Studies of “emaciation ailment” in the Bactrian camel

The clinical signs of disorder known locally as “emaciation ailment” in Bactrian camels in Haizi, Qinhai, China were defined. They included pica, emaciation, dyskinesia, deprived appetites and anemia. We found that concentrations of copper (Cu) in soil and forage from affected and  unaffected areas were similar, but the concentrations of sulfur (S) in soil and forage were significantly higher (P<0.01) in affected than in unaffected areas. Concentrations of Cu in blood, hair and liver from the affected camels were significantly lower (P<0.01) than those in unaffected camels. Fifty affected camels grazing on affected pastures were consuming an average of 136 mg of Cu/d for 80 d by a free-choice, salt-basedtrace mineral supplement. Liver Cu increased over time in all camels. However, the mean Cu content of the liver was significantly lower in the camels supplemented with salt-based trace mineral as compared with those in the healthy camels at the end of the study. Twelve affected camels were removed from the affected pastures and allocated to one of two treatments for 80 d, consisting of supplement providing 136 mg/d of either inorganic (Cu sulfate; n = 6) or organic (Availa-Cu n = 6) Cu. Liver Cu increased over time in all camels regardless of treatment; however, camels treated with Availa-Cu have higher mean liver Cu contents than those receiving Cu sulfate (163.6 ± 13.5 and 228.9 ± 26.7 μg/g, for Cu sulfate and Availa-Cu, respectively) at the end of the study. Mean Cu content in the liver of camels received Availa-Cu was significantly higher than that in supplemented camels with Cu sulfate. In all treated camels, some signs of recovery were evident in 20 - 30 days after, and appetite and vigor were improved. Thus, it is reasonable to conclude that ailments of camels in the Haizi area are caused by a secondary Cu deficiency, mainly due to high sulfur content in soil and forage.Key words: Bactrian camel, sulfur, copper, deficiency, “emaciation ailment”

Stress, Coping and Suicide Ideation in Chinese College Students

The study was to examine 1) whether stress and coping styles could significantly predict the probability of suicide ideation; 2) and whether coping styles were mediators or moderators on the association between life stress and suicide ideation. The survey was conducted in a sample of 671 Chinese college students. Approximately twenty percent students reported having suicide ideation. Life stress, active coping styles, and passive coping styles all had independent effect on the probability of suicide ideation. Passive coping styles, especially fantasizing, mediated the relation between life stress and suicide ideation. Moderation hypotheses were not supported. Implications of the findings and future directions were discussed

Stress, Coping and Suicide Ideation in Chinese College Students

The study was to examine 1) whether stress and coping styles could significantly predict the probability of suicide ideation; 2) and whether coping styles were mediators or moderators on the association between life stress and suicide ideation. The survey was conducted in a sample of 671 Chinese college students. Approximately twenty percent students reported having suicide ideation. Life stress, active coping styles, and passive coping styles all had independent effect on the probability of suicide ideation. Passive coping styles, especially fantasizing, mediated the relation between life stress and suicide ideation. Moderation hypotheses were not supported. Implications of the findings and future directions were discussed

Ferroptosis Contributes to Isoflurane Neurotoxicity

The underlying mechanisms of isoflurane neurotoxicity in the developing brain remain unclear. Ferroptosis is a recently characterized form of programmed cell death distinct from apoptosis or autophagy, characterized by iron-dependent reactive oxygen species (ROS) generation secondary to failure of glutathione-dependent antioxidant defenses. The results of the present study are the first to demonstrate in vitro that ferroptosis is a central mechanism contributing to isoflurane neurotoxicity. We observed in embryonic mouse primary cortical neuronal cultures (day-in-vitro 7) that 6 h of 2% isoflurane exposure was associated with decreased transcription and protein expression of the lipid repair enzyme glutathione peroxidase 4. In parallel, isoflurane exposure resulted in increased ROS generation, disruption in mitochondrial membrane potential, and cell death. These effects were significantly attenuated by pre-treatment with the selective ferroptosis inhibitor ferrostatin-1 (Fer-1). Collectively, these observations provide a novel mechanism for isoflurane-induced injury in the developing brain and suggest that pre-treatment with Fer-1 may be a potential clinical intervention for neuroprotection

Structural and Functional Characterization of the FadR Regulatory Protein from Vibrio alginolyticus

The structure of Vibrio cholerae FadR (VcFadR) complexed with the ligand oleoyl-CoA suggests an additional ligand-binding site. However, the fatty acid metabolism and its regulation is poorly addressed in Vibrio alginolyticus, a species closely-related to V. cholerae. Here, we show crystal structures of V. alginolyticus FadR (ValFadR) alone and its complex with the palmitoyl-CoA, a long-chain fatty acyl ligand different from the oleoyl-CoA occupied by VcFadR. Structural comparison indicates that both VcFadR and ValFadR consistently have an additional ligand-binding site (called site 2), which leads to more dramatic conformational-change of DNA-binding domain than that of the E. coli FadR (EcFadR). Isothermal titration calorimetry (ITC) analyses defines that the ligand-binding pattern of ValFadR (2:1) is distinct from that of EcFadR (1:1). Together with surface plasmon resonance (SPR), electrophoresis mobility shift assay (EMSA) demonstrates that ValFadR binds fabA, an important gene of unsaturated fatty acid (UFA) synthesis. The removal of fadR from V. cholerae attenuates fabA transcription and results in the unbalance of UFA/SFA incorporated into membrane phospholipids. Genetic complementation of the mutant version of fadR (Δ42, 136-177) lacking site 2 cannot restore the defective phenotypes of ΔfadR while the wild-type fadR gene and addition of exogenous oleate can restore them. Mice experiments reveals that VcFadR and its site 2 have roles in bacterial colonizing. Together, the results might represent an additional example that illustrates the Vibrio FadR-mediated lipid regulation and its role in pathogenesis

Original Article Diagnosis of children's attention deficit hyperactivity disorder (ADHD) and its association with cytomegalovirus infection with ADHD: a historical review

Abstract: As the most common mental disorder identified in children and teenagers, attention deficit hyperactivity disorder (ADHD) affects millions of children and their families, making it a critical health issue worldwide. This article reviewed the historical opinions about the diagnosis of ADHD and defined different subtypes of this disorder. It also summarized the current diagnostic criteria and available medications. After re-visiting the etiology of ADHD in the sense of both genetic and environment factors, it was further hypothesized that viral infection might be involved in ADHD pathogenesis. Human cytomegalovirus (HCMV) infection may be associated with ADHD, although both clinical observations and animal studies need to be performed for validation

Gut microbiota, a hidden protagonist of traditional Chinese medicine for acute ischemic stroke

Acute ischemic stroke (AIS) is one of the leading diseases causing death and disability worldwide, and treatment options remain very limited. Traditional Chinese Medicine (TCM) has been used for thousands of years to treat ischemic stroke and has been proven to have significant efficacy, but its mechanism of action is still unclear. As research related to the brain-gut-microbe axis progresses, there is increasing evidence that the gut microbiota plays an important role during AIS. The interaction between TCM and the gut microbiota has been suggested as a possible key link to the therapeutic effects of TCM. We have compiled and reviewed recent studies on the relationship between AIS, TCM, and gut microbiota, with the expectation of providing more ideas to elucidate the mechanism of action of TCM in the treatment of AIS

miR-200a attenuated oxidative stress, inflammation, and apoptosis in dextran sulfate sodium-induced colitis through activation of Nrf2

IntroductionOxidative stress and inflammatory responses are critical factors in ulcerative colitis disease pathogenesis. Nuclear factor erythroid 2-related factor 2 (Nrf2) modulates oxidative stress and suppresses inflammatory responses, and the protective benefits of Nrf2 activation have been associated with the therapy of ulcerative colitis. MicroRNA-200a (miR-200a) could target Kelch-like ECH-associated protein 1 (Keap1) and activate the Nrf2-regulated antioxidant pathway. Nevertheless, whether miR-200a modulates the Keap1/Nrf2 pathway in dextran sulfate sodium (DSS)-induced colonic damage is unknown. Here, our research intends to examine the impact of miR-200a in the model of DSS-induced colitis.MethodsPrior to DSS intervention, we overexpressed miR-200a in mice for four weeks using an adeno-associated viral (AAV) vector to address this problem. ELISA detected the concentration of inflammation-related cytokines. The genes involved in inflammatory reactions and oxidative stress were identified using quantitative reverse transcription-polymerase chain reaction (qRT-PCR), western blot, and immunofluorescence. Moreover, we applied siRNAs to weakened Nrf2 expression to confirm the hypothesis that miR-200a provided protection via Nrf2.ResultsThe present study discovered miR-200a down-regulation, excessive inflammatory activation, enterocyte apoptosis, colonic dysfunction, and Keap1/Nrf2 antioxidant pathway inactivation in mouse colitis and NCM460 cells under DSS induction. However, our data demonstrated that miR-200a overexpression represses Keap1 and activates the Nrf2 antioxidant pathway, thereby alleviating these adverse alterations in animal and cellular models. Significantly, following Nrf2 deficiency, we failed to observe the protective benefits of miR-200a against colonic damage.DiscussionTaken together, through activating the Keap1/Nrf2 signaling pathway, miR-200a protected against DSS-induced colonic damage. These studies offer an innovative therapeutic approach for ulcerative colitis

The role of Nrf2 in the pathogenesis and treatment of ulcerative colitis

Ulcerative colitis (UC) is a chronic inflammatory bowel disease involving mainly the colorectal mucosa and submucosa, the incidence of which has been on the rise in recent years. Nuclear factor erythroid 2-related factor 2 (Nrf2), known for its key function as a transcription factor, is pivotal in inducing antioxidant stress and regulating inflammatory responses. Numerous investigations have demonstrated the involvement of the Nrf2 pathway in maintaining the development and normal function of the intestine, the development of UC, and UC-related intestinal fibrosis and carcinogenesis; meanwhile, therapeutic agents targeting the Nrf2 pathway have been widely investigated. This paper reviews the research progress of the Nrf2 signaling pathway in UC