睾丸大细胞钙化性支持细胞瘤一例

患者男．25岁。双侧睾丸肿大半年余,伴咳嗽、咳痰和发热于2005年3月入院。体检：双侧睾丸上极均触及无痛性硬肿物,大小分别约1．5cm×1．5cm和0．5cm×0．2cm,可活动,与周围组织无粘连．既往无睾丸外伤史,无体态及毛发的改变。无明显内分泌疾病症状和体征。手术切除双侧睾丸肿物,病理检查：两块肿物组织境界清楚,直径分别约1．5cm和0．5cm。切面为黄白色带有分散的钙化点,切开时有沙砾感.未见包膜的浸润．也无出血和坏死灶。镜下观察：肿瘤内钙化十分显著,瘤细胞排列呈小梁状、小管状和实体性区域,呈巢状分布（图1）。间质部分为疏松的黏液样基质,部分为纤维性间质,伴有形状不规则的钙化灶（图2）。瘤细胞胞体和细胞核均较大,可见明显的核仁和丰富的嗜酸性胞质。胞质内可见不规则的深红染小体样结构。核分裂象罕见。瘤细胞问可见少量淋巴细胞浸润。未见包膜和血管浸润．也未见Reinke结晶和脂褐素沉积。免疫组织化学染色示瘤细胞S-100蛋白和α-抑制素弥漫强阳性（图3,4）,波形蛋白阳性。但平滑肌肌动蛋白（SMA）、细胞角蛋白（CK）、甲胎蛋白（AFP）、Ki-67阴性。     

急性肾梗死临床诊治分析

目的探讨急性肾梗死的临床特点、鉴别诊断及治疗要点。方法对本院收治的2例急性肾梗死的临床资料进行回顾性分析。结果1例表现为无痛性全程肉眼血尿,腹部CT平扫及强化提示左肾实性占位,考虑肾癌,经手术治疗确诊;另1例表现为左腰部胀痛不适,在外院按输尿管结石予抗感染、解痉治疗无效,后于本院行腹部B超、强化CT检查诊断为急性右肾后下部梗死,予尿激酶、静脉滴注溶栓治疗,同时予抗凝、抗感染、扩血管、止痛等对症治疗,症状逐渐治愈出院。结论急性肾梗死临床少见,且表现也各不相同,对临床表现可疑者,及时行相关检查以尽早诊治。     

人股骨头坏死微观结构及成骨、破骨细胞活性的区域性分布特征

 目的 比较人股骨头坏死标本不同区域的骨微观结构及成、破骨细胞活性。方法 收集2011年3月至2013年5月行全髋关节置换的非创伤性股骨头坏死患者术后的股骨头标本10例（Ficat Ⅳ期）,男6例,女4例;年龄40～57岁,平均47.7岁。Micro-CT扫描后,根据影像学识别骨质密度不同,将每个标本分为软骨下骨区、坏死区、硬化区、健康区,通过病理学检测、纳米压痕、实时荧光定量PCR、免疫组化染色等方法对不同区域的骨微观结构、微观力学性能及成骨、破骨细胞活性进行比较。结果 Micro-CT结果显示,股骨头坏死标本软骨下骨区及坏死区的骨小梁连续性破坏;硬化区的骨小梁数目增多,间隙变窄;正常区域骨小梁结构完整,厚度分布均匀。软骨下骨区、坏死区、硬化区和健康区骨小梁的弹性模量分别为（13.808±4.22） GPa、（13.999±3.816） GPa、（17.266±3.533） GPa和（11.927±1.743） GPa;硬度分别为（0.425±0.173） GPa、（0.331±0.173） GPa、（0.661±0.208） GPa和（0.423±0.088） GPa。抗酒石酸酸性磷酸酶（Trap）染色结果显示,软骨下骨区和坏死区可见Trap染色阳性细胞,硬化区及健康区未见Trap染色阳性细胞。免疫组化染色结果显示,骨形成相关因子Runx2和BMP2在硬化区及健康区表达高于其他区域;骨吸收相关因子RANK和RANKL在软骨下骨区及坏死区表达高于其他区域。结论 股骨头坏死塌陷过程中,骨微观结构发生明显改变,而坏死区骨小梁微观力学强度较健康区无显著降低。股骨头坏死标本中软骨下骨区及坏死区破骨细胞活性增强,硬化区成骨细胞活性增强。     

In Healthy Adults,Biological Activity of Vitamin D,as Assessed by Serum PTH,Is Largely Independent of DBP Concentrations

Vitamin D insufficiency, as measured by 25‐hydroxyvitamin D (25[OH]D) levels, has been associated with important health outcomes. The majority of vitamin D in circulation is bound to vitamin D–binding protein (DBP) and albumin, and recent genetic studies have demonstrated that serum DBP is a major determinant of 25(OH)D concentrations in adults. The impact of circulating DBP levels on vitamin D's biologic action, is unclear, but is of particular relevance to vitamin D epidemiology, because a lack of control for DBP levels could strongly influence the association of vitamin D with disease. Serum parathyroid hormone (PTH) levels can act as a biological readout of 25(OH)D activity. We therefore assessed the relationship between serum total and free 25(OH)D and PTH with and without adjusting for DBP, in 2073 subjects of European descent. Total 25(OH)D levels correlated positively (r = 0.19, p = 1.8 × 10^?17) with DBP, whereas the free 25(OH)D correlated negatively (r = ?0.14, p = 5.0 × 10^?12). Total and free 25(OH)D levels correlated negatively with PTH (r = ?0.29, p = 1.3 × 10^?39; r = ?0.26, p = 1.9 × 10^?33, respectively). Including age, body mass index (BMI), sex, estimated glomerular filtration rate, calcium, and season of blood draw as covariates, total 25(OH)D levels were significantly associated with log‐transformed PTH (lnPTH) levels (linear term: β = ?0.010, p < 0.0001, squared term: β = 0.00004, p < 0.0001) and this association was not changed by adjusting for DBP. These findings provide evidence that in a largely vitamin D–sufficient cohort, the biological effect of vitamin D on PTH levels is mainly independent of DBP concentration. Accordingly, this study may provide useful information for studies investigating the relationship between vitamin D, DBP, and disease. © 2014 American Society for Bone and Mineral Research.     

Oxidative stress increased hepatotoxicity induced by nano‐titanium dioxide in BRL‐3A cells and Sprague–Dawley rats

Extensive studies have shown that titanium dioxide (TiO₂) nanomaterials (NMs) can cause toxicity in vitro and in vivo under normal conditions. However, an adverse effect induced by nano‐TiO₂ in many diseased conditions, typically characterized by oxidative stress (OS), remains unknown. We investigated the toxicity of nano‐TiO₂ in rat liver cells (BRL‐3A) and Sprague–Dawley (SD) rat livers under OS conditions, which were generated using hydrogen peroxide (H₂O₂) in vitro and alloxan in vivo, respectively. In vitro results showed that cell death ratios after nano‐TiO₂ exposure were significantly enhanced (up to 2.62‐fold) in BRL‐3A cells under OS conditions, compared with normal controls. Significant interactions between OS conditions and nano‐TiO₂ resulted in the rapid G0/G1 to S phase transition and G2/M arrest, which were opposite to G0/G1 phase arrest in cells after NMs exposure only. In vivo results showed that obvious pathological changes in rat livers and the increased activities of four enzymes (i.e. aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase and alkaline phosphatase) owing to liver damage after nano‐TiO₂ exposure under OS conditions, compared with their healthy controls. In addition, compared with increased hepatotoxicity after nano‐TiO₂ exposure, micro‐TiO₂ showed no adverse effects to cells and rat livers under OS conditions. Our results suggested that OS conditions synergistically increase nano‐TiO₂ induced toxicity in vitro and in vivo, indicating that the evaluation of nanotoxicity under OS conditions is essentially needed prior to various applications of NMs in foods, cosmetics and potential treatment of diseases. Copyright © 2013 John Wiley & Sons, Ltd.     

吗替麦考酚酯联合泼尼松治疗老年难治性肾病综合征观察

目的：观察吗替麦考酚酯治疗老年难治性肾病综合征的疗效及安全性。方法： 老年难治性肾病综合征患者69例随机分为观察组和对照组。在口服泼尼松0.5mg·kg^-1·d^-1治疗基础上,观察组联用吗替麦考酚酯,对照组联用环磷酰胺,进行1年的随访。观察两组患者治疗前,治疗后6、12个月时24 h尿蛋白定量、血清白蛋白、血肌酐的变化情况,并记录两组药品不良反应发生情况。结果：治疗12月后,吗替麦考酚酯组24 h尿蛋白定量较环磷酰胺组明显下降（P=0.021）、血清白蛋白明显升高（P=0.039）。治疗12月后,吗替麦考酚酯组总有效率为77.14%;环磷酰胺组总有效率为52.94%。吗替麦考酚酯组较环磷酰胺组疗效明显（P=0.041）。结论：吗替麦考酚酯联合小剂量激素可有效治疗老年难治性肾病综合征,且不良反应小。     

Quantifying the Severity of a Delirium Episode Throughout Hospitalization: the Combined Importance of Intensity and Duration

Background

The ability to determine which episodes of delirium are likely to lead to poor clinical outcomes has remained a major area of challenge.

Objective

To quantify delirium severity and course over an entire hospitalization using several measures, and to evaluate their predictive validity for 30- and 90-day outcomes post-discharge.

Design

Two prospective cohort studies.

Participants

Analysis was conducted in two independent cohorts of adult patients aged ≥70.

Main Measures

Nine delirium episode severity measures were examined: (1) measures reflecting delirium intensity (peak Confusion Assessment Method-Severity [CAM-S] and mean CAM-S score), (2) a measure reflecting delirium intensity and duration (sum of all CAM-S scores, sum of all CAM-S scores on delirium days only, peak CAM-S score x days with delirium), (3) measures requiring information on delirium duration and delirium at discharge (total number of delirium days, percentage of delirium days, delirium at discharge), and (4) a measure of cognitive change. Associations of the delirium episode severity measures with 30- and 90-day post-hospital outcomes (death, nursing home placement, and readmission) relevant to delirium were examined.

Key Results

The delirium episode severity measure that required information on both delirium intensity and duration (sum of all CAM-S scores) was the most strongly associated with 30- and 90-day post-hospital outcomes. Using this measure, the relative risk [95 % confidence interval] for death at 30-days increased across levels of sum of all CAM-S scores from 1.0 (referent) to 2.1 [0.8, 5.4] for ‘low,’ to 2.9 [1.2, 7.1] for ‘moderate,’ to 6.4 [2.9, 14.0] for ‘high’ (p for trend <.01).

Conclusions

The delirium episode severity measure that included both intensity and duration had the strongest association with important post-hospital outcomes.