睡眠呼吸暂停低通气综合征( SAHS) 是一种常见病症,临床上以阻塞性睡眠呼吸暂停低通气综合征( OSAHS) 最为常见[1] 。1993 年一项基于社区人群的研究中, Young 等[2] 发现年龄介于30 ～60 岁的人群中, 以睡眠呼吸暂停低通气指数( AHI) ≥5 次/h 定义的OSAHS在女性的患病率为9% ,在男性为24% , 2% 的女性和4% 的男性同时存在嗜睡症状。越来越多的证据表明睡眠呼吸暂停可导致许多并发症, 包括行为和躯体两方面。行为并发症包括日间嗜睡、注意力下降和神经心理异常, 而躯体并发症主要包括心脑血管疾病, 尤其是高血压[3, 4] 。OSAHS 是全身多个脏器功能损害的独立危险因素, 其中心血管并发症是主要死因[5] 。如何评价OSAHS 病情严重程度, 对患者的诊断、治疗及预后判断具有非常重要的意义。目前AHI 仍然是诊断OSAHS 的金标准,但其与靶器官损害的相关性存在诸多争议。
Objective To evaluate the effects of selective serotonin reuptake inhibitors ( SSRIs) on sleep apneas in Sprague-Dawley ( SD) rats. Methods Thirty adultmale SD rats were randomly divided into two groups ( 15 rats in each group) . The treatment group and the control group were injected intraperitoneally with paroxetine ( 10 mg· kg- 1 · d - 1 ) and sterile distilled water ( 2 mL· kg- 1 · d - 1) for 7 days respectively. Parameters about sleep apnea and sleep structure were measured before and after the treatment. Results In the treatment group, there was a significant reduction of apnea index ( AI) from ( 12. 4 ±3. 7)times /hour to ( 7. 4 ±2. 2) times/ hour ( P = 0. 000) . Both post sigh apnea index ( PSAI) and spontaneous apnea index ( SPAI) were decreased significantly ( P = 0. 000 and 0. 021 respectively) in non-rapid eye movement ( NREM) sleep, but not in REM sleep. REM sleep was reduced from 8. 6% to 8. 0% ( P =0. 013) and its latency was increased from ( 54. 1 ±48. 4) min to ( 110. 9 ±43. 4) min ( P = 0. 001) in the treatment group, as well as the sleep-onset latency [ from ( 20. 7 ±9. 1) min to ( 30. 0 ±15. 7) min, P =0. 038] . Conclusion Paroxetine can reduce sleep apneas in SD rats during NREMsleep. Its effects on sleep structure include reducing REM time, increasing REM latency and sleep-onset latency.
Objective To evaluate the role of guide sheath (GS) utilization in radial endobronchial ultrasound guided transbronchial lung biopsy (EBUS-TBLB) for diagnosis of peripheral pulmonary lesions (PPLs). Methods The clinical data of patients who underwent EBUS-TBLB in Peking University First Hospital from July 2012 to June 2015 were retrospectively reviewed. The patients were divided into three groups,ie. a GS group, a non-GS group, and a double biopsy group. Results A total of 118 patients with 126 PPLs were collected. The overall diagnostic yield of EBUS-guided bronchoscopy was 60.3%. The diagnostic yield of GS group, non-GS group and double biopsy group was 65.4%(36/55), 61.5%(8/13), 59.6%(31/52), respectively. The diagnostic yield of the non-GS group was significantly lower than other two groups when PPLs≤20 mm (χ2=6.8,P=0.033), whereas no significant difference was observed when PPLs>20 mm (χ2=2.301,P=0.301). Conclusion GS significantly improves diagnostic yield in EBUS-TBLB when PPLs≤20 mm.
Objective To summarize the clinical features and prognosis of extensively drug-resistant Acinetobacter baumannii (XDRAB) bacteremia. Methods This retrospective study included patients with Acinetobacter baumannii bacteremia diagnosed and treated in RICU of this hospital during January 1, 2012 and December 31, 2015. Demographic features, clinical data, clinical outcome within 3 days and 14 days after sample collection for blood culture were collected. Results Eight patients were included, with the mean age of (62.4±18.0) years, and including 3 males and 5 females. All patients had underlying diseases, 6 patients were immune suppressed, 7 patients had been exposed to β-lactam/enzyme inhibition or carbapenems for at least 7 days within 2 weeks before blood sample collection, and 6 patients received mechanical ventilation. Lung is the main pathogen source (6 cases). Within 48 hours after blood collection, the mean acute physiology and chronic health evaluation Ⅱ (APACHEⅡ) score was 28.3±7.5, the level of serum C-reactive protein (18.2 to 231.0 mg/L) and procalcitonin (0.1 to 25.0 ng/ml) had individual differences. The 3-day mortality rate was 4/8, the death group had APACHEⅡ >25. The 14-day mortality rate was 6/8, all the patients with procalcitionin>0.5 ng/ml died. Conclusions The 14-Day mortality is associated with the severity and increased procalcitionin in XDRAB patients. Preemptive therapy is recommend for patients with multiple risk factors, receiving mechanical ventilation, and with elevated procalcitonin and high APACHEⅡ score ( >25).
ObjectiveBy detecting the expression of the long non-coding RNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) in myocardial tissue under different hypoxia patterns, to explore the possible mechanism of obstructive sleep apnea (OSA)-induced cardiovascular diseases.MethodsSD rats were randomly and equally divided into 4 groups namely a normal (N) group, a continuous hypoxia (CH) group, an intermittent hypoxia (IH) group and an intermittent hypoxia with hypercapnia (IHH) group, and were treated for 1, 2, and 3 weeks. The expression of MALAT1 and associated immune factors of the myocardial tissue were examined by qRT-PCR.ResultsAn elevation without significance was observed in those three hypoxia groups in contrast with N group after 1 week’s treatment. However, in 2 and 3 weeks’ groups, the mRNA expression of MALAT1 was significantly higher in IHH group than the other three groups (all P<0.01), while there was no significant difference among IH, CH or N groups despite an increasing tendency in IH and CH groups against N group were observed. Additionally, the expressions of hypoxia inducible factor-1α (P<0.05), Toll-like receptor 4 (P<0.01) and interleukin-6 (P<0.05) mRNA were also increased significantly in IHH group compared with IH, CH and IHH groups in 3 weeks’ treatment respectively, which were coordinated with the change of MALAT1 mRNA.ConclusionsThe expression of MALAT1 in myocardial tissue is elevated by intermittent hypoxia with hypercapnia, and the tendency is similar with hypoxia-induced inflammation factors. These findings indicate that MALAT1 is probably a regulatory factor of OSA induced myocardial immune injury.
ObjectiveTo investigate the changes of lung function after exposure to fine particulate matter (PM2.5) for 60 days and the expression of miR-146 in mice.MethodsThirty SPF BALB/c mice were treated with noninvasive tracheal instillation of fine particulate matter suspension at different doses (2.5 mg/kg, 5.0 mg/kg, 10.0 mg/kg) for 2 months (two times one week), the blank group and normal saline group were set as control groups. The mice were examined and killed on the next day after the last instillation. Histopathological changes of the lungs, pro-infammatory factors levels in the lung tissues, pulmonary functions and the relative expression of miR-146a and miR-146b in the lung tissues were detected.ResultsPeak inspiratory flow (PIF) and peak expiratory flow (PEF) were decreased significantly after PM2.5 exposure, however, lung resistance increased and maximal voluntary ventilation reduced from the general tendency without significant difference. Hematoxylin-eosin stain showed lymphocyte infiltration and macrophage infiltration by phagocytic particles, alveolar spacer widening, inflammatory response increased with the increase of PM2.5 exposure dosage. Pro-infammatory factors as interleukin-6 in the bronchoalveolar lavage fluid, interferon-γ and tumor necrosis factor-α in the lung homogenate were increased significantly by enzyme linked immunosorbent assay. The relative expressions of miR-146a and miR-146b were up-regulated remarkablely in treatment groups compared to the control group by real-time fluorescence quantitative polymerase chain reaction, which had negative relationships with PIF and PEF.ConclusionsThe lung function of mice decreases significantly after exposure to fine particulate matter, and the expression of miR-146 is up-regulated.
Objective To evaluate the value of Epworth sleepiness scale ( ESS) in evaluating the severity of obstructive sleep apnea hypopnea syndrome ( OSAHS) . Methods A total of 340 cases with suspected OSAHS were enrolled. The ESS scores and polysomnography ( PSG) monitoring data were analyzed. According to the PSG monitoring results the patients were classified into non-OSAHS, mild, moderate and severe OSAHS groups. The average ESS scores and the ratio of patients whose ESS score was ≥9 were compared among the four groups. The diagnostic value of ESS score was evaluated by ROC curve. The correlation of ESS scores with age, apnea hypopnea index ( AHI) , the lowest SpO2( LSpO2 ) and microarousal index was analyzed. Results The ESS scores had an ascending tendency as the severity of OSAHS was increased but only in the severe OSAHS cases the difference was significant statistically compared with the other three groups ( P lt; 0. 05) . The mean ESS scores in the four groups were 9. 96 ± 4. 81,10. 21 ±5. 48, 11. 48 ±5. 28 and 13. 52 ±5. 84, respectively. There was no statistical significance while comparing the ratio of patients whose ESS scores were ≥9 among the four groups. The analysis of ROC curve showed the area under the ROC curve ( AUC) was lesser( 0. 601) and a best cutoff could not be obtained. When ESS score ≥9 was made as the cutoff in screening OSAHS patients the sensitivity was 70. 0% and the misdiagnosis rate was 63. 21% . The ESS scores had positive correlation with the apnea hypopnea index ( AHI)( r =0. 240, P lt; 0. 01) and negative correlation with LSpO2 ( r = - 0. 198, P lt;0. 01) . The ESSscores had no correlation with age or the microarousal index ( P gt; 0. 05) . Conclusions The ESS score has some significance in screening severe OSAHS patients but can not exactly reflect the severity of OSAHS patients among Chinese population, suggesting ESS score has limited value in the evaluation of OSAHS severity. The ESS score ≥9 as a cutoff is not a reliable parameter to estimate the severity of OSAHS. A more effective scoring system need to be established for better screening of OSAHS patients.
Objective To detect the single nucleotide polymorphisms ( SNPs) in the upstream promoter region of chemokine like factor ( CKLF) gene and analyze their possible associations with asthma and asthma-related phenotypes. Methods Direct Sequence of the 1553bp upstream promoter region of CKLF gene was performed in 245 Chinese Han human genomic DNAs ( 119 asthmatics and 126 controls) .The frequencies of alleles, genotypes, and haplotypes were determined and the association of these SNPs with asthma were further analyzed. Results Four novel SNPs, SNP88 ( T gt; C) , SNP196 ( T gt; C) , SNP568 ( C gt;G) , and SNP1047 ( C gt; G) were found in the promoter region of CKLF. The frequency of rare allele was 0. 168 ( SNP88C) , 0. 168 ( SNP196C) , 0. 352 ( SNP568G) and 0. 167 ( SNP1047G) , respectively.Haplotypes, their frequencies and the linkage disequilibrium coefficients between SNPs were constructed.Complete linkage disequilibrium( LDs) were observed between SNP88 and SNP196, SNP88 and SNP1047,as well as SNP196 and SNP1047, respectively ( D′=1. 000, r2 = 1. 000) . SNP568 was in partial LD with the other three SNPs ( r2 = 0. 366) . No association between asthma and the SNPs was observed. Conclusions Four SNPs in the regulatory region of CKLF in Chinese Han population were firstly identified. Although no significant correlation with asthma was revealed, the SNP and haplotype information is useful for other disease association studies in the future.