Heat shock protein 90 mediates the protective effects of vericiguat on myocardial ischemia/reperfusion injury by inhibiting toll-like receptor 4 and c-Jun N-terminal kinases.

Objectives: This study aimed to investigate whether vericiguat exerts a protective effect against myocardial ischemia-reperfusion injury (MIRI) by inhibiting toll-like receptor 4 (TLR4) and c-Jun N-terminal kinases (JNK) activation and whether heat shock protein 90 (HSP90) mediates these effects.

Materials And Methods: A total of 120 male mice were randomly divided into six groups: sham, ischemia/reperfusion (I/R group), VPreC (vericiguat, 3 mg/kg, administered intravenously 12 hr before ligation), VPreC+HSP90 inhibitor geldanamycin (GA) (geldanamycin, 1 mg/kg, injected intraperitoneally 30 min before ligation), VPostC (vericiguat, 3 mg/kg, administered intravenously ten minutes before reperfusion), and VPostC+GA (geldanamycin, 1 mg/kg, injected intraperitoneally 20 min before reperfusion). The remaining five groups were subjected to 30 min of ischemia followed by two hours of reperfusion.

Light at night negatively affects mood in diurnal primate-like tree shrews via a visual pathway related to the perihabenular nucleus.

To better understand the potential health threats and underlying visual pathways of long-term light at night (LAN) exposure, we adopted a widely accepted diurnal animal model tree shrew (), which is a close relative to primates, and evaluated the deleterious effects of long-term LAN exposure. We used an early-night LAN paradigm that was established in mice to examine behavioral and physiological consequences in adult male tree shrews. We found that 3-wk LAN exposure significantly impaired the mood and long-term memory of tree shrews without affecting the general activity pattern.

Exosomal HSP90 induced by remote ischemic preconditioning alleviates myocardial ischemia/reperfusion injury by inhibiting complement activation and inflammation.

Background/aims: The activation of the complement system and subsequent inflammatory responses are important features of myocardial ischemia/reperfusion (I/R) injury. Exosomes are nanoscale extracellular vesicles that play a significant role in remote ischemic preconditioning (RIPC) cardioprotection. The present study aimed to test whether RIPC-induced plasma exosomes (RIPC-Exo) exert protective effects on myocardial I/R injury by inhibiting complement activation and inflammation and whether exosomal heat shock protein 90 (HSP90) mediates these effects.

Light modulates glucose metabolism by a retina-hypothalamus-brown adipose tissue axis.

Public health studies indicate that artificial light is a high-risk factor for metabolic disorders. However, the neural mechanism underlying metabolic modulation by light remains elusive. Here, we found that light can acutely decrease glucose tolerance (GT) in mice by activation of intrinsically photosensitive retinal ganglion cells (ipRGCs) innervating the hypothalamic supraoptic nucleus (SON).

New targets of morphine postconditioning protection of the myocardium in ischemia/reperfusion injury: Involvement of HSP90/Akt and C5a/NF-κB.

Background: Activation of the complement component 5a (C5a) and nuclear factor κB (NF-κB) signaling is an important feature of myocardial ischemia/reperfusion (I/R) injury and recent studies show that morphine postconditioning (MP) attenuates the myocardial injury. However, the mediating cardioprotective mechanisms remain unclear. The present study explores the role and interaction of heat shock protein 90 (HSP90), Akt, C5a, and NF-κB in MP-induced cardioprotection.

HSP90-Mediates Liraglutide Preconditioning-Induced Cardioprotection by Inhibiting C5a and NF-κB.

Objective: We previously showed that HSP90 is involved in postconditioning cardioprotection by inhibiting complement C5a. Here, we investigated whether HSP90-mediated C5a/NF-κB inhibition is responsible for the cardioprotection conferred by liraglutide.

Methods: Rat hearts underwent a 30 min occlusion of the anterior descending coronary artery, after which reperfusion was performed for 2 h.

Mangiferin Inhibits Human Lung Adenocarcinoma by Suppressing MiR-27b and MiR-92a.

Lung adenocarcinoma (LUAD) is one of the most prevalent malignancies. However, its mechanism and therapeutic strategy remain to be clarified. Mangiferin is a flavonoid derived from the leaves of mango trees of the lacquer family that has many pharmacological and physiological effects.

Role of HSP90 in suppressing TLR4-mediated inflammation in ischemic postconditioning.

Background: Myocardial inflammation mediated by toll-like receptor 4 (TLR4) plays an active role in myocardial ischemia/reperfusion (I/R) injury. Studies show that heat shock protein 90 (HSP90) is involved in ischemic postconditioning (IPostC) cardioprotection. This study investigates the roles of TLR4 and HSP90 in IPostC.

Ischemic postconditioning attenuates the inflammatory response in ischemia/reperfusion myocardium by upregulating miR‑499 and inhibiting TLR2 activation.

Toll-like receptor 2 (TLR2)-mediated myocardial inflammation serves an important role in promoting myocardial ischemic/reperfusion (I/R) injury. Previous studies have shown that miR‑499 is critical for cardioprotection after ischemic postconditioning (IPostC). Therefore, the present study evaluated the protective effect of IPostC on the myocardium by inhibiting TLR2, and also assessed the involvement of microRNA (miR)‑499.

Involvement of HSP90 in ischemic postconditioning-induced cardioprotection by inhibition of the complement system, JNK and inflammation.

Purpose: To investigate whether heat shock protein 90 (HSP90) is involved in complement regulation in ischemic postconditioning (IPC).

Methods: The left coronary artery of rats underwent 30 min of occlusion, followed by 120 min of reperfusion and treatment with IPC via 3 cycles of 30s reperfusion and 30s occlusion. The rats were injected intraperitoneally with 1 mg/kg HSP90 inhibitor geldanamycin (GA) after anesthesia.

Effect of solution chemistry and aggregation on adsorption of perfluorooctanesulphonate (PFOS) to nano-sized alumina.

The interaction of pollutants with nanomaterials has attracted attention due to the extensive application of nanomaterials. In this study, the adsorption behavior of PFOS on nano-alumina with different shapes was investigated. First, the adsorption isotherms and kinetics of PFOS on alumina nanoparticles (NPs) and nanowires (NWs) were measured to calculate thermodynamic parameters.

A short review on human exposure to and tissue distribution of per- and polyfluoroalkyl substances (PFASs).

PFASs are widely distributed in natural and living environment and can enter human bodies via different routes. Many studies have reported that PFASs may be associated with human diseases, such as urine acid and thyroid diseases. In this study, we reviewed PFAS levels in human bodies reported in past seven years, including blood, urine, milk, and tissues (hair and nails).

Recognition of the long range enhancer-promoter interactions by further adding DNA structure properties and transcription factor binding motifs in human cell lines.

The enhancer-promoter interactions (EPIs) with strong tissue-specificity play an important role in cis-regulatory mechanism of human cell lines. However, it still remains a challenging work to predict these interactions so far. Due to that these interactions are regulated by the cooperativeness of diverse functional genomic signatures, DNA spatial structure and DNA sequence elements.

Novel Functional Role of Heat Shock Protein 90 in Mitochondrial Connexin 43-Mediated Hypoxic Postconditioning.

Background/aims: Previous studies have shown that heat shock protein 90 (HSP90)-mediated mitochondrial import of connexin 43 (Cx43) is critical in preconditioning cardioprotection. The present study was designed to test whether postconditioning has the same effect as preconditioning in promoting Cx43 translocation to mitochondria and whether mitochondrial HSP90 modulates this effect.

Methods: Cellular models of hypoxic postconditioning (HPC) from rat heart-derived H9c2 cells and neonatal rat cardiomyocytes were employed.

Global distribution of perfluorochemicals (PFCs) in potential human exposure source-A review.

Human exposure to perfluorochemicals (PFCs) has attracted mounting attention due to their potential harmful effects. Breathing, dietary intake, and drinking are believed to be the main routes for PFC entering into human body. Thus, we profiled PFC compositions and concentrations in indoor air and dust, food, and drinking water with detailed analysis of literature data published after 2010.

Adaptation to visual stimulation modifies the burst firing property of V1 neurons.

The mean firing rate of visual cortical neurons is reduced after prolonged visual stimulation, but the underlying process by which this occurs as well as the biological significance of this phenomenon remains unknown. Computational neuroscience studies indicate that high-frequency bursts in stimulus-driven responses can be transmitted across synapses more reliably than isolated spikes, and thus may carry accurate stimulus-related information. Our research examined whether or not adaptation affects the burst firing property of visual cortical neurons by examining changes in the burst firing changes of V1 neurons during adaptation to the preferred visual stimulus.

Acute lesions of primary visual cortical areas in adult cats inactivate responses of neurons in higher visual cortices.

Psychophysical studies suggest that lateral extrastriate visual cortical areas in cats may mediate the sparing of vision largely by network reorganization following lesions of early visual cortical areas. To date, however, there is little direct physiological evidence to support this hypothesis. Using in vivo single-unit recording techniques, we examined the response of neurons in areas 19, 21, and 20 to different types of visual stimulation in cats with or without acute bilateral lesions in areas 17 and 18.