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Emotion regulation is an essential aspect of mental health and wellbeing. In fact, past studies have found associations between poor emotion regulation and several psychiatric disorders, including bipolar disorder, borderline personality disorder and complex post-traumatic stress disorder (PTSD).

During their everyday life, humans can regulate their negative emotions in different ways, most of which do not require any conscious cognitive engagement. For instance, they might take a bath, step outside for fresh air or listen to .

Researchers at Radboud University Nijmegen in The Netherlands, the Norwegian University of Science and Technology (NTNU), and University Hospital Aachen, Germany have recently carried out a study aimed at investigating the effects of a short-term on implicit emotion regulation. Their paper, published in BMC Neuroscience, specifically examined whether musical training helped people to reduce the negative emotions elicited by unpleasant or disgusting odors.

Immortality DNA strands found in humans.


Distributed stem cells (DSCs), which continuously divide asymmetrically to replenish mature tissue cells, adopt a special form of mitotic chromosome segregation. Chromosome segregation is nonrandom instead of random. DSCs cosegregate the set of sister chromosomes with the older of the two template DNA strands used for semiconservative DNA replication during the preceding S phase. Neither the responsible molecular mechanisms nor the cellular function of nonrandom segregation are known. Here, we report evidence that immortal strand chromosomes have a higher level of cytosine 5-hydroxymethylation than mortal chromosomes, which contain the younger DNA template strands. We propose that asymmetric chromosomal 5-hydroxymethylation is a key element of a cellular mechanism by which DSCs distinguish older DNA template strands from younger ones.

Immortal strands are the targeted chromosomal DNA strands of nonrandom sister chromatid segregation, a mitotic chromosome segregation pattern unique to asymmetrically self-renewing distributed stem cells (DSCs). By nonrandom segregation, immortal DNA strands become the oldest DNA strands in asymmetrically self-renewing DSCs. Nonrandom segregation of immortal DNA strands may limit DSC mutagenesis, preserve DSC fate, and contribute to DSC aging. The mechanisms responsible for specification and maintenance of immortal DNA strands are unknown. To discover clues to these mechanisms, we investigated the 5-methylcytosine and 5-hydroxymethylcytosine (5hmC) content on chromosomes in mouse hair follicle DSCs during nonrandom segregation. Although 5-methylcytosine content did not differ significantly, the relative content of 5hmC was significantly higher in chromosomes containing immortal DNA strands than in opposed mitotic chromosomes containing younger mortal DNA strands.

Recently, we found dramatic mitochondrial DNA divergence of Israeli Chamaeleo chamaeleon populations into two geographically distinct groups. We aimed to examine whether the same pattern of divergence could be found in nuclear genes. However, no genomic resource is available for any chameleon species. Here we present the first chameleon transcriptome, obtained using deep sequencing (SOLiD). Our analysis identified 164000 sequence contigs of which 19000 yielded unique BlastX hits. To test the efficacy of our sequencing effort, we examined whether the chameleon and other available reptilian transcriptomes harbored complete sets of genes comprising known biochemical pathways, focusing on the nDNA-encoded oxidative phosphorylation (OXPHOS) genes as a model. As a reference for the screen, we used the human 86 (including isoforms) known structural nDNA-encoded OXPHOS subunits. Analysis of 34 publicly available vertebrate transcriptomes revealed orthologs for most human OXPHOS genes. However, OXPHOS subunit COX8 (Cytochrome C oxidase subunit 8), including all its known isoforms, was consistently absent in transcriptomes of iguanian lizards, implying loss of this subunit during the radiation of this suborder. The lack of COX8 in the suborder Iguania is intriguing, since it is important for cellular respiration and ATP production. Our sequencing effort added a new resource for comparative genomic studies, and shed new light on the evolutionary dynamics of the OXPHOS system.

Keywords: chameleon, oxidative phosphorylation, transcriptome.

Massive parallel sequencing (MPS) enables identifying the entire set of transcribed genes (transcriptome) of understudied organisms, thus providing novel genomic resources. However, because there is no genomic reference to those organisms, the short reads generated by MPS must be de novo assembled in order to form sequence contigs, which in turn could be annotated (Kusumi et al. 2011), thus creating reference sequences for further analyses.

Circa 2010


In this review, we consider the evidence that a reduction in neurogenesis underlies aging-related cognitive deficits, and impairments in disorders such as Alzheimer’s disease (AD). The molecular and cellular alterations associated with impaired neurogenesis in the aging brain are discussed. Dysfunction of presenilin-1, misprocessing of amyloid precursor protein and toxic effects of hyperphosphorylated tau and β-amyloid likely contribute to impaired neurogenesis in AD. Since factors such as exercise, enrichment and dietary energy restriction enhance neurogenesis, and protect against age-related cognitive decline and AD, knowledge of the underlying neurogenic signaling pathways could lead to novel therapeutic strategies for preserving brain function. In addition, manipulation of endogenous neural stem cells and stem cell transplantation, as stand-alone or adjunct treatments, seem promising.

There is a progressive decline in the regenerative capacity of most organs with increasing age, resulting in functional decline and poor repair from injury and disease. Once thought to exist only in high turnover tissues, such as the intestinal lining or bone marrow, it now appears that most tissues harbor stem cells that contribute to tissue integrity throughout life. In many cases, stem cell numbers decrease with age, suggesting stem cell aging may be of fundamental importance to the biology of aging (for review, see Ref. [1]). Therefore, understanding the regulation of stem cell maintenance and/or activation is of considerable relevance to understanding the age-related decline in maintaining tissue integrity, function, and regenerative response.

The adult brain contains neural stem cells (NSCs) that self-renew, proliferate and give rise to neural progenitor cells (NPC) that exhibit partial lineage-commitment. Following several cycles of proliferation, NPC differentiate into new neurons and glia. NSCs are increasingly acknowledged to be of functional significance and harbor potential for repair of the diseased or injured brain. The dramatic decline in neurogenesis with age is thought to underlie impairments in learning and memory, at least in part. Aging is also the greatest risk factor for Alzheimer’s disease (AD), a neurodegenerative disease characterized by progressive loss of memory and cognitive decline. Alterations in neurogenesis have been described extensively in animal models of AD, and key proteins involved in AD pathogenesis are shown to regulate neurogenesis.

Breast cancer is the leading cause of cancer death in women around the world, responsible for 1700 deaths every day. Although the vast majority of breast cancers are treatable, the most aggressive subtype—triple negative breast cancer (TNBC) – has a high recurrence rate, a high potential for metastasis and shows resistance to conventional treatments, leading to very poor prognosis and survival outcomes. A team of researchers at the Research Institute of the McGill University Health Center (RI-MUHC) conducted a preclinical study and discovered a novel targeted combination therapy that efficiently reduced tumor growth in metastatic breast cancer. Published in Nature Communications, their findings could lead to the development of a novel first line targeted therapy for the treatment of TNBC, with the prospect of rapidly transitioning to clinical trials in humans.

“There is no targeted therapy for TNBC. Chemotherapy treatment can even enrich these tumors in and be detrimental to the patient, as we have shown in a previous study,” says Dr. Jean-Jacques Lebrun, senior scientist in the Cancer Research Program at the RI-MUHC and principal investigator of the study. “Filling that huge medical gap was our motivation in conducting this study.”

While most breast cancers have one of three main receptors that are like entrance gates for treatments—estrogen, progesterone and a protein called human epidermal growth factor (HER2) – TNBC has none, thus the name triple negative . Using state-of-the-art technologies such as and genome-wide molecular approaches, the team identified two pathways which could be targeted in a therapeutic strategy.

“Once the virus is recognised, the CRISPR enzyme is activated and chops up the virus,” she said.


Paris (AFP)

Scientists have used CRISPR gene-editing technology to successfully block the transmission of the SARS-CoV-2 virus in infected human cells, according to research released Tuesday that could pave the way for Covid-19 treatments.

Writing in the journal Nature Communications, researchers in Australia said the tool was effective against viral transmissions in lab tests, adding that they hoped to begin animal trials soon.

Coronavirus disease-19 caused by the novel RNA betacoronavirus SARS-CoV2 has first emerged in Wuhan, China in December 2019, and since then developed into a worldwide pandemic with 99 million people afflicted and 2.1 million fatal outcomes as of 24th January 2021. SARS-CoV2 targets the lower respiratory tract system leading to pneumonia with fever, cough, and dyspnea. Most patients develop only mild symptoms. However, a certain percentage develop severe symptoms with dyspnea, hypoxia, and lung involvement which can further progress to a critical stage where respiratory support due to respiratory failure is required. Most of the COVID-19 symptoms are related to hyperinflammation as seen in cytokine release syndrome and it is believed that fatalities are due to a COVID-19 related cytokine storm. Treatments with anti-inflammatory or anti-viral drugs are still in clinical trials or could not reduce mortality. This makes it necessary to develop novel anti-inflammatory therapies. Recently, the therapeutic potential of phytocannabinoids, the unique active compounds of the cannabis plant, has been discovered in the area of immunology. Phytocannabinoids are a group of terpenophenolic compounds which biological functions are conveyed by their interactions with the endocannabinoid system in humans. Here, we explore the anti-inflammatory function of cannabinoids in relation to inflammatory events that happen during severe COVID-19 disease, and how cannabinoids might help to prevent the progression from mild to severe disease.

Researchers have identified a specialized protein that appears to help prevent tumor cells from entering the bloodstream and spreading to other parts of the body.

“We have discovered that this protein, TRPM7, senses the pressure of fluid flowing in the circulation and stops the cells from spreading through the vascular system,” said Kaustav Bera, a Image 1: Overexpressing protein TRPM7 in cancer cells greatly reduces entry into the blood vessels. Image 2: In static conditions, cells enter microchannels, whereas 40-60% reverse direction when fluid is flowing. Courtesy of Johns Hopkins University.

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