ICU患者低磷血症临床观察与思考

回顾性分析41例低磷血症患者血磷水平与同期血气分析、血浆白蛋白(ALB)、尿素氮(BUN)等因素间关系及治疗前后急性生理和慢性健康评分(APACHE)Ⅱ的变化。结果显示脓毒症组血磷降低程度最明显,该组APACHEⅡ评分及纠正低磷血症所需时间显著高于其他基础疾病组。治疗前重度低磷血症组患者血pH、BUN显著高于轻中度低磷血症组,而PaCO2及ALB则明显低于轻中度低磷血症组;治疗前重度低磷血症组与轻中度低磷血症组间APACHEⅡ评分有显著差异,而治疗后两组间差异消失。病因治疗辅以适当补磷治疗可有效纠正低磷血症。由此得出结论,脓毒症患者易继发低磷血症。危重症患者重度低磷血症的发生与机体内酸碱环境改变及感染、高分解代谢等因素有关。低磷血症程度与疾病严重程度有关,但尚不足以成为独立的预后指标。     

磷酸肌酸钠对脓毒症患者心功能保护作用研究

探讨磷酸肌酸钠对脓毒症患者心功能保护作用。选取脓毒症患者70例随机分为常规治疗组(脓毒症常规治疗)和CP组(脓毒症常规治疗基础上加用CP),观察患者入ICU 0d、3d、7d外周血BNP水平、APACHEⅡ评分及入ICU 0d、7d LVEF、LVED、CO变化。发现入ICU 3d、7d与对照组比较BNP明显下降;CP组入ICU 7d时LVEF、CO较入ICU 0d有改善,LVED虽得到改善,但无统计学意义,治疗7d后CP组LVEF、CO较常规治疗组明显改善,APACHEⅡ评分降低、病死率降低。提示在脓毒症常规治疗基础上加用磷酸肌酸钠可改善脓毒症患者心功能,降低死亡率,改善预后。     

感染性休克患者血氨基酸浓度变化的研究

本研究观察感染性休克患者血氨基酸浓度的变化及与急性生理学和慢性健康状况评估Ⅱ(APACHEⅡ)评分、多器官功能障碍(MODS)评分、血乳酸(Lac)浓度的相关性。纳入38例感染性休克患者,测定入重症加强护理病房(ICU)后氨基酸浓度并记录APACHEⅡ评分、MODS评分、血Lac及预后,比较死亡组和存活组的氨基酸浓度。入住ICU后部分氨基酸浓度出现下降或升高,但均在正常范围内。死亡组的亮氨酸、缬氨酸、色氨酸(Trp)、甲硫氨酸(Met)、半胱氨酸、谷氨酸、脯氨酸(Pro)浓度低于存活组;死亡组的苯丙氨酸(Phe)、同型半胱氨酸浓度高于存活组。Met浓度变化与APACHEⅡ、MODS评分呈正相关;Trp浓度变化与MODS评分呈正相关;Phe浓度变化与血Lac呈正相关,Pro浓度变化与血Lac浓度呈负相关。入ICU后,感染性休克患者的血氨基酸浓度出现了不同程度的波动。Met、Trp、Phe、Pro浓度与APACHEⅡ评分、MODS评分、血Lac具有相关性。     

早期目标血糖管理下严重脓毒症患者HMGB1的变化及其临床意义

探讨早期目标血糖管理对严重脓毒症患者HMGB1变化的影响.严重脓毒症患者随机分为血糖控制A（4.4mmol/L~6.1mmol/L）、B（6.2mmol/L~8.3mmol/L）、C（8.4mmol/L~10.0mmol/L）三组.给予早期目标血糖管理,入ICU后0d、1d、3d、5d、7d采血测TNF-α、HMGB1浓度.三组TNF-α、HMGB1浓度及APACHEⅡ评分均呈下降趋势,A组HMGB1浓度及APACHEⅡ评分在第7d较B、C组明显降低（P＜0.05）.A组28d病死率较B、C组降低（P＆gt;0.05）.严重脓毒症患者在早期目标血糖管理下,显著降低HMGB1浓度,降低病死率和改善预后,HMGB1可用来评价脓毒症的严重程度及预后.     

B型尿钠肽前体N末端对全身性感染患者预后评价价值

探讨B型尿钠肽前体N末端(NT-proBNP)在全身性感染患者预后评价方面的价值,及其与APACHEⅡ评分在全身性感染患者的相关性.选取全身性感染患者32例.以28天随访结果,根据其转归分为存活组24例和死亡组8例.分别在确诊后Oh、72h采血行NT-proBNP检测,并采集数据进行APACHE Ⅱ评分.结果显示死亡组NT-proBNP(Oh)[(5 463.75±4 152.3)ng/L]明显高于存活组[(839.45±1 132.0)ng/L](P=0.016),72h后死亡组NT-proBNP[(5 676.1±3 937.4)ng/L]依然高于存活组[(843.5±866.3)ng/L](P=0.017).NT-proBNP(Oh)、NT-proBNP(72h)(P<0.05)是病死率的独立影响因素.经过对数转换的NT-proBNP(Oh)与APACHEⅡ评分明显相关(r=0.73,P<0.001).由此可见,NT-proBNP与病死率及APACHEⅡ评分呈显著正相关关系,可以作为一种常规临床检测指标来判断全身性感染患者的预后.     

重症急性胰腺炎并发急性呼吸窘迫综合征危险因素的分析

为了探讨重症急性胰腺炎(SAP)并发急性呼吸窘迫综合征(ARDS)的危险因素,回顾性分析了我院76例SAP患者入1CU时的年龄、血糖、APACHEⅡ评分等17项指标,根据是否合并ARDS对各项指标进行单因素及多因素Logistic回归分析.单因素分析显示两组在年龄、呼吸频率、血糖、感染、APAcHEⅡ评分、Ranson评分、CT评分、ICU住院日方面差异有显著性(P<0. 05),多因素Logistic回归分析显示年龄、血糖、感染、APACHEⅡ、Ranson、CT评分与SAP并发ARDS有关.故得出结论,年龄、血糖,感染、APACHEⅡ、Ranson与CT评分是SAP并发ARDS的独立危险因素.     

ICU患者低钙血症发生率调查与危险因素分析

筛查大连地区ICU患者早期低钙血症发生率,并分析其危险因素.选择自2010年9月14日至2010年9月30日新入大连市8家三级医院ICU的患者.入选44例患者中低钙血症患者20例,低钙血症发生率为45.4％.入选患者中全身性感染低钙血症发生率最高为61.1％,随后依次为其他疾病、心血管疾病、创伤和神经系统疾病.低钙血症的危险因素为蛋白水平、血磷水平、乳酸水平以及日照时间长短.     

ICU中机械通气患者胃肠道功能障碍与预后的关系

为了探讨重症加强治疗病房机械通气患者胃肠道功能障碍与预后的关系,回顾性分析了我院中心ICU收治的68例非胃肠道疾病且行有创机械通气治疗超过48h患者的临床资料,并将患者分为胃肠道功能障碍组和非胃肠道功能障碍组,用统计软件分析发生胃肠道功能障碍的相关临床因素及发生胃肠道功能障碍后对病死率的影响.结果显示,统计分析显示胃肠道功能障碍组和非胃肠道功能障碍组在机械通气天数、APACHE Ⅱ评分、MODS的发生率、病死率间存在明显差异.因此,对危重病患者应重视其胃肠道功能障碍的防治.     

重症急性胰腺炎并发急性呼吸窘迫综合征危险因素的分析

为了探讨重症急性胰腺炎（SAP）并发急性呼吸窘迫综合征（ARDs）的危险因素,回顾性分析了我院76例SAP患者入ICU时的年龄、血糖、APACHEⅡ评分等17项指标,根据是否合并ARDS对各项指标进行单因素及多因素Logistic回归分析。单因素分析显示两组在年龄、呼吸频率、血糖、感染、APACHEⅡ评分、Ranson评分、CT评分、ICU住院日方面差异有显著性（P〈0．05）,多因素Logistic回归分析显示年龄、血糖、感染、APACHEⅡ、Ranson、CT评分与SAP并发ARDS有关。故得出结论,年龄、血糖、感染、APACHEⅡ、Ranson与CT评分是SAP并发ARDS的独立危险因素。     

镇静与镇痛在ICU机械通气患者中的应用变化

探讨ICU内机械通气患者应用镇痛剂、镇静剂及肌松剂的情况及其对机械通气和预后的影响。回顾性分析我院中心ICU2006年、2007年收治的244例行有创机械通气治疗超过48h患者的临床资料,并将患者分为2006年组和2007年纽,用统计软件分析患者在年龄、性别、入ICU时APACHEⅡ评分、血糖、血浆白蛋白、基础疾病,气管插管时间、机械通气时间、ICU住院天数、镇痛与镇静剂应用的时间、机械通气时是否使用肌松剂、Ramsay评分及病死率方面是否存在差别。统计分析显示2006年组和2007年组在年龄、性剐、入ICU时APACHEⅡ评分、血糖、血浆白蛋白、是否使用肌松剂及基础疾病方面无差别;与2006年组相比2007年组患者气管插管时间、机械通气时间及ICU住院天数均缩短,镇痛与镇静剂应用时间均缩短,Ramsay评分降低,病死率下降。提示对机械通气的危重症患者应合理使用镇痛剂与镇静剂。     

金属蛋白酶-9（MMP-9）及其组织抑制物-1（TIMP-1）在胰腺癌中的表达

探讨MMP-9和TIMP—1在胰腺癌癌细胞及间质的表达与胰腺癌分化程度、分期之间的关系。采用免疫组织化学方法,检测MMP-9和TIMP—1在胰腺癌细胞及间质细胞的表达。MMP-9在胰腺癌细胞和间质组织中均有表达。TIMP—1主要表达在胰腺癌细胞中。MMP-9在胰腺癌间质细胞中的表达高于胰腺癌癌旁组织间质细胞,与胰腺癌的病理分级、分期呈正相关。结论认为MMP-9在胰腺癌间质细胞的表达可能参与胰腺癌的浸润和转移,对预后判断、诊断及治疗具有一定的意义。     

胰岛细胞再生研究的临床应用前景

胰岛细胞再生是治愈1型糖尿病和胰岛β细胞功能丧失的2型糖尿病的根本途径。体外再生和体内再生两种策略都是通过将干细胞或其他类型体细胞分化或转化为胰岛细胞后发挥胰岛素分泌功能,从而治疗糖尿病。基础研究显示,两者存在着各自的优势和面临的问题。胰岛细胞再生治疗的临床应用前景尚需要进一步加以考证。     

从抗原提呈细胞到抗原提呈小体

树突状细胞是体内专职抗原提呈细胞,在抗肿瘤免疫治疗中发挥重要作用。而exosome是树突状细胞分泌的一种膜性微囊小体,富含树突状细胞的MHC-I/II类分子、协同刺激分子等多种生物活性分子,亦在抗肿瘤免疫应答中发挥重要作用。从树突状细胞到exosome,是细胞性瘤苗向非细胞性瘤苗的飞跃,对免疫治疗研究产生极为深远的影响。     

胞外体认识之新进展

胞外体是由多种细胞分泌的一种膜性小囊泡,参与多种生理及病理生理过程。近年研究发现,由抗原提呈细胞分泌的胞外体富集MHCI/II类分子、协同刺激分子、热休克蛋白70~90等多种生物活性分子于一身,在体内外免疫调节中起关键作用。就胞外体的基本特征及其作为一种新型的亚细胞疫苗在抗肿瘤和抗病毒免疫中的应用前景予以综述。     

Effect of peripherally administered lipopolysaccharide (LPS) on GTP cyclohydrolase I, tetrahydrobiopterin and norepinephrine in the locus coeruleus in mice

Lipopolysaccharide (LPS), an endotoxin released from the outer membranes of Gram-negative bacteria, triggers cells to synthesize and release inflammatory cytokines that may progress to septic shock in vivo. We found that LPS enhances tetrahydrobiopterin (BH4) biosynthesis by inducing the biosynthetic enzyme GTP cyclohydrolase I (GCH) in vitro in the mouse neuroblastoma cell line N1E-115. Furthermore, we observed that gene expression of GCH in the locus coeruleus (LC) in mice was enhanced by peripheral administration of LPS, resulting in increased concentrations of BH4, and norepinephrine, and its metabolite 4-hydroxy-3-methoxyphenylglycol (MHPG). These results suggest that tyrosine hydroxylase (TH) activity is increased by increased content of BH4 due to enhanced mRNA expression of GCH in the LC resulting in the increase in norepinephrine in the LC during endotoxemia. LPS in blood may act as a stressor to increase norepinephrine biosynthesis in the mouse LC.     

Cytokine responses to LTP induction in the rat hippocampus: a comparison of in vitro and in vivo techniques

Because exogenous application of a number of cytokines and growth factors can alter synaptic properties, we sought to determine if endogenous cytokine expression is affected by neuronal activity. In addition, we examined whether cytokine expression is altered by the techniques used to stimulate and record from hippocampal neurons. Using semi-quantitative RNase protection and RT-PCR assays, we studied the expression of 18 cytokine, growth factor, and receptor genes in the hippocampus following the induction of Schaffer collateral-CA1 long-term potentiation (LTP). We found that various cytokines are dramatically induced following preparation of slices for in vitro recording and as a result of injury following acute electrode placement in vivo. These increases can be overcome in vivo, however, using permanent electrodes implanted three weeks prior to testing. Using this chronic preparation, we found that interleukin-6 (IL-6) mRNA was upregulated nearly 20-fold by LTP induction in vivo, marking the first demonstration of endogenous regulation of this cytokine in response to LTP. In situ hybridization for IL-6 revealed that upregulation is tightly localized near the site of stimulation and is detected only in non-neuronal cells, identified as GFAP+ astrocytes and GFAP− cells within proximal blood vessels. Coupled with previous results showing that exogenously applied IL-6 can prevent the induction of LTP, this finding suggests a mechanism by which the local release of a cytokine could regulate LTP at nearby sites.     

Pancreatic Cancer Surveillance Among High-Risk Populations: Knowledge and Intent

Pancreatic cancer is the fourth most common cancer in both men and women in the United States. It has the lowest survival rate of all cancers, largely due to the presence of non-specific symptoms, leading to diagnosis at advanced stages. While the majority of cases of pancreatic cancer are sporadic, up to 10% may be associated with an inherited predisposition. Currently, there is no standard screening protocol for pancreatic cancer, although this will change in the future as technology improves. Additionally, there is little information regarding the perceptions and intent to screen for pancreatic cancer among those with an increased risk due to a hereditary cancer predisposition syndrome, which was the objective of this study. Focus groups and individual telephone interviews were conducted, with questions focused on knowledge about pancreatic cancer and screening, perceived motivators, and perceived barriers related to each of the screening techniques currently available. Participants were recruited from the High Risk Breast Cancer and Pancreatic Cancer Registries at Huntsman Cancer Institute. The findings of this study indicated that individuals from these high-risk groups have low knowledge levels of pancreatic cancer screening, despite their desire for this information. Motivation to undergo a particular screening technique is related to whether the test is recommended by a physician, cost, degree of invasiveness, and comfort level. This information is useful to genetics professionals who counsel at-risk individuals, physicians who formulate patient care plans, and translational researchers who are developing pancreatic screening methods.     

突破制约肿瘤问题认识的瓶颈

用生物医学模式还原论方法考察肿瘤,肿瘤患者的共同特征都有癌肿,癌肿由异常细胞构成,癌细胞基因表型与正常细胞不同,肿瘤是分子疾病。用生物-心理-社会医学模式辩证法矛盾对立统一观点,从组织干细胞增殖与分化受阻的角度考察肿瘤疾病的种种现象,肿瘤起源于组织再生过程,细胞增殖与分化受阻这对矛盾贯穿肿瘤疾病始终。     

Identification of genes expressed in the amygdala during the formation of fear memory

In this study we describe changes of gene expression that occur in the basolateral complex of the mouse amygdala (BLA) during the formation of fear memory. Through the combination of a behavioral training scheme with polymerase chain reaction-based expression analysis (subtractive hybridization and virtual Northern analysis) we were able to identify various gene products that are increased in expression after Pavlovian fear conditioning and are of potential significance for neural plasticity and information storage in the amygdala. In particular, a key enzyme of monoamine metabolism, aldehyde reductase, and the protein sorting and ubiquitination factor Praja1, showed pronounced and learning-specific induction six hours after fear conditioning training. Aldehyde reductase and Praja1, including a novel alternatively spliced isoform termed Praja1a, were induced in the BLA depending on the emotional stimulus presented and showed different expression levels in response to associative conditioning, training stress, and experience of conditioned fear. Stress and fear were further found to induce various signal transduction factors (transthyretin, phosphodiesterase1, protein kinase inhibitor-alpha) and structural reorganization factors (e.g., E2-ubiquitin conjugating enzyme, neuroligin1, actin, UDP-galactose transporter) during training. Our results show that the formation of Pavlovian fear memory is associated with changes of gene expression in the BLA, which may contribute to neural plasticity and the processing of information about both conditioned and unconditioned fear stimuli.