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Category: genetics

A revolution is underway in gene editing—and at its forefront is David Liu, an American molecular biologist whose pioneering work is rewriting the building blocks of life with unprecedented precision.

A professor at the Broad Institute of MIT and Harvard, Liu was awarded a Breakthrough Prize in Life Sciences on Saturday for developing two transformative technologies: one already improving the lives of patients with severe genetic diseases, the other poised to reshape medicine in the years ahead.

He spoke with AFP ahead of the Los Angeles ceremony for the prestigious Silicon Valley-founded award.

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Continue reading “Dietary AGE Products Impact Insulin Resistance And Inflammation: Jaime Uribarri, M.D” | >

Gestational diabetes is a disorder characterized by abnormally high levels of blood glucose (also called blood sugar) during pregnancy.

Affected women do not have diabetes before they are pregnant, and most of these women go back to being nondiabetic soon after the baby is born. Gestational diabetes is often discovered during the second trimester of pregnancy.

The disease has a 30 to 70 percent chance of recurring in subsequent pregnancies.

Gestational diabetes mellitus (GDM) is influenced by both genetic and environmental factors. Polymorphisms in genes related to glucose metabolism and insulin signaling, such as TCF7L2, have been associated with increased risk. This gene influences insulin secretion and glucose production, affecting the body’s ability to regulate blood sugar during pregnancy. Other implicated genes include GCK, encoding glucokinase, and MTNR1B, involved in melatonin receptor signaling.

More information on genetic factors that contribute to the development of GDM is provided in the link below.

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A variety of genetic conditions are known to affect brain development and, consequently, might potentially exhibit behaviours related to SIDs, as they impact areas involved in sensory processing and the perceptual integration of inputs. This is the case of Williams syndrome (WS), 22q11.2 deletion syndrome (22qDS) and pseudohypoparathyroidism (PHP). Although some previous research indicates sensory processing alterations in WS [20], this area remains largely unexplored in 22qDS and PHP.

The condition 22qDS, caused by a deletion in the q11.2 region of chromosome 22, is associated with significant brain abnormalities, along with cardiac anomalies, cleft palate, immune deficiencies, cognitive difficulties, and an increased risk of psychiatric disorders such as schizophrenia [21]. Common structural alterations include hypoplasia of the corpus callosum, which impacts interhemispheric communication, and anomalies in the thalamus, affecting the relay of sensory and motor information. Additionally, structural changes in the cortical brain regions, such as variations in cortical thickness, have been observed. These structural abnormalities are linked to disruptions in neural networks and can contribute to deficits in cognitive and emotional functions, impacting development and behaviour in individuals with the syndrome [22].

WS is caused by a microdeletion in the chromosomal region 7q11.23. It is characterised by a distinctive cognitive and behavioural profile, including strong social and verbal skills, accompanied by anxiety and attention problems. Additionally, individuals with WS may present with cardiovascular anomalies, hypercalcemia in infancy, and a distinctive facial phenotype [23]. MRI studies reveal reduced brain size and a more pronounced loss of white matter compared to grey matter in WS. The posterior brain regions are notably more affected, with reduced grey matter density observed in the superior parietal lobe and hypofunction near the intraparietal sulcus, areas associated with multisensory integration and perception [24].

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A new model of Alzheimer’s disease has been proposed, which could speed up efforts to understand and cure the complex condition – while bringing all manifestations of the condition under one unifying theory.

Researchers from Arizona State University suggest that stress granules – protein and RNA clumps that form around cells in stressful conditions due to genetic and environmental risk factors – are the primary culprit behind the disease.

In their new study, the team reviewed data from multiple health databases and past papers – particularly a 2022 study on Alzheimer’s progression – to identify widespread changes in gene expression that come with it.

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1. Non-selective neurons, which respond to both pain and itch stimuli indiscriminately.

2. Stimulus-specific neurons, which were selectively activated by either pain or itch stimuli.

Furthermore, using the dual-eGRASP technique—an advanced synaptic analysis method the research team discovered that stimulus-specific neurons in the ACC receive distinct synaptic inputs from the mediodorsal thalamus (MD). This finding indicates that pain and itch are processed by independent neuronal populations within the ACC, which receive differentiated synaptic inputs, providing fundamental insights into the neural mechanisms of pain and itch processing.

To further confirm the role of these neurons, the team used chemogenetic techniques to selectively deactivate either pain-specific or itch-specific neurons. The results showed suppressing pain neurons reduced pain perception without affecting itch, and vice versa. This discovery suggests that these neurons play a direct role in shaping how we experience pain and itch.

A research team have uncovered the neural mechanisms underlying the processing of pain and itch in the anterior cingulate cortex (ACC). This study provides new insights into how the brain distinguishes between these two distinct sensory experiences.

Pain and itch are both unpleasant sensations, but they trigger different responses—pain often prompts withdrawal, while itching leads to scratching. Until now, scientists have struggled to understand how the brain processes these sensations separately, as they share overlapping neural pathways from the spinal cord to the brain.

Continue reading “How the brain distinguishes between pain and itch” | >

Wischnewski et al. demonstrate suppressed CD8+ T cell cytotoxicity in breast cancer brain metastases, contrasting with genetically identical extracranial tumors. Neutrophils and Trem2+ macrophages drive this suppression, limiting the efficacy of combined irradiation and anti-PD1 therapy, highlighting potential therapeutic targets for brain metastases.

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In this study, researchers engineered an attenuated strain, Designer Bacteria 1 (DB1), which efficiently survives and proliferates in tumor tissues while being cleared in normal tissues, achieving a remarkable “tumor-targeting” effect as well as “tumor-clearing” effect.

To understand how DB1 simultaneously achieves these effects, researchers investigated the interactions between the bacteria and tumors. They discovered that DB1’s antitumor efficacy is closely linked to tissue-resident memory (TRM) CD8+ T cells within the tumor, which are reinvigorated and expanded following DB1 therapy. Interleukin-10 (IL-10) plays a crucial role in mediating this effect, with efficacy depending on the high expression of interleukin-10 receptor (IL-10R) on CD8+ TRM cells.

To investigate the molecular mechanisms underlying the high expression of IL-10R on CD8+ TRM cells, researchers conducted a series of computational and quantitative experiments. They found that IL-10 binds to IL-10R on CD8+ TRM cells, activating the STAT3 protein and further promoting IL-10R expression. This established a positive feedback loop, enabling cells to bind more IL-10 and creating a nonlinear hysteretic effect, whereby CD8+ TRM cells “memorize” previous IL-10 stimulation during tumorigenesis. The high expression of IL-10R on CD8+ TRM cells was exploited by a bacteria-induced IL-10 surge, which activated and expanded CD8+ TRM cells to clear tumor cells.

To examine the source of IL-10 within the tumor microenvironment (TME) after bacterial therapy, researchers found that tumor-associated macrophages (TAMs) upregulate IL-10 expression following DB1 stimulation via the Toll-like Receptor 4 (TLR4) signaling pathway. Interestingly, IL-10 reduced the migration speed of tumor-associated neutrophils (TANs), aiding DB1 in evading rapid clearance. These processes depended on high IL-10R expression in tumor-associated immune cells, highlighting the critical role of IL-10R hysteresis.

A research team elucidated the mechanism behind bacterial cancer therapy using a genetically engineered bacterial strain. Their findings were published in Cell.

Exploring the use of antitumor bacteria in cancer therapy dates back to the 1860s. Despite this long history, however, clinical application of bacterial-based cancer therapy has faced significant challenges in terms of safety and efficacy.

Continue reading “Designer bacteria for cancer therapy” | >