Circuit responsible for building memories during sleep

According to a new study Neuroscientists have identified a mechanism that may help build memories during deep sleep. This study centered on the role of the nucleus reuniens, an area which connects two other brain structures involved in creating memories the prefrontal cortex and the hippocampus and may coordinate their activity during slow-wave sleep. Lead researcher said that slow-waves during sleep benefit our memories for personal experiences, likely due to coordinated activity in the prefrontal cortex and hippocampus & found that the nucleus reuniens is responsible for coordinating synchronous, slow-waves between these two structures. This means that the reuniens may play an essential role for sleep-dependent memory consolidation of events. Slow-wave sleep is the deepest stage of sleep, during which the brain oscillates at a very slow, once-per-second rhythm. It is crucial for muscle and brain recovery, and has been shown to play a role in memory consolidation. This under-studied and relatively unknown brain area likely has a substantial role in forming long-term memories while sleep.

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                                      Critical protein unlock Zika virus treatments identified

A protein that is critical in controlling replication of Zika viruses and could be important for developing therapies to prevent and treat those viruses has been identified by a researcher. The researchers found Z-DNA binding protein 1 (ZBP1) is a sensor that plays a significant role in triggering a robust immune response when it detects a viral infection within cells. Researcher found ZBP1 is essential for restricting Zika virus replication, and that it prevents Zika-associated encephalitis (inflammation of the brain) in mice. The absence of ZBP1 in mice leads to 100 percent mortality when infected with even a non-disease-producing strain of Zika Virus, the study found. Researcher discovered that when cells are infected with viruses such as Zika & respond by triggering necroptosis, a form of programmed cell death, via ZBP1 signaling. This inhibits viral replication and spread, allowing the immune system to clear the virus. This findings could present new treatment strategies for viruses that can infect the central nervous system by modulating ZBP1 expression. Manipulating a host protein already inside the genome to trigger the body's natural immune response is a better way of fighting viruses already in the brain.

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                               Chromosomal abnormalities related with recurrent miscarriage

When a couple loses a pregnancy, and especially when the same couple loses multiple pregnancies, doctors are often at a loss to explain why. For about 40 to 60 percent of couples with recurrent miscarriage (RM), the condition remains unexplained, even after costly testing. Chromosomal abnormalities rearrangements of large chunks of DNA in the genomes of one or both individuals trying to conceive are thought to be one of the major genetic causes of RM. Routine chromosome analysis can currently detect these abnormalities in about 1 in 50 couples. A new study uses a special genetic sequencing technique known as low-pass genome sequencing (GS) to look for chromosomal abnormalities in couples with RM. Low-pass GS revealed additional chromosomal abnormalities in more couples than traditional testing, increasing detection to 1 in 9 couples. RM carries an underappreciated psychological and financial burden for affected couples. Building on a previous collaboration, researchers explore further low-pass GS as a tool in clinical cytogenetics. Couples were enrolled from RM clinics at the two universities. Investigators performed chromosome analysis and low-pass GS. The team detected 127 chromosomal abnormalities using low-pass GS, accounting for approximately 12 percent of the couples and about 50 more couples than traditional chromosomal analysis detected. A technique known as pre-implantation genetic testing (PGT) can help couples with genetic abnormalities conceive through in vitro fertilization. Researcher said that results suggest that applying low-pass GS could help identify a larger subgroup of patients at increased risk of subsequent miscarriage who might take advantage of pre-implantation genetic testing.

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                                              New pain organ discovered in the skin

Researchers have discovered a new sensory organ that is able to detect painful mechanical damage, such as pricks and impacts. Pain causes suffering and results in substantial costs for society. Almost one person in every five experiences constant pain and there is a considerable need to find new painkilling drugs. However, sensitivity to pain is also required for survival and it has a protective function. It prompts reflex reactions that prevent damage to tissue, such as pulling your hand away when you feel a jab from a sharp object or when you burn yourself. Researchers have now discovered a new sensory organ in the skin that is sensitive to hazardous environmental irritation. It is comprised of glia cells with multiple long protrusions and which collectively go to make up a mesh-like organ within the skin. This organ is sensitive to painful mechanical damage such as pricks and pressure. The study describes what the new pain-sensitive organ looks like, how it is organized together with pain-sensitive nerves in the skin and how activation of the organ results in electrical impulses in the nervous system that result in reflex reactions and an experience of pain. The cells that make up the organ are highly sensitive to mechanical stimuli, which explain how they can participate in the detection of painful pinpricks and pressure. In experiments, the researchers also blocked the organ and saw a resultant decreased ability to feel mechanical pain. The discovery changes our understanding of the cellular mechanisms of physical sensation and it may be of significance in the understanding of chronic pain said by lead researcher.

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                                              Potent bacterial toxin kills MRSA bacteria

Researcher have discovered how a potent bacterial toxin is able to target and kill MRSA, paving the way for potential new treatments for superbugs. Lead researcher specifically recognizes MRSA cell walls and quickly causes the breakdown of this pathogen. The lysostaphin is able to increase the number of its molecules bound to the surface of the MRSA cell and this allows the enzyme to 'walk' along the cell walls and cause rapid breakdown. Lysostaphin is an enzyme that has been shown to eradicate Staphylococcal infections, such as MRSA, alone or in combination with antibiotics. Although it was discovered over 50 years ago, not much has been known about how it kills these infections. The researcher hope to use their findings to develop new treatments for MRSA and other antibiotic resistant superbugs which target the infection in a similar way. MRSA is a bacterial superbug that is resistant to several antibiotics and frequently spreads in hospitals where people are more susceptible to infection. Lead researcher said that Lysostaphin is arguably the most studied enzyme after lysozyme, so they are delighted that this research is able to explain the mechanism underpinning its potent antibacterial activity & this study explains how this enzyme is able to target and digest the MRSA bacteria and why it is so potent. Hospital-acquired infections caused by bacteria resistant to last resort antibiotics are on the rise, but this work could lead to the development of new treatments for these superbugs that use the same targeting mechanism.

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