2009年 · 第122卷第12期

Bronchial asthma is characterized by chronic recruitment of eosinophils in the airways. It has been reported that bronchial eosinophil recruitment and activation may even occur in mild-moderate stable asthma and that bronchial epithelium damage and airway responsiveness may be partially associated with the eosinophilic inflammatory reaction.1 There is increasing evidence that the eosinophil-rich bronchial inflammation characteristic of asthma is orchestrated, at least partly, by cytokine products of activated T lymphocytes. Of particular interest is T-helper type 2 (Th2) cell-derived interleukin-5 (IL-5). 2 This cytokine mediates the terminal differentiation of committed eosinophil precursors, activates mature eosinophils, and prolongs their survivals in culture and, presumably, at sites of allergic inflammation.3-6 IL-5 also selectively enhances eosinophil degranulation, antibody-dependent cytotoxicity, 3 and adhesion to vascular endothelium.4

Abstract：Background Tobacco use is the major risk factor for numerous health problems. However, only 5% of smokers can successfully quit without therapy owing to the highly addictive properties of nicotine. The serotoninergic system may be involved in smoking behavior because nicotine increases brain serotonin secretion, nicotine withdrawal decreases serotonin levels, and a selective serotonin reuptake inhibitor antagonizes the response to nicotine withdrawal. Serotonin transporter (5-HTT) is the most important protein, as it adjusts the serotonin concentration in the synaptic cleft. There is a polymorphism in the upstream regulatory region of the 5-HTT gene, named 5-hydroxytryptamine transporter gene-Iinked poyymorphic region (5-HTTLPR). Compared with the L allele, the S allele of the polymorphism is associated with decreased transcription efficiency of the 5-HTT gene. In this study, we investigated the relationship between this gene polymorphism and smoking behavior in Chinese males.Methods Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was performed to find 5-HTTLPR gene polymorphisms in 144 smokers and 135 age-matched healthy non-smokers. A questionnaire was completed in all recruited subjects.Results The proportion of L/L (15.3% vs 5.2%) and S/L (50.0% vs 33.3%) genotypes was significantly higher in the smokers than that in the non-smokers (χ2=21.9; P <0.01). The odds ratio (OR) adjusted by age, education, effects of family members and friends who smoke, and alcohol intake was 2.9 (95%CI 1.78-4.80). In smokers, the number of cigarettes/day (L/L vs S/L vs S/S: 28+12 vs 20±8 vs 16±6, χ2=18.5, P <0.01), smoking index (L/L vs S/L vs S/S.. 561±446vs 393±341 vs 237+901, χ2=12.5, P <0.01) and score on the Fagerstrom test for nicotine dependence (FTND) (L/L vs S/L vs S/S. 7.8±1.6 vs 6.2±9.5 vs 3.5±9.1, χ2=48.3, P <0.01) were significantly higher in smokers with an L/L or S/L genotype than that in the smokers with the S/S genotype. There were no significant differences in the proportion of starting smoking before 20 years old (P=-0.219) and those who succeeded in quitting smoking for more than 1 month (P=0.456) between individuals with different 5-HTTLPR genotypes in smokers.Conclusions 5-HTTLPR polymorphism may be associated with susceptibility to cigarette smoking in Chinese males.The proportion of theL/L and S/L genotype in smokers was higher than that in non-smokers. In smokers, the level of nicotine dependence and resultant cigarettes consumption may be much higher in individuals with an L/L or S/L genotype than those with the S/S genotype。

Abstract：Background Increased production of reactive oxygen species (ROS) is thought to play a major role in the pathogenesis of obstructive sleep apnea-hypopnea syndrome (OSAHS). The reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex is an important source of ROS. The p22phox subunit is polymorphic with a C242T variant that changes histidine-72 for a tyrosine in the potential heme binding site. This study aimed to investigate the relationship between NADPH oxidase subunit p22phox gene polymorphism and OSAHS. Methods The genotypes of p22phox polymorphism were determined by polymerase chain reaction-restriction fragment length polymorphisms (PCR-RFLP) assay in 176 unrelated subjects of the Han population in southern region of China (including 107 OSAHS subjects and 69 non-OSAHS subjects), while the plasma concentration of superoxide dismutase (SOD) was detected in the two groups, and p22phox mRNA expression in peripheral blood mononuclear cell (PBMC) was determined with reverse transcription polymerase chain reaction (RT-PCR).Results The phagocyte NADPH oxidase subunit p22phox mRNA expression was significantly increased in the OSAHS group than that in the non-OSAHS group (P<0.01). Compared with the non-OSAHS control group ((85.31±9.23) U/ml), the levels of SOD were lower in patients with OSAHS ((59.65±11.61) U/ml (P<0.01). There were significant differences in genotypes distribution in p22phox polymorphism between the two groups (P=0.02). Compared with the non-OSAHS control group, the OSAHS group had a significantly higher T allele frequency in p22phox polymorphism (P=0.03). There were independent effects of p22phox polymorphism on body mass index (BMI), neck circumference (NC), waist-to-hip ratio (WHR) in the OSAHS group, and the carriers of the T allele of p22phox polymorphism had greater NC, WHR, systolic blood pressure (SBP), diastolic blood pressure (DBP) and apnea-hypopnea index (AHI) (P <0.05), but the carriers of the T allele had lower SOD (P <0.01) and lowest SaO2 (P=0.04). There was no significant difference in p22phox mRNA expression between the OSAHS groups with or without T allele (P=0.45). Conclusions The NADPH oxidase subunit p22phox gene polymorphism may be associated with susceptibility to OSAHS, and it may be an important candidate gene for OSAHS。

Abstract：Background Previous studies show that sleep-related breathing disorder (SRBD) is common in patients with heart failure (HF) and is associated with increased mortality. This study aimed to determine whether there was significant difference of subjective daytime sleepiness between HF patients with and without SRBD.Methods We enrolled, prospectively, 195 consecutive HF patients with left ventricular ejection fractions (LVEF)≮45%and all subjects underwent polysomnography to measure the sleep structure between 2005 and 2008. Patients were then assigned to those with SRBD including obstructive and central sleep apnea (apnea-hypopnea index (AHI)≯5/hour of sleep) and those without SRBD (AHI<5/hour) according to the sleep study. The subjective sleepiness was assessed withEpworth sleepiness scale (ESS).Results Among 195 HF patients, the prevalence of obstructive sleep apnea (OSA) was 53% and of central sleep apnea (CSA) was 27%. There was no significant difference of ESS scores between patients without SRBD (NSA) and with SRBD (NSA vs OSA: 6.7±0.6 VS 7.6±0.4, P=0.105 and NSA vs CSA: 6.7±0.6 vs 7.4±0.5, ,P=0.235, respectively),indicating that SRBD patients had no more subjective daytime sleepiness. Compared with NSA, patients with SRBD had increased arousal index (Arl) (NSA vs OSA: 14.1±1.4 vs 26.3±1.5, P <0.001 and NSA vs CSA: 14.1±1.4 vs 31.3±3.5, P <0.001, respectively), more awake number after sleep onset (NSA vs OSA: 19.2±1.5 vs 26.2±1.4, P=0.01 and NSA vs CSA: 19.2±1.5 vs 36.9±4.4, P <0.001, respectively), and reduced proportion of slow-wave sleep (SWS) (NSA vs OSA: 13.8±1.7 vs 9.3±0.7, ,P=0.024 and NSA vs CSA: 13.8±1.7 vs 8.9±0.9, P=0.024, respectively). Conclusions OSA and CSA remain common in patients with HF on optimal contemporary therapy. Patients with both HF and SRBD have no significant subjective daytime sleepiness compared with patients without SRBD, despite of significantly increased awake number, arousal and decreased proportion of deep sleep stages. It is not a credible way and means to exclude SRBD in patients with HF according to the absence of subjective daytime sleepiness。

Abstract：Background Pulmonary arterial hypertension (PAH) is characterized by suppressing apoptosis and enhancing cell proliferation in the vascular wall. Inducing pulmonary artery smooth muscle cells (PASMC) apoptosis had been regarded as a therapeutic approach for PAH. Oridonin can cause apoptosis in many cell lines, while little has been done to evaluate its effect on PASMC.Methods Thirty male Sprague-Dawley rats were randomly assigned to three groups: normal control (NC); hypoxia-hypercapnia (HH); Hypoxia-hypercapnia + oridonin (HHO). Flats were exposed to hypoxia-hypercapnia for four weeks. Cultured human PASMC (HPASMC) were assigned to three groups: normoxia (NO); hypoxia (HY); hypoxia+ oridonin (HO). The mean pulmonary artery pressure, mass ratio of right ventricle over left ventricle plus septum (RV/(LV+S)), the ratio of thickness of the pulmonary arteriole wall to vascular external diameter (WT%) and the ratio of the vessel wall area to the total area (WA%) were measured. Morphologic changes of pulmonary arteries were observed under light and electron microscopes. The apoptotic characteristics in vitro and in vivo were detected. Results The mPAP, RV/(LV+S), WT%, and WA% in the HH group were significantly greater than those in the NC (P <0.01) and HHO groups (P <0.01); the activities of caspase-3 and caspase-9, and the expressions of Bex, cyt-C and apoptotic index (AI) in the group HH were less than those in the NC and HHO groups; and the expression of Bcl-2 in group HH was greater than that in the NC and HHO groups. HPASMC mitochondrial membrane potentials in group HO was lower than in group HY (P <0.01), and cyt-C in the cytoplasm, AI, and caspase-9 in the HO group were greater than that in the HY group (P <0.01), but the expression of Bcl-2 in the HO group was less than that in the HY group (P <0.05). Conclusions The results suggest that oridonin can lower pulmonary artery pressure effectively, and inhibit pulmonary artery structural remodeling by inducing smooth cell apoptosis via a mitochondria-dependent pathway。

Abstract：Background Treatment with melatonin significantly reduces lung injury induced by bleomycin, paraquat and ischemia reperfusion. In the present study, we investigated the possible protective roles of melatonin in pulmonary inflammation and lung injury during acute endotoxemia.Methods Thirty-two male Sprague-Dawley rats were randomly assigned to four groups: vehicle + saline group, melatonin + saline group, vehicle + lipopolysaccharide group, melatonin + lipopolysaccharide group. The rats were treated with melatonin (10 mg/kg, intraperitoneal injection (I.p.)) or vehicle (1% ethanol saline), 30 minutes prior to lipopolysaccharide administration (6 mg/kg, intravenous injection). Four hours after lipopolysaccharide injection, samples of pulmonary tissue were collected. Blood gas analysis was carried out. Optical microscopy was performed to examine pathological changes in lungs and lung injury score was assessed. Wet/dry ratios (W/D), myeloperoxidase activity, malondialdehyde concentrations and tumor necrosis factor-alpha (TNF-a) and interleukin-10 (IL-10) levels in lungs were measured. The pulmonary expression of nuclear factor-kappa B (NF-KB) p65 was evaluated by Western blotting. Results PaO2 in the vehicle + lipopolysaccharide group decreased compared with that in the vehicle + saline group. This decrease was significantly reduced in the melatonin + lipopolysaccharide group. The lung tissues from the saline + lipopolysaccharide group were significantly damaged, which were less pronounced in the melatonin + lipopolysaccharide group. The W/D ratio increased significantly in the vehicle + lipopolysaccharide group (6.1±0.18) as compared with that in the vehicle + saline group (3.611±0.3) (P <0.01), which was significantly reduced in the melatonin + lipopolysaccharide group (4.8±0.25) (P <0.01). Myeloperoxidase activity and malondialdehyde levels increased significantly in the vehicle + lipopolysaccharide group compared with that in the vehicle + saline group, which was reduced in the melatonin + lipopolysaccharide group. The TNF-α level of pulmonary tissue increased significantly in the vehicle + lipopolysaccharide group ((8.7±0.91) pg/mg protein) compared with that in the vehicle + saline group ((4.3±0.62) pg/mg protein, P <0.01). However, the increase of TNF-α level of pulmonary tissue was significantly reduced in the melatonin + lipopolysaccharide group ((5.9±0.56) pg/mg protein, P <0.01). Pulmonary IL-10 levels were elevated markedly in the vehicle + lipopolysaccharide group in contrast to that in the vehicle + saline group, whereas the elevation was augmented in the melatonin + lipopolysaccharide group. The nuclear localization of p65 increased markedly in the vehicle +lipopolysaccharide group and this enhancement of nuclear p65 expression was much less in the melatonin + lipopolysaccharide group.Conclusion Melatonin reduces acute lung injury in endotoxemic rats by attenuating pulmonary inflammation and inhibiting NF-KB activation。

Abstract：Background Acute rejection is one of the most important factors for prognosis following liver transplantation. With the use of potent immunosuppressants, acute rejection does not always present typical manifestations. Moreover, other complications often occur concomitantly after liver transplantation, which makes early diagnosis of acute rejection more difficult. Acute rejection is best diagnosed by liver biopsy. Differentiation of clinical manifestations and pathological features plays an important role in achieving individualized immunosuppressive treatment and prolonging long term survival of patients given orthotopic liver transplants.Methods From January 2004 to December 2006, 516 orthotopic liver transplantations were performed at the First Affiliated Hospital, Sun Yat-sen University. For patients who suffered acute rejection, clinical manifestations, histopathological features, diagnosis and anti-rejection treatment were summarized and analyzed. Results In 86 cases (16.7%), of the 516 recipients, 106 episodes of acute rejection occurred, which included 9 with histopathological borderline changes, 36 Banff Ⅰ rejections, 48 Banff Ⅱ and 13 Banff Ⅲ. Among these, 36 were cured by adjusting the dose of immunosuppressant and 65 were reversed by methylprednisolone pulse treatment. Five were methylprednisolone resistant, 3 of whom were given OKT3 treatment and 2 underwent liver retransplantation. Conclusions Due to potent immunosuppressive agents, acute rejection following an orthotopic liver transplantation lacks typical clinical manifestations and pathological features. Acute rejection is best diagnosed by liver biopsy. Designing rational individualized immunosuppressive regimen based on clinical and pathological features of acute rejection plays an important role in prolonging long term survival of patients。

Abstract：Background Laparoscopy-assisted radical gastrectomy is gaining acceptance for treating early gastric cancer. However, few reports concerning the effectiveness of laparoscopy-assisted D2 radical distal gastrectomy (LADG) for advanced gastric cancer or data comparing the results obtained after open distal gastrectomy (ODG) are yet available. The aim of this study was to evaluate the method, feasibility and clinical result of LADG for advanced gastric cancer. Methods A retrospective study was performed comparing LADG and ODG for advanced gastric cancer. Seventy-eight patients who underwent LADG were compared with 90 patients who underwent ODG in terms of pathologic findings, operative outcome, and complications.Results There was no conversion to open surgery in the LADG group and no postoperative mortality of any patients. There were no significant differences between LADG and ODG in operative time ((245±35) vs (220±20) minutes), complication rate (7.7% vs 10.0%), and number of lymph nodes (23.5±6.0 vs 21.0±7.5), while the blood loss was less after LADG ((110±2.5) vs (196+30) ml, P <0.05). The time to postoperative flatus and postoperative hospital stay were shorter after LADG ((73.0±8.5) vs (102.0±10.5) hours, and (8.6±1.2) vs (12.1±2.5) days, P <0.05, respectively). Conclusion LADG for advanced gastric cancer is feasible, safe, and minimally invasive。

Abstract：Background Increased triglyceride (TG) occurs in patients with acute coronary syndrome (ACS), and apolipoprotein AV (apoAV) has been shown to lower TG levels. In the present study, we investigated plasma apoAV level and its relationship with TG and C-reactive protein (CRP) in ACS patients.Methods A total of 459 subjects were recruited and categorized into control group (n=-116), stable angina (SA) group (n=115), unstable angina group (n=-116) and acute myocardial infarction group (n=112). Plasma apoAV level was measured by a sandwich ELISA assay.Results Compared with controls ((100.27±2.2.44) ng/ml), plasma apoAV was decreased in SA patients ((76.54+16.91) ng/ml) but increased in patients with unstable angina ((330.89±66.48) ng/ml, P <0.05) or acute myocardial infarction ((368.66±60.53) ng/ml, P <0.05). Inverse correlations between apoAV and TG were observed in the control or stable angina groups (t=-0.573 or-0.603, respectively, P <0.001), whereas positive correlations were observed in the patients with unstable angina or acute myocardial infarction (t=0.696 or 0.690, respectively, P <0.001). Furthermore, a positive relationship between apoAV and CRP was observed in the ACS patients but not in the non-ACS subjects. Conclusion The plasma apoAV concentration is increased and positively correlates with TG and CRP in ACS patients。

Abstract：Background Homoharringtonine (HH'r) is effective in treating late stage chronic myelogenous leukaemia (CML), but little is known about long term maintenance during complete cytogenetic response. Long term efficacy and toxicity profiles of low dose HHT were evaluated in this study.Methods One hundred and six patients with CML received 1.5 mg/m2 of HHT alone by continuous daily infusion for seven to nine days every four weeks. Of 79 patients in the control group, 31 were treated with interferon α (IFN-α) and 48 with hydroxycarbamide. For 17 patients who failed to achieve cytogenetic response within 12 months' treatment of IFN-α, HHT was administered. Quantitative RT-PCR was used to detect the BCR-ABL mRNA expression in 36 Philadelphia positive CML patients enrolled after 2007. Haematological and cytogenetic responses were evaluated in all patients at the 12th month of follow-up. Long term efficacy was assessed in a follow-up with a median time of 54 months (12 months-98 months).Results After 12 months of therapy, cytogenetic response rate of the HHT, IFN-α and hydroxycarbamide groups were 39/106, 14/31 and 3/48, and corresponding molecular cytogenetic response rates 6/18, 3/8 and 0. Of the 17 patients who received HHT as salvage treatment, 6 achieved cytogenetic response (3 major). At the 48 months' follow-up, cytogenetic response was maintained in 32/39 patients treated with HHT. Patients who had cytogenetic response in HHT group or treated with IFN-α also showed longer median chronic durations, which were 45 months (12 months-98 months) and 49 months (12 months-92 months) respectively, indicating a longer survival time.Conclusions Low dose HHT alone showed considerable short term and long term efficacy in the treatment of late stage CML. It may also be a good choice for patients who have failed imatinib, IFN-α treatment or haematopoietic stem cell transplantation or cannot afford these treatments。

Abstract：Background Increased signal intensity (ISI) in the spinal cord on T2-weighted MR images has been reported in some previous researches, however no study focused on the position of the ISI in the spinal cord and its potential value. The aim of this study was to investigate the correlation between ISI position and the outcome of surgical treatment for cervical spondylotic myelopathy (CSM) patients.Methods A retrospective study was conducted. Pre- and post-operative clinical status was evaluated by modified Japanese Orthopaedic Association (JOA) score. ISI was evaluated according to the T2-weighted sequences. The JOA score and the recovery ratios among patients with ISI in gray matter (group A), in both gray and white matter (group B), and ISI-negative group were compared.Results Totally 64 patients were enrolled in this retrospective study. Preoperative JOA score of ISI positive and negative group had significant difference, but the recovery ratios had no significant difference (the recovery ratios of the two groups in week 1, week 26, and week 104 were (21.54±14.65)%, (50.56±14.76)%, (59.23±13.08)% and (20.25±14.32)%, (54.46±23.16)% and (61.26±29.4)%, respectively; P>0.05). The recovery ratios of negative group and group A in week 104 were superior to group B (the recovery ratios of negative group, group A, and group B in week 104 were (61.26±E29.49)%, (65.35±11.36)%, and (50.33±10.20)%, respectively; P <0.05). Conclusions Patients with ISI in the gray matter alone on T2-weighted MR images did not have significantly different surgical outcomes compared with those without ISI. Patients with ISI in both gray and white matter had surgical outcomes that were worse than those without ISI。

Abstract：Background The critical roles of polyamines in cell growth and differentiation have made polyamine metabolic pathway a promising target for antitumor therapy. Recent studies have demonstrated in vitro that some antitumor polyamine analogues could be used as substrates and oxidized by purified recombinant human N1-acetylpolyamine oxidase (APAO, an enzyme that catabolizes natural polyamines), indicating a potential role of APAO in determining the sensitivity of cancer cells to specific antitumor analogues. This study evaluated, in vivo, the effect of APAO on cytotoxicity of antitumor polyamine analogue, N1-cyclopropylmethyI-N11-ethylnorspermine (CPENS) and its mechanism when highly expressed in human lung cancer line A549.Methods A clone with high expression of APAO was obtained by transfecting A549 lung cancer cell line with pcDNA3.1/APAO plasmid and selecting with quantitative realtime PCR and APAO activity assay. Cell proliferation was determined by MTT method and apoptosis related events were evaluated by DNA fragmentation, sub-G1/flow cytometric assay, western blotting (for cytochrome C and Bax) and colorimetric assay (for casapse-3 activity). Results A clone highly expressing APAO was obtained. High expression of APAO in A549 cells inhibited accumulation of CPENS, decreased their sensitivity to the toxicity of CPENS and prevented CPENS induced apoptosis. Conclusion These results indicate a new drug resisting, mechanism in the tumor cells. High expression of APAO can greatly decrease the sensitivity of tumor cells to the specific polyamine analogues by detoxitying those analogues and prevent analogue induced apoptosis。

Abstract：Background Hepatitis B is at particularly high risk of fibrosis progression. Unfortunately, the mechanism of hepatic fibrogenesis induced by hepatitis B virus (HBV) has not been fully understood to date. The aim of this study was to observe whether HBV can infect hepatic stellate cells (HSCs), and to examine the effects of HBV or HBV S protein (HBs) on the proliferation and collagen type Ⅰ expression of HSCs.Methods The supernatants of HepG2.2.15 cells which contained HBV-DNA or HBs were added to LX-2 cells for 72 hours. Cell survival was determined by MTT assay. HBV particles in LX-2 cells were detected by transmission electron microscopy. The expression of HBs and HBV C protein (HBc) was determined by confocal fluorescence microscopy. The expression levels of HBV-DNA were measured by real-time PCR. The cellular collagen type Ⅰ mRNA and protein levels were quantified by reverse transcription-PCR and ELISA, respectively.Results High concentrations of HBV (1.2x105-5.0x105 copies/ml) or HBs (1.25-20 μg/ml) inhibited the proliferation of LX-2 cells, while low concentrations of HBV (1.0x103-6.2x104 copies/ml) or HBs (0.04-0.62 μg/ml) promoted the proliferation. After treating LX-2 cells with HBV for 72 hours, about 42 nm HBV-sized particles and strong expression of HBs and HBc were found in the cytoplasm of LX-2 cells. HBV-DNA in the culture medium of LX-2 cells decreased at 24 hours, rose at 48 hours and thereafter, decreased again at 72 hours. The mRNA and protein expression of cellular collagen type Ⅰ in LX-2 cells were significantly increased by HBV infection but not by recombinant HBs. Conclusions HBV and HBs affect the proliferation of HSCs; HBV can transiently infect and replicate in cultured HSCs and express HBs and HBc in vitro. Furthermore, HBV can significantly increase the expression of collagen type Ⅰ mRNA and protein in HSCs。

Many philosophical and theoretical questions of sleep and dream have been written in traditional Chinese medicine literatures.' Varied approaches, including different recipes isolated from traditional herbs (2nd century, AD), auto-hypnosis (methods of self-suggestion, 1 lth century, AD), exercises and acupuncture, have been used to treat insomnia since ancient times, and they are now still used as the first-line treatment for insonmia by many physicians in China. However, the practice of modern sleep medicine in China starts from the recognition of sleep apnea。

Based on available population-based studies, Obstructive Sleep Apnea (OSA) associated with accompanying daytime sleepiness affects 3% to 7% of adult men and 2% to 5% of adult women in the general population. In some population subsets, like obese or older people, this prevalence is even higher. The health risk in OSA patients shows a strong association with acute cardiovascular events such as stroke, myocardial infarction and nocturnal sudden death.1,2 And with chronic conditions such as coronary artery disease, heart failure, and especially, systemic hypertension.3,4 In this review, prevalence and incidence of hypertension in OSA patients and the relationships between OSA and its confounders are considered, and of course, these confounders are also generally taken as risk factors for hypertension。

Alzheimer disease (AD) is characterized by the presence of β-amyloid (Aβ) plaques in the brain.1 More evidence of inflammatory parameters, such as, complement factors, proinflammatory cytokines and lymphocytes has been found to be co-localized with Aβ plaques,1,2 The research in the past decades has demonstrated abnormalities of both the humoral and cellular immune responses, suggesting an association of immunological aberration and AD. The total percentage of lymphocytes was not found to be altered, whereas the alterations of T-cell function, differentiation and subset distribution have still been unresolved.3,4 A significantly decreased function of suppressor as well as helper T-cells and natural killer (NK) cells in AD patients has been observed. Studies on lymphocyte subpopulations showed conflicting results, while other studies could not find alterations in lymphocyte subset distribution. In the present study, we assume the immune system dysregulation depending on a defective immune response which also affects lymphocyte differentiation and subset distribution. We investigated T lymphocyte subset pattems and co-stimulatory molecules, as well as B lymphocytes and NK cells in peripheral blood of AD patients and age matched healthy controls。

Pulmonary lymphangioleiomyomatosis (PLAM) is a rare disease primarily occurring in women at reproductive age, and claaracterlzed lay abnormal proliferation of immature smooth muscle cells named lymphangioleiomyomatosis (LAM) cells in the pulmonary lymphatics, blood vessels and airways, resulting in respiratory failure and death.1 It was first described by Bun'ell et al2 in 1937, and since then, more than 300 patients have been reported around the world. The first patient of PLAM in the mainland of China was reported in 1993,3 and an increasing number of patients have been described within recent years. However, misdiagnosis seems common, resulting in inappropriate therapy to this disease. Therefore, we summarized the patients reported in the mainland of China between 1993 and 2007, which may help to increase physicians' awareness of PLAM。

Randomized controlled trial (RCT) as recognized to be able to provide the most powerful and direct evidence is a highly demanded research in evidence-based medicine.1 The elements from the participants' selection, distribution, intervention, measurement, data collection and analysis to publication should strictly follow the principles of clinical epidemiology and evidence-based medicine. To improve the reporting quality of RCTs, a group of clinicians, statisticians, epidemiologists, and editors drafted theconsolidated standards of reporting trials (CONSORT) statement in 1996, which was revised in 2001, and 2008 respectively.2,3 Many leading medical journals and major international editorial groups have adopted the CONSORT statement as a guidance to authors regarding how to report their trials and to editors about how to appraise a RCT report.4,5