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Category: Research

Poor motherly care for newborn linked to a father’s gene?

Scientists from Cardiff University’s School of Biosciences reported that a father’s gene may have an impact on the quality of care that is furnished by the mother to her newborn offspring. One of the most crucial roles of a mother is being able to provide and attend to the needs of her offspring, especially during the time of conception up to the time of nursing the offspring. Good quality maternal care is essential to ensure a healthy development of the newborn and the recent study on mice suggests that a father’s gene may have an effect on the mother’s nurturing behavior towards her offspring before and after they are born.



Imprinting of genes

In humans, the zygote is a diploid cell that results from the union of two haploid sex cells. This means that the zygote will possess two copies of the genome, i.e. one coming from the mother and the other one from the father. The autosomal genes of the zygote would therefore occur in pairs or as two copies. Their expressions occur simultaneously except for a few genes whose expressions will depend on the parent-of-origin.  Depending on the parent source, one of the gene copies will be imprinted, which means it will be ”silent”. For example, a father’s gene that is imprinted will be “silent” and will not be expressed but the other copy of the gene (from the mother) will be expressed, or “vice versa“. This phenomenon is called genomic imprinting.  An imprinted gene is one in which the DNA is methylated. A methylated gene means that its expression is suppressed.1



Phlda2 gene – overview

Pleckstrin homology-like domain family A member 2 (Phlda2) gene is an example of a gene whose expression accords to the phenomenon of genomic imprinting. The gene is located in the cluster of imprinted genes on chromosome 11p15.5.2 It encodes for the Phlda2 protein. It was also found that only one copy of the Phlda2 gene is “switched on” and that the other copy of the gene that is “silent” comes from the father.3 In rodents, one of its physiological roles is identified to be associated with the regulation of the activity of the placental cells called spongiotrophoblasts, which are cells responsible for the production of placental hormones. It was reported that the Phlda2 gene controls their size, and therefore their hormone production activity. 3




Phlda2 gene – impact on mother’s behavior

Phlda2 gene activity may have an effect on the maternal care behavior


Scientists from Cardiff University’s School of Biosciences found that female mice carrying pup embryos with two active Phlda2 genes, and thus with relatively higher Phlda2 levels and probably reduced placental hormone activity, exhibited decreased nursing and grooming of pups but with an increased focus in nest building. On the contrary, mothers carrying pup embryos with lower Phlda2 levels were more focused at nurturing their pups than on nest building. They also identified corresponding changes in the brain regions essential for maternal care behavior (particularly, hippocampus and hypothalamus) of the mothers during pregnancy. Their findings implicate that the Phlda2 gene activity may have an effect on the maternal care behavior of mice.3



Based on the recent findings, scientists speculate that Phlda2 gene activity may also have an impact in human pregnancies.  Many regard motherhood as an epitome of a woman’s existence. Apparently, there are instances when the quality of maternal care provided to the child is inadequate due to various factors. If these findings are relevant to humans, then, this is a potential aspect to probe in order to understand the biology of maternal care behavior – one that involves Phlda2 gene.



— written by Maria Victoria Gonzaga



1 Genomic imprinting. (n.d.). Biology-Online Dictionary. Retrieved from
2 PHLDA2 pleckstrin homology like domain family A member 2 [Homo sapiens (human)]. (8 July 2018). National Center for Biotechnology Information, U.S. National Library of Medicine. Retrieved from
3 Creeth, H.D.J., McNamara, G.I., Tunster, S.J., Boque-Sastre, R., Allen, B., Sumption, L., et al. (2018). Maternal care boosted by paternal imprinting in mammals. PLoS Biol, DOI: 10.1371/journal.pbio.2006599

Parental chromosomes are together but still apart at first mitosis

A recent finding by a team of researchers from European Molecular Biology Laboratory on the parental chromosomes during the first mitosis of an embryo implicates a possible revision in biology textbooks. What they observed during the first mitotic division after the supposed “union” of gametes in mouse models apparently invalidates what is currently believed. Biologists assume that there is only one spindle apparatus that works to separate the two parental chromosomes during the first cell division of a mammalian zygote. It turns out that there are two. Their finding could also help explicate the common errors occurring during the first divisions in the early embryos of mammals, and possibly of humans.



Early model of mitosis in mammalian zygote

Mitosis of a human cell. In this image, the microtubules are shown in green, chromosomes (DNA) in blue, and kinetochores in red.


The first mitosis in mammals occurs during the union of male and female chromosomes. Upon fertilization, the zygote holds two parental chromosomes that unite, and then separated, triggering the formation of two cells (each with own nucleus) after the first mitosis. This marks the two-cell stage embryo.

The first mitosis is thought to proceed initially by the break-down of the nuclear envelope. This enabled the two parental chromosomes to unite thereafter. A single spindle assembly then forms. The spindles attach to the chromosomes, align them at metaphase, and then pull them apart during anaphase. The first mitosis ends at telophase where the cell divides into two cells, each with its own nucleus.



Viewing first mitosis through light-sheet microscopy

Researchers from European Molecular Biology Laboratory found out that there is not one but two spindle apparatus at work during the first mitosis of the mouse embryo. Using a light-sheet microscopy approach, they were able to conduct real-time, 3D imaging of the mouse embryo.1 Without this innovative technology, capturing an image at this stage will not be feasible because embryos are sensitive to light. With it, the researchers were able to track the chromosomes during the supposed union and saw differently what has long been held. They were surprised to find out that (1) the maternal and the paternal chromosomes assembled their own autonomous spindle structure and (2) the parental chromosomes remain in separate regions and did not mix prior to and during the first mitosis.1,2



Current model of first mitosis

Based on the current mouse embryo model, what transpires at first mitosis after the nuclear envelope disintegration post-fertilization event is that both the maternal and the paternal chromosomes form their own spindle apparatus. The mitotic spindles then attach to the chromosomes. Even so, the maternal and the paternal chromosomes remain in separate regions of the spindle. The spindles align them in a way that the maternal chromosomes align juxtapose to where the paternal chromosomes align. The two spindle apparatus then autonomously pull them apart towards opposite poles. The cell finally divides into two, where each has only one nucleus. Conversely, an erroneous axis alignment of paternal chromosomes during metaphase was observed to lead to the formation of one of the cells with multiple nuclei after the first mitosis.

The recent findings could help explain certain errors (e.g. multiple-nucleated cell) following the first mitosis. If this mechanism holds true to humans as well it could lead to new targets for treatment (particularly an erring first mitotic spindle apparatus) in a developing embryo. It might also provide an insight as to when life can be assumed to first exist — is it during the first meet-up of the male and the female chromosomes that do not mix yet… or is it that point at which they unite — but apparently occurs only after the first mitosis.



— written by Maria Victoria Gonzaga





1 Reichmann, J., Nijmeijer, B., Hossain, M. J., Eguren, M., Schneider, I., Politi, A.Z., Roberti, M.J., Hufnagel, L., Hiiragi, T. & Ellenberg, J. (2018). Dual-spindle formation in zygotes keeps parental genomes apart in early mammalian embryosScience. DOI: 10.1126/science.aar7462

2 Zielinska, A.P. & Schuh, M. (2018). Double trouble at the beginning of life. Science  361 (6398): 128-129. DOI: 10.1126/science.aau3216

Colon cancer : Independent prognostic genes and mechanisms

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

Role of selenium-fortified yogurt against aflatoxin-contaminated nuts

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



CRISPR caused gene damage? Rise and pitfall of the gene-editor

CRISPR as a gene editing tool made a prodigious leap forward in science. In 2015, it was heralded as Science’s 2015 Breakthrough of the Year.1 It stymied other impressive contenders like Ebola vaccine. It supersedes other gene-editing predecessors, such as TALENs (transcription activator-like effector nucleases) and ZFNs (zinc finger nucleases). Unlike these two, CRISPR does not need a custom protein for every targeted DNA sequence. It does, however, require a guide RNA (gRNA). Even so, the process of designing a gRNA is easier and less time-consuming than creating a custom protein. For that, it is favoured over other gene-editing tools.



The rise of a revolutionary gene-editing tool — CRISPR

CRISPR-Cas9 – a customizable tool that cuts and inserts small pieces of DNA at specific areas along a DNA strand. (Credit: Ernesto del Aguila III, National Human Genome Research Institute, NIH)


The discovery of CRISPR was indeed phenomenal. Short for clustered regularly interspaced short palindromic repeats, CRISPR swiftly opened avenues for biological and medical innovations. Initially identified as a family of viral DNA snippets, it was discovered to inherently protect bacteria against re-invading bacteriophages akin to our immune system’s adaptive immunity. This natural gene-editing system in bacteria has two key players: gRNA and Cas9 (CRISPR-associated enzyme). The gRNA finds and binds to specific DNA target. The Cas9 goes where the gRNA is, and then cuts the DNA target, disabling the latter. Now, scientists exploit it as a way to splice specific DNA targets and then replace them with a DNA that would yield the desired outcome. For instance, CRISPR can be used to correct physiological anomalies caused by gene mutations or defective genes.

CRISPR-Cas9 system. (Credit: marius walter, Wikimedia Commons under CC BY-SA 4.0 Int’l license)




CRISPR – a versatile gene-editing tool

CRISPR has been shown to have the potential to slow down the progression of cancers. It can switch off a gene in immune cells. The altered immune cells can be designed to fight cancer. In 2016, US FDA approved the clinical trial study where CRISPR technology would be used to cure patients with cancers. 2 Not only in biology and medicine, the use of CRISPR has also extended to agriculture and animal husbandry. Through it, the genes of crops and livestock can be improved. They can be made more resistant to certain diseases.




CRISPR causing gene damage?

One of the issues raised against CRISPR is ethical concerns. Similar to what was ethically raised against other gene-editing technologies, the concern is chiefly about the notion of bias and “playing God”. What are the standards that will define and permit judgment over a gene to be construed as either “good” or “bad”? But taking aside this issue, there is another issue being hurled against CRISPR. Marked of recent as “breaking news”, a study published in Nature warned about the possible pathogenic consequences of CRISPR when the researchers identified on-target mutagenesis in the form of large deletions and complex genomic rearrangements at target sites in mitotically active cells of mice and humans.3 This is not the first time that a study questioned the safety of CRISPR technology. In 2017, researchers from Columbia University reported that it led to hundreds of unexpected mutations. Nevertheless, this claim was retracted when they failed to replicate their results.4



CRISPR as a gene-editing tool wields so much potential beyond one can imagine. It is easy to use, feasible, and far-reaching. One can expect that issues would come along the way, and thus slow down its fast-paced utilization in different fields. It is a no-nonsense stumbling block for we belong in a community that moves forward through social discourse fueled by scientific nosiness and reasoning. Probing the dangers of CRISPR should be as extensive as exploring its benefits. We must be not too quick to adulate without first bringing out in the open its risks — especially ones that are as crucial as mutations and gene damage.



— written by Maria Victoria Gonzaga




1 Science News Staff. (2015). And Science’s 2015 Breakthrough of the Year is… Retrieved from

2 Reardon, S. (2016). First CRISPR clinical trial gets green light from US panel. Retrieved from

3 Kosicki, M., Tomberg, K. & Bradley, A. (2018 July 16). Repair of double-strand breaks induced by CRISPR–Cas9 leads to large deletions and complex rearrangements. Nature Biotechnology.

4 Dockrill, P. (2018 July 16). BREAKING: CRISPR Could Be Causing Extensive Mutations And Genetic Damage After All. Retrieved from

Impacts of millennium drought on butterfly faunal dynamics

Butterflies are flying colored wing insects that vary in color and pattern from individual to another individual. It has wings covered with overlapping rows of scales. Most of butterflies have developed mechanisms to   avoid predators making disguise coloration blending like leaf or bark of the tree. Some releases chemicals as a defense mechanism wherein butterfly evolved to have toxic chemicals. But recent finding due to extreme weather events and trend linked to ongoing anthropogenic climate change species shifts its dynamics. Droughts occur more often in larger spatial scale which has an effect on insects. Generally, drier and warmer climatic conditions have an impact either positive or negative to insect populations. The aim of this research is to address the knowledge gap using multi-decadal dataset of 163 butterfly species. All of this butterflies experienced millennium-scale drought.


Impacts of droughts on Butterflies

To know the faunal dynamics, investigation of phenology, species richness and diversity with its elevation gradient has been conducted. In which linear model used to understand differential sensitivity of butterflies to climate change at low and high elevation. A decade of dataset of 163 butterfly species across elevational gradient in Northern California has been considered. Results showed that a prolonged shift towards spring flight during drought years and change in phenology is evident across elevations. It also happened that the total flight window expanded at lower elevations while at higher elevation shifted and compressed. This leads the notion that fewer overall flight days at higher sites.


The millennium drought in California created across site with elevation-specific changes in flight windows and species richness. This resiliency reveals that lowest elevations are less detrimental than biotic-abiotic association at higher elevations. Most of the researchers hypothesized a mismatch between trophic levels as a result of climate change. But, results of butterflies from low elevation would suggest that at consumer trophic level need not always have negative impacts. Additionally, species at lowest elevations have access to agricultural lands though irrigation does not correlate the population dynamics during drought. Thus, there is a possibility that low elevation population buffered by irrigated crops or agricultural margin during drought.


Indeed, that at high elevation butterflies declined in number and become sensitive to dry years with warmer temperatures. Contrary to the theory that mountains offer microclimatic refugia and adapt species for climatic changes. It has been known that high latitude environments are warming faster with negative consequences to several species. But positive or have a neutral effect for other species. Consequently, this research suggests more thorough investigation about organismal responses to extreme weather. As well as on the extent wherein different habitat type may or may not buffer species populations against climate change.


Source: Prepared by Joan Tura from Springer BMC Climate Changes Responses

Volume 5:3 26 January 2018

Immune characterization of Breast Cancer Metastases

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

Prognostic biomarkers in Pancreatic Cancer

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





First Video Proof That Could Explain Antibiotic-Resistant Superbug Bacteria

Amidst the battle for supremacy, our army of immune cells relentlessly wages war against various pathogens, especially superbug bacteria. Despite the pool of ample winnings, our body still experiences defeat from time to time. We succumb to diseases as the war reels its favor towards the tenacious pathogens. Of course, we cannot allow our immune defense to be utterly defeated. Otherwise, we’d be dead. As bacteria advance by taking over much space and nutrients inside our body, we get external help through antimicrobial chemicals that scientists continue to contrive.  Unfortunately, antibiotic resistance has surfaced and turned certain strains of bacteria into a superbug – one that has become resistant to the effects of antibiotics.




Chemical warfare prior to the rise of a superbug

Antimicrobial chemicals, particularly antibiotics, came into existence as chemicals that were strategically designed and produced with the intent of killing pesky bacteria. In 1928, penicillin was discovered, which led to its use as the first natural antibiotic capable of undermining a spectrum of bacteria, if not by killing, by inhibiting their growth. Its role as a wonder drug against various bacteria caused Alexander Fleming to receive a duly recognition by winning a Nobel prize award for its discovery. Soon, more antibacterial agents came up to our defense. Antibiotics, such as penicillin and cephalosporin, destroy bacterial cell wall whereas polymyxins target bacterial cell membrane. Rifamycin, quinolones, sulfonamides, and the likes interfere with the enzymes essential to bacteria. Once again, we gained an upper hand.




Bacteria resisting: the rise of a superbug

A Scanning Electron Microscope (SEM) image of cells of the bacteria Vibrio tasmaniensis(Credit: Lewis Lab at Northeastern University. Image created by Anthony D’Onofrio, William H. Fowle, Eric J. Stewart and Kim Lewis)


While we thought we finally came up with a powerful weapon, the bacteria conjured up an amazing strategy to work in their favour — antibiotic resistance. Some of them started to morph. They evolved and mutated into new strains referred to as superbug. They became capable of resisting the drugs’ antimicrobial effects. One of their strategies is to produce β-lactamases that destroy the structure of β-lactam antibiotics (e.g. penicillin and cephalosporin). The bacteria that evolved into superbug organisms did not just live; they thrived. They multiplied and passed on to the next generation the features that could withstand a number of antibiotics.




DNA uptake by superbug bacteria

Apart from the vertical gene transfer of genes, antibiotic resistance could also be transferred through horizontal gene transfer. It is a mechanism whereby genes are taken up or transposed from one species to another, and one of the possible explanations for the rise of superbug bacteria. DNA uptake by a bacterial cell was captured for the first time in a video by a team of scientists from Indiana University. In the video1, it shows how a bacterial cell takes up DNA fragments from dead bacterial cells through its pilus. Like a harpoon, the pilus was used by the bacterium, Vibrio cholera, to catch and reel a stray DNA fragment, and then bring it inside the bacterial cell via the same pore on its cell wall. It, then, incorporates the DNA into its own genome. Accordingly, this is probably one of the mechanisms for a bacterium to turn into a superbug.

First video evidence of DNA uptake by Vibrio cholera.
(Video credit: Ankur Dalia, Indiana University, uploaded on YouTube by Group IU Biology News)


A researcher from the team, Courtney Ellison, recounted, “The size of the hole in the outer membrane is almost the exact width of a DNA helix bent in half… If there weren’t a pilus to guide it, the chance the DNA would hit the pore at just the right angle to pass into the cell is basically zero.” It appears that the pilus takes a crucial role in horizontal gene transfer. If left to chance the DNA fragment would not easily get inside the cell since the pore was too small for it to fit. Through horizontal gene transfer, those that were once sensitive to the antibiotic could later become superbug bacteria as well. As Ankur Dalia, another researcher from the same team, pointed out, “Horizontal gene transfer is an important way that antibiotic resistance moves between bacterial species….” The video that the research team captured for the first time could explain how antibiotic resistance can be acquired from one superbug bacterial species to another.




The battle is far from over. The antibiotic resistance already raised global concerns as it has rendered certain antibiotics ineffective. Pathogenic superbug bacteria have successfully armed themselves with genes that could neutralize antibiotic effects. Fortunately, scientists do not waver in determining the strategies that superbug bacteria exploit.  The recent discovery of the way by which bacteria employ to make them antibiotic-resistant superbug strains could lead to better therapeutic strikes that could counter them, hopefully, with ample success.




— written by Maria Victoria Gonzaga




1 Indiana University. (2018). IU scientists watch bacteria ‘harpoon’ DNA to speed their evolution. Retrieved from

Brief Diversions Help Keep Selective Attention in Top-notch

The ability to focus one’s attention on a specific point of interest for a given time is referred to as selective attention. Imagine a scenario wherein you can pay attention to everything. That would lead to information overload. Selective attention enables an individual to react to certain stimuli from among those occurring simultaneously. This ability is crucial particularly when you need to focus on a task you need to finish before the time is up. You tend to put much of your attention to your target and then ignore potential distractions.




Neurobiology of selective attention

Selective attention is one of the neural functions of the brain. The neurons relay the information from one neuron to the next by releasing neurotransmitters, such as acetylcholine, at the synapse. The neurons responsible for our capacity to focus are found in the lateral prefrontal cortex.1 They are also responsible for suppressing potential distractions in the background. For more neurobiological aspect and potential therapeutic targets, read Selective Attention – neurobiology and potential therapeutics.




Selective attention and inattentional blindness

While we can choose which of the things to focus on and which ones to ignore, there are also instances wherein we tend to overlook things beyond our will. One of the possible consequences of selective attention is inattentional blindness, which is the phenomenon of not being able to perceive things although they are just right in front of our eyes. Because we are focused on one thing, there is a tendency that other things escape us. For instance, you might not notice the tiniest details on your essay (e.g. misspelled words) or missed key information from a reference book.

Inattentional blindness can be perfectly demonstrated through Daniel Simons and Christopher Chabris’ invisible gorilla test. The test is a video of two basketball teams in which the viewer has to count how many times the ball is tossed around to the team members. The viewer would likely be so busy counting that the person in a gorilla suit walking back and forth on the background would easily go unnoticed. Because of selective attention, we are inclined to filter things out. We might even think that we saw everything but, in fact, we only see what we want to see. Thus, letting other salient details to slip out while on selective attention is not unusual.




Brief diversions improve selective attention

Imposing short and momentary breaks helps to rest mentally from sustained stimulations, and thereby, possibly keep up excellent selective attention.

One could easily surmise that selective attention and distractions should never go together when one wants to complete a highly demanding task. However, this seems to be the opposite based on what Atsunori Ariga and Alejandro Lleras from University of Illinois at Urbana-Champaign found in their study.2 Repetitive tasks that required prolonged selective attention could wind up to diminished quality in performance. The researchers presumed that diminishing attention per se was not the culprit to a poor performance but the constant stimulation happening in the brain. Lleras explained: “Constant stimulation is registered by our brains as unimportant, to the point that the brain erases it from our awareness.” What their study implicates is to impose short and momentary breaks to rest mentally from sustained stimulations. Brief breaks, as they proposed, will help to stay focused while doing long, arduous tasks, such as studying before an exam.2




Perhaps, we can all agree that there are times when selective attention can be a cinch and then there are also times when it is simply impossible. We can get easily distracted. There are just so many factors that prevent us from focusing on a daunting task. An emotional turmoil, for instance, is one such distraction that can be difficult to overcome. Nevertheless, these studies open up to possibilities how diversions and distractions can be put to use to uphold selective attention to tasks that need to be done over prolonged periods of time.




— written by Maria Victoria Gonzaga




1 McGill University. (2015, January 7). Having a hard time focusing? Research identifies complex of neurons crucial to controlling attention. ScienceDaily. Retrieved from
2 University of Illinois at Urbana-Champaign. (2011, February 8). Brief diversions vastly improve focus, researchers find. ScienceDaily. Retrieved June 5, 2018, from