Notes

Postmortem whole-genome sequencing over a dried blood vessels place pinpoints a novel homozygous SUOX alternative triggering singled out sulfite oxidase deficiency.
The results of this project suggest immersing students in a specialty area may be a first step in alleviating the shortage in these areas. Oxidative stress exacerbates brain damage following ischemia-reperfusion and traumatic brain injury (TBI). Management of TBI and critically ill patients commonly involves use of propofol, a sedation medication that acts as a general anesthetic with inherent antioxidant properties. Here we review available evidence from animal model systems and clinical studies that propofol protects against ischemia-reperfusion injury. However, evidence of propofol toxicity in humans exists and manifests as a rare complication, "propofol infusion syndrome" (PRIS). Evidence in animal models suggests that brain injury induces expression of the p75 neurotrophin receptor (p75NTR), which is associated with proapoptotic signaling. p75NTR-mediated apoptosis of neurons is further exacerbated by propofol's superinduction of p75NTR and concomitant inhibition of neurotrophin processing. Propofol is toxic to neurons but not astrocytes, a type of glial cell. Evidence suggests that propofol protects astrocytes from oxidative stress and stimulates astroglial-mediated protection of neurons. One may speculate that in brain injury patients under sedation/anesthesia, propofol provides brain tissue protection or aids in recovery by enhancing astrocyte function. Nevertheless, our understanding of neurologic recovery versus long-term neurological sequelae leading to neurodegeneration is poor, and it is also conceivable that propofol plays a partial as yet unrecognized role in long-term impairment of the injured brain. Copper (Cu), a transition metal, is an essential trace element in human and animal nutrition at low concentration, but Cu has toxic effects on tissues and organs at high concentration. Endoplasmic reticulum (ER) is a toxicological target in Cu poison. Thus far, no studies have focused on the relationship among copper, endoplasmic reticulum (ER) stress and apoptosis in animal and human livers. In the present study, mice treated with copper sulfate (CuSO4) were used to assess the impacts of copper on ER stress and hepatic apoptosis. A total of 240 mice were orally administered with 0 (control), 10, 20 and 40 mg/kg of CuSO4 for 42 days. The results indicated that CuSO4 at 10 mg/kg markedly induced hepatocyte apoptosis and ER stress. In addition, ER stress was characterized by the increased mRNA and protein levels of glucose-regulated protein 78 (GRP78) and 94 (GRP94). Furthermore, ER stress-triggered 3 apoptotic pathways were also activated by the increased intracellular calcium and up-regulated expression levels of genes involved in growth arrest- and DNA damage-inducible gene 153 (Gadd153/CHOP), c-Jun N-terminal kinase (JNK) and cysteine aspartate-specific protease 12 (caspase-12) signaling pathways in CuSO4-treated mice. In conclusion, CuSO4-induced ER stress can promote hepatic apoptosis in mice by activating CHOP, JNK and caspase-12 signaling pathways. Numerous studies have demonstrated adverse effects on human health after exposure to fine particulate matter (PM2.5). However, it is still not clear how the toxicological effects and the health risks vary among PM samples of different compositions and concentrations. DN02 In this study, we examined effects of region- and season-dependent differences of PM2.5 on cytotoxicity, and the contributions of PAHs, nitro-PAHs (N-PAHs) and hydroxy-PAHs (OH-PAHs) to PM2.5 toxicity by determining different toxicological indicators in three lung cell lines. The results illustrated significant differences in components concentrations and biological responses elicited by PM2.5 collected in different cities and seasons. The concentrations of most PAHs, N-PAHs and OH-PAHs were much higher in Taiyuan than in Guangzhou. PM2.5 from Taiyuan exhibited lower cell viability and higher reactive oxygen species (ROS) and interleukin-6 (IL-6) release on lung cells than those from Guangzhou. Specifically, PM2.5 collected in summer from Taiyuan caused higher levels of pro-inflammatory responses and oxidative potential than those collected in winter. The correlation analysis between 19 PAHs, 17 N-PAHs and 12 OH-PAHs and the measured indicators demonstrated that PAHs were more related to PM2.5-induced CCK-8 cytotoxicity and IL-6 release in Taiyuan while N-PAHs and OH-PAHs were more related to PM2.5-induced CCK-8 cytotoxicity and dithiothreitol (DTT)-based redox activity in Guangzhou, suggesting that the toxicity of PM2.5 from Taiyuan was mostly correlated with PAHs while the toxicity of PM2.5 from Guangzhou was closely associated with N-PAHs and OH-PAHs. These results revealed that composition differences in PM2.5 from different regions and seasons significantly accounted for the differences of their toxicological effects. Metal enriched areas represent important and dynamic microbiological ecosystems. In this study, the draft genome of a uranium (U) tolerant bacterium, Chryseobacterium sp. strain PMSZPI, isolated from the subsurface soil of Domiasiat uranium ore deposit in Northeast India, was analyzed. The strain revealed a genome size of 3.8 Mb comprising of 3346 predicted protein-coding genes. The analysis indicated high abundance of genes associated with metal resistance and efflux, transporters, phosphatases, antibiotic resistance, polysaccharide synthesis, motility, protein secretion systems, oxidoreductases and DNA repair. Comparative genomics with other closely related Chryseobacterium strains led to the identification of unique inventory of genes which were of adaptive significance in PMSZPI. Consistent with the genome analysis, PMSZPI showed superior tolerance to uranium and other heavy metals. The metal exposed cells exhibited transcriptional induction of metal translocating PIB ATPases suggestive of their involvement in metal resistance. Efficient U binding (~90% of 100 μM U) and U bioprecipitation (~93-94% of 1 mM U at pH 5, 7 and 9) could be attributed as uranium tolerance strategies in PMSZPI. The strain demonstrated resistance to a large number of antibiotics which was in agreement with in silico prediction. Reduced gliding motility in the presence of cadmium and uranium, enhanced biofilm formation on uranium exposure and tolerance to 1.5 kGy of 60Co gamma radiation were perceived as adaptive responses in PMSZPI. Overall, the positive correlation observed between uranium/metal tolerance abilities predicted using genome analysis and the functional characterization reinforced the multifaceted adaptation strategies employed by PMSZPI for its survival in the soil of uranium ore deposit comprising of high concentrations of uranium and other heavy metals.
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