Objective To analyze the multiple factors affecting the postoperative mechanical ventilation supporting time of chil-dren with congenital heart diseases ,and to preferably master the offline period and offer intervention techniques about shortening mechanical ventilation supporting time and improving efficacy .Methods A total of 217 with congenital heart diseases in 2012 from January to October were retrospectively studied to seek the factor affecting the duration of ventilation .The factors including the age ,weight ,cardiopulmonary bypass time(CBP) ,aortic cross-clamping time(ACC) ,preoperative albumin ,preoperative pulmonary infection ,preoperative pulmonary artery pressure ,postoperative complications were analyzed by the stepwise Logistic regression . Results The ventilation supporting time was 0 .5 -312 .0 h ,average(28 .42 ± 2 .99)h .Multivariate stepwise Logistic analysis showed that the postoperative complications ,preoperative pulmonary infection and CPB were mechanical ventilation use time of the main influence factors .Conclusion Postoperative complications ,preoperative pulmonary infection and CPB are the main influencing factors of mechanical ventilation supporting time .

0.05).The proportion of TR degree improved in patients of two groups in a short-term.However,the difference of TR in long-term between two groups was statistically significant(P

In order to improve doctor patient relationship and communications, the system of doctor patient communications was implemented in an all round way. First, the contents of the system were defined. Then the ways of implementing the system were fixed: improving training and changing service concepts; bringing doctor patient communications into line with quality management; making use of special survey forms for the system, and mastering a variety of communications skills. In addition, necessary organization, personnel, and regulations were put in place to guarantee the success of the system. Consequently, implementation of the system brought about pretty tangible results.

Objective To study the influencing factors of pediatric in-hospital cardiopulmonary resuscitation(CPR).Methods It was a retrospective observational study.We studied a total of 281 children who suffered in-hospital cardiopulmonary arrest(CPA).The outcome was defined as sustained return of spon-taneous circulation ﹥20 min.Results A total of 281 patients met study entry criteria.In 129 children (45.9%),return of spontaneous circulation sustained ﹥20 min and 20 cases(8.8%)survived to hospital discharge.In the univariate analysis,gender,age,weight,time of CPA happened,first cardiac rhythm,pH, blood lactate had no obvious influence on the outcome.Underlying disease,the place of CPA,personnel fac-tors,airway support,the duration of CPR,doses of adrenaline,use of bicarbonate and blood glucose level were associated with outcome.Conclusion At present,the rate of successful CPR and discharge of hospital is still low.Respiratory disease has a higher survival rate.CPR ﹥20 min,use of bicarbonate and using adrenaline≥3 doses are associated with poor outcome and an increase in mortality.

OBJECTIVE:To investigate the protective effect of Polydatin on acute lung injury following endotoxic shock in rats.METHODS:Using a rat endotoxic shock model,animals were randomly divided into4groups∶sham operation group,en?dotoxic shock group,Polydatin treatment group and Polydatin pretreatment group.MAPs(mean artery pressures)were mea?sured at given time points.At the end of the experiment,the serum,the lung tissue,and the bronchoalveolar lavage fluid(BALF)were collected.The levels of lung coefficient,lung penetrating index(LPI),the protein concentration of BALF and the content of NOS in the lung tissue were measured.Furthermore,the histologic changes of the lung were observed under light micro?scope.RESULTS:In addition to prohibiting the dropping of MAP,Polydatin could mitigate the acute lung injury induced by endotoxin which increased the levels of lung coefficient,LPI,the protein concentration of BALF and the content of NOS in lung tissue.Enough morphological evidence could be found in pathological sections.Especially,the protective effects were more ob?vious in Polydatin pretreatment group.CONCLUSION:Polydatin has prophylactic and therapeutical effects on acute lung injury following endotoxic shock and the prophylactic effect is more marked than the therapeutic one.

0.05). For all patients, the WR relapse rates were 0%(0/43) in Group A and 1.6%(1/63) in Group B and for the core patients, these rates were 0%(0/34) and 2.2% (1/46),respectively.Conclusions WR prophylactic irradiation is not advisable in treatment of cervical primary NHL, especially when chemotherapy was combined. It is to protect the major salivary glands from radiation damage and improve the patient's quality of life. However, it is extremely important to routinely examine WR by CT scan,pharyngorhinoscopy and WR biopsy to rule out primary WR NHL.

BACKGROUND: Activated by Ca2+, phospholipase A2 will aggravate the influx of Ca2+ or the release of intracellular Ca2+, and then forms a vicious circle, which results in a continuous increase in free calcium level and leads to server injury in neural cells.OBJECTIVE: To discuss the protective effects of nimodipine on acute ischemic brain injury caused by activation of phospholipase A2.DESIGN: A completely randomized controlled trial.SETTING: Intensive Care Unit (ICU) of Children's Hospital, Chongqing Medical University.MATERIALS: From January 2001 to October 2003, it was completed at the ICU of Children' s Hospital, Chongqing Medical University. Thirty male rats were selected and divided into sham operation group, ischemia group and nimodipine treated group randomly, with 10 rats in each group.METHODS: In sham operation group, the right common carotid artery was identified by blunt dissection without ligation under anesthesia in rats. In ischemia group, at 30 minutes before cerebral ischemia, 2 mL saline was injected intraperitoneally. In nimodipine treated group, at 30 minutes before cerebral ischemia, 0.2 g/L nimodipine (2 mg/kg) was injected intraperitoneally. In all the three groups, the duration between ischemia and decollation was 120 minutes. Rats were decollated under anesthesia and their brains were taken out to assess the activity of phospholipase A2, the free calcium level in brain cells, the brain water content and the changes in mRNA levels of type Ⅱ phospholipase A2 (secretive phospholipase A2) and type Ⅳ phospholipase A2 (cytoplasmic phospholipase A2) in brain tissue.pholipase A2) and type Ⅱ phospholipase A2 (cytoplasmic phospholipase A2)in brain tissue were measured in rats in all the groups.pholipsse A2 in brain tissue: In ischemia group and nimodipine treated group, the activity of phospholipase A2 were higher than that in sham operation group [(57.8 ±7.2),(42.5±6.1), (17.1±5.3)%, P＜ 0.05-0.01], and it was a litter lower in nimodipine brain cells: It was higher in nimodipine treated group and ischemia group than that in sham operation group [(775.8±105.5), (497.2±45.9), (103.8±10.3) μmol/L,P ＜ 0.05-0.01], and it was lower in nimodipine group than in ischemia group (P ＜ 0.01).that in sham operation group [(82.9±0.5), (80.0±1.1), (72.1±0.01)%, P ＜ 0.05-0.01], and it was lower in nimodipine treated group than that in ischemia group (Ppase A2 could be detected in brain tissue. And the mRNA level of type Ⅱ phospholipase A2 in brain tissue was very low. At 120 minutes after ischemia, mRNA of type Ⅱ phospholipase A2 was detectable and the expression of type Ⅱ phospholipase A2 was increased. Compared to ischemia group, the expression of type Ⅱ phospholipase A2 was not decreased in nimodipine treated group while the expression of type Ⅱ phospholipase A2 was decreased.CONCLUSION: Nimodipine is capable of decreasing the free calcium level in brain cells, the activity of phospholipase A2 in brain tissue and the brain water content after ischemia. However, it cannot significantly inhibit the expressions of type Ⅱ phospholipase A2 and type Ⅱ phospholipase A2 after cerebral ischemia.

OBJECTIVE：Analyzing the epidemic of drug risistance bacteria with extend spectrum β-lactamase(ESBLs)in children's wards to cut off the transmitting pathway and prevent the outbreak of nosocomial infections in time.METHODS：Samples，including sputum，umbilical secretion，pus，pharyngeal swab，were collected from in-hospital child patients in Departments of Newborn，Respiratory Tract Diseases，Cardiology，Nephrology，Hematology，Pediatric Surgery and ICU，then bacterial cultures and drug susceptibility test were carried out.54 strains of ESBLs E.coli and Klebsiella pneumoniae were isolated and their plasmid profiles were analysed by agarose electrophoresis.RESULTS：The percentages of ESBLs in the above-mentioned departments were 46.3，12.9，5.6，12.9，5.6，11.1，5.6 respectively.In analysis，three types of profiles were found and strains with four types of the same profile concentrated in the Newborn Department.The others were dispersed.CONCLUSION：Nosocomial infections possibly occured in the Newborn Department to some extent.

BACKGROUND: Free radicals are produced during ischemia, which can strengthen activity of lipid peroxidation; induce lesion of cell and cellular barrier, result in necrosis or apoptosis of neurons; and aggravate edema of ischemic cerebral tissue.OBJECTIVE: To observe the effects of polydatin (PD) on free radicals, lipid peroxidation, water contents and pathological morphology of brain tissue in rats with focal cerebral ischemia so as to explore its protective mechanisms.DESIGN: A randomized controlled trial.SETTING: Intensive Care Unit, Second Affiliated Hospital, Chongqing University of Medical Sciences; Pediatric Research Institute, Children's Hospital Chongqing University of Medical Sciences.MATERIALS: The experiment was carried out at the Pediatrics Medicine Institute of Chongqing Medical University from October 2001 to July 2002.Totally 48 healthy adult male Wistar rats were divided into 3 groups randomly,with 16 in each group. Group Ⅰ was sham-operated group: rats were anaesthetized, the right common carotid arteries were separated instead of being occluded. Group Ⅱ was ischemia group: to establish the right middle cerebral artery occlusion model of rats. Group Ⅲ was PD pretreatment group: polydatin (6 g/L, 12 mg/kg) were intravenously administrated 30 minutes before the onset of ischemia. Saline substituted for PD, besides, were intravenously administrated with the same way and dosage on Group Ⅰ, Group Ⅱ and Group Ⅲ.The rats were decapitated and the brains were immediately removed after cerebral ischemia 2 hours. In each group, 8 rats were chosen to be determined water contents of brain tissue, the other 8 rats were chosen to be determined levels of lipid peroxidation and free radicals in brain tissue.METHODS: According to the formula which was: wet weight-dry weight/wet weight×100%, water content of cerebral tissue was assayed. Superior liquid was taken to assay MDA with spectrophotometer thiobarbituric acid method (TBA) method, SOD activity assayed by xanthiue oxidase enzyme method, the activities of GSH-Px, CAT and NOS determined by colorimetry,the amount of protein determined by the method of Lowry. All the procedures were carried out strictly according to the instruction.malonaldehyde (MDA) and activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and nitric oxide synthase chemia, contents of SOD, GSH-Px and CAT in cerebral tissue of PD group were obviously higher than those of ichemia model group [(226.43±8.69),(193.37±11.14) NU/mg; (244.38±12.34), (211.71±16.50) μkat/g; (59.85±9.67),water in cerebral tissue of PD group were obviously lower than those of ichemia model group [(6.38±0.54), (8.63±0.78) μmol/g; (78.72±0.43)%,tivity in ischemic tissue but the results were similar to that in ischemia model group [(12.00±1.00), (12.84±1.17) μkat/g, P ＞ 0.05] in brain tissue.ed that PD alleviated the ischemia edema of cerebral ischemia.CONCLUSION: PD can alleviate the reaction of lipid overoxidation, improve the activities of antioxidant-enxymes, reduce ischemia brain edema,protect the function of cell member, bring down the damage to ischemia neurons. It shows that PD has significant cerebral protective role on focal ischemia brain damage.

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