Objective To study the clinical effectiveness analysis of early use of low molecular weight hepa-rin and aspirin in the treatment of acute cerebral infarction.Methods 120 cases with acute cerebral infarction were randomly divided into the observation group and the control group according to a random number table,with 60 cases in each group.The patients of the control group were treated with aspirin,while the patients of the observation group were given low molecular weight heparin on the basis of the control group.Both groups were treated for one month,and the therapeutic effects and adverse reactions of the two groups were compared.Results The total efficiency of the ob-servation group was 96.7%(58 /60),which was significantly higher than the 76.7%(46 /60)of the control group, the difference was statistically significant(χ2 =12.051,P =0.019);The neurological deficits after treatment of the observation group was (16.21 ±2.05 )points,which was significantly lower than (26.04 ±1.03)points of the control group,the difference was statistically significant (t =10.372,P =0.027 ).Conclusion Acute cerebral infarction early use of low molecular weight heparin and aspirin had better clinical efficacy,and it can significantly promote the recovery of neurological function in patients.

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 To investigate the curative effect of low-temperature plasma-assisted uvulopalatopharyngoplasty(UP-PP)in the patients with positional and non-positional obstructive sleep apnea-hypopnea syndrome(OSAHS).Methods Twenty-six patients with OSAHS diagnosed by polysomnography monitoring receiving the low-temperature plasma-assisted UPPP in our hospital from January 2014 to December 2015 were selected and divided into the positional OSAHS group(PPs) and non-positional OSAHS group(NPPs) according to the apnea-hypopnea index (AHI) under different sleep positional status.The AHI change before and after operation and operation effective rate were compared between the two groups.Results Theoverall AHI,supine position AHI and lateral position AHI in the PPs group all were lower than those in the NPPs group(P＜0.05),moreover the blood oxygen related indexes were higher than those in the NPPs group(P＜0.05).The overall surgical effective rate in the OSAHS patients was 73.08％ (19/26),in which the surgical effective rate was 100％ (7/7) in the PPs group and 63.16％ (12/19) in the NPPs group,the difference between the two groups had no statistical significance(P=0.13).The postoperative total AHI,supine position AHI and lateral position AHI in the two groups were decreased compared with before operation(P＜0.05);the decrease range of lateral position AHI in the NPPs group was significantly higher than that in the supine position AHI[0.96(0.86,1.00)vs.0.53(0.34,0.77),P＜0.01].78.95 ％ (15/19) postoperation patients in the NPPs group converted to PPs.Conclusion Low-temperature plasma-assisted UPPP has some effects on OSAHS patients,in which the benefit of NPPs are more apparent.