早期实施肠道内营养支持干预对ICU禁食危重患者营养状态和预后影响

目的探讨早期实施肠内营养支持干预对ICU禁食危重患者营养状态及预后的影响。方法选取2016年5月～2017年5月我院ICU收治的禁食危重患者87例,按随机数字表法分为观察组和对照组,其中观察组44例于入院24～48h内实施肠道内营养支持干预,对照组43例于入院49～72h后实施肠内营养,观察比较两组患者的营养指标及预后情况。结果观察组患者的血清前清蛋白、血清白蛋白、转铁蛋白均高于对照组,APACHEⅡ评分、死亡率低于对照组,差异均有统计学意义(P0.05)。结论早期实施肠内营养支持干预可有效改善ICU禁食危重症患者营养状态,降低死亡率,利于患者预后,值得临床推广。     

危重症患者预后的危险因素及相关指标的预后预测价值分析

目的:探讨危重症患者预后的危险因素,并分析相关指标对患者预后的预测价值。方法:对2016年4月至2018年4月上海交通大学附属第六人民医院救治的5585例ICU危重症患者病例进行回顾性分析,收集患者一般资料、初始乳酸水平、24 h乳酸水平、24 h乳酸清除率以及APACHEII评分等,采用多因素logistic回归分析危重症患者预后的影响因素,ROC曲线评估多项指标预测患者预后的价值。结果:共纳入1465例危重症患者,多因素logistic回归分析显示,住ICU平均时间长、APACHEII评分高、初始乳酸水平大于4 mmol/L、24 h乳酸清除率低、术后肾功能异常是危重症患者住院期间死亡的危险因素(P0.05),24 h乳酸清除率、APACHEII评分及初始乳酸水平三者联合评估预测患者住院死亡率的ROC曲线下面积(ROC-AUC)为0.900,高于单独检测。结论:住ICU时间、APACHEII评分、初始乳酸水平、24 h乳酸清除率、术后肾功能是危重症患者住院期间死亡的影响因素,初始乳酸水平、24 h乳酸清除率和APACHEII评分联合使用可以更好地预测危重症患者的短期预后。     

个体化营养支持对肺结核患者的影响

目的探讨个体化营养支持对肺结核患者的影响。方法将100例肺结核患者随机分为对照组和干预组各50例,对照组按照肺结核护理常规进行护理及自行饮食,干预组在肺结核护理常规基础上给予个体化营养支持干预,30天后观察比较两组患者护理干预前后身体质量指数和营养风险指数。结果个体化营养支持干预后,患者身体质量指数、NRI值均优于对照组,差异有统计学意义(P0.01)。结论个体化营养支持干预能有效改善肺结核患者的营养状况,对结核病的预后具有积极促进的作用。     

APACHEⅡ评分联合动脉血乳酸水平对危重症产妇预后的预测价值分析

摘要 目的：探讨急性生理学与慢性健康状况评分系统Ⅱ（APACHEⅡ）评分联合动脉血乳酸水平对危重症产妇预后的预测价值。方法：选取2019年3月至2022年3月期间上海市第一妇婴保健院收治的危重症产妇84例,根据住院期间危重症产妇的生存预后情况将其分为预后良好组（n=74）及预后不良组（n=10）。所有纳入本研究的危重症产妇均于入院24 h内完成APACHEⅡ评分评估;对所有危重症产妇应用动脉血气分析仪测定其动脉血乳酸水平。对比两组危重症产妇APACHEⅡ评分及动脉血乳酸水平;采用Pearson相关系数分析危重症产妇APACHEⅡ评分与其动脉血乳酸水平的相关性;单因素、多因素Logistic回归分析危重症产妇预后不良的危险因素;采用受试者工作特征（ROC）曲线分析APACHEⅡ评分、动脉血乳酸水平单项指标及联合检测对危重症产妇预后的预测效能。结果：预后不良组APACHEⅡ评分、动脉血乳酸水平均高于于预后良好组（P＜0.05）。采用Pearson相关系数分析显示,危重症产妇APACHEⅡ评分与其动脉血乳酸水平呈正相关（P＜0.05）。多因素Logistic回归分析显示年龄≥35岁、孕前体质指数（BMI）≥25 kg/m²、剖宫产、产后并发心力衰竭、高APACHEⅡ评分、动脉血乳酸水平升高是危重症产妇预后不良的危险因素（P＜0.05）。ROC曲线分析显示,APACHEⅡ评分、动脉血乳酸水平联合检测的预测效能高于单项指标检测。结论：危重症产妇动脉血乳酸水平随着APACHEⅡ评分升高而升高,两者呈正相关关系。高APACHEⅡ评分、动脉血乳酸水平升高是影响危重症产妇预后不良的危险因素,联合检测上述两项指标对危重症产妇预后的预测价值较高。     

营养支持小组对临床维持性血液透析患者营养状况的影响

目的：研究营养支持小组对临床维持性血液透析患者一般营养状况的影响及应用价值。方法：选择武汉大学中南医院收治的进行维持性血液透析患者共180例纳入研究,随机分为观察组和对照组,对照组患者给予常规营养支持,观察组在此基础上由专业的营养支持小组为患者提供专业化营养支持;分析两组患者的营养状况。结果：两组干预前相关指标无统计学差异,干预后观察组患者营养指标明显优于干预前和对照组干预后,差异显著（P＜0.05）。SGA评价结果显示观察组营养状况良好者比例明显高于对照组,差异有统计学意义（P＜0.05）。结论：临床应用专业的营养支持为维持性血液透析患者提供营养支持,可改善患者营养不良情况,促进患者营养全面提升,具有积极临床意义。     

重型颅脑损伤患者早期营养支持的研究进展

<正>重型颅脑损伤患者的病情危急且有不同程度意识障碍,死残率较高。重型颅脑损伤患者由于住院时间长,且不能自行进食,胃肠外营养不能完全满足患者的能量及各种营养成分的需要,因此早期行肠内营养支持治疗是关键环节之一。而及时、合理的营养支持对患者的苏醒、减少并发症发生、提高免疫功能及促进脑功能恢复等有重要意义~([1])。而早期营养支持方案的选择对重型颅脑损伤患者预后也至关重要~([2])。本文就重型颅脑损伤患者早期营养支持研究进展综述如下。1重型颅脑损伤患者早期营养支持的目的     

APACHE Ⅳ和APACHE Ⅱ预测危重症患者预后的比较性研究

目的:比较不同版本的急性生理和慢性健康评分(Acute Physiology And Chronic Health Evaluation,APACHE)(APACHE Ⅳ和APACHE Ⅱ)对于成人危重症患者预后评估的应用价值。方法:收集2011年1月至10月入住我院重症监护病房患者的临床资料,分别计算其入ICU24小时内的APACHE Ⅳ和APACHE Ⅱ评分,并计算其各自预测病死率,通过标准化死亡率(StandardizedMortality Ratios,SMR)来比较这两个评分系统对危重症患者预后评估的准确性。结果:本研究共纳入184例患者,死亡率为41.8%。APACHE Ⅱ得分为25±8分,预测死亡率为53.31%;APACHE Ⅳ得分为93±24分,预测死亡率为30.76%。APACHEⅡ预测死亡率比实际死亡率高(SMR为0.78,95%CI 0.614～0.972);APACHEⅣ预测死亡率比实际死亡率低(SMR=1.35,95%CI1.066～1.688)。但二者对于危重症患者死亡率的预测没有统计学差异(P>0.05)。结论:APACHE Ⅱ和APACHE Ⅳ对于危重症患者死亡率预测准确性高;与APACHE Ⅱ相比,APACHE Ⅳ无表现出更为优越的性能,二者之间的差异不存在统计学意义。     

APACHEIV和APACHEII预测危重症患者预后的比较性研究

目的：比较不同版本的急性生理和慢性健康评分（Acute Physiology And Chronic Health Evaluation,APACHE）（APACHEⅣ和APACHEⅡ）对于成人危重症患者预后评估的应用价值。方法：收集2011年1月至10月入住我院重症监护病房患者的临床资料,分别计算其入ICU24小时内的APACHEⅣ和APACHEII评分,并计算其各自预测病死率,通过标准化死亡率（Standardized Mortality Ratios,SMR）来比较这两个评分系统对危重症患者预后评估的准确性。结果：本研究共纳入184例患者,死亡率为41．8％。APACHEII得分为25±8分,预测死亡率为53．31％;APACHEⅣ得分为93±24分,预测死亡率为30．76％。APACHEII预测死亡率比实际死亡率高（SMR为0．78,95％CI0．614-0．972）;APACHEIV预测死亡率比实际死亡率低（SMR=1.35,95％CI1．066-1．688）。但二者对于危重症患者死亡率的预测没有统计学差异（P〉0．05）。结论：APACHEII和APACHEIV对于危重症患者死亡率预测准确性高;与APACHEII相比,APACHEIV无表现出更为优越的性能,二者之间的差异不存在统计学意义。     

呼吸科危重症患者应用高脂低糖肠内营养的疗效

目的：观察应用高脂低糖肠内营养对改善呼吸科危重症患者营养状况及呼吸功能的价值。方法：选取就诊于我院呼吸科的106例危重症患者,按就诊顺序分为对照组和观察组,每组53例,对照组患者给予常规营养液肠内营养支持治疗,观察组患者给予高脂低糖肠内营养液支持治疗。观察两组患者治疗后第7天和第14天的血清白蛋白、清蛋白、转铁蛋白的水平变化,免疫功能及肱二头肌皮褶厚度、上臂肌围的变化情况,营养支持前后CO2生成量、氧耗量及氧合指数等呼吸功能指标。结果：观察组患者治疗后第7天和第14天的血清白蛋白、清蛋白、转铁蛋白的水平及免疫功能明显高于对照组,差异具有统计学意义（P<0.05）,观察组患者肱二头肌皮褶厚度、上臂肌围的改善情况优于对照组（P<0.05）,观察组患者的CO2生成量、氧耗量及氧合指数均优于对照组（P<0.05）。结论：高脂低糖肠内营养治疗呼吸科危重症患者,对改善营养指标及呼吸功能具有重要意义,可以作为呼吸科重症患者的一种营养方法。     

静脉补充鱼油脂肪乳对呼吸科ICU患者炎症反应治疗作用观察

目的：探讨静脉补充鱼油脂肪乳对呼吸科ICU患者炎症反应的治疗作用。方法：选取在新桥医院呼吸科重症ICU住院并行IMV呼吸机辅助呼吸患者55例,分为2组,试验组26例、对照组29例,除采用常规治疗外,2组均采用等氮等热量肠内营养结合静脉营养给予营养支持,试验组患者给予肠内营养联合添加鱼油脂肪乳静脉营养支持,对照组给予肠内营养联合未添加鱼油脂肪乳静脉营养支持。两组患者分别在使用营养支持前1天和支持后第6天检测炎症反应指标C反应蛋白（CRP）水平,肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）水平,记录患者入住ICU时间、机械通气天数。结果：2组患者手术前 CRP、TNF-α、IL-6无显著性差异（P＞0.05）。使用营养支持后第6天试验组炎症反应指标CRP、TNF-α、IL-6浓度显著低于对照组,有统计学差异（P＜0.05）,机械通气时间明显缩短（P＜0.05）、入住ICU时间无统计学差异（P>0.05）。结论：鱼油脂肪乳能够改善呼吸系统危重症患者的炎症反应,并有益于缩短机械通气天数。     

Role for dopamine in malonate-induced damage in vivo in striatum and in vitro in mesencephalic cultures

Defects in mitochondrial energy metabolism have been implicated in the pathology of several neurodegenerative disorders. In addition, the reactive metabolites generated from the metabolism and oxidation of the neurotransmitter dopamine (DA) are thought to contribute to the damage to neurons of the basal ganglia. We have previously demonstrated that infusions of the metabolic inhibitor malonate into the striata of mice or rats produce degeneration of DA nerve terminals. In the present studies, we demonstrate that an intrastriatal infusion of malonate induces a substantial increase in DA efflux in awake, behaving mice as measured by in vivo microdialysis. Furthermore, pretreatment of mice with tetrabenazine (TBZ) or the TBZ analogue Ro 4-1284 (Ro-4), compounds that reversibly inhibit the vesicular storage of DA, attenuates the malonate-induced DA efflux as well as the damage to DA nerve terminals. Consistent with these findings, the damage to both DA and GABA neurons in mesencephalic cultures by malonate exposure was attenuated by pretreatment with TBZ or Ro-4. Treatment with these compounds did not affect the formation of free radicals or the inhibition of oxidative phosphorylation resulting from malonate exposure alone. Our data suggest that DA plays an important role in the neurotoxicity produced by malonate. These findings provide direct evidence that inhibition of succinate dehydrogenase causes an increase in extracellular DA levels and indicate that bioenergetic defects may contribute to the pathogenesis of chronic neurodegenerative diseases through a mechanism involving DA.     

Scurvy in capybaras bred in captivity in Argentine

In order to determine if the absence of vitamin C in the diet of capybaras (Hydrochoerus hydrochaeris) causes scurvy, a group of seven young individuals were fed food pellets without ascorbic acid, while another group of eight individuals received the same food with 1 g of ascorbic acid per animal per day. Animals in the first group developed signs of scurvy-like gingivitis, breaking of the incisors and death of one animal. Clinical signs appeared between 25 and 104 days from the beginning of the trial in all individuals. Growth rates of individuals deprived of vitamin C was considerably less than those observed in the control group. Deficiency of ascorbic acid had a severe effect on reproduction of another population of captive capybaras. We found that the decrease in ascorbic acid content in the diet affected pregnancy, especially during the first stages. The results obtained suggest that it is necessary to supply a suitable quantity of vitamin C in the diet of this species in captivity.     

Changes in lactate dehydrogenase activity in chicken tissues in hyperthyreosis in ontogenesis

The lactate dehydrogenase activity in reactions of lactate oxidation and synthesis was studied in subfractions of the chicken brain, heart and liver at the embryonal, early postembryonal and adult stages of development after thyroxine administration. It has been shown that during embryogenesis thyroxine predominantly enhanced the rate of lactate oxidation in the mitochondrial tissues. A marked increase in the lactate synthesis was found in cytoplasm of the adult chicken tissues. Specificity of enzyme activity alterations was detected in the chicken brain during ontogenesis after thyroxine administration.     

SSTR5 ablation in islet results in alterations in glucose homeostasis in mice

Somatostatin (SST) peptide is a potent inhibitor of insulin secretion and its effect is mediated via somatostatin receptor 5 (SSTR5) in the endocrine pancreas. To investigate the consequences of gene ablation of SSTR5 in the mouse pancreas, we have generated a mouse model in which the SSTR5 gene was specifically knocked down in the pancreatic beta cells (betaSSTR5Kd) using the Cre-lox system. Immunohistochemistry analysis showed that SSTR5 gene expression was absent in beta cells at three months of age. At the time of gene ablation, betaSSTR5Kd mice demonstrated glucose intolerance with lack of insulin response and significantly reduced serum insulin levels. Insulin tolerance test demonstrated a significant increase of insulin clearance in vivo at the same age. In vitro studies demonstrated an absence of response to SST-28 stimulation in the betaSSTR5Kd mouse islet, which was associated with a significantly reduced SST expression level in betaSSTR5Kd mice pancreata. In addition, betaSSTR5Kd mice had significantly reduced serum glucose levels and increased serum insulin levels at 12 months of age. Glucose tolerance test at an older age also indicated a persistently higher insulin level in betaSSTR5Kd mice. Further studies of betaSSTR5Kd mice had revealed elevated serum C-peptide levels at both 3 and 12 months of age, suggesting that these mice are capable of producing and releasing insulin to the periphery. These results support the hypothesis that SSTR5 plays a pivotal role in the regulation of insulin secretion in the mouse pancreas.