10年剖宫产率及指征分析

目的 :分析剖宫产率升高的原因及指征的变化。方法 :对 1991～ 2 0 0 0年 10年间 7618例剖宫产病历进行回顾性分析。结果 :平均剖宫产率 2 9.99% ,剖宫产率逐年增加 ,1991年为 2 2 .19% ,到 2 0 0 0年达 47.2 4% ,有极显著性差异 (P<0 .0 0 5)。以社会因素为手术指征的剖宫产率 ,1991年为 5.58% ,2 0 0 0年为 13 .48%明显增加 ,差异有显著性 (P<0 .0 1) ,剖宫产率上升 ,围产儿死亡率无明显下降。结论 :剖宫产并不是绝对安全的分娩方式 ,剖宫产率的增加不是一个单纯的医疗问题 ,而是一个社会问题     

孕妇血清HBV-DNA含量对预测胎儿宫内感染的临床价值

目的:探讨孕妇血清HBV-DNA含量对预测胎儿宫内感染的临床价值。方法:应用聚合酶链反应(PCR)法检 测103例乙型肝炎表面抗原(HBsAg)阳性孕妇的血清HBV-DNA含量,并对相关因素进行分析。结果:103例HBsAg阳性孕妇 的HBV-DNA检出阳性率为56%,胎儿宫内感染率为12.6％,且胎儿宫内感染率随血清HBV-DNA含量的增加而升高, HBV-DNA含量与胎儿宫内感染率呈正相关(r=0.572,P<0.01)。结论:孕妇血清HBV-DNA含量可间接预测胎儿宫内感染 的发生率。     

瘦素及胰岛素样生长因子-Ⅰ与胎儿生长受限的关系

目的　探讨瘦素及胰岛素样生长因子Ⅰ (IGF Ⅰ )与胎儿生长受限 (FGR)的关系。方法　采用放射免疫法和免疫放射法测定 30例FGR孕妇 (FGR组 )和 80例正常孕妇 (对照组 )的血清及脐血瘦素、IGF Ⅰ水平 ,并对其结果进行相关性分析。结果　FGR组血清瘦素水平与对照组比较 ,差异无显著性 (P >0 0 5 ) ;FGR组血清IGF Ⅰ水平明显低于对照组 (P <0 0 5 ) ,FGR组脐血瘦素、IGF Ⅰ水平均明显低于对照组 (P <0 0 5 ,P <0 0 1 ) ;两组孕妇血清瘦素、IGF Ⅰ水平与脐血瘦素、IGF Ⅰ水平无相关性 (r =0 1 85 ,r =0 2 6 2 ,P >0 0 5 ) ;脐血瘦素水平与新生儿出生体重呈正相关 (r =0 36 4 ,P <0 0 5 ) ,与胎盘重量无相关性 (r =0 1 94 ,P >0 0 5 ) ;脐血IGF Ⅰ水平与新生儿出生体重及胎盘重量呈正相关 (r =0 4 75 ,r =0 4 86 ,P <0 0 5 )。结论　FGR孕妇脐血瘦素水平降低与胎儿脂肪沉积减少有关 ,脐血瘦素水平可作为预测胎儿体重的一项指标。血清与脐血IGF Ⅰ的分泌相对独立 ,提示IGF Ⅰ不能通过胎盘屏障。脐血IGF Ⅰ水平降低 ,可能是导致FGR的病因之一。     

刺五加注射液致药物不良反应99例文献分析

目的：了解刺五加注射液不良反应发生的情况并分析相关因素。方法：对国内近10年使用刺五加注射液出现的99例不良反应报道进行分类统计与分析。结果：刺五加注射液所致不良反应与给药剂量、给药途经、给药速度无显著关联，主要集中发生在用药过程中30min以内，且多发生于41～60岁年龄组，女性多于男性。不良反应可累及机体多个器官系统(呼吸系统、心血管系统、消化系统、皮肤、眼结膜等)，临床表现复杂多样，主要表现为变态反应，严重者可出现过敏性休克。结论：刺五加注射液所致变态反应确切机理有待进一步研究，临床医师、药师与护士应重视刺五加注射液的不良反应。     

后巩膜收缩术治疗病理性近视黄斑劈裂

目的：评估后巩膜收缩术对病理性近视黄斑劈裂的治疗效果。方法：回顾性研究。选取2014年12月 至2017年04月在南京市第一医院眼科行后巩膜收缩术的病理性近视黄斑劈裂患者24例（45眼）,观察手术前后患者的最佳矫正视力、眼轴长度、屈光度、黄斑区视网膜劈裂高度的状况与手术并发症。对相关计量资料进行重复测量方差分析。结果：患者术前,术后1个月、3个月、6个月及12个月的黄斑区视网膜劈裂高度分别为（494±31）、（299±24）、（256±24）、（200±22）、（168±25）μm,术后各时间点与术前比较差异有统计学意义（均P<0.05）。患者术后1、3、6个月眼轴长度分别为（28.6±2.1）、（28.9±2.0）、（29.3±2.0）mm,与术前[（30.5±2.2）mm]相比差异有统计学意义（P<0.05）,术后12个月眼轴（29.8±2.1）mm,与术前相比差异无统计学意义（P>0.05）。患者术后1个月、3个月的屈光度分别为（-15.14±5.16）D、（-15.64±5.05）D,与术前[（-17.33±7.43）D]相比差异有统计学意义（P=0.013、0.048）,术后6、12个月的屈光度分别为（-15.96±4.97）D、（-17.05±5.10）D,与术前相比差异无统计学意义（P>0.05）。患者最佳矫正视力差异无统计学意义（P>0.05）。结论：针对病理性近视黄斑劈裂伴或不伴视网膜脱离的治疗,后巩膜收缩术的安全性和可行性较好。     

Effects of α1-adrenergic receptor antagonists on the development and progression of urothelial cancer

We recently demonstrated that silodosin, a selective α₁-blocker often prescribed for the symptomatic treatment of benign prostatic hyperplasia (BPH), could inactivate a c-fos proto-oncogene regulator ELK1 in bladder cancer cells possessing a functional androgen receptor (AR). However, the clinical impact of α₁-blockers on the development and progression of bladder cancer remained poorly understood. In the present study, we investigated if α₁-blockers clinically used, including silodosin, tamsulosin, and naftopidil, could prevent the neoplastic/malignant transformation and cell growth, using non-neoplastic urothelial SVHUC sublines with carcinogen/MCA challenge and bladder cancer lines, respectively. Bladder cancers in men treated with silodosin, tamsulosin, or naftopidil for their BPH were then compared. Silodosin at 1-10 µM significantly inhibited the neoplastic transformation of MCA-SVHUC-AR cells, but not that of AR-negative MCA-SVHUC-control cells. In MCA-SVHUC-AR, silodosin significantly reduced the expression levels of oncogenes (c-fos/NF-κB1) and induced those of tumor suppressors (p27/PTEN). However, tamsulosin (up to 1 µM) or naftopidil (up to 10 µM) failed to significantly inhibit the neoplastic transformation of AR-positive or AR-negative urothelial cells. Similarly, cell proliferation/migration of AR-positive bladder cancer lines was considerably inhibited only by silodosin. Meanwhile, the incidence of bladder cancer in patients with silodosin [49/540 (9.1%)] was marginally lower, compared to those with tamsulosin [64/523 (12.2%); P=0.094] or tamsulosin or naftopidil [64+28/523+236 (12.1%); P=0.082]. There were no significant differences in tumor grade/stage among the 3 cohorts. Outcome analysis revealed lower risks for disease progression of non-muscle-invasive bladder tumors in the silodosin group than in the naftopidil group (P=0.011) or tamsulosin+naftopidil groups (P=0.035). Similarly, silodosin patients with muscle-invasive tumor had lower risks for disease progression, compared with tamsulosin (P=0.006) or tamsulosin+naftopidil (P=0.028) patients. Multivariate analysis further showed that silodosin treatment in those with non-muscle-invasive tumor was associated with improved progression-free survival, compared with naftopidil (hazard ratio=0.086; 95% confidence interval=0.008-0.905; P=0.041) or tamsulosin/naftopidil (hazard ratio=0.128; 95% confidence interval=0.016-1.036; P=0.054) treatment. Our in vitro studies thus indicate that both urothelial tumorigenesis and tumor growth are inhibited by silodosin, but not by tamsulosin or naftopidil. Clinical data further suggest that even pharmacological doses (e.g. 0.1 µM) of silodosin contribute to preventing bladder cancer progression.     

Recent Advances: Osteoporosis in the “Oldest Old”

Osteoporosis and related fractures disproportionately impact patients with advanced age, those with the frailty phenotype, and those with multiple comorbidities. Recent studies report a changing incidence in fracture type among the oldest old throughout the world, a finding not satisfactorily explained by advances in treatment of lifestyle factors. A growing recognition of the importance of muscle and bone interaction is leading to improved understanding of the underlying biochemical pathways linking them and new therapeutic targets. New models of care for frail older populations, particularly after hip fracture, are being developed but have been challenged to identify appropriate outcomes to target. An appreciation for the relationship between age-related comorbidities, fracture risk, and competing mortality risk is essential for practitioners caring for the oldest-old population.     

Neuroprotective effect of carnosine in the olfactory bulb after vanadium inhalation in a mouse model

Carnosine (β‐alanyl‐L‐histidine) is synthesized in the olfactory system, has antioxidant activity as a scavenger of free radicals and has been reported to have neuroprotective action in diseases which have been attributed to oxidative damage. In neurodegenerative disorders, such as Parkinson's and Alzheimer's diseases, impairment of olfactory function has been described. Vanadium derivatives are environmental pollutants, and its toxicity has been associated with oxidative stress. Vanadium toxicity on the olfactory bulb was reported previously. This study investigates the neuroprotective effect of carnosine on the olfactory bulb in a mice model of vanadium inhalation. Male mice were divided into four groups: vanadium pentoxide (V₂O₅) [0.02 mol/L] inhalation for one hour twice a week; V₂O₅ inhalation plus 1 mg/kg of carnosine administered daily; carnosine only, and the control group that inhaled saline. The olfactory function was evaluated using the odorant test. Animals were sacrificed four weeks after exposure. The olfactory bulbs were dissected and processed using the rapid Golgi method; cytological and ultrastructural analysis was performed and malondialdehyde (MDA) concentrations were measured. The results showed evidence of olfactory dysfunction caused by vanadium exposure and also an increase in MDA levels, loss of dendritic spines and necrotic neuronal death in the granule cells. But, in contrast, vanadium‐exposed mice treated with carnosine showed an increase in dendritic spines and a decrease in neuronal death and in MDA levels when compared with the group exposed to vanadium without carnosine. These results suggest that dendritic spine loss and ultrastructural alterations in the granule cells induced by vanadium are mediated by oxidative stress and that carnosine may modulate the neurotoxic vanadium action, improving the olfactory function.     

Classification of anemia for gastroenterologists

Most anemia is related to the digestive system by dietary deficiency, malabsorption, or chronic bleeding. We review the World Health Organization definition of anemia, its morphological classification （microcytic, macrocytic and normocytic） and pathogenic classification （regenerative and hypo regenerative）, and integration of these classifications. Interpretation of laboratory tests is included, from the simplest （blood count, routine biochemistry） to the more specific （iron metabolism, vitamin B12, folic acid, reticulocytes, erythropoietin, bone marrow examination and Schilling test）, in the text and various algorithms, we propose a hierarchical and logical way to reach a diagnosis as quickly as possible, by properly managing the medical interview, physical examination, appropriate laboratory tests, bone marrow examination, and other complementary tests. The prevalence is emphasized in all sections so that the gastroenterologist can direct the diagnosis to the most common diseases, although the tables also include rare diseases. Digestive diseases potentially causing anemia have been studied in preference, but other causes of anemia have been included in the text and tables. Primitive hematological diseases that cause anemia are only listed, but are not discussed in depth. The last section is dedicated to simplifying all items discussed above, using practical rules to guide diagnosis and medical care with the greatest economy of resources and time.