[A clinical and pathological report of delayed encephalopathy after heat stroke].

Objective: To explore the clinical manifestations, dynamic neuroimaging changes and brain histopathologic characteristics of a patient with delayed encephalopathy after heat stroke. Methods: In October 2019, the clinical manifestations, electroencephalogram, cerebrospinal fluid, imaging changes and brain histopathological characteristics of a patient with brain damage caused by heat stroke were retrospectively analyzed. Results: The patient was a 40-year-old male who suddenly appeared dizziness, unconscious, high fever when working in the high temperature environment. The EEG showed diffuse slow wave activity. Early CT was normal, and abnormal signals gradually appeared in the basal ganglia region of the thalamus after a few days. In the late, the MRI found a large area of abnormal signals under the cerebral cortex, and white matter was involved. Pathological examination of brain biopsy showed that cortical neuron loss, loose white matter changes, and significant demyelination changes, while no inflammatory cell infiltration was observed in subarachnoid space, meninges, and dermal white matter. Conclusion: Imaging examination dynamic changes of the delayed encephalopathy is important in the heat stroke, and the main pathological manifestation is demyelination.

Osteocalcin prevents insulin resistance, hepatic inflammation, and activates autophagy associated with high-fat diet-induced fatty liver hemorrhagic syndrome in aged laying hens.

The aim of this study was to investigate the effects of osteocalcin (OCN) on fatty liver hemorrhagic syndrome (FLHS) in aged laying hens. Thirty 68-week-old White Plymouth laying hens were randomly assigned into conventional single-bird cages, and the cages were randomly allocated into one of 3 treatments (n = 10): normal diet (ND + vehicle, ND + V), high-fat diet (HFD + vehicle, HFD + V), and HFD + OCN (3 µg/bird, 1 time/2 d, i.m.) for 40 d. At day 30, oral glucose tolerance tests (OGTT) and insulin tolerance tests (ITT) were performed. At the end of experiment, the hens were euthanized followed by blood collection. The plasma aspartate transaminase (AST), alkaline phosphatase (ALP), total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) were measured using an automatic biochemistry analyzer. Pathological changes in the liver were examined under both light and transmission electron microscopes. The plasma inflammatory factors including interleukin-1 (IL-1), IL-6, and tumor necrosis factor-alpha (TNF-α) were analyzed by ELISA, and the gene expressions of these inflammatory factors in the liver were analyzed by real-time PCR. The level of oxidative stress was evaluated using malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) assay kits, respectively. The results showed that HFD + V hens had more severe liver hemorrhage and fibrosis than ND + V hens (P < 0.05). The ultramicrostructural examination showed that hepatocytes of HFD + V hens exhibited necrotic pyknosis showing great intracellular electron, mitochondrial swelling, shrunk nucleus, and absence of autolysosomes. Osteocalcin mitigated HFD + V-induced pathological changes in aged laying hens. High-fat diet + OCN hens had higher insulin sensitivity; lower liver concentrations of MDA (P = 0.12) but higher GSH-Px (P < 0.05); and lower blood TNF-α concentrations (P < 0.05) and mRNA expressions (P < 0.05) than HFD + V hens. These results suggest OCN functions in preventing the FLHS process in old laying hens through inhibiting excessive energy diet-induced metabolic disorder, oxidative stress, and related pathological damage.

Genetic variability of XRCC1 influences the treatment outcome of gastric cancer.

We aimed to investigate the role of XRCC1 codon 194 (Arg>Trp), 280 (Arg>His), and 399 (Arg>Gln) polymorphisms in response to chemotherapy and the overall survival of gastric cancer patients. A total of 172 patients were recruited for our study between January 2010 and March 2012. Genotyping of the three XRCC1 codons was carried out by restriction fragment length polymorphism polymerase chain reaction. By logistic regression analysis, we found that the Trp/Trp genotype of XRCC1 194 (Arg>Trp) showed a stronger association with complete or partial response to chemotherapy compared to the Arg/Arg genotype, and the adjusted odds ratio (95%CI) was 0.17 (0.05-0.58). Moreover, the Trp/Trp genotype was associated with a higher risk of death than that with the Arg/Arg genotype based on multivariate Cox proportional hazard regression analysis, and the adjusted hazard ratio (95%CI) was 4.08 (1.20-14.19). In conclusion, we found that the XRCC1 194 (Arg>Trp) polymorphism was correlated with a better response to chemotherapy and a low risk of death in patients with gastric cancer.

Telmisartan-enhanced hypercholesterolaemic serum-induced vascular endothelial growth factor expression in immortalized human umbilical vascular endothelial cells.

OBJECTIVE: To clarify whether hypercholesterolaemia can increase vascular endothelial growth factor (VEGF) expression in human umbilical vascular endothelial cells (HUVECs) through the phosphatidylinositol 3-kinase (PI3K) pathway, and whether a special angiotensin II receptor blocker, telmisartan, can attenuate VEGF expression induced by hypercholesterolaemia. METHODS: Levels of VEGF expression, PI3K activity and angiogenesis in vitro were determined by various methods after HUVECs were incubated with hypercholesterolaemic serum or combined with telmisartan and/or wortmannin. RESULTS: We found that hypercholesterolaemic serum (cholesterol > or = 0.08 mmol/L) can increase VEGF expression in HUVECs and that telmisartan cooperates with hypercholesterolaemic serum in promoting VEGF expression. The increased VEGF expression was associated with enhanced PI3K activity and could be significantly inhibited by wortmannin, a potent PI3K inhibitor. Likewise, hypercholesterolaemic serum significantly promoted angiogenesis in vitro, which could be inhibited when PI3K activity was suppressed. CONCLUSIONS: Our study suggests that hypercholesterolaemic serum induces VEGF expression through PI3K in HUVECs and that telmisartan cooperates with hypercholesterolaemia in promoting VEGF expression.

Sequestration of As by iron plaque on the roots of three rice (Oryza sativa L.) cultivars in a low-P soil with or without P fertilizer.

A pot experiment was carried out in a greenhouse to investigate the sequestration of As in iron plaques on root surface of three rice (Oryza sativa L.) cultivars. Phosphate (P) fertilization increased both plant biomass and tissue P concentrations significantly, indicating that the soils used in this study was highly P-deficient. Results from this study confirmed that low P supply improved the formation of iron plaque on rice roots. As a consequence, arsenic (As) concentrations in DCB-extracts with no P addition were significantly higher than those with P fertilization. Arsenic was highly sequestrated in iron plaque; arsenic concentration in iron was up to nearly 120 mg kg(-1), while arsenic concentrations in roots were just several mg kg(-1). Both arsenic and phosphate concentrations in iron plaque were highly positively correlated with the amounts of iron plaque (DCB-extractable Fe). Contrary to normal understanding that increasing P supply could reduced As accumulation in plants, results from the present study showed that P fertilization did not inhibit the As uptake by plants (As accumulation in aboveground), which was probably due to the fact that iron plaque formation was improved under low P conditions, thus leading to more As sequestration in the iron plaque. Thus results obtained in this study indicated that the iron plaque may inhibit the transfer of As from roots to shoots, and thus alter the P-As interaction in plant As uptake processes.

[A study on mechanism of skin penetration by cercaria of S. japonicum and screening of preventive drugs].

Mice pretreated with PG cyclo-oxygenase inhibitor aspirin, at 300 mg/kg/d x 5, and ibuprofen, at 100 mg/kg/d x 5 orally and 20 mg/kg/d x 3 intraperitoneally revealed moderate chemoprophylactic effects and the reduction of the penetration of worms by 23% when compared to controls. Daily oral administration of aspirin, at 300 mg/kg for 15 days the worms reduction increased to 41.7%. In estimation of PGE1 in cercariae of S. japonicum by radioimmunoassay, the PGE1 was 49 pg/100 cercariae. In normal mouse skin PGE1 has been measured to amount to 3105 +/- 691.7 pg/10 mg on average. In cercarial penetrated mouse skin, 1.5 hours after exposure the PGE1 assessed in 100 and 250 cercariae in the infected skin were 5506 +/- 1127.1 and 12085 +/- 2622.9 pg/10 mg respectively, which were significantly higher than that of the non-penetrated skin. These studies in conjunction with our previous work indicate that: 1.PGs, similar to S. mansoni, were probably necessary for cercarial penetration. 2.PG inhibitors could reduce cercarial penetration. Receptors antagonist etc. e.g. diphenhydramine, chlorpheniramine, atropine, practolol could not reduce cercarial penetration, but praziquantel in the pretreated mice could reduce cercarial penetration significantly. e.g. 400 mg/kg orally 2 hours prior to affection of cercariae about 100% reduction of the penetration, but if pretreated with praziquantel, 4, 8, 24, 36 hours prior to the affection the reduction penetration decreased to 51.7, 46.1, 9.4, 8.9% respectively.