Cerebellar abnormalities, particularly in Right Crus I (RCrusI), are consistently reported in autism spectrum disorders (ASD). Although RCrusI is functionally connected with ASD-implicated circuits, the contribution of RCrusI dysfunction to ASD remains unclear. Here, neuromodulation of RCrusI in neurotypical humans resulted in altered functional connectivity with the inferior parietal lobule, and children with ASD showed atypical functional connectivity in this circuit. Atypical RCrusI–inferior parietal lobule structural connectivity was also evident in the Purkinje neuron (PN) TscI ASD mouse model. Additionally, chemogenetically mediated inhibition of RCrusI PN activity in mice was sufficient to generate ASD-related social, repetitive, and restricted behaviors, while stimulation of RCrusI PNs rescued social impairment in the PN TscI ASD mouse model. Together, these studies reveal important roles for RCrusI in ASD-related behaviors. Further, the rescue of social behaviors in an ASD mouse model suggests that investigation of the therapeutic potential of cerebellar neuromodulation in ASD may be warranted.

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Coronary arterial disease is the most common cardiovascular disease. Myocardial ischemia-reperfusion injury caused by the initial interruption of organ blood flow and subsequent restoration of organ blood flow is an important clinical problem with various cardiac reperfusion strategies after acute myocardial infarction. Even though blood flow recovery is necessary for oxygen and nutrient supply, reperfusion causes pathological sequelae that lead to the aggravation of ischemic injury. At present, although it is known that injury will occur after reperfusion, clinical treatment always focuses on immediate recanalization. Mitochondrial fusion, fission, biogenesis, autophagy, and their intricate interaction constitute an effective mitochondrial quality control system. The mitochondrial quality control system plays an important role in maintaining cell homeostasis and cell survival. The removal of damaged, aging, and dysfunctional mitochondria is mediated by mitochondrial autophagy. With the help of appro-priate changes in mitochondrial dynamics, new mitochondria are produced through mitochondrial biogenesis to meet the energy needs of cells. Mitochondrial dysfunction and the resulting oxidative stress have been associated with the pathogenesis of ischemia/reperfusion (I/R) injury, which play a crucial role in the pathophysiological process of myocardial injury. This review aimed at elucidating the mitochondrial quality control system and establishing the possibility of using mitochondria as a potential therapeutic target in the treatment of I/R injuries.

The transmission of mobile wound signals along the phloem pathway is essential to the activation of wound-induced systemic response/resistance, which requires an upsurge of jasmonic acid (JA) in the distal undamaged leaves. Among these mobile signals, the electrical signal mediated by the glutamatedependent activation of several clade three GLUTAMATE RECEPTOR-LIKE (GLR3) proteins is involved in the stimulation of JA production in distal leaves. However, whether JA acts as a mobile wound signal and, if so, how it is transmitted and interacts with the electrical signal remain unclear. Here, we show that JA was translocated from the local to distal leaves in Arabidopsis, and this process was predominantly regulated by two phloem-expressed and plasma membrane-localized jasmonate transporters, At-JAT3 and AtJAT4. In addition to the cooperation between AtJAT3/4 and GLR3.3 in the regulation of long-distance JA translocation, our findings indicate that importer-mediated cell-cell JA transport is important for driving the loading and translocation of JA in the phloem pathway in a self-propagating manner.

Prostate MRI before biopsy could predict the presence of PCa and HGPCa, especially in younger patients. The incorporation of MRI in nomograms could increase predictive accuracy.