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
Epstein-Barr virus — the virus causing the kissing disease or mononucleosis — is eyed as a risk factor for contracting seven other major diseases. This is what the research team at Cincinnati Children’s Hospital Medical Center reported. The Epstein-Barr virus is contracted by kissing or by the oral transfer of saliva. Apparently, once the Epstein-Barr virus infects the body it stays there forever.
Epstein-Barr virus and mononucleosis
The Epstein-Barr virus belongs to the herpes family, Herpesviridae. It contains DNA that bears 85 genes and is surrounded by a nucleocapsid. Apart from the nucleocapsid, the virus is further bounded by a protein tegument and an outermost layer of a lipid envelope. The envelope has glycoprotein projections, which are crucial for the virus during its infection of the host cell.1 B cells, the immune cells producing antibodies, are ought to destroy them. However, the Epstein-Barr virus can outwit them by a slick mechanism. The virus invades the B cell, reprograms it, and makes it “follow” its “commands”. The virus is known for causing mononucleosis or the kissing disease. The common symptoms include fever, fatigue, sore throat, rash, and swollen lymph nodes, especially in the neck.
Epstein-Barr virus and the seven major diseases
According to the study led by three scientists, John Harley, Leah Kottyan, and Matthew Weirauch, the Epstein-Barr virus infection has been implicated to seven unrelated serious diseases.2 Previous studies by Dr. Harley and his team have already connected Epstein-Barr virus with the increased risk of developing systemic lupus erythematosus years ago. Recently, however, they found that the virus could also augment the risk of developing other serious diseases, such as multiple sclerosis, type 1 diabetes, inflammatory bowel disease, celiac disease, rheumatoid arthritis, and juvenile idiopathic arthritis.3 A person contracting the Epstein-Barr virus has a greater risk of developing them. This is because the virus produces a protein, Epstein–Barr virus nuclear antigen 2 (EBNA-2), that interacts with the human DNA, especially at genetic risk variants. 2 A genetic risk variant pertains to a variant in the DNA genome that has a potential to cause disease(s).
Epstein-Barr virus and future research
Dr. Harley and his team suspect that the EBNA2 protein from the Epstein-Barr affects a set of transcription factors. Accordingly, what the seven seemingly unrelated diseases share in common is a set of dysfunctional transcription factors, each affected by the EBNA2 protein.2 When the activity of transcription factors deviate from what they are supposed to do, the host cell (such as B cell) would not be able to carry out its normal function. This, in turn, could progress to certain diseases. With their recent finding, Dr. Harley and his team are optimistic that further intensive research could direct to finding better therapies and preventive methods such as vaccines against Epstein-Barr virus infection.
This recent finding suggests that contracting Epstein-Barr virus can lead to multiple diseases apart from mononucleosis. Therefore, this calls for more studies that aim at finding better cures and preventive measures. Currently, there is no vaccine against Epstein-Barr virus; being able to boost our immunity against the virus may help mitigate the risk to many other diseases, such as those mentioned above.
— written by Maria Victoria Gonzaga
1Odumade, O.A., Hogquist, K.A., & Balfour Jr., H.H. (2011). “Progress and Problems in Understanding and Managing Primary Epstein–Barr Virus Infections”. American Society for Microbiology. 24 (1): 193–209. doi:10.1128/CMR.00044-10
2 Harley, J.B., Chen, X., Pujato, M., Miller, D., Maddox, A., Forney, C., Magnusen, A.F., Lynch, A., Chetal, K., Yukawa, M., Barski, A., Salomonis, N., Kaufman, K.M., Kottyan, L.C., & Weirauch, M.T. (2018). “Transcription factors operate across disease loci, with EBNA2 implicated in autoimmunity.” Nature Genetics. DOI: 10.1038/s41588-018-0102-3
3 Cincinnati Children’s Hospital Medical Center. (2018). ‘Mono’ Virus Linked to Seven Serious Diseases. Retrieved from https://www.cincinnatichildrens.org/news/release/2018/mono-virus.
Celiac disease is a condition that affects the digestive systems of many individuals all over the world, and in this article, the goal is to explain it in a way that anyone can understand what’s really happening. We might even include some intense action (like in the movies).
The digestive system is a beautiful thing. We start breaking down that tasty food in our mouths by chewing it, and enzymes in our saliva even starts to break down the carbohydrates that are present in our food. It then takes the journey down your pharynx to your esophagus and ends up in the stomach. (more…)