This is first study to show that hypertriglyceridemia induces BDNF expression in the rat submandibular gland and suggests that salivary BDNF is associated with lipid metabolism.

This is first study to show that hypertriglyceridemia induces BDNF expression in the rat submandibular gland and suggests that salivary BDNF is associated with lipid metabolism.

The aim of the present study is to demonstrate the effects of inhaled methyl methacrylate (MMA) on the excitability of neurons in the area postrema (AP). We also investigated the relation between vagal afferent inputs and responding cells in the AP.

We set up two groups of experimental animals, such as rats inhaling MMA and rats inhaling room air. To visualize the changes of AP neuron excitability after inhalation of MMA for 90min, c-Fos protein expression was identified and quantified by immunohistochemical analysis. Some rats receiving ventral gastric branch vagotomy were also subjected to the abovementioned experiment.

The number of c-Fos-immunoreactive (Fos-ir) cells in the MMA group was more than six times greater than that of the control group (statistically significant, p<0.01). In vagotomized rats inhaling MMA, markedly smaller number of Fos-ir cells was identified in the AP compared to that of rats inhaling MMA without vagotomy.

These results indicate that inhalation of MMA increases neuronal excitability in the AP, suggesting that vagal afferent inputs are involved in the induction mechanism of Fos-ir cells by MMA.

These results indicate that inhalation of MMA increases neuronal excitability in the AP, suggesting that vagal afferent inputs are involved in the induction mechanism of Fos-ir cells by MMA.Apoptosis, necroptosis and pyroptosis represent three major regulated cell death modalities. Apoptosis features cell shrinkage, nuclear fragmentation and cytoplasm-blebbing. Necroptosis and pyroptosis exhibit osmotic imbalances in the cell accompanied by early membrane ruptures, which morphologically resembles necrosis. Importantly, these two lytic cell death forms facilitate the release of damage associated molecular patterns into the extracellular space leading to inflammatory response. Whereas, during apoptosis, the membrane integrity is preserved and the apoptotic cell is removed by neighbouring cells ensuring the avoidance of immune-stimulation. Viruses comprise a versatile group of intracellular pathogens, which elicit various strategies to infect and to propagate. Viruses are recognized by a myriad of pathogen recognition receptors in the human cells, which consequently lead to activation of the immune system and in certain circumstances cell-autonomous cell death. Importantly, the long-standing view that a cell death inducing capacity of a virus is equal to its pathogenic potential seems to be only partially valid. The altruistic cell death of an infected cell may serve the whole organism by ultimately curbing the way of virus manufacturing. In fact, several viruses express “anti-cell death” proteins to avoid this viral-defence mechanism. LY2874455 clinical trial Conversely, some viruses hijack cell death pathways to selectively destroy cell populations in order to compromise the immune system of the host. This review discusses the pros and cons of virus induced cell death from the perspective of the host cells and attempts to provide a comprehensive overview of the complex network of cell death signalling in virus infection.Despite the various mechanisms that involved in the pathogenesis of Alzheimer’s disease (AD), neuronal damage and synaptic dysfunction are the key events leading to cognition impairment. Therefore, neuroprotection and neurogenesis would provide essential alternatives to the rescue of AD cognitive function. Here we demonstrated that extracellular vesicles secreted from adipose-derived mesenchymal stem cells (ADSCs-derived EVs, abbreviated as EVs) entered the brain quickly and efficiently following intranasal administration, and majorly accumulated in neurons within the central nervous system (CNS). Proteomics analysis showed that EVs contained multiple proteins possessing neuroprotective and neurogenesis activities, and neuronal RNA sequencing showed genes enrichment in neuroprotection and neurogenesis following the treatment with EVs. As a result, EVs exerted powerful neuroprotective effect on Aβ1-42 oligomer or glutamate-induced neuronal toxicity, effectively ameliorated neurologic damage in the whole brain areas, remarkably increased newborn neurons and powerfully rescued memory deficits in APP/PS1 transgenic mice. EVs also reduced Aβ deposition and decreased microglia activation although in a less extent. Collectively, here we provide direct evidence that ADSCs-derived EVs may potentially serve as an alternative for AD therapy through alleviating neuronal damage and promoting neurogenesis.Pharmaceutical drugs are an important part of the global healthcare system, with some estimates suggesting over 50% of the world’s population takes at least one medication per day. Most drugs are delivered as immediate-release formulations that lead to a rapid increase in systemic drug concentration. Although these formulations have historically played an important role, they can be limited by poor patient compliance, adverse side effects, low bioavailability, or undesirable pharmacokinetics. Drug delivery systems featuring first-order release kinetics have been able to improve pharmacokinetics but are not ideal for drugs with short biological half-lives or small therapeutic windows. Zero-order drug delivery systems have the potential to overcome the issues facing immediate-release and first-order systems by releasing drug at a constant rate, thereby maintaining drug concentrations within the therapeutic window for an extended period of time. This release profile can be used to limit adverse side effects, reduce dosing frequency, and potentially improve patient compliance. This review covers strategies being employed to attain zero-order release or alter traditionally first-order release kinetics to achieve more consistent release before discussing opportunities for improving device performance based on emerging materials and fabrication methods.