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Johnston Cheng posted an update 6 months, 1 week ago
The MeHg exposure increased total mercury levels in spinal cord parenchyma, which increased lipid peroxidation and nitrite levels , and reduced antioxidant status. The proteomic analysis showed several proteins related to biological processes, cellular components and molecular functions. Moreover, according to the ORA analysis, the proteins are involved in processes such as mitochondrial activity, stress response, cytoskeleton and apoptosis. Therefore, we concluded that exposure to low doses of MeHg can activate the oxidative stress pathway and thus, modulate the status of regulation of several important proteins.Curcumin has protective effects in several acute kidney injury models, including that induced by potassium dichromate (K2Cr2O7). The protective effect of curcumin in this experimental model has been associated to the preservation of mitochondrial bioenergetics. This study is aimed at evaluating whether or not curcumin’s protective effect in mitochondrial bioenergetics is related to the modulation of mitochondrial dynamics and biogenesis. Wistar rats were treated with a single subcutaneous dose of K2Cr2O7 (12.5 mg/kg) or received curcumin (400 mg/kg/day) by oral gavage 10 days before and one day after the K2Cr2O7 injection. K2Cr2O7 induced kidney dysfunction and increased mitochondrial hydrogen peroxide production, while decreasing the respiration directly attributable to oxidative phosphorylation and mitochondrial membrane potential. In mitochondria, K2Cr2O7 increased fission and reduced fusion. Structural analysis of mitochondria in the proximal tubular cells corroborated their fragmentation and loss of crests’ integrity. Regarding mitochondrial biogenesis, K2Cr2O7 decreased peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) levels. Conversely, curcumin treatment mitigated the aforementioned alterations and increased the expression of the mitochondrial transcription factor A (TFAM). Taken together, our results suggest that curcumin can protect against renal injury by modulating mitochondrial homeostasis, mitigating alterations in bioenergetics and dynamics, possibly by stimulating mitochondrial biogenesis.Staphylococcus aureus is emerging as complicated pathogen because of its wide-ranging origin, multiple variants, and compromised antibiotic susceptibilities. Current study was planned to find lineage of hospital acquired methicillin resistant Staphylococcus aureus (HA-MRSA), and its comparative phenotypic clinico-epidemiology with vancomycin resistant S. aureus (VRSA). A total of (n = 200) samples were aseptically collected from wound, nose, and cerebrospinal fluid of patients from metropolitan and rural background hospitals along with on spot filling in of questionnaire. Phylogenetic analysis of HA-MRSA was identified by targeting mecA gene in S. aureus. At optimal tree branch length of 1.91 and evolutionary distance 0.1, high level sequence similarity (97%-99%) was observed with different strains of S. aureus isolated from both human and animal. Non-descriptive statistics at 5% probability found 61% S. aureus, while 43.44% of them were HA-MRSA, 92.62% VRSA, and 42.62% were both MRSA and VRSA. Among assumed risk factors, use of antibiotics, venous catheterization, chronic disease, pre-hospital visits, and ICU admitted patients showed significant association (p less then 0.05) with pathogen. HA-MRSA was 37.50%, 80%, and 37.50% sensitive to chloramphenicol, gentamicin, and oxacillin, respectively. While less then 50% of VRSA were sensitive against oxacillin, enoxacin, and chloramphenicol. A significant difference (p less then 0.05) of percentage responses of MRSA and VRSA at resistant, intermediate, and sensitive cadre against all antibiotics except chloramphenicol was obvious in this study. The Current study concluded higher prevalence of MRSA & VRSA, significant association of risk factors, limiting antibiotic susceptibility profile, and genetic transfer at animal-human interface which suggests further studies cum preventive strategies to be planned.Cl-amidine, a peptidylarginine deiminase inhibitor, has been shown to ameliorate the disease course and clinical manifestation in variety of disease models. Due to the beneficial effects of Cl-amidine, it has been becoming the hottest compound for the study in inflammatory diseases. However, the anti-inflammatory activity of Cl-amidine in lipopolysaccharide (LPS)-induced mouse mastitis remains unclear. In this study, we investigated the effects of Cl-amidine on LPS-induced mastitis mouse model. The mouse mastitis model was established by injection of LPS through the canals of the mammary gland. Cl-amidine was administered intraperitoneally 1 h before LPS treatment. The results showed that Cl-amidine significantly attenuated the damage of the mammary gland, which suppressed the activity of myeloperoxidase (MPO). The real-time PCR results indicated that Cl-amidine inhibited the production of TNF-α, IL-1β and IL-6 in LPS-induced mouse mastitis. Moreover, the western blot results indicated that Cl-amidine decreased the phosphorylation of IκB, p65, p38, ERK and the expression of NLRP3 in LPS-induced mouse mastitis. Furthermore, the neutrophils extracellular traps (NETs) were determined by Quant-iT picogreen dsDNA assay kit®, which suggested that Cl-amidine significantly inhibited the NETs in mouse serum. This study demonstrated that Cl-amidine decreased the pathological injury in LPS-induced mouse mastitis by inhibiting NF-κB, MAPK, NLRP3 signaling pathway and NETs release, which provides a potential candidate for the treatment of mastitis.Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) and resistant bacterial co-infection is a serious threat to pig farms. This study was aimed to determine the characteristics of the co-infection of PRRSV with resistant bacterial strains in pig farms. The presence of the PRRSV orf5 gene was confirmed by RT-PCR from 395 samples. Selleckchem IPI-549 Bacterial strains were isolated from PRRSV positive samples. Antimicrobial drug susceptibility was determined by the Kirby-Bauer method. Resistant genes were determined by PCR amplification and sequencing. The whole genome of carbapenems resistant E.coli was sequenced and analyse. A total of 75 samples were PRRSV positive, and 45 different orf5 sequences were finally determined. Phylogenetic analysis showed that 45 sequences are clustered into four groups, including JXA1-like, NADC30-like, GD-QY2-like, and CH-1a-like viruses. Twenty-one samples were identified with PRRSV and amoxicillin resistance bacterial co-infection, and 23 were found with amoxicillin resistance (including 15 Escherichia coli, 3 Klebsiella pneumoniae, 2 Haemophilus parasuis, 1 Actinobacillus pleuropneumoniae, 1 Pasteurella multocida, and 1 Proteus mirabilis).