[Study on 4 cases of mushroom poisoning with amanita and identification of poison].

Different kinds of poisonous mushrooms contain different toxic components. Acute liver injury caused by amanita mushroom is the main cause of death from poisonous mushroom poisoning in China. Consumption of poisonous mushrooms has an incubation period, there is a false recovery period in the clinical process, and the early performance is slight and does not attract enough attention from doctors, and it is easy to miss the treatment opportunity. The clinical characteristics, treatment and identification of mushrooms containing amanita in 4 patients were analyzed in order to improve clinicians' understanding of the diagnosis and treatment of mushroom poisoning and early species identification.

[CD38 dictates cardiac damage through mitochondrial apoptotic pathway under hypoxic-ischemic conditions].

Objective: To explore the mechanism of CD38-mediated cardiac damage under hypoxic-ischemic (H/I) conditions. Methods: Twenty CD38(-/-) male mice (8-week-old) and 20 wild-type (WT) male C57BL/6J mice (8-week-old) were randomly selected to construct the model of approximately 25% of the total body surface area (TBSA) burn injury. The cardiomyocytes (CMs) were separated from neonatal mice (1day) to construct the H/I injury model. Ad-CD38 adenovirus was transfected into CD38(-)/- primary CMs to callback CD38 expression. Animal experiments were grouped into WT-control group, CD38(-/-)-control group, WT-burn group, and CD38(-/-)-burn group (10 mice in each group). Primary CMs were divided into 6 groups: WT-normoxia group, CD38(-/-)-normoxia group, CD38(-/-)+Ad-CD38-normoxia group, WT-H/I group, CD38(-/-)-H/I group, CD38(-/-)+Ad-CD38-H/I group. The release of lactic dehydrogenase (LDH) from CMs and the cell viability were measured to estimate the level of myocardial injury. Ultrastructure of cardiomyocytes was examined by electron microscope. CD38 protein level and mitochondrial apoptosis-related proteins were detected by Western blot. Flow cytometry was used to detect mitochondrial reactive oxygen species (MitoSOX) of CMs under H/I condition. Cardiac function of mice was detected by ultrasonic apparatus. Results: (1) Animal experiments: The expression level of cardiac CD38 in WT-burn group was significantly higher than that in sham group (P<0.001). The heart function of CD38(-/-)-burn group was obviously better than WT-burn group [ejection fraction (EF)%: (84.70±2.31)% vs (76.10±2.96)%, shortening fraction (FS)%: (48.90±5.00)% vs (38.10±2.80)%] (both P<0.001). (2) Cell experiments: The expression level of cardiac CD38 in WT CMs under H/I condition was significantly higher than that in WT CMs under normoxia condition (P<0.05). The level of LDH, apoptotic cell and MitoSOX in CD38(-/-)-H/I group were fewer than WT-H/I group and CD38(-/-)+Ad-CD38(-)H/I group [(11.2±3.0)% vs (18.2±3.4)% and (17.6±4.0)%, (13.0±2.8)% vs (23.1±4.9)% and (23.3±6.0)%, (162±11)% vs (228±18)% and (220±18)%] (all P<0.001). The levels of cleaved-caspase3, Cytochrome-C in CD38(-/-)-H/I group were significantly lower than those in WT-H/I group and CD38(-/-)+Ad-CD38-H/I group (P<0.001). The cell viability in CD38(-/-)-H/I group was higher than that in WT-H/I group and CD38(-/-)+Ad-CD38-H/I group (0.355±0.043 vs 0.280±0.051 and 0.291±0.024) (all P<0.05). Electron microscopy results showed that structure of mitochondria in CD38(-/-)-H/I group was better than in WT-H/I group and CD38(-/-)+Ad-CD38-H/I group. Conclusion: Overexpression of CD38 contributes to cardiac damage by stimulating mitochondrial apoptotic pathway.

[Effect and mechanism of cardiac adipose triglyceride lipase overexpression on burn-induced cardiac injury].

Objective: To explore the effect and potential mechanism of cardiac adipose triglyceride lipase (ATGL) overexpression on burn-induced cardiac injury. Methods: Eight-week-old C57BL/6J mice with cardiac ATGL overexpression driven by the myosin heavy chain (MHC) promoter (MHC-ATGL burn group) and wild-type (wild-type burn group) mice were randomly chose to the following experiments with burn injury after 24 h (n=8/group), MHC-ATGL mice and wild-type mice with corresponded age and sex were included as control. Cardiac ATGL protein expression, serum levels of cardiac troponin T and cardiac kinase-MB (CK-MB), cardiac free fatty acid and reactive oxygen species were detected. The wild-type and MHC-ATGL burn groups were not only compared with their corresponded control groups, but also compared between each other. Results: The hair color and development were shown little difference between each group. ATGL protein expression is elevated in wild-type burn group (1.00±0.68 vs 3.09±0.93, P=0.023) and decreased in MHC-ATGL burn group (17.84±2.41 vs 10.36±2.22, P<0.001), while ATGL protein expression is still increased in MHC-ATGL burn group compared with wild-type burn group (P<0.001). Serum levels of cardiac troponin T and CK-MB were both elevated in wild-type burn group and MHC-ATGL burn group [(0.456±0.131) vs (0.076±0.019) µg/L and (0.219±0.089) vs (0.060±0.019) µg/L, (1 421±162) vs (221±67) U/L and (761±142) vs (221±41) U/L] (all P<0.001), while serum levels of cardiac troponin T and CK-MB was still decreased in MHC-ATGL burn group compared with wild-type burn group (P<0.001). In addition, cardiac free fatty acid was increased in wild-type burn group and little difference was found in MHC-ATGL burn group [(2.54±0.51) vs (0.46±0.27) mmol/L, P<0.001, and (0.81±0.38) vs (0.59±0.25) mmol/L, P=0.251], while cardiac free fatty acid was significant reduction in MHC-ATGL burn group compared with wild-type burn group (P<0.001). Levels of cardiac reactive oxygen species was both elevated in wild-type burn group and MHC-ATGL burn group [(1.89±0.23) vs (1.00±0.18) and (1.38±0.17) vs (0.95±0.13)] (both P<0.001), while levels of cardiac reactive oxygen was reduction in MHC-ATGL burn group compared with wild-type burn group (P<0.001). Conclusion: Cardiac ATGL overexpression may protect against burn-induced cardiac injury through reducing free fatty acid and reactive oxygen species production.

[Analysis of the prevalence and influencing factors of occupational musculoskeletal disorders among rural migrant workers in Tianjin].

Objective: To explore the prevalence of occupational musculoskeletal disorders (OMD) and its influencing factors among rural migrant workers in Tianjin, with the aim of developing strategies to improve the health condition of this specific population. Methods: Questionnaire survey was conducted among 415 rural migrant workers working in Tianjin about their fundamental state and occupational musculoskeletal disorders (OMD) during January 2015 to January 2016. Statistical methods were utilized to analyze the influencing factor. Results: A total of 415 rural migrant workers were investigated, in which young Young adults and low education level were in the majority of rural migrant workers. The prevalence of OMD for whole population, male and female were 28.92% (120/415), 33.06% (81/245) and 22.94% (39/170), respectively. Prevalence showed significant differences njin and workplace hygiene. Multivariate logistic regression analysis showed that the risks of OMD increased with age group, and decreased with higher education level. The risk of OMD among rural migrant workers with monthly income between 3000 to 5000 yuan was 2.26 times (95%CI: 1.37-3.75) higher than that of low-income workers (<3000 yuan per month). Workers engaged in housekeeping service had 2.28 times higher risk of OMD than those in manufacturing industry (95%CI: 1.06-4.89) . Conclusion: Prevalence of OMD among rural migrant workers is higher than that of general people. Age, education, monthly income, occupation are the independent influencing factors for OMD among rural migrant workers.

Association of interleukin 22 gene polymorphisms and serum IL-22 level with risk of systemic lupus erythematosus in a Chinese population.

The aim of this study was to investigate the association between the single-nucleotide polymorphisms (SNPs) of the interleukin 22 (IL-22) gene and systemic lupus erythematosus (SLE) in a Chinese population. Three IL-22 SNPs (rs2227485, rs2227513 and rs2227491) were genotyped using SNaPshot SNP genotyping assays and identified by sequencing in 314 SLE patients and 411 healthy controls. The IL-22 level of serum was assessed by enzyme-linked immunosorbent assay (ELISA) kits. Data were analysed by spss version 17.0 software. We found that rs2227513 was associated with an increased risk of SLE [AG versus AA: adjusted odds ratio (aOR) = 2·24, 95% confidence interval (CI) = 1·22-4·12, P = 0·010; G versus· A: adjusted OR = 2·18, 95% CI = 1·20-3·97, P = 0·011]. Further analysis in patients with SLE showed that the AG genotype and G allele were associated with an increased risk of renal disorder in SLE (G versus A: aOR = 3·09, 95% CI = 1·30-7·33, P = 0·011; AG versus· AA: aOR = 3·25, 95% CI = 1·35-7·85, P = 0·009). In addition, the concentration of IL-22 was significantly lower in the rs2227513 AG genotype compared with AA genotype (P = 0·028). These results suggest that rs2227513 polymorphism might contribute to SLE susceptibility, probably by decreasing the expression of IL-22.

Influence of Hydrostatic Pressure on the Corrosion Behavior of Superhydrophobic Surfaces on Bare and Oxidized Aluminum Substrates.

It is generally recognized that superhydrophobic surfaces in water may be used for corrosion resistance due to the entrapped air in the solid/liquid interface and could find potential applications in the protection of ship hull. For a superhydrophobic surface, as its immersion depth into water increases, the resultant hydrostatic pressure is also increased, and the entrapped air can be squeezed out much more easily. It is therefore predicted that high hydrostatic pressure would cause an unexpected decrease in corrosion resistance for the vessels in deep water (e.g., submarines) because of the unstable entrapped air. In this work, in order to clarify the role of hydrostatic pressure in the corrosion behavior of superhydrophobic surfaces, two typical superhydrophobic surfaces (SHSs) were prepared on bare and oxidized aluminum substrates, respectively, and then were immersed into the NaCl aqueous solutions with different depths of ∼0 cm (hydrostatic pressure ∼0 kPa), 10 cm (1 kPa), and 150 cm (15 kPa). It was found out for the SHSs on the oxidized Al, as the hydrostatic pressure increased, the corrosion behavior became severe. However, for the SHSs on the bare Al, their corrosion behavior was complex due to hydrostatic pressure. It was found that the corrosion resistance under 1 kPa was the highest. Further mechanism analysis revealed that this alleviated corrosion behavior under 1 kPa resulted from suppressing the oxygen diffusion through the liquid and reducing the subsequent corrosion rate as compared with 0 kPa, whereas the relatively low hydrostatic pressure (HP) could stabilize the entrapped air and hence enhance the corrosion resistance, compared with 15 kPa. The present study therefore provided a fundamental understanding for the applications of SHSs to prevent the corrosion, especially for various vessels in deep water.

[Clinical experience and next-generation sequencing analysis of encephalitis caused by pseudorabies virus].

Objective: To detect potential pathogens including pseudorabies virus in patients with encephalitis of unknown etiology in China and describe novel encephalitic entities. Methods: Patients with clinically suspected infectious encephalitis were enrolled in a multicenter study to identify the pathogens in PUMCH Encephalitis Program.Next-generation sequencing(NGS) of cerebrospinal fluid (CSF) was used in patients with encephalitis of unknown etiology enrolled from 2016 to 2017.The patients diagnosed as PRV encephalitis were studied to describe this novel entity. Results: The four patients(3 male, 1 male, 38-54 years old) had occupational exposure to raw park when working in the production or marketing of pork and at least one got injured during pork-cutting.Two of them were confirmed with NGS of CSF, and anti-PRV antibodies were positive in 3 patients whose serum was available for serological analysis.They all presented with an acute onset of fever, convulsion, loss of consciousness and respiratory failure within 1 to 4 days and rapidly deteriorated even on extensive treatment.All the patients needed ICU admission and 3 needed mechanical ventilation.Two patients also had bilateral retinitis.Neuroimaging revealed symmetric gray matter lesions including limbic system, basal ganglia and midbrain without obvious hemorrhage.Lumbar puncture revealed elevated intracranial pressure and lymphocytic pleocytosis [(6-64)×10(6)/L] of CSF.The patients failed to response to the treatment of acyclovir combined with intravenous immunoglobulin and steroids.Modified Rankin Score was 3, 5, 5 and 6 (died) for the 4 patients respectively on last follow-up. Conclusions: PRV could be a cause of severe encephalitis.The patients with suspected pseudorabies encephalitis (PRE) need to be tested for PRV DNA timely.Severe encephalitis with bilateral involvement of limbic system, basal ganglion, thalamus and midbrain in patient with occupational exposure indicate this emerging infectious encephalitis.

[Experimental research on mesenchymal stem cells (MSCs) therapy for autoimmune uveitis].

Autoimmune uveitis is a major cause of visual disability. Treatment of chronic and recurrent uveitis can be extremely difficult, as various complications of it could impede the long-term usage of corticosteroids and immunosuppressants. Mesenchymal stem cells are of both immunosuppressive and neurotrophic effect, and can enhance the antimicrobial ability of the body, thereby hold great promise in clinical application for treating uveitis. (Chin J Ophthalmol, 2018, 54: 712-715).

A novel intronic mutation and a missense mutation of MEN1 identified in two Chinese families with multiple endocrine neoplasia type 1.

BACKGROUND: Multiple endocrine neoplasia type 1 (MEN1) caused by MEN1 mutation is widely recognized. To date, 14 novel mutations were reported in Chinese and intronic mutations are getting more attention. AIM: To explore clinical features and MEN1 mutations in two Chinese families suffering from MEN1. METHODS: Nineteen individuals (10 males and 9 females) from two unrelated families with MEN1 were studied. Mutations of MEN1 were analyzed by direct sequencing of PCR products. In vitro splicing analysis was also performed with minigenes containing both wildtype and novel mutant fragments. Through the RNAstructure program, we analyzed the secondary structure of the wild type MEN1 pre-mRNA and then introduced T>G mutation at +2 donor splice site of intron 7. RESULTS: Clinical features of 3 patients in two families were described, and 5 individuals were proven to be carriers of MEN1 mutation without apparent symptoms. A novel splicing site mutation of the intron 7 (IVS7+2 T→G) was identified in the first family. In vitro analysis also verified this mutation caused the aberrant splicing of MEN1 mRNA. With the RNAstructure program, we could figure out that the global secondary structure as well as the number of stems and loops of pre-mRNA greatly changed after this mutation. The mutation c. 1227 C>A (C409X) was identified in another family, which also caused the truncation of menin. CONCLUSION: We reported a novel intronic mutation and a missense mutations in two Chinese families suffering from MEN1.

Characterisation and validation of a novel panel of the six short tandem repeats for genetic counselling in Chinese haemophilia A pedigrees.

Haemophilia A (HA) is the most common hereditary bleeding disorder caused by F8 gene mutation. Linkage analysis is an auxiliary strategy to direct mutation analysis for genetic counselling of HA. Here we characterize and validate a novel panel of six short tandem repeat (STR) loci for genetic counselling in Chinese HA pedigrees. The panel was analysed in 116 unrelated healthy female patients and 108 male patients, and verified in 169 unrelated pedigrees with HA. The six STR loci in the panel spanned a distance of 0.3 Mb from each side of the F8 gene. Three of them, F8Up226, F8Up146 and F8Down48, were first described here. Markers F8Up226, F8Up146, F8Int13, F8Int25, F8Down48 and DXS1073 exhibited the number of alleles 16, 9, 8, 6, 9 and 10, and heterozygosity rates of 74.8%, 44.8%, 60.9%, 42.6%, 61.7% and 62.0% respectively. Haplotype frequencies analysis suggested that the genotypes of haplotype provided a highly informative content (56.5%). The panel was informative in 167 of 169 unrelated haemophilic pedigrees with the combined diagnostic rate of 98.8%. In eight pedigrees could not be diagnosed by mutation detection linkage studies using the panel were informative in all the pedigrees and a reliable diagnosis was made in seven pedigrees. The novel panel of the six STR loci represents a high degree of informativeness and a low fraction of recombination. Linkage analysis using this panel provides an alternative strategy when direct mutation detection is not feasible for genetic counselling in Chinese HA families.

Mitochondrial apoptotic pathways: a mechanism for low androgen-induced vascular endothelial injury in male rats.

The aim of the study was to investigate the role of mitochondrial apoptotic pathways in vascular endothelial injury in male rats with low androgen. 8 week-old adult male Sprague-Dawley (SD) rats were randomly divided into 3 groups (n=6/each group): control group, castrated group (low androgen), and replacement group (given androgen after castration). After 10 weeks, endothelial structure was observed by general light microscope and transmission electron microscope (TEM) respectively. Isolated mitochondria and mitochondrial membrane potential (MMP) were detected by fluorescence to access mitochondrial function. Chromatin degradation was measured by terminal deoxynucleotidyl transferase-mediated deoxyuridine-biotin nick end labeling (TUNEL) staining method. The mRNA and protein of bcl-2, cytochrome C (Cyt C), caspase-9, and caspase-3 were analyzed for apoptosis. Cell shrinkage and condensed chromatin, less mitochondria and a fall in MMP levels were observed in the castrated group, along with more apoptotic endothelial cells. Bcl-2 level was reduced and the expression of caspase-9, caspase-3 and Cyt C were elevated in the castrated group (p<0.05). But there was no significant difference between the replacement group and the control group (p>0.05). It was concluded that low androgen caused vascular endothelial damage. It may be, at least in part, related with the activating mitochondrial apoptotic pathways.

Changes of pituitary and penile structure in male adult rats following castration and high-fat diet.

AIM: To investigate the influence of low androgen levels and high-fat diet on the structure of pituitary and penis in male rats. METHODS: Ten-week-old adult male Sprague-Dawley rats were randomly divided into 2 groups, one fed a high-fat diet the other fed a normal diet; each group consisted of 3 subgroups: controls, castrated rats (with low androgen), and castrated rats given undecanoate replenishment. After 11 weeks, the structure of pituitary and penis were observed under light microscopy. Immunohistochemistry was used to assess the expression of FSH in pituitary and cyclooxygenase-2 (COX-2) in corpora cavernosa penis. RESULTS: The structures of pituitary and penis in castrated rats were injured, and were more damaged in castration together with high-fat diet. Immunohistochemistry showed FSH expression in castrated rats pituitary while castrated rats on a high-fat diet had less positive staining than those on a normal diet. Vascular structure of corpora cavernosa penis, showed a strongly positive COX-2 expression in high-fat diet rats. CONCLUSIONS: Castration and high-fat diet could induce structural damages of pituitary and penis in male rats. Replacement with testosterone could partially restore the impaired structure. The positive expression of COX-2 implied inflammatory pathway existence on vascular structure of penis in high-fat diet and low-androgen male rats.

Rosiglitazone protects diabetic rats from liver destruction.

AIMS: To investigate whether rosiglitazone (ROS) protects diabetic rats from destructive changes in the liver. METHODS: Twenty-four Sprague Dawley rats were randomly divided into 3 groups: control (NC) group (no.=8), streptozocin (STZ)-treated diabetic (DM) group (no.=8), and STZ+ROStreated diabetic (RSG) group (no.=8). After 8 weeks, the liver structure was observed by light microscopy and transmission electron microscopy. Apoptosis was detected by TUNEL, and apoptosis index was calculated. The Fas ligand (FasL) mRNA expression of apoptosis-promoting gene and cyclooxygenase- 2 (COX-2) mRNA in the liver were detected by RTPCR. COX-2 protein in the liver was tested via immunohistochemical staining. RESULTS: Compared to NC group, DM group showed a visible fatty degeneration and inflammatory cell infiltration in the liver under microscopy. Obvious hepatocyte swelling with atrophic mitochondria was observed, and the central zone of cholangiole was severely outstretched. Meanwhile, in RSG group, the hepatocyte steatosis and inflammatory cell infiltration decreased, and the hepatic ultra-structure was markedly improved. Hepatocyte apoptosis (p<0.05) and the expression levels for hepatic COX-2 mRNA (p<0.05), FasL mRNA (p<0.01), and COX-2 protein (p<0.05) were higher in DM group compared to the NC group, while the expression level of hepatic COX-2 mRNA (p<0.05), FasL mRNA (p<0.01), COX-2 protein (p<0.05), and hepatocyte apoptosis (p<0.05) in RSG group were decreased compared to DM group. CONCLUSION: Diabetes causes severe liver injury and ROS can protect diabetic rats from liver destruction, which may be related to inhibition of the expression of COX-2 and the hepatocyte apoptosis induced by FasL gene over expression.

Somatostatin receptors SSTR2 and SSTR5 are expressed in the human thoracic duct.

Somatostatin and its analog octreotide have been used successfully to treat postoperative chylothorax, and it has been shown that octreotide binds with high affinity to somatostatin receptor (SSTR) subtypes 2 and 5. Therefore, we investigated expression of SSTR2 and SSTR5 in the human thoracic duct by immunohistochemistry. Normal rat pancreas was used as a positive control for antibodies against SSTR2 and SSTR5, and Factor VIII-related antigen, SMA, actin, elastin, or collagen type II, III, IV or V antibodies were used to identify cell types and structures within the human thoracic duct. The antibodies against SSTR2 and SSTR5 worked well and yielded positive staining in control rat islets. In the human thoracic duct, SSTR2 was present in smooth muscle cells and some scattered structures which were stained by antibodies against Factor VIII-related antigen, SMA, actin, elastin or collagen type II, III, IV or V. SSTR5 was also present in smooth muscle cells. The presence of SSTR2 and SSTR5 in the human thoracic duct sheds light on the mechanism of somatostatin and octreotide use in the successful treatment of chylothorax and offers new molecular pathways to explore for potential future therapies.

[Preliminary study on the relationship between different blood glucose levels and periodontitis in patients with diabetes mellitus type 2].

Objective: To determine the correlation between the diabetes mellitus control and periodontitis. Methods: This study was a cross-sectional survey using stratified system sampling model design. The target population was the patients with diabetes investigated from May to July 2018 in Huangpu District of Shanghai. In the present study, severe periodontitis was defined as at least at two sites in different quadrants with probing depth (PD)≥6 mm and clinical attachment loss (CAL)≥ 5 mm. Edentulous induced by periodontitis were also classified as severe periodontitis and the others were classified as non-severe periodontitis subjects. Diabetes control levels were divided into the following three groups: poorly controlled group [glycated hemoglobin (HbA1c)>7.5% and fasting blood glucose (FPG)>7.0 mmol/L], well controlled group (6.5%≤HbA1c≤7.5％ or 6.1 mmol/L≤FPG≤7.0 mmol/L) and ideally controlled group (HbA1c<6.5% and FPG<6.1 mmol/L). SPSS 25.0 was used for statistical analysis. Chi square test was used for demographic data and frequency distribution, α=0.05, two-sided test. Ordinal regression model was used for PD and diabetes control status to balance confounding factors (including age, gender, education and smoking status). After matching the propensity scores between severe periodontitis group and non-severe periodontitis group, logistic regression analysis was used to analyze the level of diabetes control and periodontitis. Results: A total of 5 220 adults over the age of 18 with a medical history of diabetes participated in the survey, of which 3 064 subjects with diabetes mellitus type 2 (T2DM) who were given both oral and laboratory examinations and were included in this study. Statistics showed that the prevalence of moderate and severe periodontitis was 10.57% (324/3 064). In the severe periodontitis group, 79.01% (256/324) of the subjects were over 65 years old, 55.56% (180/324) were male, 58.33% (189/324) had lower education level than high school level, and 21.91% (71/324) were smokers, which were significantly higher than those in the non-severe periodontitis group (P<0.01). In different T2DM status groups, the percentage of severe periodontitis increased with the aggravation of T2DM status. In severe periodontitis group, the proportion of patients with poor glycemic control was higher. T2DM patients with poor glycemic control accounted for 68.52% (222/324) in severe periodontitis group, which was significantly higher than the proportion of non-severe periodontitis group of 60.99% (1 671/2 740) (P<0.05). The regression coefficient of PD was 0.191, and PD had a significant negative effect on the level of blood glucose (P<0.01). There was a significant positive correlation between diabetes glycemic control and severe periodontitis (OR=2.800, P<0.05). Conclusions: In Huangpu District of Shanghai, among T2DM patients, the age of severe periodontitis group was higher than that of non-severe periodontitis group, most of them were male, with lower education level and higher proportion of smoking. The severity of diabetes was related to periodontitis and the proportion of severe periodontitis was higher in patients with poor glycemic control.

Telbivudine preserves T-helper 1 cytokine production and downregulates programmed death ligand 1 in a mouse model of viral hepatitis.

Telbivudine is an orally bioavailable L-nucleoside with potent and specific anti-hepatitis B virus activity. The higher rate of hepatitis B e antigen (HBeAg) seroconversion during telbivudine treatment than other potent anti-HBV agents suggests a potential immunomodulatory effect. We sought to determine the effects of telbivudine on the immune system, particularly on cytokine production and T-cell response, using an animal model with mouse hepatitis virus strain 3 (MHV-3)-induced hepatitis. The effects of telbivudine on virus replication and cytokine production were investigated in vitro using MHV-3-infected macrophages, and the effects on T-cell response were investigated in vivo in an MHV-3-induced viral hepatitis model. Telbivudine had no effect on MHV-3 replication in macrophages. However, the production of tumour necrosis factor-alpha and interleukin-12 was increased significantly in MHV-3-induced macrophages treated with telbivudine. In vivo survival was enhanced in telbivudine-treated mice, with marked normalization in clinical conditions and histological lesions. Serum levels of interferon-gamma were elevated significantly after telbivudine treatment in MHV-3-infected C3H mice. In contrast, serum interleukin-4 levels were decreased significantly. Furthermore, telbivudine treatment enhanced the ability of T cells to undergo proliferation and secrete cytokines but did not affect cytotoxicity of infected hepatocytes. Of note, we found that telbivudine treatment suppressed programmed death ligand 1 expression on T cells. The results demonstrate the immunomodulatory properties of telbivudine, independent of its antiviral activity, in a mouse model of MHV-3-induced hepatitis.

Enhancement of charge-mediated magnetoelectric coupling in Fe3O4/SrTiO3/Ba0.6Sr0.4TiO3 heterostructure.

The in-plane magnetic hysteresis loops of Fe3O4/SrTiO3(STO) and Fe3O4/STO/Ba0.6Sr0.4TiO3(BSTO) heterostructures have been investigated at 200 K under various electric fields. The bottom BSTO layer of the STO/BSTO bilayer is used to improve the dielectric properties of the top STO layer. The polarization of the STO/BSTO bilayer is ∼78% larger than that of the STO layer at room temperature due to the improvement of surface topography and the contribution of electrostatic interlayer coupling. A significant enlargement (∼70%) in the magnetoelectric response of Fe3O4/STO/BSTO heterostructure has been achieved at 200 K and 300 kV cm-1 after introducing the BSTO layer, since the STO/BSTO bilayer with larger dielectric constant supplies more polarization charges at its interface to the Fe3O4 layer than the STO layer. It indicates that the dielectric bilayer improves the polarization and thus benefits the magnetoelectric coupling in the multiferroic heterostructure.

The effects of rosiglitazione on renal artery endothelium in diabetic rats.

BACKGROUND: Macrovascular disease is a common complication of Diabetes Mellitus (DM). Study of renal artery endothelium may serve as a surrogate for cardiovascular and renal vascular disease. OBJECT: This study is to elucidate (1) how about the changes of renal endothelial ultrastructures it is in different time of diabetes animals (2) Whether PPARgamma ligand (such as rosiglitazone: ROS) could improve endothelium destruction in diabetes. METHODS: Streptozoticin (STZ) induced diabetic rats were stratified by age groups from 6 to 10 weeks of age and were paired with age-matched control non-diabetic rats. Further, another group of diabetic rats were treated with ROS and matched with non-treated diabetic rats. RESULT: The renal artery endothelium of diabetic rats was partially coarse, distended, cracked and destroyed. The Vascular Endothelial Structure Score (VESS) was 34.5 in diabetic rats compared with non-diabetic control male rats (P=0.001). The older rats demonstrated more endothelial wall damage, more pronounced in male rats. Compared with non-treated control diabetic rats, ROS prevented diabetic endothelial damage (VESS=4.6, P=0.001). CONCLUSION: Renal artery endothelium damage in STZ induced diabetic rats was significantly attenuated by rosiglitazone.