OBJECTIVE:To analyze bacteria distribution and drug resistance of pediatric severe sepsis in our hospital,and to provide reference for clinical rational use of antimicrobial agents. METHODS:57 pediatric severe sepsis patients were collected from pediatric intensive care unit of our hospital during Jan. 2014 to May 2015. The results of pathogen culture and drug sensitivity tests were analyzed retrospectively. RESULTS:Of 57 children,pathogen were detected in 18 cases(31.58%). A total of 91 pathogen were detected,of which there were 24 strains of Gram-positive(G+)bacteria(26.37%)mainly including Staphylococcus and Entero-coccus,60 strains of Gram-negative (G-) bacteria (65.93%) mainly including Klebsiella pneumoniae and Acinetobacter calco-acetcus-A. baumannii complex and 7 strains of fungus (7.69%) as Candida. 4 strains of methicillin-resistant Staphylococcus,22 strains of carbapenems-resistant K. pneumoniae,21 strains of multi-drug resistant K. pneumoniae and 7 strains of multi-drug resistant A. calcoacetcus-A. baumannii complex were all detected. Methicillin-resistant Staphylococcus,Staphylococcus aureus and Streptococ-cus pneumoniae were sensitive to vancomycin and linezolid,with resistant rate of 0. K. pneumoniae was completely resistant to ampi-cillin sodium and sulbactam sodium,piperacillin sodium and tazobactam sodium,imipenem and cephalosporin,with resistant rate of 100%. Resistant rate of A. calcoacetcus-A. baumannii complex to major common antimicrobial agents was higher than 50%. Esche-richia coli was resistant to cefotaxime,and resistant rates of other antimicrobial agents were lower than 40%. CONCLUSIONS:Main pathogen of pediatric severe sepsis is G- bacteria in our hospital,and carbapenems-resistant K. pneumoniae is detected,to which should be pay attention. The multiple drug-resistant treatment should be adopted for pediatric severe sepsis caused by multiple drug-re-sistant bacteria. Antimicrobial agents should be selected rationally according to pathogen type and the results of drug sensitivity test.

Contraindications ; Humans ; Infant ; Infant, Newborn ; Promethazine ; adverse effects

OBJECTIVE:To explore the role of clinical pharmacists participating in drug therapy for patients with severe infec-tions. METHODS:Clinical pharmacists participated in drug treatment for a patient with tropical candidemia and assisted physicians to adjust anti-infective treatment plan. According to the results of blood culture,clinical pharmacists suggested Piperacillin sodium and tazobactam sodium for injection 3.75 g,ivgtt,q8 h+Caspofungin acetate for injection 50 mg (initial dose of 70 mg),ivgtt, qd,for symptomatic treatment;increased the daily dose of Caspofungin acetate for injection to 50 mg,ivgtt,bid due to plasma ex-change;Caspofungin acetate for injection 50 mg,ivgtt,qd+Amphotericin B for injection 0.1 mg/kg,ivgtt,qd for anti-infective plan due to the possible“contradiction”of echinocandins;closely monitored ADR,such as allergy,erythra,renal function injury. RE-SULTS:Physicians adopted the suggestions of clinical pharmacists,vital sign of patient kept stable,and tropical candidemia was not detected in the blood culture;the patient was transferred to general ward for further treatment. CONCLUSIONS:Based on the results of blood calture,clinical symptoms and the characteristics of drug effects,clinical pharmacists participated in the treatment for the patient with severe infection,retrieved related treatment guideline,assisted physicians to adjust anti-infective plan and close-ly monitored possible ADR so as to guarantee the effectiveness and safety of anti-infective treatment.

One hundred and fifty eight post-stroke patients in the recovering period were divided into intervention group (78 cases) and control group (80 cases).Patients in intervention group received home rehabilitation service provided by general practitioners (GP) for 6 months,while patients in control group received routine rehabilitation.After 6-months,the scores of self-rated health measurement scale (SRHMS) in intervention group were significantly higher than those of control group (P ＜0.01);the visiting time and frequency,medical costs and time of caregiving were decreased (P ＜ 0.01);and the satisfaction score of the patients in intervention group was 97％.The results show that home rehabilitation service can improve effectiveness of rehabilitation for post-stroke patient in recovering period.

0.05). Only tumor classification and cell differentiation were proved to be independent factor determing the outcome (P

Objective To investigate the effects of C-terminal fragment of parathyroid hormonerelated protein (PTHrP107-139) on bone mineral density (BMD), bone histomorphometry and biomechanical properties in ovariectomized (OVX) rats and its effect on bone metabolism is also explored. Methods Forty 4-month old female Wistar rats in which 30 were ovariectomized and then divided into 3 groups: the placebo, the PTHrPC and the CT groups, the other 10 rats were Sham-operated as the control group (Sham). Five weeks later, the rats of PTHrPC and CT groups were subcutaneously injected with PTHrP107-139 (40 μg/kg) and Salmon Calcitonin (15 U/kg) respectively once every other day. The rats of the placebo and sham groups were injected with 0.2 ml saline once every other day. After treatment of 12 weeks, all rats were sacrificed and all samples were collected and analyzed. Results ① Compared with the placebo, the BMD and bone strength of PTHrPC and CT groups were significantly increased (P<0.05). ② Histomorphometry revealed that the tetracycline labeled bone surfaces, osteoid surfaces, mineral apposition rate and bone resorption rate were remarkably decreased in PTHrPC, and CT groups comparing with those of the placebo group. Conclusion Cter-minal PTHrP107-139 is effective in increasing the BMD, bone strength and quality when administered intermittently to ovariectomy-induced osteoporotic rats. Its increasing in bone quality may relate to reducing bone turnover and inhibiting resorption.

Objective To investigate the therapeutic effects of human parathyroid hormone related protein (PTHrP1-34) on osteoporosis of ovariectomized osteoporotic rats. Methods Sixty 4-month-old female Wislar rats were involved in this study and 40 of them were ovariectomized and another 20 received sham operation. After 6 weeks of ovariectomy the osteoporosis model was confirmed by examing 10 ovariectomized and sham-operated rats. The 30 osteoporotic rats were randomly divided into 3 treatment groups, i.e. PTHrP, estradiol and placebo. Human 40 ?g/kg PTHrP1-34 was subcutaneously injected once daily to PTHrP group and the estradiol group was injected with 40 ?g/kg estradiol benzoate once every 3 days.The placebo and shamoperated rats were given 0.2 ml saline every 3 days. The bone mineral density (BMD), bone histomorphology, the bone weight of dry and ash and serum Ca,P,alkaline phosphatase (ALP) were measured after 3 months' therapy. Results After 6 weeks of ovariectomy, the lumbar BMD of ovariectomized rats were significantly declined compared with those of the sham-operated rats. After 12 weeks treatment the femoral and lumbar BMD and the rate of bone weight of dry and ash in the PTHrP group were increased obviously compared with those of placebo groups.There was no significant difference between PTHrP group and estradiol group, in PTHrP group the percent age of trabecular area,trabecular width,osteoblast surface and mineral apposition rate were obviously higher than those in placebo group.Conclusion Treatment with 40 ?g/kg dose of hPTHrP1-34 administered once daily is effective in treating ovariectomy-induced osteoporosis.

Background and purpose: Lysine specific demethylase 1(LSD1) is an important chromatin modifier. It epigenetically regulates gene expression pattern through chromatin modification and participates in maintenance of tumor malignant properties, such as oncogenesis, development, invasion, migration and metabolic transformation. SIRT3 (sirtuin 3) is a mitochondria localized tumor suppressor and regulates tumor metabolic transformation and oxidative stress. The correlation between LSD1 and SIRT3 has never been reported before. This study aimed to elucidate the correlation between LSD1 and SIRT3 with gene transcriptional regulation methods. Methods: RNA interference technique, co-immunoprecipitation assay(CoIP), chromatin immune-precipitation assay(ChIP) and ifrelfy luciferase activity assay were employed to elucidate the correlation between LSD1 and SIRT3 in pancreatic cancer. Results:mRNA and protein levels of SIRT3 were signiifcantly elevated in LSD1 knock-down PANC-1 cells. LSD1 interacts with PGC-1α, an important regulator of SIRT3 gene expression. LSD1 and PGC-1αoccupied the same region in SIRT3 promoter region through ChIP analysis. Luciferase activity assay validated LSD1 as a negative regulator of PGC-1αin SIRT3 gene transcriptional regulation. Conclusion:LSD1, as an important tumor promoter, negatively regulates the expression of tumor suppressor gene SIRT3, these results provide important clues for the role that LSD1 plays in aberrant metabolism and oxidative stress.

OBJECTIVETo explore efficacy enhancing and detoxification roles of Jiedu Quyu Zishen Recipe (JQZR) in treating systemic lupus erythematosus (SLE) by studying its effect on Toll like receptor 9 (TLR9) signal pathway of murine macrophage cells after JQZR stimulated CpG oligodeoxynucletide (CpG ODN).

METHODSMurine macrophage cells in vitro cultured were randomly divided into 4 groups, i.e., the blank serum group, the CpG ODN stimulus group, the CpG ODN + dexamethasone group, the CpG ODN + medicated serum group. Murine macrophage cells were collected after 24-h intervention. The expression of TLR9, myeloid differentiation factor 88 (MyD88), NF-KB, IFN-α mRNA were analyzed by RT-PCR. The expression of TLR9 and NF-κB protein were analyzed by Western blot. Changes of the NF-KB transcriptional activity were assayed by Dual-Luciferase reporter assay system.

RESULTSmRNA expressions of TLR9, MyD88, NF-κB, and IFN-α, protein expressions of TLR9 and NF-κB, and NF-κB transcriptional activities were enhanced, showing statistical difference when compared with those of the blank serum group (P <0. 05, P <0. 01). Compared with the CpG ODN stimulus group, mRNA expressions of MyD88, NF-κB, and IFN-α, the protein expression of NF-κB and the NF-κB transcriptional activities decreased in the CpG ODN + dexamethasone group with statistical difference (P <0. 01). Compared with the CpG ODN stimulus group, mRNA expressions of TLR9, MyD88, NF-κB, and IFN-α, protein expressions of TLR9 and NF-κB, and NF-κB transcriptional activities were decreased in CpG ODN+ medicated serum group with statistical difference (P <0. 01).

CONCLUSIONEfficacy enhancing and detoxification roles of JQZR in treatment of SLE might be realized through regulating TLR9 signal pathways.

Animals ; Cell Line ; Drugs, Chinese Herbal ; pharmacology ; Humans ; Macrophages ; metabolism ; Mice ; Myeloid Differentiation Factor 88 ; NF-kappa B ; RNA, Messenger ; Signal Transduction ; Toll-Like Receptor 9 ; metabolism

AIM: To study the distribution of C46T polymorphism of factor Ⅻ(FⅫ) in Chinese Han population and the association of the polymorphism with coronary artery disease(CAD) and acute coronary syndrome(ACS). METHODS: Selected coronary angiography was performed in 168 CAD patients and 210 controls. Genetype of FⅫ was typed by mutagenically separated polymerase chain reaction assay(MSPCR). RESULTS: FⅫ allelic frequencies of C and T were 29.8%, 70.2% and 31.4%, 68.6% in CAD and controls, respectively(P>0.05). Genetype distribution was in accordance with Hardy-Weinberg equilibrium. The frequency of CC, CT, TT in CAD and control was 8.7%, 40.5%, 50.0% and 5.2%, 52.6%, 42.2%. The association between FⅫ genetype and CAD(χ~2=6.393, P<0.05) was observed. As compared with the CC group, the CT genetype was a protective factor for CAD(OR 0.43, 95% CI 0.19-0.97). When compared to stable coronary artery disease, the frequency of TT genetype is significant less in ACS group(45.0% vs 62.5%, χ~2=4.200, P<0.05). The distribution of genetype in C46T was no significant difference among the numbers of stenosed coronary artery. CONCLUSION: The C46T polymorphism of FⅫ is association with CAD in Chinese Han population. The C→T mutation may be a protective factor against CAD and ACS.