Adolescent ; Adult ; Aged ; Charcoal ; administration & dosage ; therapeutic use ; Enema ; Female ; Gastric Lavage ; Humans ; Male ; Middle Aged ; Organophosphate Poisoning ; Retrospective Studies ; Treatment Outcome ; Young Adult

Congresses as Topic ; Humans ; Infection ; Nose Diseases ; microbiology ; Nose Neoplasms ; Rhinitis, Allergic ; Rhinitis, Allergic, Perennial

Child, Preschool ; Humans ; Male ; Tricuspid Valve Insufficiency ; etiology ; Tricuspid Valve Prolapse ; congenital

Objective To study the protective effect of compound nitroglycerin gel on rats with skin ulcer wound and its action mechanism. Methods Skin ulcer modle of 54 rats was established.Then the rats were randomly divided into three groups (n=18 each), including model control group, Jin wan hong group, and compound nitroglycerin gel group. Wound healing process and healing time were recorded.At the day 7 and 14 after the model was established, the number of fibroblasts and new blood capillaries of granulation tissue from center of the wound were measured,and RT-PCR was used to detect mRNA expression levels of VEGF, Ang1 andHIF-1α. Results As compared with model control group [(24.17±5.91) days], healing time of skin in the compound nitroglycerin gel group was significantly shorter [(14.67±3.76) days, P<0.01].The numbers of fibroblasts (61.20±7.56) and new blood capillaries (9.35±1.43) were increased, and mRNA expression levels of VEGF (1.692±0.196), HIF-1α (1.527±0.174) and Ang1 (1.548±0.203) were remarkably up-regulated on 7th day (P<0.05 or P<0.01).While on 14th day, the numbers of fibroblasts (28.00±5.96) and new blood capillaries (4.20±1.30) were decreased and the mRNA expression levels of VEGF (1.156±0.123), HIF-1α(1.021±0.105) and Ang1 (1.034±0.134) were significantly down-regulated (P<0.05 or P<0.01) . Conclusion Compound nitroglycerin gel can treat skin ulcer wound via regulating the numbers of fibroblasts, new blood capillaries and VEGF/Ang1/HIF-1α signal transduction pathway.

AIM: To investigate the signal transduction mechanism of Chlamydia pneumoniae (Cpn) in down-regulating the expression of ATP binding cassette A1 (ABCA1) and ATP binding cassette G1 (ABCG1),the key molecules in cholesterol efflux and atherogenesis,from THP-1-derived macrophages. METHODS: Cpn was propagated in Hep-2 cells. THP-1 monocytes were induced into macrophages by 160 nmol/L phorbol myristate acetate (PMA) for 48 h,and were randomly allocated into 4 groups to incubate continually: control group,50 mg/L low density lipoprotein (LDL); Cpn infection group,Cpn (1×10~6 IFU) and 50 mg/L LDL; Cpn and SP600125 (a special JNK inhibiter) group,THP-1 macrophages were previously treated with different concentrations (1-20 μmol/L) of SP600125 for 1 h,and then infected with Cpn (1×10~6 IFU) and 50 mg/L LDL; SP600125 group,SP600125(20 μmol/L)and 50 mg/L LDL. The expressions of ABCA1/ABCG1 and peroxisome proliferator-activated receptor γ (PPARγ) from each group were detected then. The cholesterol efflux was detected by enzyme-fluorescence. The expressions of ABCA1/ABCG1 and PPARγ mRNA and protein were determined by RT-PCR and Western blotting,respectively. RESULTS: Cpn not only down-regulated the ABCA1/ABCG1 expression,but also down-regulated the expression of PPARγ,which regulated the ABCA1/ABCG1 genes transcriptions. However,the mentioned effects of Cpn infection were restrained by the special JNK inhibitor SP600125 in a dose-dependent manner. CONCLUSION: Chlamydia pneumoniae may down-regulate ABCA1/ABCG1 expression from THP-1-derived macrophages via JNK-PPARγ signal transduction pathway.

Objective:To investigate the effects of Chlamydia pneumoniae(Cpn) on SR-A1 and CD36 expression in THP-1-derived macrophages and role of c-Jun NH_2-terminal signal transduction pathway in the process.Methods:Cpn was propagated in Hep-2 cells.THP-1 monocytes were induced into macrophages by 160 nmol/L phorbol myristate acetate(PMA)for 48h,and were randomly allocated into four groups to be incubated continually: control group;Cpn infection group;Cpn and SP600125(a JNK inhibiter)group and SP600125 group.Lipid droplets in cytoplasm were observed by oil red O staining.The contents of intracellular cholesterol ester were detected by enzyme-fluorescence.The expression of SR-A1 and CD36mRNA and protein were determined by RT-PCR and Western blot, respectively. Results:THP-1-derived macrophages infected with Cpn resulted in large accumulation of lipid droplets and foam cell formation when co-cultured with LDL.Meanwhile,the expression of SR-A1 mRNA and protein were up-regulated by Cpn infection (P<0.05).However,the expressions of CD36 mRNA and protein in THP-1-derived macrophages infected with Cpn were unchanged.Moreover,the up-regulation of SR-A1 and foam cell formation induced by Cpn could be restrained by the JNK inhibiter SP600125 in a dose-dependent manner,and SP600125 had little impact on the expression of CD36 in THP-1-derived macrophages infected with Cpn.Conclusion:The up-regulation of SR-A1 but not CD36 expression is involved in mechanisms of Cpn inducing foam cell formation.And Chlamydia pneumoniae up-regulates the expression of SR-A1 via the JNK signal transduction pathway.This may be a novel mechanism for the foam cell formation induced by Cpn.

Objective To investigate the role of c-Jun N-terminal kinase (JNK) signal transduction pathway on the up-regulation of the expression of acyl-coenzyme A: cholesterol acyltransferasel (ACAT1) induced by Chlamydia pneumoniae (C. pn), and to discuss the mechanism of macrophages-derived foam cell formation induced by C. pn. Methods C. pn was propagated in Hep-2 cells. THP-1 monocytes were induced into macrophages by 160 nmol/L phorbol myristate acetate(PMA) for 48 h, and were randomly allocated into four groups to be incubated continually: control group, C. pn infection group, C. pn and SP600125 (a special JNK inhibitor)group and SP600125 group. Lipid droplets in cytoplasm were observed by oil red O staining. The contents of intracellular cholesterol ester were detected by enzyme fluorescence analysis. The expressions of ACAT1 mRNA and protein were determined by reverse transcriptase polymerase chain reaction(RT-PCR) and Western blot, respectively. Results Compared with the control group, the expressions of ACAT1 mRNA and protein were up-regulated in C. pn infection group [(4.16±0.26) vs. (2.17±0.18), (1.20±0.10)vs. (0.61±0.03), both P<0.05], and C. pn-induced foam cell formation was observed. The expressions of ACAT1 mRNA and protein and the foam cell formation were inhibited by SP600125 in a concentration-dependent manner (r = - 0.92, P<0.05; r= - 0. 96, P<0.05, respectively). Conclusions The up-regulation of ACAT1 expression is induced by C. pn via JNK signal transduction pathway, which is involved in the mechanism of C. pn-induced macrophage-derived foam cell formation.

Objective To investigate the mechanisms of Chlamydia pneumoniae (C. pn)-induced foam cell formation, the expression of ATP binding cassette transporter AI ( ABCA1 ) and perexisome prolif-erator-activated receptor γ (PPARγ) were examined. Methods THP-1 monneytes were induced into mac-rophages after the addition of 160 nmol/L phorbol myristate acetate (PMA) for 72 h. THP-1-dorived macro-phages when co-cuhured 50 mg/L low density lipoprotein (LDL) were designated randomly in four groups: control (uninfected) group, C. pn infection group, rosiglitazone + C. pn infection group and rosiglitazone group. Lipid droplets in cytoplasm were observed by oil red O staining. The contents of intracellnlur choles-terol ester were detected by enzyme-flnoreseence. The expression of ABCA1, PPARγ, mRNA and protein were determined by RT-PCR and Western blot, respectively. Results C. pn down-regulated the expression of ABCA1, PPARγ at mRNA and protein levels in a concentration-dependent manner in THP-1-derived mac-rophages when co-incubated with LDL. Resiglitazone not only concentration-dependently alleviated the down-regulation of ABCA1 expression by C. pn infection (P<0.05), but also markedly suppressed the accumula- tion of lipid droplets and cholesteryl ester by C. pn at higher concentrations ( 10 and 20 μaol/L). Condu-sion C. pn induces foam cell formation by down-regulating the expression of ABCA1 via PPART pathway, which may provide a new evidence for the development and progression of atherosclerosis initiated by C. pn infection.

Objective To summarize the experience of emergency treatment and cosmetic repair of facial trauma.Methods The clinical materials of 584 wounds from 291 cases of facial trauma,recruited in hospital from January 2010 to August 2012,were summed up retrospectively.The principles of medical aesthetics and plastic and cosmetic surgery were followed.A high pressure douching technique was employed to carry out thorough debridement,but occasion of the debridement did not emphasize with intensive attention.A wound without skin and soft tissue defect was sutured accurately according to tissue zonation with a new suture technique,and the needle distance or side distance was limited in 0.2 cm to 0.3 cm.Otherwise,the wound was repaired by full-thickness skin graft or various flaps according to the repair principle ofrather near than further,rather simple than complicated.Attention was paid to rehabilitation care.Results After debridement,328 wounds were sutured directly,147 wounds were repaired by full-thickness skin grafting and 109 wounds by various flaps.A total of 571 wounds healed on the first stage,and the healing rate reached 97.8％.The wounds were in satisfactory apposition and without obvious cicatrix.Five senses did not appear in malposition and deformity.The other 13 wounds did not heal because of bad taking of skin grafts and flaps or wound splitting.Among them,4 wounds were repaired by second operation,and 9 wounds healed by changing dressings.By means of rehabilitation care,scar hyperplasia and pigmentation appeared slightly in those 13 wounds.A total of 454 wounds from 217 cases were followed up.The results showed good appearance and slight cicatrix hyperplasia,a pigmentation in different degree appeared in 11 wounds covered by skin grafting.In addition,eyebrow excalation,auricle excalation or total lose appeared in 12 cases.Conclusion During treating emergency cases of facial injuries,if an idea cosmetic repair of traumais followed,the theory of aesthetics and the techniques of plastic and cosmetic surgery are fully used,a multiple-discipline cooperation is brought into full play,and a prompt and accurate treatment is put into practice,the aim of cosmetic repair would come true.

In this assay, the reaction kinetics, optimum temperature, pH and various influential factors of ATP microbial rapid detection reagent by bioluminescence were studied. The results showed that it's enough for detection system to have 40 ~ 50?g/mL D-Luciferin. The light production decreased fastest in the first minute of reaction, then began to decay slowly. The optimal reaction temperature was 24℃~25℃and the optimal pH was pH 7.2 -7.4 in the reaction system. In addition, when stored at 4℃for 45h, the dissolved reagent solution could keep its 86% activity. When preserved at 25℃, the enzyme activity decreased less for 1h, and degraded gradually as time went by and only left 53. 5% of its activity after 6. 5h. While stored at 33℃, the enzyme activity decreased quickly with the time and only left 59. 1% after 1. 5h. The result indicated that storage temperature was a very important influential factor to the activity of reagent Meanwhile, different chemical substance such as acid, alkali, salt and surfactants inhibited the ATP bioluminescent reaction. When the concentration of NaCl reached 1. 5g/L, it could inhibit 52. 5% light production. Triton X-100, acid, and alkali also had some effects on the reaction, while CTAB, SDS and TCA would inhibit the bioluminescent reaction seriously.