Effects of long working hours and the night shift on severe sleepiness among workers with 12‐hour shift systems for 5 to 7 consecutive days in the automobile factories of Korea

We investigated the effects of 12‐hour shift work for five to seven consecutive days and overtime on the prevalence of severe sleepiness in the automobile industry in Korea. [Correction added after online publication 28 Nov: Opening sentence of the summary has been rephrased for better clarity.] A total of 288 randomly selected male workers from two automobile factories were selected and investigated using questionnaires and sleep‐wake diaries in South Korea. The prevalence of severe sleepiness at work [i.e. Karolinska Sleepiness Scale (KSS) score of 7 or higher] was modeled using marginal logistic regression and included theoretical risk factors related to working hours and potential confounding factors related to socio‐economic status, work demands, and health behaviors. Factors related to working hours increased the risk for severe sleepiness at the end of the shift in the following order: the night shift [odds ratio (OR): 4.7; 95% confidence interval (CI): 3.6–6.0)], daily overtime (OR: 2.2; 95% CI: 1.7–2.9), weekly overtime (OR: 1.6; 95% CI: 1.0–2.6), and night overtime (OR: 1.6; 95% CI: 0.8–3.0). Long working hours and shift work had a significant interactive effect for severe sleepiness at work. Night shift workers who worked for 12 h or more a day were exposed to a risk of severe sleepiness that was 7.5 times greater than day shift workers who worked less than 11 h. Night shifts and long working hours were the main risk factors for severe sleepiness among automobile factory workers in Korea. Night shifts and long working hours have a high degree of interactive effects resulting in severe sleepiness at work, which highlight the need for immediate measures to address these characteristics among South Korean labor force patterns.     

汗腺癌病理分级的预后意义

目的：探讨汗腺癌不同病理组织学分级对复发和转移及预后的影响。方法：参照Ｂｌｏｏｍ－Ｒｉｃｈａｒｄｓｏｎ乳腺癌分级标准对１０５例汗腺癌进行分级，并探讨其与复发、转移和预后间的关系。结果：在１０５例汗腺癌中，属分化型者４２例，属低分化型者６３例，两者复发率、多次复发率、区域淋巴结转移率和远处转移率及死亡率比较，提示在多次复发、远处转移方面差异有显著性，在预后方面差异非常显著。结论：将汗腺癌按腺管形成多少、核的多形性和核分裂数进行病理组织学分级，对选择治疗、估计预后具有很大的指导意义     

17βE2对切除卵巢兔动脉粥样硬化与血液流变学的作用

目的: 探讨17βE₂对卵巢切除(OVX)兔的AS斑块、血脂代谢及血液流变学的影响。方法: 34只成熟未孕雌兔分为4组:A为NC;B为Sham+CHO;C为OVX+CHO;D为OVX+CHO+17βE₂。喂养12周,喂养前与12周后测定血脂TC、TG、HDL-C、LDL-C、ApoA1、ApoB;测定全血粘度、血浆粘度、AIRC及纤维蛋白原。喂养12周后处死,测定AS斑块面积与主动脉总面积百分比。结果: ①AS斑块面积与主动脉总面积之比,A、B、C、D组分别为0.02±0.00、0.42±0.15、0.67±0.23、0.12±0.11,B组小于C组(P＜0.05)、D组明显小于C组(P＜0.01)。②血脂TC、TG、LDL-C、ApoB,B、D组明显小于C组(P＜0.01)。③血液流变学:全血粘度、血浆粘度AIRC与纤维蛋白原D组明显低于C组(P＜0.01)。结论: 17βE₂能抑制脂质斑块沉积,改善血脂代谢,减轻高脂血症,改善血液流变学。这可能是雌激素抑制AS形成的部份机理。     

API2-MALT1融合基因变异体在粘膜相关淋巴组织结外边缘区B细胞淋巴瘤中的分布及凋亡的关系

目的探讨API2-MALT1融合基因变异体在粘膜相关淋巴组织结外边缘区B细胞淋巴瘤(extranodal marginal zone B—cell lymphoma of mucosa—associated lymphoid tissue，MALT)中的分布特点及其转录与肿瘤凋亡的关系。方法将逆转录-聚合酶链反应和巢式聚合酶链式反应结合，检测62例不同部位MALT淋巴瘤中API2-MALT1融合基因的多种变异体；通过TdT介导脱氧核苷酸缺口末端标记技术进行肿瘤细胞的原位凋亡检测；通过逆转录-聚合酶链反应和免疫组化染色检测API2的mRNA和蛋白水平。结果62例MALT淋巴瘤中28例检出API2-MALT1融合基因(45．16％)，为变异体A1446-M1123或A1446-M814，但未检出A1446-M541和A1446-M1150。A1446-M1123(18／28)的检出明显多于A1446-M814(10／28)。融和基因转录在甲状腺MALT淋巴瘤中检出最低，在其它部位的分布无差异。在API2-MALT1^ 组(API2-MALT1mRNA表达阳性组)肿瘤凋亡水平明显高于API2-MALT1^-组(API2-MALT1mRNA表达阴性组)，API2的mRNA和蛋白水平低于阴性组。A1446-M1123^ 与A1446-M814^ 病例之间凋亡和API2的变化无差异。结论MALT淋巴瘤中t(11；18)(q21；q21)的发生有部位差异，A1446-M1123可能是中国人MALT淋巴瘤中API2-MALT1融合基因变异体的主要类型。API2-MALT1融合基因转录与MALT淋巴瘤的凋亡水平和API2的变化有关。     

应用PCR技术检测恙螨体内恙虫病立克次体动态和经卵传递的研究

本文应用聚合酶链反应技术检测恙虫病立克次体实验感染的恙螨体内立克次体的动态变化，通过人工腹腔接种而感染的恙螨成虫，恙虫病立克次体至少能在其体内生存３６０天和经卵传递４代；通过未食幼虫叮咬病小鼠而感染的恙螨，经饱蚴、若蛹、若虫、成蛹和成虫阶段，恙虫病立克次体检测均呈阳性，至少能在成虫期体内生存２７０天和经卵传递１代。     

Pleiotropic genomic variants at 17q21.31 associated with bone mineral density and body fat mass: a bivariate genome-wide association analysis

Osteoporosis and obesity are two severe complex diseases threatening public health worldwide. Both diseases are under strong genetic determinants as well as genetically correlated. Aiming to identify pleiotropic genes underlying obesity and osteoporosis, we performed a bivariate genome-wide association (GWA) meta-analysis of hip bone mineral density (BMD) and total body fat mass (TBFM) in 12,981 participants from seven samples, and followed by in silico replication in the UK biobank (UKB) cohort sample (N = 217,822). Combining the results from discovery meta-analysis and replication sample, we identified one novel locus, 17q21.31 (lead SNP rs12150327, {"type":"entrez-nucleotide","attrs":{"text":"NC_000017.11","term_id":"568815581"}}NC_000017.11:g.44956910G > A, discovery bivariate P = 4.83 × 10⁻⁹, replication P = 5.75 × 10⁻⁵) at the genome-wide significance level (ɑ = 5.0 × 10⁻⁸), which may have pleiotropic effects to both hip BMD and TBFM. Functional annotations highlighted several candidate genes, including KIF18B, C1QL1, and PRPF19 that may exert pleiotropic effects to the development of both body mass and bone mass. Our findings can improve our understanding of the etiology of osteoporosis and obesity, as well as shed light on potential new therapies.Subject terms: Genome-wide association studies, Gene expression profiling     

Inhibition of experimental autoimmune tubulointerstitial nephritis in Brown-Norway rats by (15S)-15-methyl prostaglandin E1. Analysis of the effect of prostaglandin E1 on the induction of the humoral immune response and the elicitation of humorally mediated inflammation.

Brown-Norway (BN) rats develop tubulointerstitial nephritis (TIN) after immunization with bovine tubular basement membrane (TBM) and adjuvants. Daily subcutaneous injections (either on Days 0-7 or Days 0-14) of (15S)-15-methyl prostaglandin E1 (M-PGE1) at a dose of 1 mg/kg/day markedly inhibited or completely abrogated the development of both the acute polymorphonuclear (Day 10) and the subsequent mononuclear (Day 14) inflammatory phases of BN rat TIN. Circulating anti-TBM antibody in Days 0-7 M-PGE1-treated rats was moderately diminished on Day 8 after immunization but not on Day 14. Circulating anti-TBM antibody in Days 0-14 M-PGE1-treated rats was only slightly diminished on Day 14. In experiments to test the effect of M-PGE1 on the elicitation phase of humorally mediated inflammation, M-PGE1 inhibited the acute inflammatory response observed 6 hours after intradermal injection of particulate TBM into TBM-sensitized BN rats. The inflammation in these skin tests was demonstrated by passive transfer experiments to be humorally mediated. The inhibition of acute humorally mediated intradermal inflammation was not attributable to neutropenia, because M-PGE1 caused a significant neutrophilia as demonstrated by peripheral blood smears. Although the inhibition of TIN in Days 0-14 M-PGE1-treated rats may have been due, in part, to dysfunction of the elicitation phase of humorally mediated inflammation, the inhibition of TIN in Days 0-7 M-PGE1-treated rats was more likely secondary to the diminished induction of either humoral or cellular immunity.     

Expression of interleukin-18 by nasopharyngeal carcinoma cells: a factor that possibly initiates the massive leukocyte infiltration

Interleukin-18 (IL-18) is a single-chain cytokine that is produced by various cells. With interleukin-12 (IL-12), it synergistically stimulates activated T cells and natural killer (NK) cells to produce interferon-gamma (IFN-gamma). Nasopharyngeal carcinoma (NPC) is the most common form of nasal and nasopharyngeal malignancy, and in NPC tumor tissues there is an intense leukocyte infiltration comprising predominantly T cells and macrophages. We previously showed an increased expression of IFN-gamma in the infiltrating T cells. To identify the cells that provide IL-12 and IL-18 for stimulating the expression of IFN-gamma in activated T cells, NPC cell lines CNE-2 and HK-1, as well as biopsies obtained from NPC and control individuals, were examined. CNE-2 and HK-1 cells were found to express messenger RNA encoding IL-18, but not IL-12. Secreted IL-18 was detected in the culture supernatant. Addition of a caspase-1 inhibitor decreased the secretion level, indicating that this IL-18 secretion was caspase-1 dependent. Moreover, the in vitro IL-18 production in NPC cell lines correlated with the NPC tumor cells in situ. NPC tumor cells in the biopsies produced IL-18, as detected by immunohistochemistry and immunofluorescent double staining. In contrast, IL-18 expression was not observed in the control biopsies. We suggest that IL-18 secreted by NPC tumor cells plays a role in initiating the leukocyte infiltration process. IL-18 stimulates T cells and NK cells to produce IFN-gamma, which consequently activates macrophages and other immune cells to secrete chemokines to start a leukocyte recruitment cascade.