Medicago sativa is a perennial flowering plants that belongs to a legume family. This plant is known in forage crop, grazing, silage, green manure and cover crop. Medicago sativa develops potential for medicinal uses and thrive mostly in an arid climate. The aim of this particular research is to determine the floral traits and pollinators visitation activities that affect pollen limitations. It also identifies possible effects of resource allocation on pollen supplementation and the impacts of pollen on flower opening.
Medicago sativa floral traits and pollinators
Plant reproduction is limited due to pollen resources, floral traits and pollinator activities. Medicago sativa was observed at about 120 hours by collecting pollens and nectars. The pollinator type was then noted. It was then recorded the visitation frequency and behavior of flowers based on insects as effective pollinators or occasional pollinators. The pollinators then, captured using insect nets to find out the presence of pollen grains.
The result shows a positive relationship between pollinators visitation frequency and the number of open flowers. It also found out that, it is more efficient for pollinators to visits opening flowers. Since, filaments of Medicago sativa will dry easily particularly in an arid regions. Moreover, flowers of Medicago sativa was completely open and the pollen released between 09:00 to 14:00 hours. Additionally, some insects identified as effective pollinators because it can collect more pollen and visit more often. However, a reduction of pollinators will decline the amount of pollens and reduced the probability of cross pollen transfer.
Overall, this research found out that pollen resources is the limiting factor for the reproductive success of Medicago sativa. It also shows that resource reallocation can increase pollen limitation and plants might reallocate among flowers. However, insufficient pollen deposition is typically caused by pollinators assemblage, visitation and abundance. In which flowers is the main effects of resource limitations and pollinators plays an important role in outcrossing.
Source: Prepared by Joan Tura from BMC Ecology
Volume 18:28 August 29, 2018
One of the hallmarks of old age is vascular aging. Researchers found that a biomolecule, β-Hydroxybutyrate (BHB), can serve as a key to turning the time around. Apparently, BHB has anti-aging effects on the vascular system.
β-Hydroxybutyrate – a biomolecule
β-Hydroxybutyrate is a biomolecule with a chemical formula, C4H803. Many regard it as a ketone; however, under a strict definition, it would not technically fit as a ketone. That is because its carbonyl carbon binds to only one instead of two other carbon atoms. Nonetheless, BHB appears to be physiologically related to other ketone bodies (such as acetate and acetoacetate) based on the metabolic aspect. For instance, the tissue level of BHB rises during calorie restrictions, fasting, prolonged intense workout, and when following a ketogenic diet.1 Accordingly, BHB level occurs the highest among the three circulating ketones in the body.
β-Hydroxybutyrate – biological sources
The body naturally produces BHB through the process of ketogenesis. Low-carb diet and fasting lead to the rise of BHB level. Firstly, the body breaks down fatty acids to produce acetyl CoA. This precursor goes through a series of reactions leading to acetoacetate synthesis. In turn, the acetoacetate circulates via the bloodstream, and subsequently reaches the liver. The BHB-dehydrogenase enzyme in the liver reduces the acetoacetate to BHB. 1
Another biochemical pathway that leads to the synthesis of this biomolecule uses butyrate. The body metabolizes butyrate and produce D-β-hydroxybutyrate through the aid of the enzyme, hydroxybutyrate-dimer hydrolase.
β-Hydroxybutyrate – biological action
In humans, D-β-hydroxybutyric acid is one of the major endogenous agonist of hydroxycarboxylic acid receptor 2 (HCA2), a receptor protein encoded by the HCAR2 gene. It binds to and activates HCA2. Upon activation, HCA2 can inhibit the breakdown of fats and mediates niacin-induced flushing. Moreover, it induces the dilation of blood vessels.
Based on recent research, BHB might serve as a biomolecule that could help turn time around for the vascular system. Old age faces an increased risk to cancer and cardiovascular diseases since the vasculature ages as well. Dr. Ming-Hui Zou, director at Georgia State University, explains. “When people become older, the vessels that supply different organs are the most sensitive and more subject to aging damage….”2
β-Hydroxybutyrate – vascular study
Zou et al. 2, 3 conducted a study on vascular aging, exploring the link between calorie restrictions and delayed vascular aging. Accordingly, calorie restrictions averted vascular aging.
They found that BHB, the biomolecule naturally produced from the liver, has anti-aging effects, particularly on endothelial cells. The endothelial cells line the interior surface of the vascular system. Based on the results, BHB promoted mitosis of endothelial cells, thus, pre-empting vascular aging.3 Furthermore, they saw that BHB binds to a certain protein, which stimulates a series of reactions that consequently rejuvenate, thus, keep the blood vessels young.2
BHB could eventually become a biomolecular tool that promotes mitosis of endothelial cells. In being able to do so, it could help prevent endothelial cell senescence. Hence, this potential rejuvenating effect on the vascular system may soon become valuable not just in keeping the blood vessels young but also in preventing cardiovascular diseases related to old age.
— written by Maria Victoria Gonzaga
1 Martins, N. (2018 Sept. 26). Beta-hydroxybutyrate or BHB –All You Need to Know. Retrieved from https://hvmn.com/blog/exogenous-ketones/beta-hydroxybutyrate-or-bhb-all-you-need-to-know
2 Georgia State University. (2018 Sept. 10). Researchers Identify Molecule With Anti-Aging Effects On Vascular System. Retrieved from https://www.technologynetworks.com/neuroscience/news/fasting-molecule-delays-vascular-aging-309380
3 Han, Y. M., Bedarida, T., Ding, Y., Somba, B. K., Lu, Q., Wang, Q., Song, P., & Zou, M.H. (2018). β-Hydroxybutyrate Prevents Vascular Senescence through hnRNP A1-Mediated Upregulation of Oct4. Molecular Cell, 71(6):1064-1078.e5. https://doi.org/10.1016/j.molcel.2018.07.036
We often hear that stress can be unsettling as it could make us ill when it becomes chronic and overwhelming. However, is there really a biological ratification behind it? Is it scientifically founded? Apparently, independent studies hinted a biological connection indicating how stress can cause biological damage, and eventually lead to certain ailments. And, the mitochondrial DNA — the genome in the mitochondrion appears to play a role.
Biological features of mitochondria
The mitochondrion (plural: mitochondria) is an organelle that supplies molecular energy for various biological activities. In essence, this rod-shaped structure found within the cell accounts for the generation of ATP, the cell’s major energy source. Thus, the mitochondrion is known to be the “powerhouse of the cell“.
Through the process of cellular respiration, glucose (a monosaccharide) is “churned” to extract energy, primarily, in the form of ATP. Firstly, a series of reactions leads to the conversion of glucose to pyruvate. Then, it uses pyruvate, converting it into acetyl coenzyme A for oxidation via enzyme-driven cyclic reaction called Krebs cycle. Finally, a cascade of reactions (redox reactions) involving the electron transport chain leads to the production of ATPs (via chemiosmosis).
The mitochondria have their own genetic material, called mitochondrial DNA. Because of this, the mitochondrion is regarded as semi-autonomous and self-reproducing organelle. It means it can manufacture its own RNAs and proteins. Generally, we inherit the mitochondrial genome maternally, as opposed to the nuclear genome that we inherit from both parents.
Mitochondrial fate during stress
When confronted with a stressful situation, our body responds intrinsically. We tend to breathe fast. The heartbeat goes wild. Our muscles tense up. And, we sweat profusely. All these responses (so-called “fight-or-flight“) can be an arduous task as they abruptly demand energy. When triggered for so long, eventually, we feel exhausted. Sooner or later, stress sets in and it takes its toll on our health.
The mitochondria work for an extended time just to meet up the spike of demand for energy. In effect, they become vulnerable to damage from too much work. Inopportunely, the mitochondria have limited repair mechanisms unlike the nucleus.1 And in the end, it results in the disruption of the organelle, thereby, releasing the mitochondrial DNA into the cytoplasm. Eventually, the genetic material reaches the bloodstream where they become genetic cast-offs.
Mitochondrial DNA cast-offs
The ejected mitochondrial DNA, apparently, becomes genetic wastes and stress might have something to do with this outcome. This theory came about based on a series of studies. Firstly, Gong et al. found that chronic mild stress resulted in mitochondrial damage in hippocampus, hypothalamus, and cortex in mouse brains.2
Secondly, another team of researchers (Lindqvist et al.) reported that individuals who had recent suicide attempt had higher plasma level of freely circulating mitochondrial DNA in blood than those of healthy individuals.3
Thirdly, Martin Picard (a psychobiologist at Columbia University), together with his team, observed similar findings in their participants exposed to a stressful situation. Accordingly, their participants – healthy men and women – were asked to defend themselves against a false accusation. Their blood samples were taken before and after the interview. The researchers found that the mitochondrial DNA in the serum of the participants increased twice 30 minutes after the test. 1 Picard explained that the mitochondrial DNA might have acted like a hormone. Furthermore, he theorized that the ejection of these genetic cast-offs might have mimicked the adrenal gland cells releasing cortisol in response to stress. 1
Mitochondrial DNA as an inflammatory factor
Zhang et al. observed that circulating mitochondrial DNA triggered inflammatory responses. Accordingly, the genetic cast-offs can bind to TLR9 (a receptor) on the immune cell. This binding might have incited the immune cell to respond the same way as they do when reacting with antigens. It might have stimulated the cell to release cytokines that call for other immune cells to the site. 1
So far, these conjectures from independent studies disclose the possible direct biological damage due to stress. There could be a biological insinuation that stress could play a part in the manifestation of ill-health conditions. And, the upsurge of circulating mitochondrial DNA cast-offs is one of them. More information and studies on mitochondrial DNA are delineated on a report on mental health published in Scientific American.
— written by Maria Victoria Gonzaga
1 Sheikh, K. (2018 Sept 13). Brain’s Dumped DNA May Lead to Stress, Depression. Scientific American. Retrieved from https://www.scientificamerican.com/article/brain-rsquo-s-dumped-dna-may-lead-to-stress-depression/
2 Gong, Y. Chai, Y., Ding, J. H., Sun, X. L., & Hu, G. (2011).Chronic mild stress damages mitochondrial ultrastructure and function in mouse brain. Neuroscience Letters, 488 (1): 76-80. https://doi.org/10.1016/j.neulet.2010.11.006
3 Lindqvist, D., Fernström, J., Grudet, C., Ljunggren, L., Träskman-Bendz, L., Ohlsson, L., & Westrin, Å. (2016). Increased plasma levels of circulating cell-free mitochondrial DNA in suicide attempters: associations with HPA-axis hyperactivity. Translational Psychiatry, 6 (12), e971–. http://doi.org/10.1038/tp.2016.236
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
Seaweeds are macroscopic multicellular algae that have been used as food since ancient time. It was originated in Japan and then China particularly to the people who lived near the coastal areas. In addition to its nutritional value, seaweeds are rich source of structurally diverse bioactive compounds including polysaccharides, phlorotannins and pigments. Because of this, the demand increases in the global trade wherein Korea is the major producers. In traditional Korean cuisines seaweeds used as soup, snack, pickle, vegetable and salad. Hence, this present research focuses on the edible green and red seaweeds found in Korea.
Green and Red Seaweeds Bioactive Compounds
Green seaweeds used to treat stomach disorders and hangovers because it contains 55% polysaccharides, 30% proteins, 13% ash and 1% lipids. It also have micro mineral such as calcium, manganese, iron, selenium, sodium, phosphate and potassium. Additionally, green seaweeds also used to treat wastewater and have significant medicinal value for rheumatism, high blood pressure and diabetes. In recent findings it has potentials bioactive properties to treat cancers and diabetes mellitus. Also it contains essentials oil to inhibit foodborne pathogens, anti-inflammatory, antioxidant and blood lipid reduction. Moreover, it has been used in traditional medicine for sunstroke, urinary diseases and hyperlipidemia. It is also useful to reduce eutrophication in mariculture waters that helps the survival rate productivity of shrimps and prawns.
Red seaweeds are the main source of hydrocolloids and contain vitamins A, B and C. It is also a rich source of carbohydrates particularly galactose and glucose. These red seaweeds are popularly known in agar production. And used as a raw material in bio-ethanol industry due to its high level of ethanol extraction efficiency. Likewise, both red and green seaweeds contain antioxidants properties due to its hydroxyl radical scavenging activity. That is responsible for neuro-protection against oxidative stress. In all, seaweeds have potential properties for anticancer, anti-diabetic, anti-obesity, anti-inflammatory, antimicrobial and anti-coagulant.
Therefore, seaweeds are vital source of food and medicine on different applications. The presences of secondary metabolites are potential to develop as functional materials due to its promising bioactive properties. Korea is one of the biggest consumers and producers wherein people mostly incorporate seaweeds on daily diets. This research suggests that increase consumption offers healthy benefits as well as utilization of seaweed materials as functional ingredients.
Source: Prepared by Joan Tura from BMC Fisheries and Aquatic Sciences
Volume 21:19, 6 April 2018
One of the crucial needs that arise during or after a devastating natural disaster is the availability of the “universal” blood type O. The increased demand for blood surges following the aftermath of a catastrophy. Storms, hurricanes, and earthquake calamities are major causes for an abrupt call for blood donations. Researchers from the University of British Columbia headed by Stephen Withers knew so well the gravity of this need that they are adamant in finding a way to somehow curb the limitations hampering the availability of a universal, friendlier blood type. Withers and his team recently identified a potential enzyme candidate that appears to be efficient and at the same time cost-effective in converting blood types into type O.
Blood group systems overview
The blood is the circulating fluid in our body that performs multifarious functions. Its major functions are for transporting nutrients, delivering oxygen, moves metabolic byproducts for excretion, providing immune defense, and homeostasis. It is comprised mainly of plasma (55%) and cellular elements (45%) (e.g. red blood cells and white blood cells). The red blood cells (RBCs) are the major cellular component of the blood and are essential for their role in delivering oxygen throughout the body. The white blood cells (WBCs), in turn, are involved in the detection of non-self particles (antigens) and the subsequent immune action against them.
Blood type (or blood group) is a classification system used to identify which type the blood belongs to. The blood type is determined based on the presence (or absence) and types of antigens present on the cell surface of the RBCs. Various blood classification systems are used to classify types; however, the ABO and the Rh systems are the most important ones. The ABO system is used to classify blood into types A, B, AB, and O. The Rh system, in turn, is used to denote blood as either positive (+) or negative (-) based on the presence and absence of the Rh factor, respectively.
Why type O blood?
Type O blood is considered as the universal blood because it has neither A nor B antigens on the surface of the RBCs. Type AB blood, in contrast, has both A and B antigens. If A antigens are present on the cell surface of the RBCs, the blood is typified as type A whereas type B has B antigens. Determining blood type is important because blood administered into the body that does not match with the innate blood type can trigger an immune response. Transfusion involving a blood type different from one’s own can instigate the WBCs of the body to attack the transfused blood cells, and this could lead to serious effects. Thus, an individual with type A (Rh-), for instance, can receive transfusions of type A (Rh-) and type O (Rh-). Based on this precept, type O (especially Rh-) can be administered to any blood type.
Metagenomics for creating a universal type of blood
Blood banks constantly need type O. Withers and his team focused their research works in searching for enzymes that can convert types A and B to type O by applying metagenomics. Accordingly, they found enzymes from the human gut that apparently can turn type A and B into O as much as thirty times more efficiently than previously identified enzymes.1 Withers said, “We have been particularly interested in enzymes that allow us to remove the A or B antigens from red blood cells. If you can remove those antigens, which are just simple sugars, then you can convert A or B to O blood.”
In reaching their goal, they focused on mucins, which are glycoproteins secreted by the mucous membranes in the gut wall. These mucins in the gut wall display a number of sugars, including antigen A and antigen B. They found that the gut microbiome can cleave these sugars from the gut wall and use them as food source. Using metagenomics, they identify genes from these gut microbial species that code for proteins that cleave target antigens on the cell surfaces of RBCs. Thus, type A blood, for instance, can be converted into type O blood through the enzymes that remove antigen A from the RBCs. The goal is to identify the most economical, most efficient, and safest enzyme that can be used to turn donated blood into a particular type as needed.
Disastrous events take so much of human properties and lives. Apart from the apparent destruction of homes and livestock as an aftermath of natural calamities, blood donations become crucial to save lives of the people needing blood transfusions. Suddenly, life takes a stance on the edge between survival and death. Blood transfusions have to be extensive, safe, and economical. Although research on how to turn blood types into a more universal type has still a long way to go before it can be approved for medical use, this is a significant development.
— written by Maria Victoria Gonzaga
1 American Chemical Society. (2018, August 21). Gut bacteria provide key to making universal blood (video). American Chemical Society.. Retrieved from https://www.acs.org/content/acs/en/pressroom/newsreleases/2018/august/gut-bacteria-provide-key-to-making-universal-blood-video.html?_ga=2.17288057.1746138702.1535160738-1328130083.153516073
Scientists are excited over a gene-silencing drug that recently won an approval from the US Food and Drug Administration (FDA). This approval is historic because it is the first of its kind. The drug works by silencing genes that otherwise lead to the production of damaged proteins associated with certain diseases. The drug is called patisiran and it recently got its approval for use to treat the hereditary transthyretin amyloidosis, a fatal rare hereditary condition associated with damaged nerves.
Gene basis of hereditary transthyretin amyloidosis
The hereditary transthyretin amyloidosis is a rare and fatal hereditary condition that manifests as an autosomal dominant neurodegenerative disease. Because it is dominant, this means that the offspring inheriting the defective autosomal gene will acquire the condition. A defective transthyretin (TTR) gene located on human chromosome 18q12.11 is the genetic cause. The most common type of mutation is the replacement of valine by methionine at position 30.
A normal, functional TTR gene codes for transthyretin (TTR) protein that is involved in the transportation of thyroxine (thyroid hormone) and retinol (vitamin A). TTR protein is produced mainly in the liver, and is then secreted into the bloodstream. TTR proteins from a defective TTR gene tend to misfold and stick together, forming amyloids. This building-up of amyloids in tissues is called amyloidosis. In hereditary transthyretin amyloidosis, pathogenic amyloids form especially in the peripheral nervous system, which may eventually lead to a progressive sensory and motor polyneuropathy.
Gene silencing by RNA interference
Normally, the cell performs what is now known as RNA interference (RNAi). It is also known as quelling, co-suppression, and post-transcriptional gene silencing. In this process, the RNA molecules inhibit the translation of a gene. They do so when they neutralize targeted mRNA molecules. RNAi is different from CRISPR, which is a gene-editing tool that makes use of a guide RNA. CRISPR is used to switch off a gene and has a potential therapeutic use to treat cancers. It also had FDA approval in 2016 for use in a clinical trial study. However, recent studies on CRISPR raised issues about its safety since it was found to cause unexpected mutations that involve large deletions and complex genomic rearrangement at target sites.2 To learn more about CRISPR, read: CRISPR caused gene damage? … Unlike CRISPR, the RNAi is presumed not to bring permanent changes to DNA.3
Patisiran as gene-silencing drug
Patisiran is RNA-based drug that recently received the first FDA approval for use as a gene-silencing tool. People with hereditary transthyretin-mediated amyloidosis can now be treated with it. The drug interferes with the production of transthyretin. It doses so by preventing the mRNA involved in the translation of the gene that codes for the problematic protein. This is good news to people with such fatal rare condition. FDA has now approved a drug that can be administered to them. The downside, though, is the chillingly high cost. The cost of the therapy is estimated to be about $450,000 in a year.4
New therapeutic technologies that delve into the molecular and gene mechanisms hold so much promise especially in conditions that until now lack an efficacious treatment. RNAi is a precise gene-silencing tool and scientists are excited in its historic FDA approval. This means that it is a glorious start for contemporary therapies involving targeted gene silencing and alterations. The cost of the therapy may be encumbering but it is still a step forward, certainly a scientific feat to reckon.
— written by Maria Victoria Gonzaga
1 TRANSTHYRETIN; TTR. (n.d.). OMIM.org. Retrieved from https://omim.org/entry/176300
2 Gonzaga, M. V. (17 July 2018). CRISPR caused gene damage? Rise and pitfall of the gene-editor. Biology-Online.org. Retrieved from https://www.biology-online.org/crispr-caused-gene-damage-rise-pitfall-gene-editor/
3 Nield, D. (14 Aug. 2018). A First of Its Kind Gene-Silencing Drug Just Got Historic Approval From The FDA. ScienceAlert. Retrieved from https://www.sciencealert.com/first-drug-silencing-genes-approved-by-fda-for-disease-treatment
4 Lipschultz, B. & Cortez, M. (10 Aug. 2018). Rare-Disease Treatment From Alnylam to Cost $450,000 a Year. Bloomberg. Retrieved from https://www.bloomberg.com/news/articles/2018-08-10/alnylam-wins-first-u-s-drug-approval-in-rare-genetic-disease
Colon Cancer is the third most deadly cancer worldwide. There were more than 1.4 million cases each year and 694,000 deaths globally. The treatment of colon cancer includes chemotherapy, surgery and radiation therapy. However, advances in diagnosis and treatment leads to development and improvement in survival. Numerous data point out that genetic changes function as vital role in the development of colon and rectal cancer. In which regulatory molecules mRNA affects various molecular and cellular target including cancer cells. That is why, development in research used mRNA as based diagnostic biomarkers for colon cancer in human. Furthermore, certain kind of mRNA used to predict survival in colon cancer patients. As well as a better knowledge of molecular mechanisms and associated gene is important for early diagnosis and treatment.
ULBP2 a novel prognostic biomarker in Colon Cancer
ULBP2 is a potential biomarker in colon cancer survival. Previous study shows that matrix metalloproteinase-9 reveals as an important marker for postoperative prognosis in colorectal cancer patients. Also extracellular matrix plays a vital role in cancer progression in which it provides structural and biochemical support in cells. Despite from all of these, digestion is also considered to have a major role related to cancer preventive activity. Additionally, an in vitro of peptides gastrointestinal digestion can inhibit colon cancer cells proliferation and inflammation. Moreover, recent study showed that up and down regulated mRNAs are largely amass in extracellular matrix and digestion. As a result, it would entails that abnormality of extracellular matrix and digestion takes part in colon cancer progression.
Furthermore, the Wnt signaling pathway gives clinical importance on various diseases including colon cancer. Since alteration of this pathway are mostly observed in colorectal cancer with microsatellite instability. So, inhibiting this pathway might be helpful strategy for targeting chemotherapy-resistance cells. Also drug metabolism determined resistance of colorectal cancer resorcinol-based heat shock protein 90 inhibitors. Therefore, Wnt signaling and drug metabolism are both important pathway enriched by up and down regulated mRNAs.
Prognostic biomarkers are very important and have the power to change the course of disease if only knew beyond prognostic factors. In this research ULBP2 gene that encodes cell surface glycoprotein located at chromosome 6 demonstrates prognostic biomarker for colon cancer. High level of ULBP2 is deemed independent indicator for overall survival and identified as the sole outstanding mRNA.
Source: Prepared by Joan Tura from BMC Biological Research
Volume 51:10 March 29, 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