Objective To describe the characteristics of and emergency treatment for and outcomes of critical ill children with 2009 influenza A caused by H1N1 virus strain. Method A prospective observational study of 3 pediatric patients with severe influenza A of H1N1 virus strain complicated with acute respiratory distress syndrome (ARDS) from November to December 2009. Results The H1N1 virus strain was confirmed by using realtime reverse transcription polymerase chain reaction (Real-time RT-PCR). Two patients survived and one died. Fever and cough were the onset symptoms. The systemic responses to influenza A at first were relatively mild. The tragic deterioration occurred all of a sudden with cyanosis all over the lips and dyspnea. The roentgenography showed bilateral multiple tabular pulmonary effusion and diffuse opaque shadows. The length of time required to confirm the diagnosis of ARDS from the symptom onset was 4 to 6 days. All patients were severely hypoxic with the ratio of PaO2 to 0.7-0.9 fraction of inspired oxygen (FiO2) to be 70- 100 mmHg at admission to PICU. In order to avoid injury to the lung, the protective ventilation strategy was carried out with low tidal volume (6 mL/kg) and adequate pressure,and conservative fluid management. Conclusions The H1N1 strain influenza virus A is characterized by pyrexia, cough and other respiratory symptoms in the early stage of critically ill children. In a few days, cough increased along with a sudden burst of cyanotic lips and shortness of breath, highly suggesting ARDS. Timely oxygen therapy and respiratory support, conservative fluid management, and the prophylaxis of secondary infection may be the essential measures. More clinical data are needed to clarify the critical features and to evaluate the emergency therapy for H1N1 influenza A in critically ill children.

Objective To investigate the clinicalmanifestation,monitoring and therapeutic measure of severe enterovirus 71 ( EV71 ) infection in children.MethodsForty-five cases of severe EV71 infectionwere admitted in our PICU from May 2010 to Sep 2011.The vital sign and arterial blood pressure,central venous pressure,mixed venous oxygen saturation,dynamic non-invasive heart function and urine volume were monitored.Forty-five cases were divided into 3 stages according to clinical manifestation:( 1 ) nervous system involvement stage; (2) respiratory system involvement stage; ( 3 ) circulatory system involvement stage ( compensation and decompensation).We adopted individualized remedy measure according to different stages.ResultsIn 45 cases,38 cases discharged from hospital,the cure rate was 84.4％.Among all the 38 cases,nervous system involvement was found in 19 cases,respiratory system involvement was found in 12 cases,circulatory system involvement was found in 7 cases.Seven cases died,who had circulation failure.ConclusionWe should identify severe EV71 infection early.Positive control of high fever,appropriate liquid treatment,control of high blood pressure,early respiratory support,preventment of circulation failure are the key measures for treatment.Individualized monitoring and treatment are effective in children with severe EV71 infection.

Objective To evaluate the effect of 131 iodine(131I) therapy in medium and large goiter with hyperthyroidism in order to investigate the influence of pretreatment with antithyroid drugs (ATD) methimazole(MMI) and propylthiouracide (PTU) on 131I therapy.Methods A total of 338 hyperthyroidism patients (136 cases for male,202 cases for female) with thyroid mass greater than 40 grams were treated with 131I in the People's Hospital of Sichuan Province.Thyroid function,thyroid 131I uptake ratio and thyroid imaging were measured before treatment were measured 1-3 months later after administration of 131I,and they were followed up for 6 months to 4 years.Results There were statistical difference between pretreatment and 3 months later of 131I therapy in terms of free triiodothyronine (FT3),(Free thyroxine) FT4.The level of FT3 decreased from (31.9 ± 16.2) pmol/L to (7.8 ±8.5) pmol/L(t =23.9,P =0.000) and level of FT4 decreased from (58.8 ± 22.2) pmol/L to (19.4 ± 16.9) pmol/L(t =25.4,P =0.000).Among 338 patients,109 patients (32.2％) were developed hypothyroidism,and 91 patients (26.9％) were cured,91patients (26.9％) with improved state,20 patients(5.9％) with ineffective and 27 patients(8.0％) with relapse after administration of 131I.The total effective rate was 94.1％ (318/338).Thyroid weight,levels of FT3,FT4,thyroglobulin antibody(TGA),thyroid microsomal antibody(MCA) in effective group were (49.8 ± 9.97) g,(32.5 ± 16.3) pmol/L,(59.5 ± 22.2) pmol/L,(43.6 ± 35.3) ％,(30.1 ± 22.6) ％ respectively,and were (56.9±15.7) g,(22.8 ± 12.8) pmol/L,(47.9 ±20.3) pmol/L,(22.8±30.0)％,(15.3 ±20.5)％ respectively in ineffective group.There were statistically significant differences between the ineffective group and effective group (t =2.932,2.602,2.287,2.501,2.766 ; P =0.000,0.010,0.023,0.013,0.006).Logistic regression analysis was showed that weight of thyroid and serum FT3 were the most important factors in affecting 1131 therapy.Conclusion 131 I therapy for medium and large-sized goiter with hyperthyroidism is safe and effective.ATD may not reduce the effectiveness of subsequent 131I of hyperthyroidism.Thyroid weight and FT3 are the key influential factors in affecting 131I.

Objective: To explore the echocardiographic cardiac geometric morphology and hemodynamics in premature infants at different gestational age with the inlfuencing factors.
Methods: A total of 150 premature infants and 150 full-term control infants were enrolled in this study. Based on gestational age, premature infants were divided into 3 groups:①(28-32+6 ) weeks,②(33-34+6 ) weeks,③(35-36+6) weeks; and full term control infants were divided into 2 groups:①’(37-38+6) weeks and②’ (39-41+6) weeks respectively. An iE33 Philips ultrasound examination was conducted to measure left ventricular end-diastolic diameter (LVEDD), LVESD, interventricular septum thickness, posterior wall thickness, left ventricular end-diastolic volume (LVEDV), LVESV, stroke volume, LVEF, left ventricular fractional shortening (LVFS), cardiac output, stroke index, cardiac index, left ventricular mass, left ventricular mass index (LVMI), left ventricular relative wall thickness, left ventricular remodeling index (LVRI) and LVEDVI.
Results: With adjusted body surface area, all parameters for cardiac geometric morphology and hemodynamics were similar among different groups,P>0.05. The day-old age (P=0.001), height (P=0.001) and body weight for low weight born infant (P=0.012), for normal weight born infant (P=0.003), for giant infant (P=0.016) were the independent inlfuencing factors for LVMI. The impact of anthropometry and the basic life indexes were similar on LVRI among groups (χ2=42.88,P=0.076), while the covariates were different on LVMI among groups (χ2=123.6,P<0.001).
Conclusion: Cardiac morphology and hemodynamics measured by echocardiography has important clinical meaning for assessing the development and maturity of neonatal hearts in premature infants.

OBJECTIVEThe objective of this paper was to study the change of P38MAPK and Fas in the apoptosis of THP-1 cells induced by allicin.

METHODThe proliferation inhibition rates of THP-1 cells after various treatments were examined by MTT assay. Apoptosis rate was determined with Annexin V- FITC/PI double staining by flow cytometry. The expression and distribution change of the phosphorylation p38MAPK (P-p38MAPK) were detected by immunohistochemical staining. The changes of P-p38 MAPK and Fas proteins were detected by Western blot.

RESULTThe proliferations of leukemia cell line THP-1 are inhibited by allicin. MTT assay showed that allicin can inhibit the proliferation of the THP-1 cell, and the inhibition was dependent on both dose and time. The IC50 of 72 hours was 12.8 mg x L(-1). Apoptosis rate detected by Annexin V-FITC/PI was proportional to the concentration of the allicin. After the immunohistochemical staining test, the P-p38MAPK was located in the cell nucleus and plasma, showing deep brown, when adding allicin to THP-1 cell. Western blot test showed that the P-p38MAPK proteins expression was proportional to the concentration of Allicin and was also dose dependent. The levels of P-p38MAPK in negative control group, 1/2 IC50 of 72 hours group and IC50 of 72 hours group were 0.259 8 +/- 0.013 2, 0.61 2 +/- 0.008 3 and 0.505 6 +/- 0.005 5 respectively, and the levels of Fas proteins were 0.287 4 +/- 0.008 9, 0.426 8 +/- 0.007 9 and 0.597 1 +/- 0.010 9 respectively. The difference was statistically significant when compared with the negative control group (P < 0.01).

CONCLUSIONAllicin can significantly induce THP-1 cells apoptosis, and its mechanism may be related to the activation of P38MAPK/Fas.

Apoptosis ; drug effects ; Cell Line, Tumor ; Humans ; Neoplasms ; drug therapy ; metabolism ; physiopathology ; Phosphorylation ; Signal Transduction ; drug effects ; Sulfinic Acids ; pharmacology ; p38 Mitogen-Activated Protein Kinases ; genetics ; metabolism

OBJECTIVE: To assess the association of single nucleotide polymorphisms (SNPs) of microRNA-146a (miR-146a) with clinical features of rheumatoid arthritis (RA). METHODS: In 126 patients with RA and 102 matched healthy controls, SNPs of miR-146a rs2910164 locus were determined with a high-resolution melting method. The association of such polymorphisms with disease activity score in 28 joints (DAS28) and clinical features of RA was assessed. RESULTS: The distribution of SNPs of miR-146a rs2910164 among RA patients did not differ from that of the control group. No significant association was found between miR-146a rs2910164 polymorphism with DAS28. However, RA patients with a GG genotype had a greater chance to develop extra-articular manifestations (P<0.01). CONCLUSION Polymorphisms of miR-146a rs2910164 locus is not an independent risk factor for RA, though its GG genotype may be associated with extra-articular manifestations of RA.
Arthritis, Rheumatoid ; genetics ; Case-Control Studies ; Genetic Predisposition to Disease ; Genotype ; Humans ; MicroRNAs ; genetics ; Polymorphism, Single Nucleotide