造血干细胞移植病人极期阴囊处皮肤损伤的护理

白细胞是人体防御细菌入侵的重要防线,中性粒细胞占白细胞总数50%～70%,机体抵御病原体,特别是处于化脓性细菌入侵的第一线,是一道天然免疫屏障。病人极期白细胞及中性粒细胞计数持续下降,一般有头晕、乏力、四肢酸软、食欲减退、低热、失眠或极度衰弱等非特异性症状[1,2]。尤其是病人虚弱多汗,阴囊处皮肤的特性及经钴60全身照射对皮肤的特异性损害,导致阴囊处发生皮肤损伤的几率增加。此期病人易发生     

白藜芦醇对人角膜上皮细胞炎症和氧化应激损伤的保护作用

目的：探讨白藜芦醇(RSV)对人角膜上皮细胞(HCECs)炎症和氧化应激损伤的保护作用。

方法：用肿瘤坏死因子-α(TNF-α)诱导HCECs发生炎症反应，设对照组、TNF-α组、RSV+TNF-α组； 用H₂O₂诱导HCECs发生氧化应激反应，设正常组、H₂O₂组、RSV+H₂O₂组。采用MTT法检测细胞活力； RT-qPCR及酶联免疫吸附测定(ELISA)法检测相关炎症因子IL-1、IL-6、IL-8的表达； 免疫荧光染色法及Western blot法检测核因子-κB p65(NF-κB p65)的核转位； 2''，7''-二氯荧光黄双乙酸盐(DCFH-DA)荧光探针法检测细胞内活性氧(ROS)水平。

结果：在HCECs炎症反应中，RT-qPCR及ELISA结果均显示，与对照组相比，TNF-α组的HCECs IL-1、IL-6、IL-8的表达水平均显著升高。RSV预处理细胞后，以上指标较TNF-α组显著下降； 免疫荧光染色及Western blot结果均显示，TNF-α组NF-κB p65核转位增加，而RSV预处理细胞后NF-κB p65核转位受到抑制。在HCECs氧化应激反应中，MTT和DCFH-DA荧光探针染色结果分别显示，H₂O₂刺激使HCECs活力显著下降，HCECs内ROS的产生增多。而RSV 预处理后，细胞活力显著上升，且RSV抑制了H₂O₂诱导的HCECs内ROS的产生。

结论：RSV对HCECs的炎症和氧化应激反应具有抑制作用，RSV通过抑制NF-κB通路激活以抑制炎症反应。     

Extraskeletal osteosarcoma of penis: A case report

Extraskeletal osteosarcoma (EOS) is rare and commonly arises in the retroperitoneum, limbs, head and neck. There is no significant difference between EOS and other malignant tumors in soft tissue. Localized pain and swelling are the common presenting symptoms. Clinical diagnosis of EOS is difficult, imaging techniques may be helpful and careful, and the histopathological analysis is necessary. The common histological variants of EOS include: osteoblastoma, chondroblastoma, and fibroblastoma, and other unusual subtypes were reported occasionally. It should be distinguished with myositis ossificans, malignant mesenchymoma, giant cell tumor and parosteal osteosarcoma. We present an EOS arising in the penis. The primary site and histological category of the tumor were extremely rare. We hope the case will be helpful to the recognition of clinical signs, iconography and histopathology of EOS.     

The protective effect of melatonin on smoke‐induced vascular injury in rats and humans: a randomized controlled trial

Smoking is one of the most harmful lifestyles in the world. Very few studies have investigated the effects of melatonin in smoke‐induced vascular injury. This study was designed to investigate whether melatonin could protect rats and humans from smoke‐induced vascular injury. 32 male rats and a double‐blind randomized controlled trial (RCT) containing 63 participants formed the subjects of this study. In rats, 10 mg/kg of melatonin was intraperitoneally injected. Blood samples and abdominal artery were harvested two weeks later. Melatonin decreased the expression of platelet endothelial cell adhesion molecule‐1 (CD31), intercellular adhesion molecule‐1 (ICAM‐1), vascular cell adhesion molecule‐1 (VCAM‐1) and endothelin‐1 (ET‐1) compared with the smoke exposed group (P < 0.05), whereas endothelial nitric oxide synthase (eNOS), nuclear erythroid 2‐related factor 2 (Nrf2), NAD(P)H quinone oxidoreductase 1 (NQO‐1), catalytic glutamate cysteine ligase (GCLC) and heme oxygenase‐1 (HO‐1) recovered markedly (P < 0.05). In humans, 3 mg/day of melatonin was taken orally by the participants. Blood samples were drawn at baseline and after two weeks of treatment. Compared with the oral placebo group, melatonin decreased the concentration of fibrinogen (Fbg) (P = 0.04) and free fatty acids (FFA) (P = 0.04) in smokers, along with the decreased expression of ICAM‐1, VCAM‐1 and ET‐1 (P = 0.004, P = 0.001, P < 0.0001, respectively). In contrast, Nrf2 and HO‐1 expression were markedly increased (P = 0.0001, P = 0.0049, respectively) after smokers took melatonin orally. In summary, our present data suggest that melatonin could ameliorate smoke‐induced vascular injury.     

Day-to-Day Variation in Food Intake and Energy Expenditure in Healthy Women: The Dietitian II Study

Because day-to-day food intake varies, we tested the hypothesis that ad libitum food intake and energy expenditure show corrective responses over periods of 1 to 10 days in healthy young women. Food intake and accelerometry measurements were collected daily for 17 days in 15 young women. Total daily energy expenditure (TDEE) using doubly labeled water was also measured. The daily deviations in macronutrient and energy intake and energy expenditure from the average values were compared with the deviations observed over succeeding intervals to estimate the corrective responses. The intraindividual coefficients of variation for energy intake averaged ±25%, ranging from 16% to 34%. TDEE had a coefficient of variation of 8.3%, and accelerometry had a coefficient of variation of 8.4% (range=4.6% to 16.4%). Energy expenditure by accelerometry (2,087±191 kcal/day) was not significantly different from TDEE (2,128±177 kcal/day), but reported daily energy intake was 20.4% lower (1,693±276 kcal/day). There were significant corrective responses in energy from fat and total energy intake. This occurred from Days 3 to 6, with a peak at Day 5 that disappeared when data were randomized within each subject. Human beings show corrective responses to deviations from average energy and macronutrient intakes with a lag time of 3 to 6 days, but not 1 to 2 days. These corrective responses are likely to play a role in bringing about weight stability.