Objective To observe the changing characteristics of plasma lysophosphatidic acid (LPA) or acidia phospholipid (AP) levels in patients with obstructive sleep apnea syndrome-associated(OSAS)acute cerebral infarction and to explore the pathophysiological mechanisms of OSAS-related stroke so as to provide basis for clinical antithrombotic therapy. Methods Thirty-six patients of OSAS, 32 patients of OSAS-related acute stoke and 36 patients of acute stoke without OSAS diagnosed by clinical and accessory examinations were enrolled in the current study. Thirty-eight age-matched healthy subjects were recruited as controls. The changes of the plasma LPA and AP levels were measured. Results Within 24 hours after symptom onset, the plasma LPA and AP levels in the OSAS-related acute cerebral infarction group (LPA(3. 78 ±0. 56) μmol/L; AP(7. 63 ± 1. 38) μmol/L) were significantly higher than those in the OSAS group(LPA(3. 17 ±0. 65) μmol/L; AP(6. 60 ± 1. 20) μmol/L) ,the not OSAS-related acute cerebral infarction group (LPA (3. 40 ± 0. 59)μmol/L; AP (6. 41 ± 1. 37)μmol/L) and the control group (LPA(2.76±0.45)μmol/L;AP(4.52±0. 83) μmol/L (P < 0. 01)) . The levels of LPA and AP in the OSAS group and the not OSAS-related acute cerebral infarction group were significantly higher than those in the control group(P<0. 01). Seven days after symptom onset, the plasma LPA and AP levels in the OSAS-associated acute cerebral infarction group (LPA(3.08 ± 0. 58) μmol/L; AP(6. 15 ±1. 14)μmol/L) were still higher(P < 0. 01) . The plasma LPA levels were not significantly different among the OSAS-related acute cerebral infarction group, the not OSAS-related acute cerebral infarction group and the control group 21 days after symptom onset, whereas the plasma AP levels in the OSAS-related acute cerebral infarction group (5. 04 ± 0. 83) μmol/L were still significantly higher than those in the not OSAS-related acute cerebral infarction group (4. 57 ± 0. 94) μmol/L and the control group (P < 0.05). Conclusions The significantly elevated plasma LPA and AP levels in patients with OSAS suggested that platelets in vivo are in an activated state and in cerebral ischemia and hypoxia state, especially for the OSAS-related acute cerebral infarction patients. The activated state of platelet may persist for a long time, thus the time window for antithrombotic therapy may be longer.

Objective To explore the influencing factors of the onset of autism spectrum disorder in male children.Methods Totally 151 male children with autism spectrum disorder were selected as case group and 119 healthy male children matched with the age of the case group in the same administrative region were taken as the control group.All children were assessed with the questionnaire for children's autism etiology and risk factors.Results (1) The differences in children having anorexia and partial eclipse (x2 =50.763,P＜0.01),father's age during pregnancy (x2 =11.441,P=0.043),place of pregnancy (x2 =50.763,P＜0.01),hypertension of pregnancy (x2 =5.693,P=0.026),intrauterine hypoxia (x2 =9.332,P=0.002),umbilical cord around the neck(x2 =18.483,P＜0.01),parents smoking and drinking history during pregnancy (x2 =13.660,P=0.008),parental smoking (x2 =12.901,P=0.005) and alcohol consumption (x2 =8.386,P=0.039) during pregnancy,birth height of child (x2 =8.870,P=0.031),amniotic fluid pollution (x2 =4.561,P=0.043),participation time of artificial feeding,major caregivers,delayed development indicators in infants and young children and whether or not the harmonious parent-child relationship were statistically significant(P＜0.05).(2) Children with anorexia and partial diet (OR =12.284,95％ CI =2.768-54.507),living in rural areas during pregnancy (OR =17.251,95％ CI =1.899-1 56.745),parents' history of smoking and drinking (OR =6.191,95％ CI =1.678-22.838),and intrauterine hypoxia during pregnancy (OR=38.859,95％CI=2.944-512.930) may be risk factors for male autism spectrum disorder.Conclusion To correct children's anorexia bias,improve the living environment in pregnancy,reduce pregnancy complications and avoid exposure to tobacco and alcohol pollution during maternal pregnancy can be an effective entry point for the prevention and control of autism spectrum disorders in male children.