师范院校贫困新生与非贫困新生心理健康状况的比较

目的:比较师范院校贫困新生与非贫困新生的心理健康状况。方法:于2005-10在衡阳师范学院完成调查。采用整群抽样横断面调查方法,以衡阳师范学院2005级3089名新生为调查对象,运用症状自评量表对其进行集体测查。在统一指导语下,学生根据最近1周内的自我感觉答题,独立完成,当场收卷。结果数据运用光电阅读机(OMR2000)输入计算机心理测评工具箱标准版V3.0系统进行总分和因子分的统计。量表中没有回答的项目记为"没有",5个以上项目未答者视为问卷无效以及总分低于95分的问卷因缺乏可靠性均不进行分析。所有数据输入电脑后用SPSS11.0软件进行统计分析;群体差异比较用t和Z检验。结果:共发放3089份问卷,收回有效答卷2994份,有效率为96.92%,其中贫困新生有效答卷510份,占17.03%。问卷结果显示,师范院校贫困新生在人际关系、偏执和精神病性3项因子上的得分分别为1.86±0.54,1.70±0.48和1.58±0.43,明显高于非贫困新生(1.78±0.51,1.65±0.46,1.53±0.39,t=3.34,2.02,2.92,P<0.05)。从阳性因子的人数比率来看,师范院校贫困新生在总分阳性的人数比率为0.28,明显低于非贫困新生(0.33,Z=-2.27,P<0.05);而在人际关系、偏执和精神病性3项因子阳性的人数比率分别为0.35,0.30,0.16,明显高于非贫困新生(0.31,0.24,0.13,Z=1.73,2.72,1.71,P<0.05)。结论:师范院校贫困新生的整体心理健康状况并不比非贫困新生差,但是在人际关系敏感、偏执和精神病性3个问题上明显比非贫困新生要严重。     

Prevalence of healthcare device-associated infection using point prevalence surveys of antimicrobial prescribing and existing electronic data

This study extended a previously described method for the prevalence of healthcare-associated infection, based on point prevalence surveys of antimicrobial prescribing and electronic data, to estimate the prevalence of device-associated infections. In June 2009, the six-month point prevalence survey of antimicrobial prescribing was carried out in accordance with the European Surveillance of Antimicrobial Consumption Protocol. For patients receiving antimicrobials the presence of devices was recorded. A census on device use was carried out concurrently in the relevant hospitals. We selected patients receiving antimicrobials, started >48h after admission and who had a device, or who were without a device but were receiving antimicrobials for the treatment of bloodstream infection, urinary tract infection, or pneumonia. From existing positive microbiological and radiology reports, these patients were assessed for the presence of device-associated infection according to specified definitions. Of 1354 patients surveyed, 253 (19%) were receiving antimicrobial for treatment; of these, 189 also had devices and 172 (only 13% of all patients surveyed) needed individual assessment for the presence of device-associated infection. It took about 5min per patient to check electronic microbiology and/or radiology reports. Twenty-three patients met the criteria for device-associated infection. The prevalence of catheter-associated urinary tract infection, central-line-associated bloodstream infection, local vascular access infection, and ventilator-associated pneumonia was 3.9%, 3.1%, 3.8% and 11.6%, respectively. This is a simple method, which can be adopted in other hospitals, to estimate the prevalence of device-associated infection using pre-existing data.     

克隆测序确认HLA新等位基因B*3712

目的：由于技术原理的限制，目前尚不能对所有的HLA等位基因进行严格的区分，特别是以往没有发现的新基因序列只能通过测序的方法解决，然而，当遇到等位基因杂合时，测序给出的结果仍然无法确认新的序列改变发生在等位基因的哪一侧，这时需要用分子生物学方法分离杂合子然后进行测序才能确定新的基因序列。采用基因克隆方法确认HLA新等位基因。 方法：实验于2006-01／05在河南省红十字血液中心HLA实验室，美国海军骨髓库HLA实验室完成。造血干细胞血样由中华骨髓库提供。采用荧光微珠HLA分型方法对中华骨髓库捐献者血样进行HLA分型检测，无法给出确切结果的摸棱两可结果标本用基因克隆（TOPO TA Cloning）、DNA测序的方法确认新的HLA基因序列。 结果：通过克隆分离杂合等位基因，再进行测序确认发现新的序列与B^＊3709相比，出现4个核苷酸改变：1．355nt C〉A，2．363nt C〉G，3．412nt G〉A，4．477ntC〉G，而且均发生在H哺B基因外显子3（exon3）。4处改变引起氨基酸编码改变：①编码95CTC〉ATC，氨基酸改变L〉1（亮氨酸〉异亮氨酸）。②97AGC〉AGG．S〉R（丝氨酸〉精氨酸）。③114GAC〉AACD〉N（天门冬氨酸〉天冬酰胺）。（9135GCC〉GCGA=A无氨基酸改变。 结论：①新的基因序列已经在GenBnak注册，被WHO的HLA因子命名委员会得到正式命名为HLA-B^＊3712基因。②基因克隆是确认HLA新基因的根本方法。     

Peripheral blood dendritic cell subtypes are significantly elevated in subjects with asthma

Background Dendritic cells (DCs) are crucial for the processing of antigens, T lymphocyte priming and the development of asthma and allergy. Smokers with asthma display altered therapeutic behaviour and a reduction in endobronchial DC CD83 expression compared with non‐smokers with asthma. No information is available on the impact of smoking on peripheral blood DC profiles. Objective Determine peripheral blood DC profiles in subjects with and without asthma with differing smoking histories. Methods Forty‐three asthmatics (17 smokers, nine ex‐smokers and 17 never–smokers) and 16 healthy volunteers (nine smokers and seven never–smokers) were recruited. Spirometry, exhaled nitric oxide and venesection was performed. DC elution was by flow cytometry via the expression of DC surface markers [plasmacytoid (pDC) (BDCA‐2, CD303), type 1 conventional (cDC) (BDCA‐1, CD1c), and type 2 cDC (BDCA‐3, CD141)]. Results Subjects with asthma displayed increases in all DC subtypes compared with normal never‐smokers: [type 1 cDCs – asthma [median% (IQR)]: 0.59% (0.41, 0.74), normal never‐smokers: 0.35% (0.26, 0.43), P=0.013]; type 2 cDCs – asthma: 0.04% (0.02, 0.06), normal never‐smokers: 0.02% (0.01, 0.03), P=0.008 and pDCs – asthma: 0.32% (0.27, 0.46), normal never‐smokers: 0.22% (0.17, 0.31), P=0.043, and increased pDC and type 1 cDCs compared with normal smokers. Smoking did not affect DC proportions in asthma. Cigarette smoking reduced pDC proportions in normal subjects [normal never–smokers: 0.22% (0.17, 0.31); normal smokers: 0.09% (0.08, 0.15), P=0.003]. Conclusions and Clinical Relevance This study shows for the first time that subjects with asthma display a large increase in peripheral blood DC proportions. Cigarette smoking in asthma did not affect the peripheral blood DC profile but did suppress pDC proportions in non‐asthmatic subjects. Asthma is associated with a significant increase in circulating DCs, reflecting increased endobronchial levels and the importance of DCs to the development and maintenance of asthma. (Clinical trials.gov identifier: NCT00411320) Cite this as: M. Spears, C. McSharry, I. Donnelly, L. Jolly, M. Brannigan, J. Thomson, J. Lafferty, R. Chaudhuri, M. Shepherd, E. Cameron and N. C. Thomson, Clinical & Experimental Allergy, 2011 (41) 665–672.     

Irreversible inhibitors of the EGF receptor may circumvent acquired resistance to gefitinib

Non-small cell lung cancers (NSCLCs) with activating mutations in the kinase domain of the epidermal growth factor receptor (EGFR) demonstrate dramatic, but transient, responses to the reversible tyrosine kinase inhibitors gefitinib (Iressa) and erlotinib (Tarceva). Some recurrent tumors have a common secondary mutation in the EGFR kinase domain, T790M, conferring drug resistance, but in other cases the mechanism underlying acquired resistance is unknown. In studying multiple sites of recurrent NSCLCs, we detected T790M in only a small percentage of tumor cells. To identify additional mechanisms of acquired resistance to gefitinib, we used NSCLC cells harboring an activating EGFR mutation to generate multiple resistant clones in vitro. These drug-resistant cells demonstrate continued dependence on EGFR and ERBB2 signaling for their viability and have not acquired secondary EGFR mutations. However, they display increased internalization of ligand-activated EGFR, consistent with altered receptor trafficking. Although gefitinib-resistant clones are cross-resistant to related anilinoquinazolines, they demonstrate sensitivity to a class of irreversible inhibitors of EGFR. These inhibitors also show effective inhibition of signaling by T790M-mutant EGFR and killing of NSCLC cells with the T790M mutation. Both mechanisms of gefitinib resistance are therefore circumvented by irreversible tyrosine kinase inhibitors. Our findings suggest that one of these, HKI-272, may prove highly effective in the treatment of EGFR-mutant NSCLCs, including tumors that have become resistant to gefitinib or erlotinib.     

Routine Mobilization of the Splenic Flexure is not Necessary During Anterior Resection for Rectal Cancer

Purpose Splenic flexure mobilization is widely considered to be an essential component of anterior resection for rectal cancer. It was our hypothesis that selective splenic flexure mobilization would reduce operative times without increasing morbidity or affecting cure. Methods A total of 100 consecutive patients with rectal cancer (mean 8 (range, 4–15) cm from anal verge) who underwent anterior resection for cure between 1996 and 2002 had splenic flexure mobilization only as required to achieve a tension-free anastomosis. Operative time, postoperative morbidity, pathologic findings, and recurrence rates were recorded. Results There were no clinicopathologic differences between those who had splenic flexure mobilization (n = 26) and those who did not (n = 74). Mean operative time in the splenic flexure mobilization group was longer, 167 (range, 130–200) minutes vs. 120 (range, 95–180) minutes in the nonmobilized group (P = 0.023). Mean length of specimen resected was longer in the splenic flexure mobilization group: 36 vs. 18 cm (P = 0.008). Anastomotic complications (4 percent), local recurrence (7 percent, median follow-up, 38 months), perioperative morbidity (32 percent) and mortality (2 percent), and survival did not differ between the two groups. Conclusions Routine splenic flexure mobilization is not required for safe anterior resection in patients with rectal cancer. Avoiding splenic flexure mobilization results in shorter operative times and does not increase postoperative morbidity, anastomotic leakage, or local recurrence. Presented at the Freyer Surgical Meeting, Galway, Ireland, September 2 to 3, 2005.     

Immune reconstitution in severe combined immunodeficiency disease after lectin-treated, T-cell-depleted haplocompatible bone marrow transplantation

We describe our 9-year experience with lectin-treated T-cell-depleted haplocompatible parental bone marrow transplantation (BMT) for 24 patients with severe combined immunodeficiency disease (SCID). Nineteen of 21 evaluable patients had T-cell engraftment; 2 of 11 patients tested had B-cell and monocyte engraftment. Fourteen of 24 (58%) patients are alive 7 months to 9.8 years post-BMT. Seventeen of 24 patients received pretransplant conditioning with chemotherapy and/or total body irradiation, and 8 of 24 received more than one transplant. Patients who received conditioning had a survival rate of 61% versus 57% for those who received no conditioning. None received graft-versus- host disease (GVHD) prophylaxis and no patient had acute or chronic GVHD greater than grade I. Kinetics and follow-up of immune recovery were analyzed in 14 patients who are greater than 1 year from transplant. Half of the patients showed evidence of T-cell function by 3 months and normal T-cell function by 4 to 7 months post-BMT. On average, T-cell numbers and subsets became normal 10 to 12 months posttransplant. Recovery of B-cell function was more delayed, although in most patients B-cell numbers and IgM levels were normal by 12 months post-BMT. B-cell function, as determined by isohemagglutinin titers or specific antibodies to pneumococcal polysaccharide, keyhole limpet hemocyanin, or tetanus toxoid, became normal in 10 of 14 patients 2 to 8 years post-BMT. Seven of the 14 are off gammaglobulin therapy. Production of isohemagglutinins tended to predict recovery of antibody response to pneumococcal polysaccharide (P < .064). Based on these results, we believe that haplocompatible BMT is an effective, curative treatment for patients with SCID who lack an HLA-matched related donor.