nasal cavity and paranasal sinuses all drain to the upper deep cervical lymph nodes, either directly or through the retropharyngeal lymph nodes. [3] The back of the nasal floor probably drains to the parotid lymph nodes. [3]

The nerve supply to the nose and paranasal sinuses comes from two branches of the trigeminal nerve (CN V): the ophthalmic nerve (CN V1), the maxillary nerve (CN V2), and branches from these. [3] [13]

In the nasal cavity, the nasal mucosa is divided in terms of nerve supply into a back lower part (posteroinferior), and a frontal upper part (anterosuperior). The posterior part is supplied by a branch of the maxillary nerve – the nasopalatine nerve which reaches the septum. Lateral nasal branches of the greater palatine nerve supply the lateral wall. [13]

The frontal upper part is supplied from a branch of the ophthalmic nerve – the nasociliary nerve, and its branches – the anterior and posterior ethmoidal nerves. [13]

Most of the external nose – the dorsum, and the apex are supplied by the infratrochlear nerve, (a branch of the nasociliary nerve). [3] [13] The external branch of the anterior ethmoidal nerve also supplies areas of skin between the root and the alae. [13]

The alae of the nose are supplied by nasal branches of CN V2, the infraorbital nerve, and internal nasal branches of infraorbital nerve that supply the septum and the vestibule. [41] [13]

The maxillary sinus is supplied by superior alveolar nerves from the maxillary and infraorbital nerves. [13] [42] The frontal sinus is supplied by branches of the supraorbital nerve. [13] The ethmoid sinuses are supplied by anterior and posterior ethmoid branches of the nasociliary nerve. [13] The sphenoid sinus is supplied by the posterior ethmoidal nerves. [13]

Movement Edit

The muscles of the nose are supplied by branches of the facial nerve. The nasalis muscle is supplied by the buccal branches. It may also be supplied by one of the zygomatic branches. The procerus is supplied by temporal branches of the facial nerve and lower zygomatic branches a supply from the buccal branch has also been described. The depressor septi is innervated by the buccal branch, and sometimes by the zygomatic branch, of the facial nerve. The levator labii superioris alaeque nasi is innervated by zygomatic and superior buccal branches of the facial nerve. [3]

Smell Edit

The sense of smell is transmitted by the olfactory nerves. [3] Olfactory nerves are bundles of very small unmyelinated axons that are derived from olfactory receptor neurons in the olfactory mucosa. The axons are in varying stages of maturity, reflecting the constant turnover of neurons in the olfactory epithelium. A plexiform network is formed in the lamina propria, by the bundles of axons that are surrounded by olfactory ensheathing cells. In as many as twenty branches, the bundled axons cross the cribriform plate and enter the overlying olfactory bulb ending as glomeruli. Each branch is enclosed by an outer dura mater that becomes continuous with the nasal periosteum. [3]

Autonomic supply Edit

The nasal mucosa in the nasal cavity is also supplied by the autonomic nervous system. [3] Postganglionic nerve fibers from the deep petrosal nerve join with preganglionic nerve fibers from the greater petrosal nerve to form the nerve of the pterygoid canal. Sympathetic postganglionic fibers are distributed to the blood vessels of the nose. Postganglionic parasympathetic fibres derived from the pterygopalatine ganglion provide the secretomotor supply to the nasal mucous glands, and are distributed via branches of the maxillary nerves. [3]

Development of the nose Edit

In the early development of the embryo, neural crest cells migrate to form the mesenchymal tissue as ectomesenchyme of the pharyngeal arches. By the end of the fourth week, the first pair of pharyngeal arches form five facial prominences or processes - an unpaired frontonasal process, paired mandibular processes and paired maxillary processes. [43] [44] The nose is largely formed by the fusion of these five facial prominences. The frontonasal process gives rise to the bridge of the nose. The medial nasal processes provide the crest and the tip of the nose, and the lateral nasal processes form the alae or sides of the nose. The frontonasal process is a proliferation of mesenchyme in front of the brain vesicles, [43] and makes up the upper border of the stomadeum. [44]

During the fifth week the maxillary processes increase in size and at the same time the ectoderm of the frontonasal process becomes thickened at its sides and also increases in size, forming the nasal placodes. The nasal placodes are also known as the olfactory placodes. This development is induced by the ventral part of the forebrain. [43] [44] In the sixth week the ectoderm in each nasal placode invaginates to form an indented oval-shaped pit, which forms a surrounding raised ridge of tissue. [44] Each nasal pit forms a division between the ridges, into a lateral nasal process on the outer edge, and a medial nasal process on the inner edge. [43] [44]

In the sixth week the nasal pits deepen as they penetrate into the underlying mesenchyme. [43] At this time, the medial nasal processes migrate towards each other and fuse forming the primordium of the bridge of the nose and the septum. [44] The migration is helped by the increased growth of the maxillary prominences medially, which compresses the medial nasal processes towards the midline. Their merging takes place at the surface, and also at a deeper level. [43] The merge forms the intermaxillary segment, and this is continuous with the rostral part of the nasal septum. The tips of the maxillary processes also grow and fuse with the intermaxillary process. The intermaxillary process gives rise to the philtrum of the upper lip. [43]

At the end of the sixth week the nasal pits have deepened further and they fuse to make a large ectodermal nasal sac. This sac will be above and to the back of the intermaxillary process. Leading into the seventh week, the nasal sac floor and posterior wall grow to form a thickened plate-like ectodermal structure called the nasal fin. [44] The nasal fin separates the sac from the oral cavity. Within the fin, vacuoles develop that fuse with the nasal sac. This enlarges the nasal sac and at the same time thins the fin to a membrane - the oronasal membrane that separates the nasal pits from the oral cavity. [44] During the seventh week the oronasal membrane ruptures and disintegrates to form an opening - the single primitive choana. The intermaxillary segment extends posteriorly to form the primary palate which makes up the floor of the nasal cavity. [44] During the eighth and ninth weeks a pair of thin extensions form from the medial walls of the maxillary process. These extensions are called the palatine shelves that form the secondary palate. [43] [44] The secondary palate will endochondrally ossify to form the hard palate - the end-stage floor of the nasal cavity. During this time ectoderm and mesoderm of the frontonasal process produce the midline septum. The septum grows down from the roof of the nasal cavity and fuses with the developing palates along the midline. The septum divides the nasal cavity into two nasal passages opening into the pharynx through the definitive choanae. [43] [44]

At ten weeks, the cells differentiate into muscle, cartilage, and bone. Problems at this stage of development can cause birth defects such as choanal atresia (absent or closed passage), facial clefts and nasal dysplasia (faulty or incomplete development) [45] or extremely rarely polyrrhinia the formation of a duplicate nose. [46]

Normal development is critical because the newborn infant breathes through the nose for the first six weeks, and any nasal blockage will need emergency treatment to clear. [47]

Development of the paranasal sinuses Edit

The four pairs of paranasal sinuses - the maxillary, ethmoid, sphenoid, and frontal, develop from the nasal cavity as invaginations extending into their named bones. Two pairs of sinuses form during prenatal development and two pairs form after birth. The maxillary sinuses are the first to appear during the fetal third month. They slowly expand within the maxillary bones and continue to expand throughout childhood. The maxillary sinuses form as invaginations from the nasal sac. The ethmoid sinuses appear in the fetal fifth month as invaginations of the middle meatus. The ethmoid sinuses do not grow into the ethmoid bone and do not completely develop until puberty. [44]

The sphenoid sinuses are extensions of the ethmoid sinuses into the sphenoid bones. They begin to develop around two years of age, and continue to enlarge during childhood. [13]

The frontal sinuses only develop in the fifth or sixth year of childhood, and continue expanding throughout adolescence. Each frontal sinus is made up of two independent spaces that develop from two different sources one from the expansion of ethmoid sinuses into frontal bone, and the other develops from invagination. They never coalesce so drain independently. [44]

Respiration Edit

The nose is the first organ of the upper respiratory tract in the respiratory system. Its main respiratory function is the supply and conditioning, by warming, moisturising and filtering of particulates of inhaled air. [22] Nasal hair in the nostrils traps large particles preventing their entry into the lungs. [1]

The three positioned nasal conchae in each cavity provide four grooves as air passages, along which the air is circulated and moved to the nasopharynx. [48] The internal structures and cavities, including the conchae and paranasal sinuses form an integrated system for the conditioning of the air breathed in through the nose. [48] This functioning also includes the major role of the nasal mucosa, and the resulting conditioning of the air before it reaches the lungs is important in maintaining the internal environment and proper functioning of the lungs. [49] The turbulence created by the conchae and meatuses optimises the warming, moistening, and filtering of the mucosa. [50] A major protective role is thereby provided by these structures of the upper respiratory tract, in the passage of air to the more delicate structures of the lower respiratory tract. [48]

Sneezing is an important protective reflex action initiated by irritation of the nasal mucosa to expel unwanted particles through the mouth and nose. [51] Photic sneezing is a reflex brought on by different stimuli such as bright lights. [52] The nose is also able to provide sense information as to the temperature of the air being breathed. [53]

Variations in shape of the nose have been hypothesised to possibly be adaptive to regional differences in temperature and humidity, though they may also have been driven by other factors such as sexual selection. [54]

Sense of smell Edit

The nose also plays the major part in the olfactory system. It contains an area of specialised cells, olfactory receptor neurons responsible for the sense of smell (olfaction). Olfactory mucosa in the upper nasal cavity, contains a type of nasal gland called olfactory glands or Bowman's glands which help in olfaction. The nasal conchae also help in olfaction function, by directing air-flow to the olfactory region. [50] [55]

Speech Edit

Speech is produced with pressure from the lungs. This can be modified using airflow through the nose in a process called nasalisation. This involves the lowering of the soft palate to produce nasal vowels and consonants by allowing air to escape from both the nose and the mouth. [56] Nasal airflow is also used to produce a variety of nasal clicks called click consonants. [57] The large, hollow cavities of the paranasal sinuses act as resonating chambers that modify, and amplify speech and other vocal vibrations passing through them. [58] [59]

One of the most common medical conditions involving the nose is a nosebleed (epistaxis). Most nosebleeds occur in Kiesselbach's plexus, a vascular plexus in the lower front part of the septum involving the convergence of four arteries. A smaller proportion of nosebleeds that tend to be nontraumatic occur in Woodruff's plexus. Woodruff's plexus is a venous plexus of large thin-walled veins lying in the posterior part of the inferior meatus. [39]

Another common condition is nasal congestion, usually a symptom of infection, particularly sinusitis, or other inflammation of the nasal lining called rhinitis, including allergic rhinitis and nonallergic rhinitis. Chronic nasal obstruction resulting in breathing through the mouth can greatly impair or prevent the nostrils from flaring. [60] One of the causes of snoring is nasal obstruction, [61] and anti-snoring devices such as a nasal strip help to flare the nostrils and keep the airway open. [60] Nasal flaring, is usually seen in children when breathing is difficult. [62] Most conditions of nasal congestion also cause a loss of the sense of smell (anosmia). This may also occur in other conditions, for example following trauma, in Kallmann syndrome or Parkinson's disease. A blocked sinus ostium, an opening from a paranasal sinus, will cause fluid to accumulate in the sinus.

In children the nose is a common site of foreign bodies. [63] The nose is one of the exposed areas that is susceptible to frostbite. [64]

Because of the special nature of the blood supply to the human nose and surrounding area, it is possible for retrograde infections from the nasal area to spread to the brain. For this reason, the area from the corners of the mouth to the bridge of the nose, including the nose and maxilla, is known as the danger triangle of the face. [13]

Infections or other conditions that may result in destruction of, or damage to a part of the nose include rhinophyma, [65] skin cancers particularly basal-cell carcinoma, [66] paranasal sinus and nasal cavity cancer, [67] granulomatosis with polyangiitis, [33] syphilis, [68] leprosy, [34] recreational use of cocaine, [69] chromium and other toxins. [70] The nose may be stimulated to grow in acromegaly, a condition caused by an excess of growth hormone. [71]

A common anatomic variant is an air-filled cavity within a concha known as a concha bullosa. [72] In rare cases a polyp can form inside a bullosa. [73] Usually a concha bullosa is small and without symptoms but when large can cause obstruction to sinus drainage. [74]

Some drugs can be nasally administered, including drug delivery to the brain, and these include nasal sprays and topical treatments. [53] [75] [76] The septal cartilage can be destroyed through the repeated inhalation of recreational drugs such as cocaine. This, in turn, can lead to more widespread collapse of the nasal skeleton. [77]

Sneezing can transmit infections carried in the expelled droplets. This route is called either airborne transmission or aerosol transmission. [78]

Surgical procedures Edit

Badly positioned alar cartilages lack proper support, and can affect the function of the external nasal valve. This can cause breathing problems particularly during deep inhalation. [79] The surgical procedure to correct breathing problems due to disorders in the nasal structures is called a rhinoplasty, and this is also the procedure used for a cosmetic surgery when it is commonly called a "nose job". For surgical procedures of rhinoplasty, the nose is mapped out into a number of subunits and segments. This uses nine aesthetic nasal subunits and six aesthetic nasal segments. A septoplasty is the specific surgery to correct a nasal septum deviation.

A broken nose can result from trauma. Minor fractures may heal on their own. Surgery known as reduction may be carried out on more severe breaks that cause dislocation. [80]

Several nasal procedures of the nose and paranasal sinuses can be carried out using minimally-invasive nasal endoscopy. These procedures aim to restore sinus ventilation, mucociliary clearance, and maintain the health of the sinus mucosa. [81] Some non-nasal surgeries can also be carried out through the use of an endoscope that is entered through the nose. These endoscopic endonasal surgeries are used to remove tumours from the front of the base of the skull. [82]

Swollen conchae can cause obstruction and nasal congestion, and may be treated surgically by a turbinectomy. [83]

Some people choose to have cosmetic surgery (called a rhinoplasty) to change the appearance of their nose. Nose piercings, such as in the nostril, septum, or bridge, are also common. In certain Asian countries such as China, Japan, South Korea, Malaysia, Thailand and Bangladesh, rhinoplasties are commonly carried out to create a more developed nose bridge or a "high nose". [84] Similarly, "DIY nose lifts" in the form of re-usable cosmetic items have become popular and are sold in many Asian countries such as China, Japan, South Korea, Taiwan, Sri Lanka and Thailand. [85] [86] [87] A high-bridged nose has been a common beauty ideal in many Asian cultures dating back to the beauty ideals of ancient China and India. [88] [89]

In New Zealand, nose pressing ("hongi") is a traditional greeting originating among the Māori people. [90] However it is now generally confined to certain traditional celebrations. [91]

The Hanazuka monument enshrines the mutilated noses of at least 38,000 Koreans killed during the Japanese invasions of Korea from 1592 to 1598. [92]

Nose-picking is a common, mildly taboo habit. Medical risks include the spread of infections, nosebleeds and, rarely, perforation of the nasal septum. When it becomes compulsive it is termed rhinotillexomania. The wiping of the nose with the hand, commonly referred to as the "allergic salute", is also mildly taboo and can result in the spreading of infections as well. Habitual as well as fast or rough nose wiping may also result in a crease (known as a transverse nasal crease or groove) running across the nose, and can lead to permanent physical deformity observable in childhood and adulthood. [93] [94]

Nose fetishism (or nasophilia) is the sexual partialism for the nose. [95]

Clive Finlayson of the Gibraltar Museum said the large Neanderthal noses were an adaption to the cold, [96] Todd C. Rae of the American Museum of Natural History said primate and arctic animal studies have shown sinus size reduction in areas of extreme cold rather than enlargement in accordance with Allen's rule. [97] Therefore, Todd C. Rae concludes that the design of the large and prognathic Neanderthal nose was evolved for the hotter climate of the Middle East and Africa and remained unchanged when they entered Europe. [97]

Miquel Hernández of the Department of Animal Biology at the University of Barcelona said the "high and narrow nose of Eskimos and Neanderthals" is an "adaption to a cold and dry environment", since it contributes to warming and moisturizing the air and the "recovery of heat and moisture from expired air". [98]

    , a nose crippled by excessive resection of the inferior and/or middle turbinates of the nose , an Ayurvedic technique of nasal cleansing , the Scottish Gaelic word for nose and the name of some hills in the Scottish Highlands

This article incorporates text in the public domain from page 992 of the 20th edition of Gray's Anatomy (1918)


Ability to detect directional gaze is not unique to humans

The ability to detect the direction of someone's gaze is not unique to humans, as had been previously thought, according to new research.

The contrasting color patterns of our eyes, which help us see where others are looking, was thought to be unique in humans but has been found to be present in chimpanzees and bonobos by scientists working at the University of St Andrews, the Department of Biological Sciences National University of Singapore, and Leiden University in the Netherlands.

It has been suggested that the difference between the white of our eyes, the sclera, and our colorful irises allows others to detect the direction of our gaze—something that many of our other skills, such as social learning, seem to depend on. The sclera of apes' eyes is often darker, and because of this, researchers have long argued that their gaze was 'hidden' or cryptic and that other apes would not be able to see where they are looking.

The new study, "Scleral pigmentation leads to conspicuous, not cryptic, eye morphology in chimpanzees," published today (Monday 2 September 2019) in Proceedings of the National Academy of Sciences of the United States of America found that ape eyes have the same pattern of color differences we do, suggesting that they could also follow each other's gaze.

Before humans had language, our ancestors may have relied on the gaze of those around them to help communicate dangers or other useful information. "They couldn't say 'look over there' but a look in the direction of a predator might be enough, as long as it was possible to follow the direction of their gaze," said lead author Juan O Perea-García of the Department of Biological Sciences National University of Singapore.

Senior author Dr. Cat Hobaiter, a field primatologist and lecturer in the School of Psychology and Neuroscience at the University of St Andrews, said: "Understanding where someone is looking seems to be key to understanding what they're interested in, what they're thinking about. For a long time researchers have suggested that the colour of other apes' eyes means that they hide this information we've shown that's not the case."

Bonobos, like humans, have paler sclera and darker irises, but chimpanzees have a different pattern: very dark sclera, and paler irises. Both color patterns show the same type of contrast seen in human eyes and could help other apes find out where they are looking.

Dr. Hobaiter said: "The idea that chimpanzees couldn't see where other chimpanzees were looking always puzzled me. I've spent years working with wild apes and I find it quite easy, and I'm sure they're much better at it than I am."


Are nosebleeds unique to humans? - Biology

Each of us has felt afraid, and we can all recognize fear in many animal species. Yet there is no consensus in the scientific study of fear. Some argue that ‘fear’ is a psychological construct rather than something discoverable through scientific investigation. Others argue that the term ‘fear’ cannot properly be applied to animals because we cannot know whether they feel afraid. Studies in rodents show that there are highly specific brain circuits for fear, whereas findings from human neuroimaging seem to make the opposite claim. Here, I review the field and urge three approaches that could reconcile the debates. For one, we need a broadly comparative approach that would identify core components of fear conserved across phylogeny. This also pushes us towards the second point of emphasis: an ecological theory of fear that is essentially functional. Finally, we should aim even to incorporate the conscious experience of being afraid, reinvigorating the study of feelings across species.


Blushing Response

Felix Wirth / Getty Images

In his book "The Expression of Emotions in Man and Animals," Charles Darwin said that "blushing is the most peculiar and the most human of all expressions." It is part of the "fight or flight response" of the sympathetic nervous system that causes the capillaries in human cheeks to dilate involuntarily in response to feeling embarrassment. No other mammal has this trait, and psychologists theorize that it has social benefits as well. Given that it is involuntary, blushing is considered to be an authentic expression of emotion.


Cell biology and pathology of podocytes

As an integral member of the filtration barrier in the kidney glomerulus, the podocyte is in a unique geographical position: It is exposed to chemical signals from the urinary space (Bowman's capsule), it receives and transmits chemical and mechanical signals to/from the glomerular basement membrane upon which it elaborates, and it receives chemical and mechanical signals from the vascular space with which it also communicates. As with every cell, the ability of the podocyte to receive signals from the surrounding environment and to translate them to the intracellular milieu is dependent largely on molecules residing on the cell membrane. These molecules are the first-line soldiers in the ongoing battle to sense the environment, to respond to friendly signals, and to defend against injurious foes. In this review, we take a membrane biologist's view of the podocyte, examining the many membrane receptors, channels, and other signaling molecules that have been implicated in podocyte biology. Although we attempt to be comprehensive, our goal is not to capture every membrane-mediated pathway but rather to emphasize that this approach may be fruitful in understanding the podocyte and its unique properties.

Figures

The function of podocytes is…

The function of podocytes is based on their intricate cell architecture. ( a…

Podocyte plasma membrane proteins and…

Podocyte plasma membrane proteins and a canonical pattern of injury. Shown is an…

Reversible and irreversible consequences of…

Reversible and irreversible consequences of dysregulated podocyte signaling. ( a ) Dysregulated signaling…

An example of pathways at…

An example of pathways at the intersection of AT1R and TRPC signaling at…


Results and Discussion

General features of the genome and orthologue analyses

Individual features of the bed bug genome analyses are provided as Supplementary Information (Supplementary Figs 1–42 Supplementary Notes 1–22 Supplementary Data 1–33). Our final draft assembly comprises 650.47 Mb of total sequence in 1,402 scaffolds and 45,073 contigs (N50 lengths 7.17 Mb and 23.5 kb, respectively Supplementary Data 1). This is 25% smaller than the predicted genome size of 864.5 Mb (determined through comparison with other insects by propidium iodide analyses Supplementary Note 17) and is likely due to unassembled heterochromatin and other repetitive regions. We predicted 13,953 genes using a custom MAKER annotation pipeline tuned for arthropod genomes and this was improved to 14,220 through manual curation. A total of 1,352 gene models representing gene families of interest, including 273 cuticle proteins and 114 chemoreceptors were manually curated, confirming gene identity and revealing where automated gene structures needed correction (Supplementary Note 1). To assess the completeness of the assembly and gene prediction, we analysed the predicted genes and genome assembly for benchmarking sets of universal single-copy orthologues (BUSCOs 18 ). In addition, the presence of a complete Hox cluster and all expected autophagy genes was documented, two categories that are known to be conserved among insect genomes (Supplementary Notes 10 and 12). In general, the C. lectularius gene set and genome has slightly more missing BUSCOs, ∼ 10%, compared with the genomes of seven other arthropods, but is still relatively complete (Supplementary Data 28). We therefore concluded that the data set for C. lectularius is sufficiently comprehensive for further downstream analyses.

In addition, we characterized homologous and orthologous relationships between genes in relation to those of other sequenced arthropods using a previously described orthology delineation approach employed by OrthoDB 19 . The analyses were performed with the 45 arthropod species included in OrthoDB7 (http://www.orthodb.org). Over 80% of C. lectularius genes have orthologues in at least one arthropod species (Fig. 1). Of these, 1,734 were universal single-copy orthologues across eight species, which were used to determine the maximum-likelihood phylogeny. As expected, our analyses of these eight arthropod genomes placed another hemipteran, the pea aphid Acyrthosiphon pisum, as the sister species of C. lectularius (Fig. 1). It is worth noting that A. pisum has more than twice as many genes due to extensive gene duplication in >2,000 gene families 20 . Large-scale transcription factor analyses revealed 634 putative transcription factors and we were able to infer DNA-binding motifs for 214 (34% Supplementary Note 22).

The phylogenetic analysis places C. lectularius as a sister species to another hemipteran, Acyrthosiphon pisum. The phylogeny is built using RAxML and it is based on the 1,734 single-copy orthologues that are present in all eight species. All nodes in the phylogenetic tree have 100% bootstrap support, while the branch length unit is substitutions per site. There are 1,734 genes that are present as single copy in all eight species tested. Another 4,187 of the C. lectularius genes are found in varying copy number in the other seven species, while 2,433 are found in the majority of species (that is, in 5–7 species) and 2,153 genes are found in ≥2 species (that is, in 2–4 species). Moreover, 1,147 genes have an orthologue in an arthropod other than the selected seven species. Last, 2,285 genes are lineage specific and do not have an orthologue in any other arthropod species.

Host location, obligate blood feeding and immunity

Bed bugs are obligate blood feeders, and unlike mosquitoes and many other blood-feeding insects, all immature stages and both sexes of adults rely exclusively on blood for nutrition and water 5,6,7 . C. lectularius prefers humans as hosts but accepts a range of other vertebrate hosts 5,7 . The association with humans in the built environment, coupled with their crepuscular/nocturnal activity and the complete reduction in wings, predicts specialized mechanisms for host location, acceptance, and blood ingestion and digestion. Bed bugs are equipped with small compound eyes that protrude prominently from the lateral head capsule and object recognition is suspected to play a role in host detection 21 . Consistent with low-resolution landscape vision, the bed bug genome contains one member each of the ultraviolet- and broadband long-wavelength-sensitive rhabdomeric opsin subfamilies in line with that of most other hemipteran genomes sequenced (Supplementary Note 9), as well as crepuscular insect species in general 22 . Circadian clock genes in C. lectularius appear to encode both Drosophila- and mammalian-like proteins (Supplementary Note 5), with notable absence of sequences for CRY1 and JET, which are necessary in Drosophila for the light input pathway to the clock 23,24 . Cimex may thus represent a valuable model in circadian rhythm research, particularly for organisms that inhabit low-light or -dark environments.

Olfactory and gustatory processing in insect sensilla depends on three families of chemoreceptors: odourant, gustatory and ionotropic receptors 25 . Olfactory receptors play critical roles in mate finding, host location and navigation through a dark environment using the sense of smell. The major functions of gustatory receptors (GRs) are to mediate gustation—most importantly to detect sweet (phagostimulatory) and bitter (deterrent) tastants—as well as to sense carbon dioxide 26 . Ionotropic receptors evolved from ionotropic glutamate receptors in ancestral animals, and are involved in both olfaction and gustation 27 . We idenified 48 genes encoding 49 olfactory receptors, 24 genes encoding 36 GRs and 30 ionotropic receptor genes (Fig. 2a Supplementary Note 4). This repertoire of chemosensory genes is substantially reduced relative to that of phytophagous hemipterans (for example, pea aphid), extending a similar trend noted in the genome sequences of other blood-feeding insects (Fig. 2a). Moreover, the intermediately sized repertoire of bed bug chemoreceptors is in line with the moderate complexity of its chemical ecology, being an obligate blood feeder such as tsetse flies (Glossina morsitans) 28,29 , but having a broader host range that encompasses many vertebrates, whereas Pediculus humanus humanus (body louse) feeds only on humans 30 . We found no sugar receptors in the Cimex genome, as previously documented in other obligate blood feeders, including tsetse flies 28,29 and lice 30 . This finding also explains the lack of phagostimulation by glucose in C. lectularius 31 . Remarkably, Cimex has four GRs related to a conserved lineage of carbon dioxide receptors found in flies, moths, beetles and a termite 32 , but that are absent from the pea aphid, hymenopteran species and blood feeders such as Pediculus 30 (Supplementary Note 4). The Cimex chemosensory gene families appear to have few expansions and slow evolving members (Supplementary Figs 2–4), suggesting a comparatively stable chemosensory ecology. We also found 11 odourant-binding proteins that appear to be highly species specific in C. lectularius, and 14 chemosensory proteins that are more conserved relative to other blood-feeding insects 33 .

(a) Genes associated with chemical reception among multiple insect species. Zootermopsis nevadensis (b) Genes associated with saliva function among multiple insect species. (c) Phylogeny of cathepsin D genes among multiple insect species. Sequences derived from Cimex lectularius (Cl) are denoted with red triangles and those derived from Rhodnius prolixus (Rp) are denoted with orange triangles. Other insect cathepsin D proteins represent those of Triatoma infestans (Ti), Acyrthosiphon pisum (Ap), Anopheles gambiae (Ag), Drosophila melanogaster (Dm), Pediculus humanus corporis (Ph), Apis mellifera (Am), Nasonia vitripennis (Nvi), Tribolium castaneum (Tc), Callosobruchus maculatus (Cm), Sitophilus zeamais (Sz), Chrysomela tremula (Ct), Maconellicoccus hirsutus (Mh), Nematostella vectensis (Nve), Culex quinquefasciatus (Cq) and Aedes aegypti (Aa).

One of the major obstacles in the acquisition of a blood meal is host haemostasis, the physiological process that prevents blood loss through platelet aggregation, fibrin crosslinking, vasoconstriction and local immune responses. The bed bug genome builds upon previous sialotranscriptome and proteome studies 34 and contributes to our understanding of bed bug saliva complexity and unique adaptations of blood-sucking insects. Of interest, Cimex appears to have expanded salivary apyrases, proteins involved in the inhibition of ADP-dependent platelet aggregation, including two Cimex-type apyrases 35 . In addition, 12 members of the inositol polyphosphate phosphatase family that act as nitric oxide carriers, and 6 members of the Ap4a_hydrolase family, the largest number in any insect genome, were identified (Fig. 2b Supplementary Note 18). This expanded array of salivary proteins likely permits bed bugs to stealthily feed repeatedly on the same host without inflicting pain.

Vertebrate blood is an excellent source of proteins and lipids, but it is deficient in specific micronutrients, has high water content, and its digestion requires a suite of specific digestive enzymes (Fig. 2c). Analysis of the C. lectularius genome revealed 187 potential digestive enzymes (Supplementary Data 12). C. lectularius has fewer serine proteases than most insects, but a similar repertoire to blood-feeding Rhodnius (kissing bug) and Pediculus (Supplementary Note 7 (refs 30, 36)). Of interest is a large expansion of genes associated with cathepsin D (Fig. 2c), an aspartic protease adapted for acidic pH 35 . A similar expansion, albeit of different specific cathepsin D genes, has been found in Rhodnius and deemed critical for optimal blood digestion 36,37 .

Removal of excess water from the blood meal is essential for proper digestion and aquaporins (AQPs) appear to be critical for this process 38 . Bed bugs possess seven or eight AQP genes, which are within the 6–8 range common for most insects 38 (Supplementary Note 3). Among peptide hormones and amine receptors, we documented a full complement of diuretic and antidiuretic hormones and their receptors that serve to precisely initiate and terminate postprandial diuresis (Supplementary Note 14). Unlike Rhodnius 39,40 , C. lectularius has only one capa gene encoding antidiuretic neuropeptide hormone.

Like blood-feeding ticks and triatomine bugs, but unlike most other blood-feeding insects, bed bugs can survive long periods of starvation between blood meals 5,6 . This adaptation requires nutrient conservation (for example, lower metabolism) and mechanisms to prevent excessive water loss and dehydration-induced mortality 5,6 . The latter is specifically dependent on differential expression of aquaporins and heat-shock proteins 38 (Supplementary Notes 3 and 11). In general, genes for heat-shock proteins and autophagy are similar in Cimex and other insect species, suggesting that their differential expression is likely responsible for the extreme dehydration and starvation tolerance noted in bed bugs. These gene sequences will facilitate the discovery of other physiological and behavioural mechanisms underlying the extreme dehydration and starvation tolerance of bed bugs.

The bed bug genome shows strong candidates for the key members of the Toll, Imd and Jak/STAT immune pathways, although the C. lectularius repertoire is arguably more sparse for those pathways than in holometabolous insects 41 . Recognition proteins are under-represented, as are antimicrobial peptides (two recognition proteins and two defensins and a cluster of three diptericin-like peptides Supplementary Data 29), although the latter are notoriously difficult to identify by sequence similarity. The RNA interference pathway is represented in the C. lectularius genome with multiple paralogues for Dicer, Argonaute and other enzymes required for this defence pathway.

Symbiosis and lateral gene transfer

Obligate hematophagy can result in significant deficiencies in specific micronutrients that are poorly represented in blood. Wolbachia, a common endoparasite that can affect growth and reproduction in many insect species 42 , has evolved a symbiotic nutritional relationship with C. lectularius 8,9 . Wolbachia provides the bed bug with a cocktail of specific B vitamins that are critical for reproduction and development 8,9 . We annotated genes associated with B vitamin metabolism and determined, as with other insects, that bed bugs possess the genes necessary for B vitamin salvage and conversion after their ingestion in blood or synthesis by Wolbachia (Supplementary Note 19).

A computational pipeline 43 was used to detect bacterial scaffolds within the assembly as well as candidate LGTs from bacteria to the bed bug. The nearly complete Wolbachia endosymbiont of C. lectularius was assembled into 16 scaffolds (Supplementary Data 21). In addition, the nearly complete genome of a Staphylococcus associate of bed bugs was assembled into 15 scaffolds, which include three plasmids and a ∼ 3.16-Mb chromosome (Supplementary Data 21). On the basis of high-sequence similarity of chromosomal scaffolds, this bacterium is a close relative of S. xylosus, an associate of the skin of humans and other animals 44 . Staphylococcus bacteria are commonly found in bed bugs based on two microbiome surveys 12,45 , including on the male genitalia and inside the female body, and we report here the first draft genome of this C. lectularius associate. There is evidence of sexual transmission of Staphyloccus 12 . Further studies are necessary to determine whether this bacterium is routinely acquired from human hosts or is a strain specifically adapted to Cimex. A third scaffold was assembled with homology to the bacterium Pectobacterium carotovorum. This bacterium is typically associated with plants, and the scaffold is only 250 kb in size, whereas P. carotovorum genomes are typically ∼ 5 Mb. Further, the scaffold does not contain a ribosomal locus, and therefore this bacterium is unlikely to be an endosymbiont of Cimex with a severely reduced genome size. Given that coverage of this scaffold is similar to the genome coverage (Supplementary Data 21), we speculate that this may be a large lateral gene insertion in Cimex however, further study is needed to resolve this question.

The bed bug shows evidence of extensive bacterial LGTs in its genome. In addition to the case described above, there are 805 candidate LGTs of size >100 bp that appear to be scattered throughout the bed bug genome (Fig. 3). This is the largest number of candidate LGTs found in screening of 14 arthropod genomes using this pipeline. LGTs from the genus Arsenophonus (n=459 or 57%) are the most commonly found, followed by Wolbachia (n=87 or 10.9%). Other genera represented include Sodalis, Hamiltoniella and Peptoclostridium. The large number of Arsenophonus LGTs found is uncommon in insect genomes so far screened, with numbers typically ranging from 0–22. Arsenophonus is a widely distributed arthropod-associated bacterium 46 , but has not been reported in Cimex and no scaffolds for this bacterium were detected in the genome assembly. The type species A. nasoniae 47 has a sequenced genome 48 . It causes male killing in a parasitoid wasp, whereas phenotypic effects of other Arsenophonus are less well understood. The second most common source of candidate LGTs in Cimex is Wolbachia, which is a known mutualistic endosymbiont. Wolbachia sequences from this symbiont assembled into a nearly complete genome with high sequence coverage. Because of the presence of Wolbachia bacteria in Cimex, it is possible that some apparent LGTs are due to assembly errors joining Wolbachia and Cimex sequences. However, examination of junctions between eukaryotic and prokaryotic sequences for spanning sequence reads and cloned paired ends strongly supports that nearly all of these are legitimate LGT events. In addition, LGT–eukaryotic sequence junctions were amplified for five of six candidates, confirming their presence in the genome (Supplementary Fig. 42). The LGTs found in Cimex appear to be unique insertions, as no matches were found to the closest published insect genome (A. pisum). Comparative studies among C. lectularius populations and related species will be important to determine whether there is genomic variation in LGTs among bed bugs.

(a) Number of candidate LGTs identified. (b) Length of candidate LGTs in bins spanning 10 bp.

The typical pattern of LGT evolution is expected to be insertion (most likely due to non-homologous DNA repair mechanisms) followed by degradation and loss. In this way, LGTs are similar to nuclear mitochondrial DNA insertions found in the genome of most eukaryotes 49 . However, bacterial LGTs can also evolve into functional eukaryotic genes, providing novel biochemical functions in the eukaryote 50 . Most candidate LGTs in C. lectularius show no or only traces of gene expression in RNA-seq data from adult males and females, and are thus unlikely to be functional. An exception is a Wolbachia LGT on scaffold 132, which encodes a patatin-like gene. Bacterial patatin-like genes have lypolytic properties and can be involved in pathogenicity of some bacteria 51,52 . This LGT shows high expression in adult males but no expression was detected in adult females. While the function and detailed male expression pattern of this gene remain to be determined, we speculate that it may be involved in the unusual insemination mechanism of Cimex.

Genes associated with pesticide resistance

A major factor for the increased prevalence of bed bugs in the past two decades, and a contributing factor to the immense difficulties in eradicating infestations, has been the pervasiveness of pyrethroid resistance 4,53,54,55,56 . Resistance can result from multiple mechanisms that include target-site mutations, differential gene expression, alterations in the permeability of the cuticle or digestive tract and behavioural changes 4,57,58,59 . Transcriptomic evidence supports the presence of multiple resistance mechanisms in bed bug populations 4 . To fully understand these potential mechanisms, we manually annotated genes associated with pesticide resistance, including cuticular proteins that can impede pesticide penetration and enzymes that can detoxify pesticides.

V419L and L925I mutations in the voltage-gated sodium channel α-subunit gene have been identified and shown to be responsible for deltamethrin (a pyrethroid) resistance in bed bugs 60 . Molecular analysis of bed bug populations from across the USA and Europe found that >80% and >95% of the respective populations contained V419L and/or L925I mutations in the voltage-gated sodium channel gene, indicating widespread distribution of target-site-based pyrethroid resistance 7,61 . Previous studies showed that higher expression of genes coding for metabolic enzymes including P450s, carboxylesterases and glutathione-S-transferases and a reduction in penetration due to higher expression of cuticular protein genes are likely responsible for insecticide resistance of bed bugs 4,59 .

Insect genomes code for four distinct clades of P450s called clans: the CYP2, 3, 4 and Mito clan. The C. lectularius genome contains 58 genes and one pseudogene coding for P450 enzymes (Supplementary Data 22). Relatively few insect P450s with known or suspected physiological functions are significantly conserved across species 53 , and these tend to be involved in biosynthesis of hydrocarbons that cover the insect exoskeleton and prevent desiccation (CYP4G subfamily 4 ). Most bed bug P450s (36/58 genes) are members of the highly diverse CYP3 clan these genes lack clear orthologous relationships and thus are likely involved in species-specific functions. Several transcriptomic analyses have demonstrated substantial overexpression of some bed bug P450s in a manner that was correlated with metabolic resistance to the pyrethroid insecticide deltamethrin 4,54,58 . Four of the P450 genes identified in the Cimex genome (CYP397A1, CYP398A1, CYP4CM1 and CYP6DN1) are known to be overexpressed in deltamethrin-resistant populations 4 . Knockdown in the expression of these four P450 genes by RNA interference caused a reduction in deltamethrin resistance levels 4,62 . In addition, RNA interference of cytochrome P450 reductase, which encodes a co-enzyme required for P450 activity, reduced deltamethrin resistance levels in resistant populations of Cimex 62 . These results indicate that P450s play an important role in Cimex insecticide resistance.

ATP-binding cassette (ABC) transporters play important roles in the shuttling of a wide variety of substrates including hormones, ions, sugars, amino acids, vitamins, peptides, polysaccharides, lipids and insecticides 63 . In a recent study, the expression of 8 out of 27 contigs coding for ABC transporters was elevated in pesticide-resistant Cimex populations relative to susceptible populations 54 . We identified 24 additional ABC transporters (Supplementary Data 23) in total, Cimex encodes 51 ABC transporters belonging to all eight known classes. Interestingly, 25 of the 51 transporters belong to ABCG/H class, members of which are known to be involved in transport of xenobiotics 63 . Three of the ABC transporters identified in the Cimex genome (ABCG20-3, ABCG23-5 and ABCH-B previously named ABC8, ABC9, ABC10 and ABC11 based on transcriptome analysis 54 ) are overexpressed in the epidermis in 21 field-collected resistant populations relative to susceptible populations 4 . In addition, knockdown of ABCG20-3 (ABC8 and ABC9 are encoded by this gene) reduced deltamethrin resistance 4 . With the complete set of ABC transporter genes, future studies will be able to fully assess their contribution to insecticide resistance.

Carboxylesterases are critical in the metabolic breakdown of insecticides 64 . We identified 30 carboxylesterase genes in the Cimex genome (Supplementary Data 24). Half of them are located in a single cluster in scaffold 81, suggesting significant gene duplication, and one carboxylesterase, CLE11776 (previously named ClC21331), is expressed at very high levels in most of the 21 field-collected populations tested 4 . We also identified 12 glutathione-S-transferase genes in the Cimex genome, which was similar to the number identified previously by transcriptome studies 58 (Supplementary Data 25).

The bed bug cuticle plays a substantial role in resistance to insecticides this is thought to be due (at least in part) to changes in the expression of cuticle proteins in resistant strains 4,54,59 . Using the criteria established by Willis 65 , we identified 273 genes that encode putative cuticle proteins (Supplementary Note 6). Of these, 169 genes could be placed in one of eight families (CPR, CPRL, CPF, CPFL, CPAP1, CPAP3, TWD and Dumpy), with an additional 104 proteins consisting of repeated low-complexity sequences (AAPV/GGY) commonly associated with cuticle proteins but without a defining conserved domain (Supplementary Data 10). Approximately, 70% of bed bug cuticle protein genes were arranged in clusters ranging from 3 to 19 genes (Supplementary Data 11 Supplementary Fig. 6) clusters were largely type specific and emphasize the potential for regulatory changes that might influence the expression of the entire cluster.

As in other insects, the CPR family represents the largest single family of putative cuticle protein genes found in the bed bug genome. The 121 CPR-type genes we identified (Supplementary Fig. 7) are slightly more than in Drosophila 66 but fewer than in the silkworm Bombyx mori 67 or the malaria mosquito Anopheles gambiae 68 . We note a bed bug-specific expansion in this family consisting of a novel 10 gene cluster whose members encode two chitin-binding domains each similar gene structures were not identified in the pea aphid or any of the dipteran genomes.

Traumatic insemination

Among the >40 independent evolutionary events in different lineages leading to traumatic mating, bed bugs are among the best-studied cases 69 . Females evolved a novel organ that reduces the physical trauma of copulation by means of a dense aggregation of the super-elastic protein resilin 70 . Intriguingly, our genome analysis revealed a recent expansion in pro-resilin genes, with 13 such genes containing the pro-resilin characteristics of a chitin-binding domain and consisting of >20% glycine. The pro-resilin gene CPR57 is over 600 amino acids with >40% glycine (Supplementary Figs 7,8). A similar diversification of the resilin gene family is not seen in the related pea aphid (six genes even though there are a similar number of CPR-type cuticle proteins, ∼ 115 (refs 65, 66)) nor is it seen in other blood-sucking insects that experience the enormous stretching of the cuticle to accommodate the blood meal (Aedes, Pediculus, and Anopheles 2–6 genes), indicating lineage-specific adaptive significance of the resilin gene family.

Conclusions

The sequencing, assembly, annotation and manual analyses of the C. lectularius genome provide an important and timely resource for understanding the biology of this human ectoparasite, as summarized in Fig. 4. It also will serve as a gateway for the discovery of new targets for control of bed bug populations. This reference genome sequence is of a bed bug strain that is common in laboratory cultures and collected before the introduction of pyrethroid insecticides. What triggered the current bed bug resurgence, and did bed bugs originate from one or multiple sources? This genome sequence will facilitate the discovery of molecular markers and single-nucleotide polymorphisms that will enable research to address these questions. There are many related Cimex species that specialize on non-human vertebrate hosts. Comparative genomic studies should reveal specific chemosensory and digestive specializations that define anthropophagy in C. lectularius. Even host-associated differentiation within this species requires further genomic studies to understand why one lineage of C. lectularius prefers humans and another lineage prefers bats, and how the two remain genetically differentiated even within the same home.

Red, general characteristics of bed bugs black, key aspects identified and expanded by genome sequencing and manual curation.

Traumatic insemination has evolved multiple times in various unrelated taxa. The sequenced bed bug genome will serve as an important resource for studies on male-expressed gene networks that ensure sperm transfer despite the female’s immune response and other female-expressed pathways that may facilitate cryptic choice of mates. Most haematophagous arthropods have been implicated as vectors of human or animal pathogens, but bed bugs have not. Pathogenic organisms have been isolated from bed bugs, and bed bugs have been shown experimentally to be competent vectors, for example, of American trypanosomes. However, no evidence exists of disease transmission by bed bugs in the field. The sequenced genome will enable studies on mechanisms that actively hinder or do not support vertebrate pathogen survival, proliferation and transmission in bed bugs. Finally, allergenic proteins excreted by anthropophilic arthropods (for example, cockroaches and house dust mites) tend to serve as aetiologic agents of human allergic disease and asthma. Bed bug infestations reach densities of thousands of individuals per home, which may generate high levels of specific antigens. The sequenced genome will provide a platform for the identification and characterization of bed bug-produced allergens that may negatively affect the health and well-being of those whose economic status, unfortunately and almost certainly, ensures that humans and bed bugs will remain closely associated for the foreseeable future.


Nuclear techniques confirm unique biology of human eye lens

Age-related cataract and a reduction in the ability to focus (presbyopia) are very common vision problems in older people. New research from ANSTO has provided evidence to confirm the long life of an important biomolecule in the human eye lens which may be relevant for the study of age-related diseases and conditions.

E-life has recently published a manuscript from a group of researchers from the University of Wollongong, the Illawarra Health and Medical Research Institute, Queensland University of Technology and ANSTO.

Surprisingly, the human eye lens, whose function is to focus light onto the retina, does not lose and replace cells during an entire lifespan, according to co-investigator, research scientist Vladimir Levchenko of the Institute for Environmental Research.

"It is the first time that it has been shown that the molecule, a lipid, without access to metabolic machinery, lives longer than other lipids in the body," said Levchenko, who collaborated with key investigator, neuroscientist Dr Jennifer Hughes and others on the paper.

Radiocarbon dating is most well-known for establishing the age of samples, such as sediment, coral or archaeological artefacts, but it can also be used to gain forensic information about biological processes.

Levchenko used accelerated mass spectroscopy (AMS) on the ANTARES accelerator at the Centre for Accelerator Science to measure the amount of a specific isotope, carbon-14, present in the lenses of fourteen donors. He and Hughes extracted lipids from the nucleus of the lens for the analysis.

A measurement of the amount of carbon-14 in a class of molecules allows you to date biosynthesis and the time the system stopped exchanging carbon with its surroundings.

The carbon-14 content of the lens thus reflects the atmospheric content of carbon-14 when the lens crystallines were formed. Precise radiocarbon dating is made possible by comparing the carbon-14 content of the lens crystallines to the so-called bomb pulse.

The investigators found that the level of carbon-14 in the nucleus of the lenses reflected the amount of carbon-14 in the atmosphere of the year of birth. The donors had birth dates from 1948 to 1993. Because the level of carbon-14 was found to be an accurate predictor of birth, it indicated the absence of lipid turnover during the human lifespan.

Radiocarbon dating can be used with human tissue because of a development known as the bomb pulse. Between 1955 and 1963 above-ground nuclear testing generated increased concentrations of radioactive carbon-14 in the earth's atmosphere.

After a 1964 moratorium on above ground testing, atmospheric levels of Carbon-14 began falling as the radioactivity passed from the atmosphere into the oceans and the biosphere. Virtually every organism living since the 1950's is labelled with higher than normal levels of carbon-14, including humans.

The rapid year-to-year changes in atmospheric levels of carbon-14 within this time frame, combined with rapid transfer of atmospheric carbon-14 into the food chain through photosynthesis, mean that the distribution of bomb-derived carbon-14 within the humans depends upon birth year, diet, and the dynamics of tissue replacement within the human body. The radiocarbon content of tissues is fixed at the time of death.

Although radiocarbon dating has been used previously to estimate the age of human tissue, these results represent the first evidence that lipids live for a long time.

The lens has a unique pattern of growth in which fibre cells are added to the lens that is present from birth. Newly-formed fibre cells capture and enclose pre-existing cells. This unique pattern of growth may explain the lack of molecular turnover, according to investigators.

Different classes of lipids appear to have relative chemical stability under the conditions experienced within the lens. The lipid, a sphingomyelin, is more abundant than another type of phospholipid in the human lens. Lipids in the core of the nucleus are as old as the lens itself.

Only humans have a quantity of this lipid in the lens.

The new data correlates with earlier studies that established the content of sphingomyelin remains relatively stable over time.

Lipids are known to be critical to cellular function in the body and, generally, lipid turnover is rapid. A breakdown in lipid regulation has been linked to disease. The new research indicates activity which is counter to this association.

Although it is not known if other long-lived lipids are present in other tissue, the findings may prove to be important in understanding the development of age-related diseases.