Lifeboat Foundation

Gastrointestinal (GI) disorders account for about 10% of all consultations in primary care and have a major impact on quality of life and health care resources. Gastro-oesophageal reflux disease (GERD), H. pylori infection, irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), coeliac disease, antibiotic-associated diarrhea (ADA), infectious diarrhea, are some common GI disorders.

The efficacy of probiotics in preventing and treating gastrointestinal disorders has received considerable attention in recent years. This article will shed light on how probiotics are more or less effective in treating different gastrointestinal disorders.

Indian Burden and Factors Affecting GI Disorders The prevalence of self-reported gastrointestinal disorders in India is around 18%. Whereas the prevalence of gastroesophageal reflux disease (GERD) ranges from 2.5% to 7.1% in most population-based studies in Asia.

Malaria is one of the most widespread and devastating infectious diseases across the globe. This mosquito-borne parasitic disease killed approximately 619,000 people in 2021 alone, many of them children in Africa. In one of the deadliest forms of malaria, known as cerebral malaria, the patient experiences severe neurological symptoms, such as seizures and coma. Although only a small fraction of people who fall ill with malaria also experience cerebral malaria, the condition is lethal without treatment. Among hospitalized patients with the condition, death rates range between 15 and 20%. In a new paper, recently published in Science Translational Medicine, researchers from the National Institute of Allergy and Infectious Diseases (NIAID), part of the NIH, and their colleagues studied children with cerebral malaria in Malawi to better understand the underlying causes of these devastating symptoms in the hope of developing improved treatments.

Researchers know that the symptoms of cerebral malaria are caused when the brain swells within the confines of the skull, eventually impinging upon the brainstem, which causes breathing to stop. However, researchers have been unsure how malaria infection leads to brain swelling. Some researchers hypothesized that the main cause was a weakening of the blood-brain barrier, which would allow fluid to seep into the brain and cause it to swell. Others speculated that the primary driver behind the swelling was inside the blood vessels themselves. Red blood cells infected with P. falciparum, the parasite which causes malaria, can become “sticky,” adhering to the walls of blood vessels. Partial blockages inside the cerebral veins could slow the flow of blood leaving the brain, causing the blood vessels themselves to become engorged and expand the brain from within.

To distinguish between these two hypotheses, NIAID researchers and their collaborators used non-invasive imaging techniques to study the flow of blood within the brains of 46 children who had been hospitalized for cerebral malaria at the Pediatric Research Ward of Queen Elizabeth Central Hospital in Blantyre, Malawi. As a comparison, they also studied 33 children with uncomplicated malaria and 26 healthy children from the local region. By using a light-based external monitoring tool (called near-infrared spectroscopy, or NIRS) the researchers were able to measure the amount of hemoglobin in the children’s brains. They reasoned that if excess fluid was the cause of brain swelling, then the hemoglobin concentration would be low, due to dilution. Alternatively, if the blood vessels were engorged with blood, then the hemoglobin concentration would be high.

Commercial platforms for protein therapeutics are being built on academic research that has expanded the genetic code behind cell-based translation.

Antibiotic resistance is a major danger to public health that threatens to claim the lives of millions of people per year within the next few decades. Years of necessary administration and excessive application of antibiotics have selected for strains that are resistant to many of our currently available treatments. Due to the high costs and difficulty of developing new antibiotics, the emergence of resistant bacteria is outpacing the introduction of new drugs to fight them. To overcome this problem, many researchers are focusing on developing antibacterial therapeutic strategies that are “resistance-resistant”—regimens that slow or stall resistance development in the targeted pathogens. In this mini review, we outline major examples of novel resistance-resistant therapeutic strategies. We discuss the use of compounds that reduce mutagenesis and thereby decrease the likelihood of resistance emergence. Then, we examine the effectiveness of antibiotic cycling and evolutionary steering, in which a bacterial population is forced by one antibiotic toward susceptibility to another antibiotic. We also consider combination therapies that aim to sabotage defensive mechanisms and eliminate potentially resistant pathogens by combining two antibiotics or combining an antibiotic with other therapeutics, such as antibodies or phages. Finally, we highlight promising future directions in this field, including the potential of applying machine learning and personalized medicine to fight antibiotic resistance emergence and out-maneuver adaptive pathogens.

The use of antibiotics is central to the practice of modern medicine but is threatened by widespread antibiotic resistance (Centers for Disease Control and Prevention (U.S.), 2019). Antibiotics are a selective evolutionary pressure—they inhibit bacterial growth and viability, and antibiotic-treated bacteria are forced to either adapt and survive or succumb to treatment. The stress of antibiotic treatment can enhance bacterial mutagenesis leading to de novo resistance mutations (Figure 1A), promote the acquisition of horizontally transferred genetic elements that confer resistance, or trigger phenotypic responses that increase tolerance to drugs (Davies and Davies, 2010; Levin-Reisman et al., 2017; Bakkeren et al., 2019; Darby et al., 2022;). Additionally, antibiotic treatment can select for the proliferation of pre-existing mutants already in the population (Figure 1B).

Research led by the Department of Anthropology and School of Biomedical Sciences, Kent State University, Ohio, has investigated neuropeptide Y innervation in an area of the brain called the nucleus accumbens of various primate species, including humans. The research was focused on understanding its role in brain evolution and any implications for human health, particularly regarding addiction and eating disorders.

In a paper, “Hedonic eating, obesity, and addiction result from increased neuropeptide Y in the nucleus accumbens during human brain evolution,” published in PNAS, the researchers suggest that the combination of increased neuropeptide Y (NPY) and dopamine (DA) within the human nucleus accumbens (NAc) may have allowed for enhanced brain development. This same configuration may have also made humans exceptionally vulnerable to eating disorders and substance abuse, hinting at addictive traits having a deep evolutionary origin.

NPY plays a role in the reward system, emotional behavior and is associated with increased alcohol use, drug addiction and fat intake. The NAc brain region is central to motivation and action, exhibiting one of the highest densities of NPY in the brain and is of great interest to researchers investigating brain-related promoters of addiction.

UK researchers have developed a new publicly accessible database, and they hope to see it shrink over time. That’s because it is a compendium of the thousands of understudied proteins encoded by genes in the human genome, whose existence is known but whose functions are mostly not.

The database, dubbed the “unknome,” is the work of Matthew Freeman of the Dunn School of Pathology, University of Oxford.

The University of Oxford is a collegiate research university in Oxford, England that is made up of 39 constituent colleges, and a range of academic departments, which are organized into four divisions. It was established circa 1096, making it the oldest university in the English-speaking world and the world’s second-oldest university in continuous operation after the University of Bologna.

Machines don’t have eyes, but you wouldn’t know that if you followed the progression of deep learning models for accurate interpretation of medical images, such as x-rays, computed tomography (CT) and magnetic resonance imaging (MRI) scans, pathology…

Vanderbilt researchers have developed a way to more quickly and precisely trap nanoscale objects such as potentially cancerous extracellular vesicles using cutting-edge plasmonic nanotweezers.

The practice by Justus Ndukaife, assistant professor of electrical engineering, and Chuchuan Hong, a recently graduated Ph.D. student from the Ndukaife Research Group, and currently a postdoctoral research fellow at Northwestern University, has been published in Nature Communications.

Optical tweezers, as acknowledged with a 2018 Physics Nobel Prize, have proven adept at manipulating micron-scale matter like biological cells. But their effectiveness wanes when dealing with nanoscale objects. This limitation arises from the diffraction limit of light that precludes focusing of light to the nanoscale.

This device can generate deep-UV light with a very narrow wavelength range that is safe for humans but lethal for germs.

A new device that can generate deep-ultraviolet (UV) light to kill germs without harming humans has been developed by a team of researchers from Osaka University, Japan. The device uses a novel method of combining two visible photons into one deep-UV photon inside a thin waveguide made of aluminum nitride, a material that has nonlinear optical properties.

The research, named “229 nm far-ultraviolet second harmonic generation in a vertical polarity inverted AlN bilayer channel waveguide,” has been published in the journal Applied Physics Express.