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Objective To investigate whether lidocaine can reverse Kupffer cell dysfunction in diabetic mice, as well as the mechanism of lidocaine in affecting liver abscess formation by improving the phagocytic function of Kupffer cells. Methods C57BLKS/J db/db mice were divided into diabetes control group and diabetes+lidocaine group, and C57BLKS/J db/m mice were divided into non-diabetes control group and non-diabetes+lidocaine group, with 5 mice in each group. All mice were fed with the suspension of Klebsiella pneumoniae . Kupffer cells were collected from each group and were cultured in vitro; an electron microscope was used to measure the change in ultrastructure, and Kupffer c ells were measured in terms of the levels of inflammatory mediators, the expression level of intercellular adhesion molecule-1 (ICAM-1), the chemotactic function of neutrophils, and phagocytic function; liver abscess formation was also observed. The Kruskal-Wallis H test was used for comparison of continuous data between multiple groups, and the Mann-Whitney U test was used for further comparison between two groups; the chi-square test was used for comparison of categorical data between groups. Results Compared with the non-diabetic mice, the diabetic mice had significant reductions in mitochondria and rough endoplasmic reticulum, endoplasmic reticulum dilation, mitochondrial swelling, and an increase in lipid droplets in Kupffer cells. Compared with the non-diabetes control group, the diabetes control group had significant increases in the levels of nitric oxide (NO) (4.95±0.06 μmol/L vs 1.34±0.13 μmol/L, P 0.05). Compared with the diabetes control group, the diabetes+lidocaine group had significant reductions in the levels of NO (3.35±0.28 μmol/L vs 4.95±0.06 μmol/L, P 0.05). Conclusion Lidocaine can inhibit Kupffer cell inflammatory response and improve the phagocytic function of Kupffer cells in diabetic mice, thereby exerting a protective effect on Kupffer cells, but it had no effect on liver abscess formation.
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Objective: To observe the inhibitory effect of metformin on the inflammatory response of Kupffer cells (KCs) of liver in the diabetic mice, and to explore its improvement on the phagocytic function of KCs. and to elucidate the protective mechanism of metformin on the KCs in the diabetic mice. Methods: The C57BLKS/J db/db mice were divided into diabetes group and diabetes metformin group, and die C57BLKS/J db/m mice were divided into non-diabctcs group and non-diabctcs + metformin group. 8 micc in cach group. The KCs were culturcd in vitro and the changcs of ultrastrusturcs of KCs were observed by transmission electron microscope. The levels of intcrleukin 6 (1L-6), tumor necrosis factor a (TNF-a) and y-intcrfcron (INF-7) in the KCs were detected by EL1SA. The expression levels of intercellular adhesion molecule 1 (ICAM-1) protein in the KCs was detected by Western blotting method. Transwcll chamber assay was used to detect the neutrophil chemotaxis ability of the KCs. and the phagocytic ability of KCs was observed under inverted microscope. Results: The number of mitochondria and rough endoplasmic reticulum (RER) in the KCs of the diabetic micc was reduced, the RER expanded, the mitochondria swelled, and die lipid droplets were increased. Compared with non-diabctcs group, the levels of 1L-6 , TNF-a. INF-y and the expression level of ICAM-1 in die KCs of the micc in diabetes group were significantly increased ( P<0. 05)s the neutrophil chemotaxis ability of the KCs was enhanced ( P<0. 05). and the phagocytic ability was decreased ( P< 0. 05). Compared with diabetes group, the levels of 1L-6, TNF-a, INF-y and the expression level of ICAM-1 in the KCs in diabetes + metformin group were significandy decreased ( P<0. 05)s the neutrophil chemotaxis ability was decreased ( P∗. 0. 05), and the phagocytic ability was enhanced ( P∗C0.05). Conclusion: Metformin can inhibit the inflammatory response of KCs in the diabetic mice and improve its phagocytic function and protect the KCs.
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Objective:To observe the inhibitory effect of metformin on the inflammatory response of Kupffer cells (KCs) of liver in the diabetic mice, and to explore its improvement on the phagocytic function of KCs, and to elucidate the protective mechanism of metformin on the KCs in the diabetic mice.Methods:The C57BLKS/J db/db mice were divided into diabetes group and diabetes+metformin group, and the C57BLKS/J db/m mice were divided into non-diabetes group and non-diabetes+metformin group, 8mice in each group.The KCs were cultured in vitro and the changes of ultrastrustures of KCs were observed by transmission electron microscope.The levels of interleukin 6 (IL-6) , tumor necrosis factorα (TNF-α) andγ-interferon (INF-γ) in the KCs were detected by ELISA.The expression levels of intercellular adhesion molecule 1 (ICAM-1) protein in the KCs was detected by Western blotting method.Transwell chamber assay was used to detect the neutrophil chemotaxis ability of the KCs, and the phagocytic ability of KCs was observed under inverted microscope.Results:The number of mitochondria and rough endoplasmic reticulum (RER) in the KCs of the diabetic mice was reduced, the RER expanded, the mitochondria swelled, and the lipid droplets were increased.Compared with non-diabetes group, the levels of IL-6, TNF-α, INF-γand the expression level of ICAM-1in the KCs of the mice in diabetes group were significantly increased (P＜0.05) ;the neutrophil chemotaxis ability of the KCs was enhanced (P＜0.05) , and the phagocytic ability was decreased (P＜0.05) .Compared with diabetes group, the levels of IL-6, TNF-α, INF-γand the expression level of ICAM-1in the KCs in diabetes+metformin group were significantly decreased (P＜0.05) ;the neutrophil chemotaxis ability was decreased (P＜0.05) , and the phagocytic ability was enhanced (P＜0.05) .Conclusion:Metformin can inhibit the inflammatory response of KCs in the diabetic mice and improve its phagocytic function and protect the KCs.
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Objective To investigate the incidence of autoimmune and nonautoimmune thyroid diseases in patients with breast cancer.Methods Clinical and ultrasound evaluation of thyroid gland,detection of serum thyroid hormone and related antibodies,and fine-needle aspiration of thyroid gland were performed in 100 breast cancer patients and 100 control individuals during the period from 2004 to 2008.Results The mean values of anti-thyroid peroxidase antibodies were significantly higher in breast cancer patients than that in control individuals [(104.56±21.54) U/ml vs (22.16±4.65) U/ml,(P=0.030)].The incidence rates of autoimmune and nonautoimmune thyroid diseases were higher in breast cancer patients than that in control individuals[38 ％ (38/100) vs 17 ％ (17/100),P=0.0009,26 ％ (26/100) vs 9 ％ (9/100),P =0.0016,respectively].Conclusion The results indicate an increased incidence of autoimmune and nonautoimmune thyroid diseases in breast cancer patients.
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ObjectiveTo explore the relationship among the aggressive behavior,hostile attribution bias and childhood trauma in schizophrenic patients.Methods 135 schizophrenic patients were tested with Modified Overt Aggression Scale (MOAS),the Chinese-version of the Ambiguous Intentions Hostility Questionnaire (AIHQ-C) and Childhood Trauma Questionnaire (CTQ).According to the score of the MOAS,the patients were divided into the aggressive group ( n =58 ) and the non-aggressive group ( n =77 ).The hostile attribution bias and the childhood trauma were compared between the two groups,and correlation and hierarchical regression analysis were used to investigate the relationships of the variables.ResultsCompared with the non-aggressive patients,the aggressive patients had significantly higher AIHQ-C total hostility bias score (6.27 ± 1.20 vs 5.90 ± 0.97,P ＜0.05 ),total blame bias score (8.04 ± 1.97 vs 6.91 ± 2.10,P ＜ 0.01 ) and total aggression bias score ( 6.17 ±1.02 vs 5.59 ± 1.04,P ＜ 0.01 ).Correlation analysis showed that the MOAS score,AIHQ scores and the total score of CTQ were significantly positively correlated with each other ( r =0.171 ～ 0.350,P ＜ 0.05 ～0.01 ).Regression analysis indicated the hostile attribution bias directly predicted the aggressive behavior( β =0.342,P ＜0.05) and completely mediated the relationship between the childhood trauma and the aggressive behavior.ConclusionThe aggressive behavior in schizophrenic patients is associated with the experience of childhood trauma and the attribution style.The childhood trauma indirectly influences the aggressive behavior by the mediating of the hostile attribution bias.
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Objective To explore the influence of Toxoplasma tachyzoites infection on motility of human spermatozoa in vitro, and explain its possible mechanism. Methods Semen samples obtained from 10 healthy volunteers by masturbation were prepared by the swim-up technique. The samples were then inoculated at 37 ℃ with different concentrations of live Toxoplasma tachyzoites varying among 1?103/ml (Group A), 1?104/ml (Group B), 1?105/ml (Group C), 1?106/ml (Group D), 1?107/ml (Group E) and Group F containing Ham’s F-10 only as the negative control. Motion parameters were analysed by Computer-aided sperm analyzer(CASA) in 0 hour, 1 hour, 2 hours, 4 hours respectively. Modalities of spermatozoa and possible adherence and/or agglutination were observed under the light microscope. Results Distinct adhesion of spermatozoa to Toxoplasma tachyzoites and agglutination were noticed. In all the motion parameters, progressive motility was affected most and dependent upon the incubation time and tachyzoites concentration. Progressive motility showed a significant difference between Group E and the control (P