Should Stage T2 Esophageal Squamous Cell Carcinoma Be Subclassified?

Background

In patients with esophageal squamous cell carcinoma (ESCC), pathologic examination allows T2 tumors to be further subclassified according to whether the circular or longitudinal muscle layers are invaded. Therefore, we aimed to investigate whether subclassifying the T2 stages can aid in determining the prognosis for patients with ESCC.

Methods

The clinical and pathologic characteristics of 85 ESCC patients with T2 tumors who underwent thoracoscopic esophagectomy between 2008 and 2013 were retrospectively analyzed. Univariate and multivariate analyses were performed to identify prognostic factors. The Kaplan–Meier method was used to compare survival differences with respect to each prognostic factor.

Results

Thirty-nine patients had tumors invading the circular muscle layer and were designated as having T2a disease. The remaining 46 patients had T2b disease, with tumors invading the longitudinal muscle layer. The overall 1-, 3-, and 5-year survival rates were 96.1, 53.8, and 36.4 %, respectively, with a median survival of 39.0 months. Univariate analysis indicated that sex, smoking history, grade, location, and tumor length did not significantly influence on survival. Only T stage (P = 0.017) and N stage (P = 0.003) were associated with survival. The results of multivariate Cox proportional hazard regression analysis showed that T stage (P = 0.045) and N stage (P = 0.003) were independent prognostic factors.

Conclusions

N stage and subclassified T stage are independent prognostic factors in patients with T2 tumors. Therefore, we concluded that T2 tumors can be subclassified further into T2a and T2b stages, and patients with different T2 stages may have different prognoses.     

Green tea polyphenols protect spinal cord neurons against hydrogen peroxide-induced oxidative stress

Green tea polyphenols are strong antioxidants and can reduce free radical damage. To investigate their neuroprotective potential, we induced oxidative damage in spinal cord neurons using hydrogen peroxide, and applied different concentrations(50–200 μg/mL) of green tea polyphenol to the cell medium for 24 hours. Measurements of superoxide dismutase activity, malondialdehyde content, and expression of apoptosis-related genes and proteins revealed that green tea polyphenol effectively alleviated oxidative stress. Our results indicate that green tea polyphenols play a protective role in spinal cord neurons under oxidative stress.     

通心络胶囊治疗高血压合并肾损害患者的疗效观察

目的：观察通心络胶囊治疗高血压合并肾损害患者的疗效。方法；将60例高血压合并肾损害患者随机均分成治疗组（A组）和对照组（B组），A组患者接受通心络胶囊每次3片，每天3次。连续16周。两组病人均联合应用降压药治疗。治疗前后查血糖、血脂、BUN、Cr、24h尿蛋白定量，并作对比。结果；两组病人治疗前后血糖、血脂无变化（P〉0．05）。两组病人治疗后血压均显著低于治疗前（P〈0．05），但组间比较无显著性差异。B组治疗后24h尿蛋白定量有一定程度减少，但无统计学差异（P〉0．05）。A组治疗后24h尿蛋白定量显著低于治疗前（P〈0．05）。两组BUN、Cr均有降低，但组问比较无统计学差异。结论：通心络胶囊能改善肾血管内皮功能，从而能使高血压肾损害患者的尿蛋白减少。     

Structure–function relationship between Bruch’s membrane opening-minimum rim width and perimetry in open-angle glaucoma subtypes

Graefe's Archive for Clinical and Experimental Ophthalmology - To seek the threshold value of Bruch’s membrane opening-minimum rim width (BMO-MRW) where visual field (VF) damage occurs in...     

A myofibroblast–mast cell–neuropeptide axis of fibrosis in post‐traumatic joint contractures: An in vitro analysis of mechanistic components

Previous studies have implicated a myofibroblast–mast cell–neuropeptide axis of fibrosis in pathologic joint capsules from post‐traumatic contractures. The hypothesis to be tested is that joint capsule cells (JC) from human elbows with post‐traumatic contractures and their interactions with mast cells (MC) and neuropeptides in the microenvironment underlie the pathogenesis of contractures. The hypothesis was tested using an in vitro collagen gel contraction model. The JC were isolated from human elbow capsules and mixed with neutralized PureCol collagen I. The gels were treated in various ways, including addition of MC (HMC‐1), the neuropeptide substance P (SP), an NK₁ receptor (SP receptor) antagonist RP67580 and the mast cell stabilizer ketotifen fumarate (KF). The collagen gels were released from the wells and gel size (contraction) was measured optically at multiple time points. The JC contracted collagen gels in a dose‐dependent manner. This was enhanced in the presence of MC and increased further with SP. Increasing concentrations of the SP receptor antagonist, RP67580 or the mast cell stabilizer, KF decreased the magnitude of contraction. These observations identify putative mechanistic components of a myofibroblast–mast cell–neuropeptide axis of fibrosis in the joint capsules in post‐traumatic contractures and potential prophylactic or therapeutic interventions. © 2014 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 32:1290–1296, 2014.     

Inhibition of Cathepsin K Increases Modeling‐Based Bone Formation,and Improves Cortical Dimension and Strength in Adult Ovariectomized Monkeys

Treatment with the cathepsin K (CatK) inhibitor odanacatib (ODN) protects against bone loss and maintains normal biomechanical properties in the spine and hip of ovariectomized (OVX) preclinical models. Here, we characterized the effects of ODN on the dynamics of cortical modeling and remodeling, and dimension and strength of the central femur in adult OVX‐rhesus monkeys. Animals were treated with vehicle or ODN (6 or 30 mg/kg, once per day [q.d., p.o.]) in prevention mode for 21 months. Calcein and tetracycline double‐labeling were given at 12 and 21 months, and the femoral cross‐sections were subjected to dynamic histomorphometric and cement line analyses. ODN treatment significantly increased periosteal and endocortical bone formation (BFR/BS), accompanied with an increase in endocortical mineralizing surface (102%, p < 0.01) with the 6 mg/kg dose. ODN at both doses reduced remodeling hemiosteon numbers by 51% and 66% (p < 0.05), respectively, and ODN 30 mg/kg numerically reduced activation frequency without affecting wall thickness. On the same endocortical surface, ODN increased all modeling‐based parameters, while reducing intracortical remodeling, consistent with the observed no treatment effects on cortical porosity. ODN 30 mg/kg markedly increased cortical thickness (CtTh, p < 0.001) and reduced marrow area (p < 0.01). Lastly, ODN treatment increased femoral structural strength (p < 0.001). Peak load was positively correlated with the increases in bone mineral content (BMC) (r² = 0.9057, p < 0.0001) and CtTh (r² = 0.6866, p < 0.0001). Taken together, by reducing cortical remodeling‐based and stimulating modeling‐based bone formation, ODN significantly improved cortical dimension and strength in OVX monkeys. This novel mechanism of CatK inhibition in stimulating cortical formation suggests that ODN represents a novel therapeutic approach for the treatment of osteoporosis. © 2014 American Society for Bone and Mineral Research.     

阿朴吗啡神经保护作用的途径：随机对照动物实验

目的：观察急性注射10 mg/kg R-阿朴吗啡后的神经保护作用.方法：实验于2004-06/2005-03在武装警察部队总医院完成.结合微量透析法,26只Wistar大白鼠急性皮下注射阿朴吗啡10 mg/kg,通过水杨酸钠诱捉法来清除6-羟基多巴胺或1-甲基-4-苯基吡啶离子产生的羟自由基.透析液的2,3-双羟基安息香酸含量用高效液相色谱电化学法检测.结果：26只大鼠均进入结果分析.6-羟基多巴胺或氧化产物干预2,3-双羟基安息香酸形成,这种显著增加持续到整个试验.6-羟基多巴胺灌注3 h后,仍达基线值（180.9 nmol/L）的350%.在1-甲基-4-苯基吡啶离子（5mmol/L）灌注中,2,3-双羟基安息香酸水平降低和持续增加到基线值（50.8 nmol/L）的160%,显著增加透析液中2,3-双羟基安息香酸水平.结论：急性注射阿朴吗啡,不能清除6-羟基多巴胺或1-甲基-4-苯基吡啶离子产生的羟自由基,说明阿朴吗啡神经保护的作用不是通过抗羟自由基作用.