The underlying characteristics of sleep behavior and its relationship to sleep-related cognitions: a latent class analysis of college students in Wuhu city, China.

The aim of this study was to gain insight into the sleep quality of college students and related factors from a new perspective by using Latent Class Analysis (LCA). A total of 1,288 college students from four universities in Wuhu city participated in the study. LCA was used to identify the classes of sleep behaviors. Differences in class membership related to selected research factors were examined using multinomial logistic regression analysis.Four distinct classes of behaviors were identified: (1) good sleep (Class 1, 31.8%), (2) prolonged sleep latency (Class 2, 49.1%), (3) sleep disturbances and daytime dysfunction (Class 3, 6.8%), (4) multiple poor sleep behavior (Class 4, 12.3%). The latent classes of sleep behavior were correlated with the DBAS-16 total score (rs = -0.109, P < 0.001). Learning pressure and mental state during the day could affect overall sleep (Class 2, Class 3 and Class 4), and female students were at higher risk of severe sleep problems (Class 3 and Class 4), while bedtime exercised could improve mild sleep problems (Class 2). The sleep behavior of college students in Wuhu city has obvious class heterogeneity, and different influencingfactors may affect sleep to varying degrees. In addition, our research provides a basis for targeted intervnetion in college student's sleep. .

Association of Immune Factors with Drug-Resistant Tuberculosis: A Case-Control Study.

BACKGROUND Presently, studies of factors associated with drug-resistant tuberculosis (TB) focus on patients' socio-demographic characteristics and living habits, to the exclusion of biochemical indicators, especially immune factors. This study was carried out to determine whether immune factors are associated with drug-resistant TB. MATERIAL AND METHODS A total of 227 drug-resistant pulmonary TB patients and 225 drug-susceptible pulmonary TB patients were enrolled in this study. Information on socio-demographic characteristics and biochemical indicators were obtained through their clinical records. Non-conditional logistic regression was used to analyze the association of these indicators with drug-resistant TB. RESULTS There were significant differences in re-treatment, marital status, alanine aminotransferase (ALT), blood uric acid (BUA), carcino-embryonic antigen (CEA), T-spot, and CD3 and CD4 counts between the 2 groups. In multivariable analysis, re-treatment [Odds Ratio (OR)=5.290, 95% Confidence Interval [CI]=2.652-10.551); CD3 (OR=1.034, 95% CI=1.001-1.068); CD4 (OR=1.035, 95% CI =1.001-1.070) and IgM (OR=1.845, 95% CI=1.153-2.952) were associated with drug-resistant TB. CONCLUSIONS These results suggest the need for greater attention to re-treatment cases and immune function when treating drug-resistant TB.

PDTC attenuate LPS-induced kidney injury in systemic lupus erythematosus-prone MRL/lpr mice.

Lipopolysaccharide (LPS) from bacteria can accelerate and exacerbate lupus nephritis (LN) and induce infiltrating inflammatory cells in kidney in animal models. Pyrrolidine dithiocarbamate (PDTC) is known to exert anti-inflammatory effects. Monocyte chemoattractant protein-1(MCP-1) is upregulated by various stimuli, including LPS, high glucose, and hyperosmolality. However, the molecular mechanisms of transcriptional regulation of the MCP-1 protein expression with LPS are poorly understood. Expression of MCP-1 was examined by western blot and enzyme-linked immunosorbent assay, respectively. The activity of nuclear factor (NF)-kappaB was measured by western blot. These mice have uncontrolled proliferation of T cells, an impaired response to T cell mitogen and produce autoantibodies against nuclear antigens, including DNA. We found that after LPS treatment for 14 weeks, LPS increased MCP-1 protein expression in kidney, which was significantly suppressed by antioxidant PDTC. The expression of NF-κB, pERK, pJNK and MCP-1 were increased, pp38 expression was decreased significantly, concomitantly with sera anti-dsDNA, MCP-1 and the acceleration of severity of autoimmune kidney injury. LPS induce markedly neutrophil infiltration in the glomerulus, especially around the mesangial region. PDTC reduced the number of infiltrating inflammatory cells and severity of kidney injury via inhibiting NF-κB and p38 MAPK activity. They also markedly prevented LPS-induced pJNK and MCP-1. Therefore, MCP-1 may be responsible for the recruitment and activation of leukocytes in diseased kidneys in female MRL/lpr mice. In this study, the long-term administration of PDTC had impacts on the prevention of end-stage organ damage induced by LPS treated. We demonstrated that PDTC inhibited LPS-induced monocyte migration and attenuated LPS-induced p38 MAPK activation. Based on these data we infer that PDTC inhibits LPS-induced MCP-1 expression, secretion and function through inhibition of NF-κB and p38 MAPK activity. Our study suggests that MAPK is an important therapeutic target of monocyte recruitment and accumulation within the glomerulus in inflammatory renal disease. These results suggest that PDTC protects against kidney inflammation of SLE at least in part via NF-κB and MAPK signaling pathways induction, and that inhibitory action on anti-dsDNA may be associated with the protective mechanism of PDTC. In summary, PDTC pretreatment attenuates LPS-induced kidney injury in female MRL/lpr mice through regulating NF-κB and MAPK signaling pathways. Our results indicate that LPS induces MCP-1 mainly through activating NF-κB and its downstream MAPK, and that such effect was inhibited by PDTC, suggesting the efficacy of PDTC in preventing kidney fibrosis in lupus-prone mice. Therefore, appropriate inhibition of NF-κB activation may attenuate the kidney injury in lupus-prone mice.

[Studying the lipid peroxidation index, morphology and apoptosis in testis of male BALB/c mice exposed to polybrominated diphenyl ether (BDE-209)].

OBJECTIVE: To explore the lipid peroxidation and the testicular morphological change induced by decabrominated diphenyl ether (BDE-209) in male BALB/c mice. METHODS: Twenty one male BALB/c mice were randomly divided into three groups: the high exposure group (500 mg/kg BDE-209), the low exposure group (200 mg/kg BDE-20) and control group (normal saline). The mice were exposed by gavage one time a day for 6 weeks, then were sacrificed. Body weight, testis weight, malonyldialdehyde (MDA), total superoxide dismutase (T-SOD) and glutathione (GSH) in testis were examined. The morphological alteration of testis was observed. TUNEL assay was used to detect the apoptosis in testicular cells. RESULTS: Body weight and testis weight in high and low exposure groups were (21.6140 +/- 2.3550) g, (20.8000 +/- 1.7630) g and (0.1859 +/- 0.0349) g, (0.1718 +/- 0.0266) g, respectively, which were significantly lower than those (27.7570 +/- 1.2880) g and (0.2302 +/- 0.0335) g in the control group (P < 0.05); the testis coefficient in high exposure group was (0.8640% +/- 0.1706%), which was significantly higher than that (0.8329 +/- 0.1386%) in the control group (P < 0.05). The GSH level and SOD activities of testis in 2 BDE-209 groups were 0.044 +/- 0.006, 0.039 +/- 0.005 nmol/mg prot, and 0.735 +/- 0.179, 0.907 +/- 0.198 U/mg prot, respectively, which were significantly lower than those (0.052 +/- 0.067) mol/mg and (1.161 +/- 0.188) U/mg in the control group (P < 0.05). The levels of MDA in 2 BDE-209 groups were (2.365 +/- 0.339) and (1.752 +/- 0.366) nmol/mg prot, which were significantly higher than that (1.173 +/- 0.232 nmol/mg prot) in control group (P < 0.05). there were significant differences of SOD and MDA levels between high exposure group and low exposure group (P < 0.05). Histological examination showed that the number of spermatogenic cells and layer were decreased significantly in 2 exposure groups as compared with control group. TUNEL assay showed that apoptosis cells appeared in 2 exposure groups. CONCLUSION: BDE-209 changed lipid peroxidation in male BALB/c mice testis and caused toxic effects on the testis.

[Effects of mitogen-activated protein kinases signaling pathway proteins on kidney injury in mice exposed subchronically to cadmium].

OBJECTIVE: To explore the effects of mitogen activated protein kinase (MAPK) and extracellular signal-regulated kinases (ERK) on kidney injury in female BALB/c mice exposed to cadmium. METHOD: Twenty-one female BALB/c mice were randomly divided into 3 groups, i.e. control group, low Cd exposure group (2.5 µmol/kg) and high Cd exposure group (10 µmol/kg) were exposed to normal saline, 2.5, 10 µmol/kg Cd, respectively, 3 times a week for 14 weeks. The kidney slice were stained by HE, PAS and Masson staining to observe the morphological changes. The expression levels of pERK, ERK, pp38, p38, pJNK and JNK proteins in kidneys were tested by Western blot assay. RESULTS: The ratios of pERK/ERK, pp38/p38, pJNK/JNK in high Cd group were higher than those in the control group (P < 0.05). The ratio of pERK/ERK in low Cd group was higher than control group (P < 0.05). The expression levels of bcl-2, bax proteins and the ratio of bcl-2 to bax in Cd exposure groups decreased significantly, as compared with the control group (P < 0.05). The impairment of renal glomeruli and tubules were observed in HE, PAS and Masson staining slices of kidneys in mice exposed to Cd. CONCLUSION: CdCl2 may induced renal injury by affecting the expression levels of MAPK.

[Effect of exposure to higher decabrominated diphenyl ether (PBDE-209) on learning and memory functions of BALB/c mice].

OBJECTIVE: To investigate the effects of exposure to decabrominated diphenyl ether (PBDE-209) on learning and memory of BALB/c mice. METHODS: Eighteen female BALB/c mice were randomized divided into 3 groups and gavaged with peanut oil in the control groups and 300, 1500 mg x kg(-1)xd(-1) PBDE-209 in peanut oil daily in two exposed groups respectively for 4 weeks. The learning and memory ability of mice were tested by the Morris water maze and the shuttling box respectively. The body weight and organs index were measured and the acetylcholinesterase and butyrylcholinesterase activity in brain were determined. The liver histopathological examination was performed. RESULTS: The heart index in high dose PBDE-209 group was higher than that of the low dose PBDE-209 group (P < 0.05). The results of Morris water maze showed that escape latency period was significantly shorter than the control group (F = 3.134, P < 0.05). The swimming time in the second quadrant of low dose PBDE-209 group was (15.78 +/- 10.92) s, significantly shorter compared with the swimming time in the second quadrant of the control group's [(28.80 +/- 8.67) s] (P < 0.05). There was no significant difference in the times of active avoidance in the shuttling between three groups (F = 3.423, P = 0.06). There were no significant differences in acetylcholinesterase and butyrylcholinesterase activity in brain of PBDE-209 groups compared with the control group (P > 0.05). Histologically liver damages in structure such as adipose degeneration and swelling were observed in PBDE groups. CONCLUSION: Exposure to PBDE-209 slightly impairs the space learning and memory ability of BALB/c mice, and it has some hepatotoxicity.

[Oxidative stress of decabromodiphenylether in mice brain tissue].

OBJECTIVE: To study the oxidative stress induced by decabromodiphenylether (PBDE-209) in the cerebral cortex, hippocampus, cerebellum and striatum of mice. METHODS: Twenty-eight male BALB/c mice were randomized divided into four groups with seven mice in each: solvent control, blank control, low (200 mg/kg) and high (500 mg/kg) dose groups. Test substances were administered by gavage and mice were sacrificed 6 weeks after treatment. Malonyldialdehyde (MDA), total superoxide dismutase (T-SOD) and glutathione (GSH) in cerebral cortex, hippocampus, cerebellum and striatum were examined. RESULTS: The content of MDA in cerebral cortex, cerebellum, striatum and hippocampus in high dose group was (92.25 ± 36.64), (4.24 ± 1.15), (12.92 ± 4.30), (12.12 ± 6.39) nmol/mg pro respectively, higher than that in blank group [(56.713 ± 6.44), (2.42 ± 1.41), (4.05 ± 2.23), (4.91 ± 1.60) nmol/mg pro] and the difference was statistically significant (P < 0.05); T-SOD activity in cerebral cortex, cerebellum and striatum in low dose group was (182.48 ± 11.59), (6.67 ± 1.56), (35.48 ± 21.98) U/mg pro respectively, lower than that in blank group [(277.76 ± 106.70), (18.02 ± 16.40), (63.57 ± 20.83) U/mg pro] and the difference was statistically significant (P < 0.05); in high dose group the T-SOD activity in hippocampus was(59.26 ± 37.09) U/mg pro, lower than that in blank group [(93.28 ± 21.75) U/mg pro] and the difference was statistically significant (P < 0.05); The content of GSH in cerebral cortex, cerebellum and striatum in high dose group was (40.98 ± 13.19), (3.55 ± 1.55), (24.46 ± 11.30) mg/g pro respectively, lower than that in blank group [(75.79 ± 26.51), (8.01 ± 3.23), (44.52 ± 13.15) mg/g pro and the difference was statistically significant (P < 0.05); while the content of GSH in hippocampus was not decreased significantly compared with the blank group (P > 0.05). CONCLUSION: PBDE-209 could induce oxidative stress in nervous tissue. The tissue oxidative damage might be one of the primary mechanisms of neurotoxicity of PBDE-209.