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Testosterone therapy is associated with reduced risk of acute kidney injury, kidney failure with renal replacement therapy, and cardiovascular events in men with diabetes and hypogonadism

Testosterone deficiency is common in men with diabetes. Effects of testosterone therapy on kidney failure and cardiovascular outcomes in diabetic men remain poorly understood. Our aim was to assess whether testosterone therapy is associated with reduced risk of acute kidney injury and kidney failure requiring replacement therapy in men with diabetes and hypogonadism compared to matched untreated men with diabetes.

Participants were recruited from the TriNetX Research Collaborative network. We identified 26,027 diabetic men with hypogonadism treated with testosterone and matched them 1:1 using propensity score matching to 26,027 untreated diabetic men with hypogonadism. Primary outcomes were acute kidney injury and kidney failure requiring replacement therapy (dialysis or transplantation). Secondary outcomes included myocardial infarction, ischemic stroke, atrial fibrillation, and all-cause mortality. Cox proportional hazard models were used over a mean follow-up of 3.3 years.

Men had a mean age of 58 years (SD 12), with 71% being non-Hispanic White. Testosterone-treated men had significantly lower risk of acute kidney injury (HR: 0.93 [95% CI 0.87–0.98], p = 0.01) and kidney failure with replacement therapy (HR: 0.81 [95% CI 0.72–0.92], p = 0.001) compared to untreated men. Testosterone therapy was also associated with reduced risk of myocardial infarction (HR: 0.85 [95% CI 0.78–0.93], p 0.0001), ischemic stroke (HR: 0.88 [95% CI 0.80–0.97], p = 0.01), atrial fibrillation (HR: 0.91 [95% CI 0.85–0.98], p = 0.01), and all-cause mortality (HR: 0.85 [95% CI 0.79–0.91], p 0.0001).

Astrocytes are critical for fear memory

The team used a mouse model to understand how fear learning as a mechanism takes place in the brain, how fear-related memories can be retrieved, and the contribution of neurons versus astrocytes to fear learning.

Using fluorescent activity sensors, the team watched astrocytes respond in real time as fear memories were formed and later retrieved. As those memories were extinguished, astrocyte activity diminished. When the researchers then selectively increased or suppressed the signals astrocytes send to neighboring neurons, the strength of fear memories shifted in parallel, demonstrating that astrocytes are not just passive bystanders, but active participants in shaping fear.

Change in astrocyte activity also influenced neural circuits. When the astrocyte activity was disrupted, neurons could no longer form normal fear-related activity patterns and effectively transmit information about appropriate defensive reactions to brain regions that help control defensive behavior. These findings challenge neuron-centric models of fear by showing that fear memories aren’t produced by neurons alone.

The impact of disrupting astrocytes rippled beyond the amygdala. The manipulations also influenced how fear signals were relayed to the prefrontal cortex, a brain region that is key for decision-making. This suggests that astrocytes not only influence encoding of fear memories by the amygdala, but also how the brain uses those memories to determine appropriate responses to fearful situations.

Knowing that astrocytes play a key role in the retrieval of fear memories will reshape therapeutic interventions for disorders driven by persistent fearful memories such as post-traumatic stress disorder, anxiety disorders and phobias, the author said. If astrocytes help determine whether fear memories are expressed or successfully extinguished, then targeting astrocyte-related pathways, rather than neural pathways, could eventually complement neuron-focused therapies.

Picture a star-shaped cell in the brain, stretching its spindly arms out to cradle the neurons around it. That’s an astrocyte, and for a long time, scientists thought its job was caretaking the brain, gluing together neurons, and maintaining neural circuits.

Continue reading “Astrocytes are critical for fear memory” | >

Inositol Requiring Enzyme 1α Mediates Hypertension and Vascular Remodeling

A single genetic “switch” may be the secret to how the body’s cleanup crew grows up and keeps our organs running smoothly.

Scientists at the University of Liège have identified a crucial genetic regulator that allows macrophages to fully mature and help maintain healthy organs. This regulator, known as MafB, acts as a “molecular switch” that turns specific genes on or off at the right time and in the right cells.

By carefully controlling this genetic activity, MafB enables the development of macrophages that defend the body and support normal organ function. When MafB is missing, macrophages do not work as they should and lose their ability to carry out their protective duties.

Russia forges nuclear steel to brave 1112°F for next-gen reactors

It could solve the corrosion and thermal challenges of lead-cooled reactors.

The development of this steel was conducted under the “Breakthrough” (Proryv) project, which focuses on the implementation of a closed nuclear fuel cycle using fast neutron reactors.

The new steel provides corrosion resistance and thermal stability at temperatures up to 600°C (1,112°F).

According to Sergei Logashov, Director of the Institute of Materials Science at CNIITMASH, the material was designed using computer modeling and data from heavy liquid metal coolant systems.

Enhancement of Patient-Centered Lung Cancer Screening: The MyLungHealth Randomized Clinical Trial

The MyLungHealth randomized trial found that digital tools improved eligibility assessment and CT ordering for LungCancer screening, but gains in scan completion were limited.

Question Does adding a patient-facing, electronic health record (EHR)–integrated tool to a clinician-facing clinical decision support system improve the identification and ordering of lung cancer screening?

Findings In this randomized clinical trial of 31 303 adults aged 50 to 79 years with uncertain or documented eligibility for lung cancer screening, the EHR-integrated tool significantly increased the identification of screening-eligible patients and the ordering of low-dose computed tomography lung cancer screening.

Meaning Combining patient-facing and clinician-facing decision support in primary care may enhance lung cancer screening by improving eligibility identification and computed tomography scan ordering.

Clinical Implications of Left Atrial and Ventricular Reverse Remodeling After Atrial Fibrillation Ablation in Patients With Systolic Dysfunction

AFib ablation promotes LA/LV reverse remodeling.

Read this study about how combined assessment better stratifies distinct trajectories in systolic dysfunction. @MasatoOkada1105

BackgroundCatheter ablation of atrial fibrillation (AF) is an effective treatment to achieve left atrial (LA) and left ventricular (LV) reverse remodeling in patients with systolic dysfunction. However, the relationship between LA and LV reverse remodeling (LARR and LVRR) and their clinical implications remains unclear.

Liquid Crystal Monomers Released from LCD Displays Accumulate in Endangered Marine Cetaceans Triggering Health Concerns

Liquid crystal monomers (LCMs), critical substances of liquid crystal displays in consumer electronics, are persistent pollutants, posing potential threats to marine ecosystems. Despite their bioaccumulative potential, their occurrence and possible biological impacts on marine megafauna remain understudied. We investigated LCM occurrence in Indo-Pacific humpback dolphins (Sousa chinensis) and finless porpoises (Neophocaena phocaenoides) collected from the South China Sea (2007–2021) and assessed their toxicity through in vitro assays using established dolphin cell lines. By employing robust source-tracing methodologies, we provide the first evidence that LCMs from household electronics and coastal e-waste accumulate in cetacean tissues, including blubber, muscle, and, critically, brain tissues, demonstrating blood–brain barrier penetration, a previously undocumented phenomenon of LCMs in mammalian wildlife. The temporal trend of LCM burden in porpoise blubber is correlated with shifts in global liquid crystal display production. Transcriptomic profiling revealed LCM-induced DNA damage, cell cycle arrest, and impaired cell division in cetacean cells. These findings suggest that LCMs may pose potential risks to the nervous system and other organs of marine mammals, warranting further investigation into their toxicological effects and possible implications for human health. By bridging critical gaps among everyday electronics, LCM contamination, and marine conservation, this study highlights the need for urgent regulatory actions and improved e-waste governance to mitigate ecological and public health risks.

N-Terminal Actin-Binding Site of Lmod2 Promotes Controlled Pointed End Elongation

Larrinaga & colleagues discovered how a heart muscle protein fine-tunes muscle contraction by acting like a “leaky cap” & controlling how important muscle fiber components (actin filaments) grow. Learn how disrupting this control causes actin filaments to grow unusually long, perturbing the beating of the heart at.

BACKGROUND: Lmods (leiomodins) are critical for the assembly and maintenance of thin filaments in striated muscles by allowing thin filament elongation at the pointed ends. Lmod2’s elongation function has been linked to both actin-binding sites (ABSs) 2 and 3, while the existence and function of an N-terminal ABS1 has been debated. METHODS: To elucidate the little-known role of Lmod2’s ABS1, we created a mutant (F64D/L69D/W72D/W73D: Lmod2-quadruple mutant) predicted to decrease the binding of ABS1 to actin. We analyzed the effect of the mutations using several in vitro, cellular, and in vivo assays. RESULTS: By disrupting the interaction of Lmod2 ABS1 with actin in isolated cardiomyocytes and in mice, we engineered a super Lmod2 that results in remarkably longer thin filaments.

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