Notes

Viral as well as Host Qualities Underlying the Roots regarding Zoonotic Coronaviruses in Softball bats.
Nanoparticulate titanium dioxide (Nano-TiO
) has been widely used in food industry, and it has been demonstrated to have adverse effects on mice and human stomach, but its mechanism is rarely concerned. The aim of this study is to determine the effects of nano-TiO
on the stomach and confirm the role of oxidative stress and apoptosis in the mice gastric damage caused by nano-TiO
, as well as its molecular mechanisms.

Mice were continuously exposed to nano-TiO
with 1.25, 2.5 and 5mg/kg bw by intragastric administration for 9 months in the present study. The ultrastructure, levels of reactive oxygen species (ROS) and peroxides, activities of antioxidant enzymes and mitochondria-related enzymes, ATP contents as well as apoptosis-related factors expression in mice stomach were examined.

Oxidative stress, apoptosis and nano-TiO
aggregation were found in gastric mucosal smooth muscle cells after nano-TiO
exposure. Nano-TiO
exposure also resulted in the over-production of ROS and peroxides, decrease of ATP production and activities of antioxidant enzymes and mitochondria-related ATPases, upregulation of apoptosis-related factors including γH2AX, Cyt c, caspase 3, and p-JNK expression, and down-regulation of Bcl-2 expression in mice stomach.

The gastric toxicity of mice induced by chronic exposure to low dose nano-TiO
may be associated with oxidative stress and mitochondria-mediated apoptosis in mice.
The gastric toxicity of mice induced by chronic exposure to low dose nano-TiO2 may be associated with oxidative stress and mitochondria-mediated apoptosis in mice.We designed this work to examine the curative role of L-carnitine (LCAR) in a rat model of cisplatin (CDDP)-induced kidney injury. We induced kidney injury in rats by a single intraperitoneal injection of 5 mg/kg of CDDP. Fifteen days post injection, rats were orally supplemented with 354 mg/kg of LCAR for another 15 days. Kidney tissues were subjected to histo-biochemical analysis along with mRNA gene expression quantification for cytoskeleton proteins encoding genes (vimentin, nestin, and connexin 43) by real-time reverse transcription polymerase chain reaction. LCAR reversed CDDP-induced renal structural and functional impairments. LCAR significantly declined serum urea and creatinine concentrations, restored oxidant/antioxidant balance, reversed inflammation, and antagonized caspase 3-mediated apoptotic cell death in renal tissues. Moreover, LCAR effectively down-regulated cytoskeleton proteins mRNA levels, reflecting amelioration of CDDP-provoked podocyte injury. We concluded that LCAR has a favorable therapeutic utility against CDDP-induced kidney injury.Traumatic brain injury (TBI) is an insult to the brain from an external mechanical force, leading to temporary/permanent secondary injuries, i.e. impairment of cognitive, physical, and psycho-social functions with altered consciousness. The leading mechanism responsible for neuronal damage following TBI is an increase in oxidative reactions initiated by free radicals generated by the injury along with various other mechanisms. Nerolidol is reported to have potent antioxidant and anti-neuroinflammatory properties. The present study was designed to explore the neuroprotective effect of nerolidol in weight-drop-induced TBI in rats. Animals were injured on the 1st day by dropping a free-falling weight of 200 gm from a height of 1 m through a guide pipe onto the exposed skull. After 14 days of injury, nerolidol (25, 50, and 100 mg/kg, i.p.) treatment was given for the next 14 days. Locomotor activity and motor coordination were evaluated using an actophotometer and rotarod, respectively. Cognitive impairment was observed through the Morris Water Maze and Object Recognition Test. On the 29th day, animals were sacrificed, and their brains were collected for the biochemical estimation. The weight drop model significantly decreased locomotor activity, motor coordination, increased Acetylcholinesterase (AChE) activity, oxidative stress, and induced cognitive deficits in TBI rats. Nerolidol significantly improved locomotor activity, reversed motor incoordination and cognitive impairment, and reduced the AChE activity and oxidative/nitrosative stress. The present study demonstrates the promising neuroprotective effects of nerolidol, which might improve the quality of life of TBI patients.Myotonic dystrophy (DM) is a genetic disorder featured by muscular dystrophy. It is caused by CUG expansion in the myotonic dystrophy protein kinase gene that leads to aberrant signaling and impaired myocyte differentiation. Many studies have shown that microRNAs are involved in the differentiation process of myoblasts. The purpose of this study was to investigate how the miR-322/miR-503 cluster regulates intracellular signaling to affect cell differentiation. The cell model of DM1 was employed by expressing GFP-CUG200 or CUGBP Elav-like family member 1 (Celf1) in myoblasts. Immunostaining of MF-20 was performed to examine myocyte differentiation. qRT-PCR and western blot were used to determine the levels of Celf1, MyoD, MyoG, Mef2c, miR-322/miR-503, and mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK/ERK) signaling. Selleckchem GSK1120212 Dual luciferase assay was performed to validate the interaction between miR-322/miR-503 and Celf1. CUG expansion in myoblasts impaired the cell differentiation, increased the Celf1 level, but it decreased the miR-322/miR-503 levels. miR-322/miR-503 mimics restored the impaired differentiation caused by CUG expansion, while miR-322/miR-503 inhibitors further suppressed. miR-322/miR-503 directly targeted Celf1 and negatively regulated its expression. Knockdown of Celf1 promoted myocyte differentiation. Further, miR-322/miR-503 mimics rescued the impaired differentiation of myocytes caused by CUG expansion or Celf1 overexpression through suppressing of MEK/ERK signaling. miR-322/miR-503 cluster recover the defective myocyte differentiation caused by RNA-toxic via targeting Celf1. Restoring miR-322/miR-503 levels could be an avenue for DM1 therapy.Cigarette smoke (CS) is one of the severe risk factors for the development of the pulmonary disease. However, the underlying mechanisms, especially the CS-induced the human bronchial epithelial cells (BEAS-2B) apoptosis related to endoplasmic reticulum stress (ERS) and autophagy, remains to be studied. This study aims to investigate the relationship between ERS and autophagy in apoptosis induced by CS condensate (CSC). BEAS-2B cells were stimulated with 0.02, 0.04 and 0.08 mg/ml CSC for 24 h to detect the ERS, autophagy and apoptosis. Then, ERS and autophagy of BEAS-2B cells were inhibited, respectively, by using 4-PBA and 3-MA, and followed by CSC treatment. The results showed that CSC decreased cell viability, increased cell apoptosis, elevated cleaved-caspase 3/pro-caspase 3 ratio and Bax expressions, but decreased Bcl-2 expressions. The GRP78 and CHOP expressions and LC3-II/LC3-I ratio were dose-dependently increased. The structure of the endoplasmic reticulum was abnormal and the number of autolysosomes was increased in BEAS-2B cells after CSC stimulation.
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