When allergy season looms, some people with serious hypersensitivity to allergens tend to be apprehensive of what may come. Some would rather stay indoors than risking the odds of sucking up triggers that could instigate severe allergic reactions. Apart from triggers from the environment, other common factors for allergy include food, medication, certain toxins, venom from insect stings or bites, stress, and heredity. How does an allergy manifest? Which cells are involved in forming an allergic reaction?
The immune system
The immune system protects the body from foreign substances (generally referred to as antigens) that could pose a threat to our well-being. It prevents harmful bacteria, viruses, parasites, etc. from invading and causing harm. The white blood cells (also called leukocytes) constantly scout for antigens in order to destroy or disable them. The white blood cells include lymphocytes, neutrophils, basophils, eosinophils, monocytes, macrophages, mast cells, and dendritic cells.
Allergy – overview
An allergy is a state of hypersensitivity of the immune system in response to an allergen (i.e. a substance capable of inciting an allergic reaction). In this regard, several white blood cells play a role in mounting an allergic reaction.
In summary, the entry of an allergen into the body triggers an antigen-presenting cell, such as a dendritic cell. The dendritic cell takes up the allergen, process it, and then present its epitopes through its MHC II receptor on its cell surface. It, then, migrates to a nearby lymph node, waiting for a T lymphocyte to recognize it.
Upon recognition, the T lymphocyte may differentiate into a Th2 cell (type 2 helper T cells), which is capable of activating B lymphocyte. B lymphocyte, when activated, matures into a plasma cell that could synthesize and release IgE antibody in the bloodstream. Some of the circulating IgE may bind to mast cell and basophil. Thus, re-entry of such allergen could incite the IgE on mast cells and basophils to recognize its epitope. In effect, this activates the mast cell or basophil to release inflammatory substances (e.g. histamine, cytokines, proteases, chemotactic factors) into the bloodstream.
Anaphylaxis – a dreadful allergic reaction
The allergic reaction mounted by the immune system is supposed to protect the body. However, the allergens perceived by the body as a threat are generally harmless. The body tends to overly react to the allergens, and so leads to symptoms. Histamine, for instance, brings about the common symptoms of allergy: pain, heat, swelling, erythema, and itchiness.
Anaphylaxis is the most severe form of allergic reaction. It can occur rapidly and it affects more than one body system, such as respiratory, cardiovascular, cutaneous, and gastrointestinal systems. It occurs as a result of the release of inflammatory substances from mast cells and basophils upon exposure to an allergen. Within minutes to an hour, symptoms could manifest as a red rash, swelling, wheezing, lowered blood pressure, and in severe cases, anaphylactic shock.
In the presence of breathing difficulties, racing heart, weak pulse, and/or a change in voice, the situation is precarious. It calls for an immediate medical attention.
Why does anaphylaxis occur? IgE-mediated anaphylaxis is the common form of anaphylaxis. Initial exposure to an allergen leads to the release of IgE so that re-exposure to the allergen leads to its identification and the eventual activation of mast cells and basophils. Apart from immunologic factors, though, other causes of anaphylaxis are non-immunologic. For example, temperature (hot or cold), exercise, and vibration may cause anaphylaxis. In this case, IgE is not involved. Rather, these agents directly cause the mast cells and the basophils to degranulate.
Novel mechanism identified
Recently, a team of researchers1,2 found a novel mechanism that could explicate the hasty allergic reaction during anaphylaxis. They were first to uncover a mechanism involving the dendritic cells. Accordingly, a set of dendritic cells seem to “fish” allergens from the blood vessel using their dendrites. The dendritic cell near the blood vessel takes up the blood-borne allergen. Rather than initially processing it, and then presenting the epitope on its surface, it hands over the allergen inside a micro-vesicle to the adjacent mast cells.
Mast cells, unlike basophils that are in the bloodstream, are located in tissues, such as connective tissue. Thus, the question as to how the mast cells detect blood-borne allergen could be answered by the recent findings.
Rather than being internalized by the dendritic cells for processing, the allergen was merely taken into a micro-vesicle that budded off from the surface of dendritic cells. This, thus, saves time. It cuts the process, leading to a much rapid allergic reaction.
However, these findings were observed in mouse models. Therefore, the researchers have yet to observe if this novel mechanism also holds true on humans. If so, this could lead to possible therapeutic regulation of allergies, especially the most dreadful form, anaphylaxis.
— written by Maria Victoria Gonzaga
1 Choi, H.W., Suwanpradid, J. Il, Kim, H., Staats, H. F., Haniffa, M., MacLeod, A.S., & Abraham, S. N.. (2018). Perivascular dendritic cells elicit anaphylaxis by relaying allergens to mast cells via microvesicles. Science 362 (6415): eaao0666 DOI: 1126/science.aao0666
2 Duke University Medical Center. (2018, November 8). Using mice, researchers identify how allergic shock occurs so quickly: A newly identified immune cell mines the blood for allergens to directly trigger inflammation. ScienceDaily. Retrieved November 22, 2018 from www.sciencedaily.com/releases/2018/11/181108142440.htm
When sadness reeks in and you feel as if you are all by yourself, think again. That is because you are never alone. As a matter of fact, millions of microorganisms reside in our body day in and out. They are the normal flora. Our body is a world of microscopic living entities that inhabit our body without essentially causing a disease. Rather, they live in us in harmonious mutualism. Thus, our body is not ours alone. Hence, we can say we are not absolutely sterile from the moment we are born.
Typically, the body has about 1013 cells and harbors about 1014 bacteria.1 The multifarious yet specific genera of bacteria that predominate the body is referred to as the normal flora. In essence, the normal flora thrives in a host in a mutualistic lifestyle. The microbes take advantage from living stably in the body. In return, they confer benefits to the human host. For instance, their presence helps prevent other more harmful microbes from colonizing the host. Some of them biosynthesize products that the human body can use. Nevertheless, an immunocompromised host could suffer in cases when these bacteria became overwhelming in number, and thereby cause detectable harm, like infections or diseases.
Normal flora in the gut
Microbes that normally thrive in the gut are greater in density and diversity compared with those in other body parts. Nevertheless, they vary in density depending on the location in the gastrointestinal tract. For instance, the stomach harbors about 103 to 106/g of contents whereas the large bowel of the large intestine has about 109 to 1011/g of contents. The normal flora in the stomach has fewer normal microbial inhabitants due to its acidity. The ileum of the small intestine contains a moderate microbial number, i.e. 106 to 108/g of contents.1
Some of the various bacterial species of the normal gut flora includes the anaerobes, Enterococcus sp., Escherichia coli, Klebsiella sp., Lactobacillus sp., Candida sp., Streptococcus anginosus and other Streptococcus sp.. Some of these bacteria aid in the production of bile acid, vitamin K, and ammonia since they possess the necessary enzymes.
Certain normal gut bacteria can become pathogenic. They could cause a disease when opportunity presents such as when changes in their microbiota favor their growth. Be that as it may, a healthy individual would not be usually harmed by their presence. Thus, question arises — why our immune armies do not, by and large, act against the normal flora as aggressively as they would in the presence of more harmful pathogens.
Karen Guillemin, a professor of biology and one of the authors of a paper that appeared in a special edition of the journal eLife, was quoted3: “One of the major questions about how we coexist with our microbial inhabitants is why we don’t have a massive inflammatory response to the trillions of the bacteria inhabiting our guts.”
Guillemin and her team of scientists reported that they uncovered a novel anti-inflammatory bacterial protein they referred to as Aeromonas immune modulator (AimA). Accordingly, AimA is a protein produced by a common gut bacterium, Aeromonas sp., in the animal model, zebrafish. The researchers found that AimA alleviated intestinal inflammation and extended the lifespan of the zebrafish from septic shock.2 Furthermore, they described it as an immune modulator that confers benefits to both bacteria and the zebrafish host.
The newly-discovered protein seems to be the first of its kind. Nevertheless, it is structurally similar to lipocalins, a class of proteins that, in humans, modulate inflammation. Based on their findings, the removal of this protein caused more intestinal inflammation in the host and the destruction of the normal Aeromonas gut bacterium. The reintroduction of AimA reverted to “normal”, i.e. the host, relieved from inflammation and Aeromonas’ typical density, restored. AimA appears to represent a new set of bacterial effector proteins. And, Guillemin referred to them as mutualism factors.3
Guillemin and her team postulate that many more of these mutualism factors exist even in humans, and yet to be found. These mutualism factors may have therapeutic potential for use in modulating inflammation especially in medical conditions such as sepsis and certain metabolic syndromes.
— written by Maria Victoria Gonzaga
1 Davis, C. P. (1996). Normal Flora. In: Baron S, editor. Medical Microbiology. 4th edition. Galveston (TX): University of Texas Medical Branch at Galveston. Retrieved from [link]
2 Rolig, A. S., Sweeney, E. G., Kaye, L.E., DeSantis, M. D., Perkins, A., Banse, A. V., Hamilton, M.K., & Guillemin, K. (2018). A bacterial immunomodulatory protein with lipocalin-like domains facilitates host–bacteria mutualism in larval zebrafish. eLife. [link]
3 University of Oregon. (2018, November 6). Novel anti-inflammatory bacterial protein discovered: Newly discovered protein alleviates intestinal inflammation and septic shock in an animal model. ScienceDaily. Retrieved from [link]
Blacked-legged Kittiwakes are pelagic gulls that often feed on fish and macro-zooplankton at the ocean surface. They breed in colonies ranging from few to thousands of pairs which prominently observed in their open, sea-cliff nesting habitats. Blacked-legged Kittiwakes are the most popular models for research because they can be easily monitored and captured. They also considered as prime indicators of fluctuating conditions in marine ecosystem. The purpose of this research is to collect live sperm of blacked-legged Kittiwakes using a non-invasive method. Also, be able to provide information on suitable extenders and timing in relations to the breeding phenology. Additionally, it will offer informations to different disciplines including veterinary science, conservation biology, ecotoxicology and evolutionary biology.
Sperm collection of Blacked-legged Kittiwakes
Sperm of blacked-legged Kittiwakes were obtained by firmly massaging the lower back and the tail base of the male bird. Since, the researchers observed that during mating the male tend to wag their tails thus, releasing the sperm naturally. After massaging the handler lift the tail, clear the feathers around cloaca and gently squeeze the cloacal area. While doing this a capillary tube placed on the top of the cloaca to collect directly the translucent liquid. Then, verified directly to the laboratory under the microscope.
The result demonstrates a successful collection of live sperm under field condition of blacked-legged Kittiwakes for the first time. In which the researchers discovered two extenders suitable for maintaining the sperm however, undiluted sperm also performed well in terms of survival. Since, seminal fluids alone are sufficient enough to maintain the sperm alive. Though, the researchers still recommend using sperm extenders since it is necessary to dilute highly concentrated ejaculates. Also, extenders are necessary on sperm quality examination when comparing experimental groups and sperm production.
Blacked-legged Kittiwakes are strictly monogamous and stores semen inside their body unlike passerine birds that stores semen in seminal glomera. Interestingly, one has to keep in mind that sperm quality may vary seasonally. So, the researchers suggest that one should statistically account for this effects using date relative to laying eggs. Also the researchers recommends to target specific time window when the birds are about to copulate but not after copulation within a day.
Source: Prepared by Joan Tura from BMC Avian Research
Volume 9:24, 14 July 2018
Porphyromonas gingivalis is a bacterium commonly associated in periodontitis a chronic inflammatory disease in the oral cavity. Periodontium is composed of periodontal ligament, cementum, alveolar bone and gingiva. Porphyromonas gingivalis is a gram-negative bacterium that contains toxic components. It is characterized by the presence of edema and destruction of tissue supporting the teeth. In which periodontal bacteria enters into circulation that leads to bacteremia and system dissemination of bacterial products. Moreover, Porphyromonas gingivalis can promotes systemic effects through expression of inflammatory mediators like pro-inflammatory cytokines. As a consequence it is confirmed to be associated with systemic diseases such as diabetes, respiratory disease and cardiovascular disease.
Potential effects of Porphyromonas gingivalis
Neurodegenerative diseases have been recognized as the major cause of cognitive and behavioral damage. It is known that peripheral infections could activate microglial cells within the nervous system enhancing development of neurodegeneration. Thus, the inflammatory molecules in the brain could be enhanced by periodontitis that increase inflammatory levels promoting the development of Alzheimer’s disease. In this particular research Porphyromonas gingivalis infection may impair cognition by elevating expression of pro-inflammatory cytokines. It is also shown that the infected mice displayed impaired memory and learning abilities. Elevated levels of pro-inflammatory mediators in the blood can lead to direct or indirect transport to the brain.
Periodontal infection caused by Porphyromonas gingivalis promotes neuro-inflammatory response via releasing pro-inflammatory cytokines. In which inflammation induces alterations in neurovascular functions causing increased in blood brain barrier permeability and aggregation of toxins. In brain trauma, infection and presence of endogenic abnormal protein aggregates can activate secretions of TNF-α. That plays a pivotal role in the development and functions of central nervous system. Moreover, aging is also associated to chronic inflammation which exerts additional stress to the brain nerve cells. Additionally, during systemic inflammation the functions of the blood-cerebrospinal fluid barrier were also significantly affected.
Therefore, Porphyromonas gingivalis periodontal infection may induce age-dependent brain inflammation. Also periodontitis can cause memory impairment which has a similar effect on the development of Alzheimer’s disease. Furthermore, aging is the major risk factor of Alzheimer’s disease and is correlated with elevated glial responsiveness. And in due course might increase the brain’s susceptibility to injury and disease.
Source: Prepared by Joan Tura from BMC Immunity and Aging
Volume 15:6, January 30, 2018
Aflatoxins produced by a certain molds that are poisonous carcinogens which grow mostly in soil, hay, decaying plants and grains. It can affect livestock and human as natural contaminants in foods like peanuts and corn meal. There are four types of aflatoxins these are B1, B2, G1 and G2 in which all are teratogenic, carcinogenic and immunosuppressive. Its toxic effect might be due to the generation of free radicals resulting into lipid peroxidation that damage biological system. On the other hand yogurt is produced from the bacterial fermentation of milk. In which bacteria produces lactic acid that acts on milk protein to give yogurt its texture and tart flavor. However, yogurt contains plenty of probiotic bacteria that offer benefits as microflora in the intestines. It also helps boost immune response and suppress carcinogenesis since fermented dairy products contain live lactic acid bacteria.
Selenium-fortified yogurt protects against aflatoxin toxicity
Yogurt has been known as therapeutic to various disorders including lactose intolerance, indigestion, intoxication, gastroenteritis, kidney, liver disorders and cancer. Selenium added to yogurt considered as the basic trace elements vital for normal growth and development in humans and animals. It also acts as anti-oxidant as well as improves nutritional values. Additionally, selenium has both enzymatic and structural functions that protect harmful reactive oxygen and minimized the production of hydrogen peroxide from aflatoxins. Ingestion of aflatoxins leads to weight loss due to the change in digestive enzymes activity that causes malabsorption of nutrients.
Aflatoxins will impair the biosynthesis of protein which results to the degranulation of the endoplasmic reticulum. It also caused liver fibrosis and poses health risk to humans and livestock. In this research , a positive results shows that selenium-fortified yogurt suppress the level of aflatoxins in rats. It also proved that with selenium contents inhibit the activity of enzymes related to carcinogenesis. Since yogurt improves intestinal mucosa and microflora that influence intestinal barrier. These yogurt bacteria inhibit the peroxidation of lipids by foraging reactive oxygen.
Therefore, consumption of nuts infected with aflatoxins caused toxicity mainly at the kidney and liver. But intake of selenium-fortified yogurt can definitely suppress against aflatoxins toxicity. In general, application of probiotic bacteria and selenium is vital and viable therapeutic approach to improve safety in food industry. Indeed, it is recommended to eat fresh nuts to avoid aflatoxins along with selenium-fortified yogurt to lessen its toxicity.
Source: Prepared by Joan Tura from BMC Agriculture and Food Security
Volume 7:21, June 2018
Breast cancer is the occurrence of lumps or thickening of the surrounding tissues of the breast mostly in women. Yet it also occurs rarely in men. It leads to the changes in shape and appearance of the breast. As well as the changes of skin like peeling, scaling and crusting of the surrounding nipples. Nowadays, extensive support for breast cancer awareness has helped generate advances in treatment and diagnosis. In which survival rates increased while the death rates continuously declining. Due to some factors such as personalized approach for treatment, early detection and have better knowledge of the disease. In this particular research a tumor-infiltrating lymphocytes has been evaluated to convey prognostic information of the breast cancer metastases. Assess its levels, immune composition and ligand expression in metastatic lesions.
Tumor-infiltrating lymphocytes as an Immunogenicity of Breast cancer
Evidences suggest the potential of tumor-infiltrating lymphocytes as biomarker in breast cancer metastatic stage. Even at onset of disease it proves as prognostic biomarker in human epidermal growth factor receptor positive with breast cancer. 94 patients have been studied retrospectively with metastatic breast cancer. Younger women showed significant lowered tumor-infiltrating lymphocytes compared to older patients above 50 years of age. Generally tumor-infiltrating lymphocytes are low but have been recognized significantly at high level with patients having this disease. Moreover, previous reports indicate that at secondary or recurrence of disease a lower tumor-infiltrating lymphocytes level occurs.
Analysis of the characteristics of tumor immune infiltrate differs across metastatic sites. It also suggests that cutaneous tissues might harbor permissive immune microenvironment for tumor growth. In which immune heterogeneity across metastatic sites need to be explored because it is relevant in treatment and immunotherapy. Other factors that are significant to tumor-infiltrating lymphocytes composition are those patients treated with multiple lines of chemotherapy. Indeed, heavily pretreated patients might have an impaired antitumor cytotoxic activity of the immune system.
Therefore, tumor-infiltrating lymphocytes showed strong prognostic value in breast cancer patients. Further examinations of its relevance as biomarker reflect a general activation of the immune system. Thus, it indicates that tumor-infiltrating lymphocytes is a simple method that effectively appreciates the immune activation status of tissue negative tumor. Certainly, given the availability of standardized method of the assessment, this immune marker is technically simple and clinically reliable. Finally, tumor-infiltrating lymphocytes provide novel hypothesis-generating data with regards to immune composition and complex interplay with breast cancer metastatic setting.
Source: Prepared by Joan Tura from Springer BMC Breast Cancer Research
Volume 20:62, 22 June 2018
Pancreatic cancer started at the tissue of the pancreas – an organ in the abdomen that lies behind the lower stomach. Pancreas releases hormones that helps in maintaining the sugar level in the blood and assist in digestion. Pancreatic cancer is hardly detected at early stage and it is recorded as third deadliest cancer in the United States. Some of its symptom includes weight loss, diabetes, jaundice, blood clots, depression and fatigue. However, it is usually characterized at late stage that has been already metastasized. Current therapy of this disease involves adjuvant chemotherapy, surgical resection and radiotherapy. Yet despite of the advancement of the clinical management and therapy the outcome remains unsatisfactory to the patients. So, this novel research of prognostic biomarker helps pancreatic cancer treatment to maximize survival and avoid toxicity.
miRNAs as Prognostic Biomarkers for Pancreatic Cancer
Due to poor prognosis of pancreatic cancer early detection methods have been developed. To have an effective treatment options as well as the importance of critical biomarkers. However, miRNAs shows significance for early detection and diagnosis. It divulges to have great potentials as prognostic biomarkers in pancreatic cancer. miRNAs are small non-coding RNA with 18-22 nucleotides in length that have been known to be associated with tumorigenesis. It is also linked to apoptosis, cell cycle control, proliferation, chemoresistance, metastasis and invasion. This miRNAs modulates key targets and pathways in signaling as well as its unusual expression are associated with chemoresistance.
In terms of chemotherapeutic treatment of pancreatic cancer miRNAs elevated expression inhibits the anti-tumor activity. miRNAs is related to gemcitabine resistance by inhibiting tumor suppressor gene phosphatase and tensin homologue thereby activating the PI3K/AKT pathway. It is also showed that miRNAs expression correlates with prolong overall survival benefits from chemotherapeutic treatment. Additionally, down regulation of miRNAs is responsible for progression of various malignancies including pancreas, breast, prostate, lung and liver cancer. It contains anti-cancer role via modulating targets implicated in cell cycle, apoptosis and DNA repair.
Therefore, it is clear that pancreatic cancer utilizes various mechanisms to maintain a highly resistant phenotype. miRNAs epigenetic controls allow cells to quickly adapt to the genotoxic stress caused by chemotherapy. It is also quickly modulates the mRNA translation in pancreatic cancer cells in response to chemotherapeutic treatment. As a result, various kinds of miRNAs showed great potentials as prognostic biomarkers in pancreatic cancer. Optimistically, these biomarkers will form a solid foundation to have better clinical treatment strategies.To avoid toxicity and enhance the survival rate benefits.
Source: Prepared by Joan Tura from Springer BMC Biomarkers Research
Volume 6:18, 2018
When someone says “I could die of a broken heart…”, chances are, that person may be truly risking life from a broken heart – a condition referred to as broken heart syndrome. The emotional agony can be likened to a physical pain. Apparently, it was only recently that it gained stalwart attention from researchers as they began to probe the pathobiology behind a broken heart syndrome.
Broken heart syndrome – overview
Hearing stories of a person in severe emotional distraught from a loved one’s death and then died not long after is not uncommon. How much of losing a loved one, a gut-wrenching rejection, or an austere betrayal could lead to death no longer surprise us. Deep sorrow certainly takes a toll. Death is inevitable but dying from a broken heart syndrome is something that is treatable and preventable, thus, is escapable. Inopportunely, the pathobiological aspect of a broken heart syndrome has not been fully unmasked. What is known about it so far is the fact that severe emotional stress is capable of triggering the transient weakening of the heart muscle, turning the latter fatally dysfunctional.
Pathology of Broken heart syndrome
The medical term for broken heart syndrome is takotsubo cardiomyopathy. The condition was first described in Japan in 19901 and the name is derived from”takotsubo“, which when translated means an “octopus trap“. It is so because the left ventricle of the heart of a person with broken heart syndrome is shaped like a contraption pot used for catching octopuses. Its apex balloons or bulges out while its base remains as is. As a result, the heart with temporarily enlarged apical ventricle cannot function as it should. Consequently, blood is not pumped properly and this leads to angina (chest pain) and shortness of breath, which are symptoms typical of a heart attack. Because of this, broken heart syndrome can be easily mistaken as a heart attack. The difference lies in the arteries. A true heart attack is due to an occlusion in the artery. In broken heart syndrome, arteries are not obstructed. Also, the ventricle is only temporary dysfunctional and therefore may normalize again if given enough time to rest and recuperate.
Biology of a broken heart syndrome
Unraveling the mysteries of broken heart syndrome is a recent biological pursuit. Consequently, the precise mechanism is not yet clear. Experts presume a surge in adrenaline and other stress hormones since the condition is often associated with emotional stressful events (n.b. it has also been reported to happen during euphoric events, e.g. winning a lottery). The overwhelming presence of these hormones might have stunned the heart and triggered structural changes in the myocytes and/or the coronary blood vessels.2 In a study published in Psychoneuroendocrinology, researchers found that bereaved individuals have higher levels of pro-inflammatory cytokines.3
A person who went through a broken heart syndrome and survived it could attest how the struggle had been real. Having to go through an intensely stressful event could plausibly cloud one’s drive and enthusiasm for life. Research on the pathobiology behind broken heart syndrome is understandably new, and as such inadequate for now.
— written by Maria Victoria Gonzaga
1 Akashi, Y.J., Nef, H.M,, Möllmann, H., & Ueyama, T. (2010). “Stress cardiomyopathy”. Annu. Rev. Med. 61: 271–86. Doi:10.1146/annurev.med.041908.191750
2 Harvard Women’s Health Watch. (2018). Takotsubo cardiomyopathy (broken-heart syndrome). Retrieved from https://www.health.harvard.edu/heart-health/takotsubo-cardiomyopathy-broken-heart-syndrome.
3 Fagundes, C.P., Murdock, K.W., LeRoy, A., Baameur, F., Thayer, J.F., & Heijnen, C. (2018). Spousal bereavement is associated with more pronounced ex vivo cytokine production and lower heart rate variability: Mechanisms underlying cardiovascular risk? Psychoneuroendocrinology 93:65-71. doi: 10.1016/j.psyneuen.2018.04.010.
Imagine a child inside a womb with a sex yet to be decided not by the pair of sex chromosomes but by the ambient temperature – well, that is how the sex of red-eared slider turtle (Trachemys scripta elegans) and other reptile species is determined. Whether the baby red-eared slider turtle develops into a male or female will depend on the ambient temperature of the nest. The eggs hatching from a cooler nest will be males whereas those in a warmer nest will be females. Nevertheless, scientists recently identified the molecular basis associated with the temperature-dependent sex determination in red-eared slider turtle.
Temperature-dependent sex determination in red-eared slider turtle
In humans, the sex of the offspring is determined by the pair of chromosomes inherited from the parents. At fertilization, the sex of the embryo is already determined. A female embryo would have two X chromosomes whereas a male embryo would have X and Y chromosomes. This mechanism of sex-determination is referred to as genotypic sex determination (GSD). This is also how the sex of many animals, including certain reptiles, is determined. Another mechanism is temperature-dependent sex-determination (TSD). It is when the temperature predicts the sex of the developing embryo. This is observed in many reptiles, such as crocodiles, alligators, and turtles. In red-eared slider turtle, for instance, their sex can be predicted depending on the incubation temperature. There is a critical period during which the embryonic development is thermosensitive. Red-eared slider turtle eggs hatching from cooler nests will all be males whereas those hatching from warmer nests will all be females.1
Molecular basis of sex-determination in red-eared slider turtle
How the temperature causes the baby red-eared slider turtle to turn into male or female is a long-time enigma. The phenomenon of TSD was observed for more than 50 years ago and since then scientists have attempted to dig further into the molecular level of TSD. Are there genes involved in the process, and if there are, which genes? Researchers from Duke University and Zhejiang Wanli University in China published their study on red-eared slider turtle.2 Eggs incubated at 32 °C hatched as females while those incubated at a cooler temperature (26 °C) hatched as males. When they silenced the Kdm6b gene the eggs that supposedly would develop into males at a cooler temperature (26 °C) hatched as females. Knockdown of Kdm6b red-eared slider turtle babies developed ovaries rather than testes.
The molecular role of red-eared slider turtle Kdm6b gene
Kdm6b gene appears to be the key gene essential to turning on the switch of “maleness” in red-eared slider turtle. The activity of this gene is vital during the critical period of gonad development. It became more active at cooler incubation temperature and then “silent” at a warmer temperature. 1 The gene promotes directly the transcription of the male sex-determining gene, Dmrt1. It does so by coding for a protein that removes the trimethylation of the histone, H3K27, near the promoter region of Dmrt1. 2 The methyl tags of the histone repress DNA activity and therefore removing them would allow expression of the genes along the DNA molecule.
This study was unable to identify the temperature-sensing trigger since the Kdm6b and its protein were not inherently sensing temperature changes. 1 For now, the molecular basis of the temperature-dependent sex-determination in the red-eared slider turtle as described above has not reached completion. Nonetheless, what was currently discovered in the red-eared slider turtle may serve as a model to understand the underlying mechanism in other reptile species where the temperature is a major sex-determining factor.
— written by Maria Victoria Gonzaga
1 Duke University. (2018). How turning down the heat makes a baby turtle male: Scientists start to crack 50-year puzzle of how temperature influences a hatchling’s sex. ScienceDaily. Retrieved from www.sciencedaily.com/releases/2018/05/180510203722.htm
2 Ge, C., Ye, J., Weber, C., Sun, W., Zhang, H., Zhou, Y., Cai, C., Qian, G., & Capel, B. (2018). The histone demethylase KDM6B regulates temperature-dependent sex determination in a turtle species. Science 360 (6389): 645.
Respiratory failure is an outcome from inadequate gas exchange wherein arterial oxygen and carbon dioxide not at normal levels. A drop of oxygen is called hypoxemia while the rise in arterial carbon dioxide is hypercapnia. Respiratory failure includes abnormal blood gases, increased of breathing and increased respiratory rate. In obstetric patients a complicated conditions occurs resulting to various complications and several physiological changes. That is why risk of complication in pregnancy with respiratory failure considered challenge for positive maternal and neonatal outcomes.
Causes in Maternal Respiratory failure
The main causes of respiratory failure were postpartum hemorrhage, peripartum period, preeclampsia and pneumonia during pregnancy. In which the oxygen reserve impairment during pregnancy causes fast desaturation leading to fetal hypoxia. Many of the patients showed improvement after delivery in partial pressure of arterial oxygen. But some exhibited high incidence of neonatal respiratory distress syndrome. Neonatal complications were commonly caused by sepsis and meconium aspiration syndrome as well as impairment in neurological development.
Acute respiratory distress syndrome is classified as mild to severe injuries from aspiration, trauma and multiple transfusions. It is also a condition of newborn having dyspnea with cyanosis that is often related to surfactant deficiency. However, preterm infant retinas showed incomplete retinal vascularization. On the other hand obstetric patients showed 74% having maternal respiratory failure complications while 25.4% to non-obstetric patients.
Indeed, early delivery might improve maternal oxygenation and reduce mortality rate. However maternal respiratory failure may not always improve after the delivery wherein deleterious sepsis and lung injury persist after delivery. Additionally a detailed examination is needed to follow up the neonates in the future. Using the risk categories whether normal, questionable and abnormal, if the mental developmental index is <70 then the neonates are suspected to have mental retardation.
Source: Prepared by Joan Tura from Journal of the Formosan Medical Association
Volume 117, Issue 5, May 2018, Pages 413-420