Objective To investigate the effect of 3 concentrations of sevoflurane pretreatment on acute lung injury induced by endotoxin in rats. Methods Thirty-six male SD rats were randomly divided into 6 groups:a control group(Group A), a sevoflurane group(Group B), a 3.6% sevoflurane pretreatment group(Group C), a 2.4% Sevoflurane pretreatment group(Group D), a 1.2% sevo sevoflurane pretreatment group(Group E), and lipopolysaccharide (Group F).The rats were killed 6 h after lipopolysaccharide (LPS) or saline injection.Histological examinations of the lung tissues were performed with light microscope. Lung wet/dry weight (W/D) ratio, myeloperoxidase (MPO) activity, and intercellular adhesion molecule 1 (ICAM-1) mRNA expression were assayed. Results Introvenous LPS significantly aggravated lung tissue damage,increased lung W/D ratio, MPO activity, and lung ICAM-1 mRNA expression compared with the control group(P＜0.05). Precondition with 2.4% sevoflurane significantly attenuated the above mentioned changes induced by LPS (P＜0.05). The 3.6% LPS (Group C) significantly attenuated lung tissue damage and decreased MPO activity,lung ICAM-1 mRNA expression compared with the Group F (P＜0.05),but no significant change in lung W/D ratio was seen (P＞0.05). MPO activity was significantly decreased in Group E (P＜0.05), but lung W/D ratio and lung ICAM- 1 mRNA expression had no significant changes (P＞0.05).Conclusion Precondition with 2.4% sevoflurane can reduce LPS induced lung injury in rats. Decreased expression of ICAM-1 and less accumulation of neutrophils were participated in its mechanism.

Objective To screen the conservative,stable and specific DNA signature sequence in the plasmid of Yersinia pestis.Methods Specific validation trials and stability of the qualification test were carried out to 40 strains of Yersinia pestis,47 strains of non-Yersinia pestis of home and wild types of rodent in Yunnan,by using 32 DNA sequences derived from Yersinia pestis in the plasmid and conventional PCR technology,and Yersinia pestis vaccine strain EV76 as a positive control.Results Four pairs of relatively conservative,stable and specific DNA marker genes were screened:YPMT1.05c,YPMT1.03c,YPMT1.42 and YPMT1.04c.Conclusions The 4 pairs of Yersinia pestis DNA signature sequences can be used for rapid diagnosis of plague.

Adult ; Cardiovascular Diseases ; physiopathology ; Cardiovascular Physiological Phenomena ; Case-Control Studies ; Female ; Heart ; physiopathology ; Humans ; Pregnancy ; Sports ; Stress, Psychological ; physiopathology

Animals ; Female ; Fluorosis, Dental ; blood ; etiology ; Glutathione Peroxidase ; blood ; Male ; Malondialdehyde ; blood ; Myocytes, Cardiac ; pathology ; ultrastructure ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Sinoatrial Node ; pathology ; ultrastructure ; Sodium Fluoride ; poisoning ; Superoxide Dismutase ; blood

AlM: To investigate the association between the degree of anterioruveitis and related factors including inflammatory markers as well as sacroiliac joint imaging in patients with ankylosing spondylitis ( AS) .
METHODS: Anterior changes evaluated by slit lamp, erythrocyte sedimentation rate ( ESR ) , C - reactive protein ( CRP ) and magnetic resonance imaging of 55 cases with AS associateduveitis were retrospectively analyzed. A modified endotoxin-induced uveitis ( ElU ) clinical standard was used for uveitis grading. SPARCC sacroiliac scoring was used to evaluate bone edema of sacroiliac joint. The correlation between the degree of uveitis and sacroiliitis was assessed.
RESULTS: ln the 55 patients with AS, ElU grading scored 2-10, and SPARCC index scored 0-22. Further analysis showed that the severity of uveitis was significantly correlated with ESR (r=0. 869, P<0. 001) and CRP (r=0. 485, P<0. 001). The degree of anterior uveitis in AS patients was not correlated with inflammation of sacroiliac joint (r=0. 237, P=0. 081).
CONCLUSlON: Local autoimmunity of uveitis and sacroiliac joint inflammation with subsequent bone formation in AS might be mutually independent processes.

Objective To observe the influence of coal burning fluorosis on learning and memory ability in rats and reveal its possible mechanisms. Methods Healthy 48 SD rats were divided into control, low-fluoride and high-fluoride group. All rats in fluoride exposed groups were fed with the eom polluted by drying processes with burning coal containing high level of fluoride obtained from the endemic fluorosis area to produce the animal model of fluorosis. The experiment period were 3,6 mouths, respectively. The ability of leaning and memory was measured by Morris test and cholinesterase activity detected by photometric method at 3 or 6 month after experiment, respectively. Results Fluoride contents signifieantlly influenced the escape latency, the numbers of crossing the platforms and the time of staying the platforms(the value of F was 29.29,6.47,6.50, respectively, P<0.01).In addition, the numbers of crossing the platforms and the time of staying the platforms were influenced by the exposed time(the value of F was 16.11,45.59, P<0.01). Furthermore, the fluoride contents and the exposed time had an interaction between the numbers of crossing the platforms and the time of staying the platforms (the value of F was 4.67,5.68, P<0.05 or<0.01). Three months after the experiment, the mean values of escape latency [(14.71± 4.85)s] of rats in highly fluoride exposed group were significantly prolonged as compared with controls [(9.28±4.22)s]; 6 month after the experiment, the mean values of escape latency[(12.42±8.03)s, (17.48± 8.05)s] of rats in both groups exposed to fluoride were significantly prolonged as compared to controls [(7.04± 3.29)s, P<0.05]. The decreased numbers of crossing the platforms[(1.62±0.87)number] and the declined time of staying the platforms[(16.70±5.02)s] were found in the rats exposed to high fluoride as compared to controls [(3.53±1.67 )number, (23.33±5.35)s, P<0.05]. The fluoride contents obviously influenced the activities of acetylcholinesterase and butylcolinesterase (the value of F was 12.83,13.27, P<0.01). On the other hand, the times of breeding also influnced the activities of butylcolinesterase (the value of F was 16.26, P<0.01). In 3 months of the experiment, the activities of butylcolinesterase [(0.55±0.12)kU/g] in low fluoride exposed group were significantly decreased in comparison with controls[(0.73±0.10)kU/g, P<0.05]. The activities of acetylcholinesterase[(0.62±0.42)kU/g] and butylcolioesterase[(0.58±0.10)kU/g] in high fluoride group were significantly decreased as compared to eontrois[(1.41±0.52), (0.73±0.10)kU/g, P<0.05]. The correlation analysis showed that there was a negative correlation between the cholinesterase and the escape latency(r=-0.68, P< 0.01), and a positive correlation between the cholinesterase and the time of staying the platforms(r=0.57, P< 0.01). Conclusions The ability of learning and memory in rats with coal buring fluorosis was decreased, which might be connected to the decreased activity of cholinesterase in a dose-effect correlation.

Objective To investigate the effects of quetiapine on serum levels of brain-derived neurotrophic factors ( BDNF) and the correlation between BDNF and psychiatric symptoms and cognitive function in patients with first-episode schizophrenia. Methods Eighty patients with first-episode schizophrenia ( treatment group) were treated with quetiapine orally for 4 weeks,at initial dose of 100 mg·d-1 and average dose of (580±120) mg·d-1 . The psychiatric symptoms were evaluated by using the positive and negative syndrome scale ( PANSS) . The cognitive function was assessed by using Wisconsin cards sort test ( WCST) . The serum BDNF level was detected with enzyme-linked immunosorbent assay ( ELISA) . Results The serum level of BDNF was markedly lower in schizophrenic patients before[(13. 72±8. 79) ng·mL-1,P<0. 01] and after treatment[(18. 02±9.06) ng·mL-1,P<0.05]in comparison with normal controls(23. 67±10. 13) ng·mL-1]. After treatment,the PANSS total scores and subscale scores decreased,WCST number of categories and the number of correct answers increased,and the number of wrong answers reduced. There was a positive correlation between the serum BDNF and negative symptoms ( SANS) ( r= 0. 54, P=0. 032),and the number of correct answers. Conclusion The quetiapine significantly increases serum level of BDNF in schizophrenia patients,which correlates positively with improvements in symptoms and cognitive function.

OBJECTIVETo observe the effect of total flavonoids of Oldenlendia difflusa (FOD) on NF-kappaB and IL-8, TNF-alpha, IL-10 expressions of ulcerative colitis (UC) model rats, and explore its immunological mechanism of anti-UC.

METHODSixty Kunming male mice with the average weight of (20 +/- 2) g were randomly divided into six groups. The control group (cont) was orally administered with distilled water. Whereas the remaining five groups were fed with 4% dextran sulphate sodium (DSS) solution for seven days to induce acute UC, and orally administered with the following drugs: distilled water (for the DSS group), SASP at dose of 500 mg x kg(-1) x d(-1) for the DSS + SASP group, FOD at dose of 60 mg x kg(-1) x d(-1) for the DSS + FOD-H group, FOD at dose of 40 mg x kg(-1) x d(-1) for the DSS + FOD-M group, and FOD at dose of 26.7 mg x kg(-1) x d(-1) for the DSS + FOD-L group. During the modeling and drug administration, the mice were scored for DAI. Seven days later, the mice were put to death, and their colonic tissue samples were collected to evaluate colonic mucosal lesions. The NF-kappaB p65, IL-8, TNF-alpha, IL-10 expressions were tested by immunohistochemical staining and ELISA.

RESULTSeven-day feeding with 4% DSS solution could successfully induce acute UC in mice. Compared with the cont group, the DSS group showed significantly higher DAI and colonic mucosal lesions, remarkable increase in NF-kappaB p65, IL-8, TNF-alpha expression in colonic tissues, and notable decrease in IL-10 expression (P < 0.05). FOD could prevent acute UC in mice included by DSS. Seven-day administration of 60 mg x kg(-1) x d(-1) or 40 mg x kg(-1) x d(-1) FOD could completely or partially resist the above mentioned changes caused by DSS. Compared with the DSS group, the DSS + FOD-H group and the DSS + FOD-M group showed reduction in colonic mucosal lesions, down-regulation in IL-8, TNF-alpha and NF-kappaB p65 expressions and up-regulation in IL-10 expression (P < 0.05).

CONCLUSIONFOD could significantly resist UC in mice. Its mechanism may be related to the inhibition of NF-kappaB p65 activation, the reduction of IL-8 and TNF-alpha expressions and the increase in the anti-inflammatory factor IL-10.

Animals ; Anti-Inflammatory Agents ; administration & dosage ; Colitis, Ulcerative ; drug therapy ; genetics ; immunology ; Drugs, Chinese Herbal ; administration & dosage ; Flavonoids ; administration & dosage ; Humans ; Interleukin-8 ; genetics ; immunology ; Male ; Mice ; NF-kappa B ; genetics ; immunology ; Oldenlandia ; chemistry ; Transcription Factor RelA ; genetics ; immunology ; Tumor Necrosis Factor-alpha ; genetics ; immunology

Adult ; Herpes Zoster ; etiology ; Herpesvirus 3, Human ; genetics ; Humans ; Male ; Middle Aged ; Mutation

Acupuncture Therapy ; Adult ; Aged ; Combined Modality Therapy ; Facial Paralysis ; therapy ; Female ; Humans ; Male ; Middle Aged ; Moxibustion ; Punctures ; Young Adult