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Hedonic eating is controlled by dopamine neurons that oppose GLP-1R satiety

Hedonic eating is defined as food consumption driven by palatability without physiological need. However, neural control of palatable food intake is poorly understood. We discovered that hedonic eating is controlled by a neural pathway from the peri–locus ceruleus to the ventral tegmental area (VTA). Using photometry-calibrated optogenetics, we found that VTA dopamine (VTADA) neurons encode palatability to bidirectionally regulate hedonic food consumption. VTADA neuron responsiveness was suppressed during food consumption by semaglutide, a glucagon-like peptide receptor 1 (GLP-1R) agonist used as an antiobesity drug. Mice recovered palatable food appetite and VTADA neuron activity during repeated semaglutide treatment, which was reversed by consumption-triggered VTADA neuron inhibition.

Does Methylene Blue Impact Lifespan?

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Spinning into antibiotic resistance: The flagella’s hidden role

A new study from the Faculty of Medicine at the Hebrew University of Jerusalem sheds light on how bacterial motion influences the spread of antibiotic resistance. Led by Professor Sigal Ben-Yehuda and Professor Ilan Rosenshine from the Department of Microbiology and Molecular Genetics, the research uncovers a direct connection between the rotation of bacterial flagella—structures used for movement—and the activation of genes that enable bacteria to transfer DNA to one another.

This process, known as bacterial conjugation, is a key mechanism by which genetic traits, particularly antibiotic resistance, are shared among bacterial populations. While conjugation has traditionally been associated with attaching to solid surfaces, the team investigated pLS20, a widespread conjugative plasmid in Bacilli species, which behaves differently. The study shows that in liquid environments, where bacteria rely on movement to navigate, the rotation of flagella acts as a mechanical signal that turns on a set of genes required for DNA transfer.

The researchers discovered that this signal triggers gene expression in a specific subset of donor cells, which then form clusters with recipient bacteria. These multicellular clusters bring the two types of cells into close contact, facilitating the transfer of genetic material.

Abstract: Understanding the pathogenesis of NUP98-fusion mediated leukemia—

Suming Huang & team show the HoxBlin c long non-coding RNA serves as an oncogenic regulator that controls 3D nuclear organization, chromatin accessibility and gene transcription related to leukemogenesis.

The figure shows H&E staining of sternum and spleen from WT and B-ALL HoxBlin c Tg mice.


1Division of Pediatric Hematology/Oncology, Department of Pediatrics, Pennsylvania State University College of Medicine, Hershey, Pennsylvania, USA.

2Department of Molecular Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA.

3Genetics Branch, Center for Cancer Research, National Cancer Institute (NCI), NIH, Bethesda, Maryland, USA.

Advances in Acute Myeloid Leukemia: Recently Approved Therapies and Drugs in Development

Acute myeloid leukemia (AML) is one of the most common types of leukemia in adults, with an average first diagnosis at age 68, and has historically carried poor prognosis due to various genetic alterations and abnormalities that complicate…

The scientist rewriting DNA, and the future of medicine

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.

Dietary AGE Products Impact Insulin Resistance And Inflammation: Jaime Uribarri, M.D

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Genetic factors in Gestational Diabetes

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.

Sensory Processing Challenges in Children with Neurodevelopmental Disorders and Genetic Conditions: An Observational Study

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].