Objective To study the role of kallikrein 8 (KLK 8) in the pathogenesis of cerebral white matter injury induced by intrauterine infection.Method The pregnant Sprague Dawley rats were randomly assigned into two groups:the observation group and the control group.The rats in the observation group received intraperitoneal injection of lipopolysaccharide (500 μg/kg) by at day 18 and 19 of pregnancy,while the control group received the same dose of saline.The morphology of white matter of the newborn rats were observed at 1 d,3 d,7 d and 14 d after birth.The expression of KLK 8 in the hippocampus was examined using Western blot and reverse transcription-polymerase chain reaction (RTPCR);the concentration of KLK 8 in the serum was measured using enzyme linked immunosorbent assay (ELISA) method at the same time.Result In the observation group,the brain tissue was loose and edematous,the cerebral white matter was weakly stained,and the number of cells reduced.The expressions of KLK 8 in hippocampus in the observation group were higher than the control group [1 d:(0.24 ±0.01) vs.(0.23±0.01),3 d:(0.72±0.02) vs.(0.55±0.04),7 d:(1.08±0.04) vs.(0.84±0.04)],the differences were statistically significant (P ＜ 0.05).The expressions of KLK 8 mRNA in hippocampus of the observation group [1 d:(0.013 ±0.003),3 d:(0.032 ±0.002),7 d:(0.060 ±0.005)] were higher than the control group [1 d:(0.008 ±0.002),3 d:(0.016 ±0.002),7 d:(0.026 ±0.002)],the differences were also statistically significant (P ＜ 0.05).The serum KLK 8 concentration at 1 d,3 d,and 7 d were (5.13 ±0.24) μg/L,(6.46 ±0.24) μg/L,and (7.77 ±0.30) Iμg/L in the observation group,higher than the control group (4.73 ±0.25) μg/L,(5.65 ±0.29) μg/L,and (6.66 ±0.46) μg/L),the differences were also statistically significant (P ＜ 0.05).Conclusion KLK 8 may be involved in the pathogenesis of white matter injury induced by intrauterine infection.

Objective To investigate the effect of fluvastatin on the expressions of caspase-12,CCAAT/enhancer-binding protein homologous protein(CHOP), and c-Jun N-terminal kinases (JNK) in ischemia-reperfusion brain injury in rats.Methods Forty two rats were randomly divided into sham operation group (6 rats), ischemia-reperfusion (I/R) group (18 rats), and fluvastatin (Flu) group (18 rats).The rats of I/R and Flu groups were molded by modified Longa intraluminal thread, then put to death at 2 h occlusion and 24 h reperfusion point.Expressions of caspase-12, CHOP, and JNK were detected with immunohistochemistry and Western blot.Results Immunohistochemistry and Western blot showed that the expressions of caspase-12, CHOP, and JNK were increased at 24 h reperfusion.Compared to I/R group, the expressions of caspase-12 and CHOP in Flu group were decreased significantly (all P ＜0.01);and the expression of JNK had no difference between I/R and Flu groups(P ＞ 0.05).Conclusions The increased expression of caspase-12, CHOP, and JNK showed that endoplasmic reticulum stress was involved in the pathological process of ischemia-reperfusion brain injury.Fluvastatin could inhibit the expression of caspase12 and CHOP, and could delete endoplasmic reticulum stress (ERS) in ischemia-reperfusion brain injury.

Objective To assess cerebrovascular reserve capacity in patients with obstructive sleep apnea-hypopnea syndrome(OSAHS).Methods One hundred and fourteen patients with OSAHS and 43 normal persons were enrolled in this study.The patients were divided into mild,moderate,severe according to apnea hypopnea index (AHI) and LSaO2 (lowest arterial oxygen saturation).All the patients and normal persons were routinely examined using transcranial Doppler (TCD) and end-tidal carbon dioxide partial pressure(ETCO2) to evaluate cerebrovascular reserve.Hypercapnia was induced by inhaling the CO2 which produced by the patients themselves,and hypocapnia was elicited by voluntary hyperventilation.Results CVR in the severe and moderate OSAHS were significantly lower than that in the control group [ (1.80 ± 1.34) ％/mm Hg and (1.43 ±1.05)％/mm Hg vs (2.93 ±0.93)％/mm Hg,P ＜0.05] when patients in the condition of hypocapnia.And there was no significant difference on CRV between the mild OSAHS group and control group [ (2.53 ±1.83 ) ％/mm Hg vs ( 2.93 ± 0.93 ) ％/mm Hg,P ＞ 0.05 ].When patients in the condition of Hypercapnia,CRV in the severe and moderate OSAHS were also significantly lower than that in the control group [ ( 1.83 ±1.32) ％/mm Hg and (1.08 ± 1.00)％/mm Hg vs (3.32 ± 1.53)％/mm Hg,P ＜ 0.05),AHI was negatively correlated with the cerebrovascular reserve at the condition of hypercapnia and hypocapnia (r=-0.665,-0.721; P ＜ 0.05 ).Conclusion Inhaling CO2 is a effective method for assessing CVR.Cerebrovascular reserve capacity is associated with AHI.Reduced CVR causes hemodynamics change being severe hypoxia in the moderate and severe OSAHS.

Objective To observe the changes of PECAM-1,Bcl-2 and Bax expressed by ischemic cerebrum of adult rats after focal cerebral ischemia. Methods Middle cerebral artery occlusion (MCAO) models were made by operation with Longa suture method in Wistar rats. The expression levels of PECAM-1,Bcl-2 and Bax at the 6th,12th,18th,24th,48th,72nd hour after MCAO were detected by immunohistochemistry staining. Results The expression levels of PECAM-1,Bcl-2 and Bax in cerebrum were significantly increased after MCAO. The expression levels of Bcl-2 we、re up to the peak at the 12th hour after MCAO, while the levels of Bax and PECAM-1 were up to the peak at the 24th and 48th hour after MCAO. At the 72nd hour after MCAO, the expression levels of PECAM.1.Bcl-2 and Bax were still higher than that in the control group(all P＜0.001).Conclusions PECAM-1,Bcl-2 and Bax participate in the different pathological stages of focal cerebral ischemia.

Objective To investigate the clinical features and the gene mutation of patients with spinocerebellar ataxia type3 and type7.Methods The trinucleotide repeat mutations were detected by polymerase chain reaction (PCR),agarose gel electrophoresis method,and DNA sequencing in 13 patients,4 related members and 4 common members from 3 spinocerebellar ataxia families.Results Among the 13 patients,four patients had SCA3/MJD(CAG) n expansion mutation(n = 65 ～ 74),nine patients had SCA7 allele expansion for 40 ～ 52 times.Patients with type 3 or 7 showed significant difference in nervous system injury.Conclusion The difference of clinical feature might be used in diagnosis of SCA3/MJD and SCA7,but genotype determination would be the only method of definite diagnosis.

Objective:To compare the neonatal end tidal carbon dioxide pressure(PetCO 2) and its correlation with arterial carbon dioxide pressure(PaCO 2) monitored by non-invasive mask, accessory flow nasal catheter and invasive mechanical ventilation. Methods:From October 2017 to January 2020, 53 cases of newborn who were needed respiratory support treatment in our hospital were selected.PetCO 2was detected at admission, respiratory support and after weaning, including nasal catheter, non wound mask and invasive ventilation, and at the same time matching analysis of the corresponding with PaCO 2artery blood gas analysis. Results:(1) PetCO 2monitored by mask was lower than PaCO 2[(40.41 ± 10.21) mmHg vs.(42.85 ± 10.32) mmHg(1 mmHg=0.133 kPa), t=11.88, P<0.01], and there was a significant positive correlation between PetCO 2and PaCO 2( r=0.97, P<0.01); the mean bias of PetCO 2monitored by mask was(1.20 ± 2.31) mmHg, only 4.5%(5/110) was outside the 95% confidence interval.(2) PetCO 2monitored by nasal catheter was also lower than the mean PaCO 2[(40.93 ± 10.55) mmHg vs.(42.01 ± 10.50) mmHg, t=4.12, P<0.01], showing a significant positive correlation( r=0.96, P<0.01); the mean bias of PetCO 2monitored by nasal catheter was(2.44 ± 2.56) mmHg, and only 4.6%(7/150) was beyond the 95% confidence interval.(3) PetCO 2of neonates with endotracheal intubation and mechanical ventilation was also lower than PaCO 2[(43.33±10.26) mmHg vs. (49.37±11.34) mmHg, t=13.83, P<0.01], and there was also a significant positive correlation between the two groups, which was lower than that of neonates with non-invasive ventilation( r=0.94, P<0.01). The mean PetCO 2bias for neonates with invasive positive pressure ventilation was(0.90±0.82) mmHg, and only 3.9%(2/51) were outside the 95% confidence interval.(4) According to gestational age, the PetCO 2of early and late preterm infants was(37.25±11.32) mmHg and(39.58±10.37) mmHg, respectively, which were lower than that of full-term infants[(42.69±10.66) mmHg], and there was a positive correlation between PetCO 2and PaCO 2in all three groups.The correlation between PetCO 2and PaCO 2in early preterm infants was the lowest among the three groups( r=0.89, P<0.01). Conclusion:The monitoring of PetCO 2through nasal catheter, mask and invasive ventilation has a good correlation and consistency with the level of PaCO 2in neonates, which can accurately reflect the level of PaCO 2in neonates.The correlation between PetCO 2and PaCO 2in neonates with non-invasive ventilation is better than that in neonates with invasive ventilation.The correlation between PetCO 2and PaCO 2in late preterm infants and term infants is better than that in early preterm infants.

Subarachnoid hemorrhage (SAH) is the third common type of stroke in the world,and its mortality and disability rates have declined over the past few decades due to the advances in neuroimaging technology and endovascular interventional therapy and promotion of healthy physical examination,but long-term neurological deficits and cognitive impairment of the patients have not significantly improved,which may be related to the white matter injury (WMI) after SAH.Little attention has been paid to WMI after SAH in the past,which may be an important reason for the poor prognosis of the patients with SAH.The neuroin-flammation response is an important pathophysiological process after SAH,and the neuroinflammation after SAH can aggravate WMI.This article reviews the relationship between neuroinflammation and WMI after SAH in order to deepen the understanding of its effects on cognitive function after SAH.

Background Environmental noise pollution is serious, and there are few studies on the effects of long-term noise exposure during sleep on cognitive function and possible biological clock mechanism. Objective To explore the cognitive impairment induced by noise exposure during sleep in mice and possible biological clock mechanism, and to provide a theoretical basis for the protection against noise exposure. Methods Twenty male C57BL/6J mice were randomly divided into a control group and a noise-exposed group, 10 mice in each group. The noise-exposed group was exposed to sleep-period noise using a noise generator for 12 h (08:00–20:00) per day for a total of 30 d. The calibrated noise intensity was set at 90 dB. No intervention was imposed on the control group. At the end of the noise exposure, cognitive function of mice was examined using the new object recognition experiment and the open field test, and the hippocampal tissue damage of mice were evaluated by Nissl staining, ionized calcium binding adaptor molecule 1 (Iba1) immunofluorescence staining, and real-time fluorescence quantitative PCR for inflammatory factors and biological clock genes. Oxidative stress indicators in the hippocampus of mice were also detected by assay kit. Results After noise exposure during sleep period, the results of new object recognition experiment showed that the discrimination index of mice in the noise-exposed group was 0.06±0.04, which was significantly lower than that of the control group (0.65±0.13) (P<0.05). The results of open field test showed that the central activity distance of the noise-exposed group was (242.20±176.10) mm, which was significantly lower than that of the control group, (1548.00±790.30) mm (P < 0.05), and the central activity time of the noise-exposed group was (0.87±0.64) s, which was significantly lower than that of the control group, (6.00±2.86) s (P < 0.05). The Nissl staining results showed that compared with the control group, neurons in the hippocampus of the noise-exposed mice were shrunken, deeply stained, disorganized, and loosely connected. The immunofluorescence results showed that microglia in the hippocampus of the noise-exposed mice were activated and the expression of Iba1 was significantly increased compared with those of the control group (P<0.05). The real-time PCR results of showed that the mRNA levels of the biological clock genes Clock, Per2, and Rev-erbα were significantly increased compared with those of the control group (P<0.05), and the mRNA level of Per1 was significantly decreased compared with that of the control group (P<0.05); and the mRNA levels of IL-18, IL-6, iNOS, and NLRP3 in the hippocampal tissues of mice were significantly increased compared with those of the control group (P<0.05). The results of oxidative stress evaluation showed that compared with the control group, reduced glutathione content was significantly reduced in the noise-exposed group (P<0.001). Conclusion Noise exposure during sleep period can lead to the destabilization of biological clock genes in hippocampal tissues and trigger hippocampal neuroinflammation, which can lead to the activation of microglia and cause cognitive impairment in mice.