Perioperative nutritional support and fluid therapy in patients with liver diseases

The prevalence of liver dysfunction and malnutrition is common among patients with obstructive jaundice or cirrhosis, the poor nutrition status in patients with indications for hepatic resection increases the risk of postoperative complications and/or mortality. Hepatic surgery significantly affects body’s metabolism and environment. Therefore, it is very important for patients with liver diseases undergoing hepatic surgery to receive essential nutritional support and fluid therapy during perioperative period. There are several principles in nutritional support and fluid therapy that surgeons need to pay attention to, for example, time, nutritional approach, fluid volume, choice of fat emulsions and amino acids. Some issues, such as albumin and plasma application, choice of crystalloid and colloid, liver protective therapy, also need further attention.     

穴位艾灸联合耳穴压豆治疗妊娠剧吐临床研究

目的:观察穴位艾灸联合耳穴压豆治疗妊娠剧吐的临床疗效。方法:选取100例妊娠剧吐患者为研究对象,按随机数字表法分为观察组和对照组各50例。对照组给予静脉补液治疗,观察组在此基础上给予穴位艾灸联合耳穴压豆治疗,2组均治疗7~10 d。比较2组临床疗效、症状评分、妊娠剧吐评分(HGS)、胃动素水平、β-人绒毛膜促性腺激素(β-HCG)水平、尿酮体转阴时间及电解质指标水平。结果:观察组总有效率为98.00%,高于对照组的80.00%(P<0.05)。治疗后,2组呕吐、恶心、进食障碍评分均较治疗前降低(P<0.05),观察组上述3项症状评分均低于对照组(P<0.05)。治疗后,2组HGS及β-HCG水平均较治疗前降低(P<0.05),胃动素水平均较治疗前升高(P<0.05);观察组HGS及β-HCG水平均低于对照组(P<0.05),胃动素水平高于对照组(P<0.05);观察组尿酮体转阴时间短于对照组(P<0.05)。治疗后,2组血钾、血钠水平均较治疗前升高(P<0.05),观察组血钾、血钠水平均高于对照组(P<0.05);2组二氧化碳结合力均较治疗前降低(P<0.05),观察组二氧化碳结合力低于对照组(P<0.05)。结论:穴位艾灸联合耳穴压豆治疗妊娠剧吐,可显著改善患者的临床症状及电解质失衡状况,促进胃肠运动,降低复发率。     

Cholesteryl ester transfer protein in human brain

Summary The evidence that apolipoproteins are found in the cerebrospinal fluid and low-density lipoprotein receptor is found in the brain suggests that the brain may have an active lipid transport system. In plasma, cholesteryl ester transfer protein mediates the exchange and net transfer of cholesteryl ester and triglycerides among lipoproteins. Cholesteryl ester transfer activity was measured in the cerebrospinal fluid and plasma of ten neurologically normal subjects. Cholesteryl ester transfer activity was readily detectable in cerebrospinal fluid (7.4±13% cholesteryl ester was transferred per 20 μl), and this activity was completely abolished with specific antibody against the plasma cholesteryl ester transfer protein. The concentration of cholesteryl ester transfer activity in the cerebrospinal fluid was about 12% of that found in plasma, whereas the concentration of albumin in cerebrospinal fluid was only about 0.6% of that in plasma, suggesting direct synthesis of cholesteryl ester transfer protein within the brain. Cholesteryl ester transfer activity was found in conditioned medium from human neuroblastoma and neuroglioma cells and sheep choroid plexus. The data suggest that cholesteryl ester transfer protein is synthesized and secreted in the brain. This protein could play an important role in the transport and redistribution of lipids within the central nervous system. Deceased January 1991     

Acrylamide exposure impairs blood-cerebrospinal fluid barrier function

Previous studies show that chronic acrylamide exposure leads to central and peripheral neu- ropathy. However, the underlying mechanisms remained unclear. In this study, we examined the permeability of the blood-cerebrospinal fluid barrier, and its ability to secrete transthyretin and transport leptin of rats exposed to acrylamide for 7, 14, 21 or 28 days. Transthyretin levels in cerebrospinal fluid began to decline on day 7 after acrylamide exposure. The sodium fluorescein level in cerebrospinal fluid was increased on day 14 after exposure. Evans blue concentration in cerebrospinal fluid was increased and the cerebrospinal fluid/serum leptin ratio was decreased on days 21 and 28 after exposure. In comparison, the cerebrospinal fluid/serum albumin ratio was increased on day 28 after exposure. Our findings show that acrylamide exposure damages the blood-cerebrospinal fluid barrier and impairs secretory and transport functions. These changes may underlie acrylamide-induced neurotoxicity.     

CSF α-synuclein and UCH-L1 levels in Parkinson's disease and atypical parkinsonian disorders

IntroductionThere is an unmet need for biomarkers for Parkinson's disease (PD) and atypical parkinsonian disorders (APD). α-Synuclein, linked to the pathogenesis of PD, is a promising biomarker candidate in need of further investigation. The ubiquitin carboxy-terminal hydrolase L1 (UCH-L1), a pivotal component of the ubiquitin proteasome system which seems to be disturbed in PD, may also be involved in the pathogenesis of this disorder.MethodsWe investigated cerebrospinal fluid (CSF) α-synuclein and UCH-L1 levels from 22 healthy controls, 52 patients with PD, 34 with multiple system atrophy (MSA), 32 with progressive supranuclear palsy, and 12 with corticobasal degeneration.Resultsα-Synuclein levels were significantly decreased in PD and in MSA compared with controls, and in synucleinopathies compared with tauopathies. UCH-L1 levels were significantly decreased in PD, MSA as well as PSP compared with controls, and in PD compared with APD (p < 0.001). Both markers discriminated PD well from controls (p < 0.0001; area under the curve [AUC] = 0.82 and 0.89, respectively). Additionally, CSF α-synuclein separated patients with synucleinopathies from those with tauopathies (p = 0.015; AUC = 0.63), whereas CSF UCH-L1 discriminated between PD and APD (p = 0.0003; AUC = 0.69). Interestingly, α-synuclein and UCH-L1 levels were strongly correlated in PD and synucleinopathies, and weakly in tauopathies. No correlation was found in controls.ConclusionsCSF levels of α-synuclein and UCH-L1 show distinct patterns in parkinsonian syndromes. Their combined determination may be useful in the differential diagnosis of parkinsonian disorders and provide key to understanding their pathoetiology and clinical course. Further large studies are needed to validate our findings.     

The clinical use of cerebrospinal fluid biomarker testing for Alzheimer's disease diagnosis: A consensus paper from the Alzheimer's Biomarkers Standardization Initiative

BackgroundCerebrospinal fluid (CSF) biomarkers β-amyloid 1-42 (Aβ_1-42), also expressed as Aβ_1-42:Aβ_1-40 ratio, T-tau, and P-tau_181P, have proven diagnostic accuracy for mild cognitive impairment and Alzheimer's disease (AD). How to use, interpret, and disclose biomarker results drives the need for standardization.MethodsPrevious Alzheimer's Biomarkers Standardization Initiative meetings discussed preanalytical issues affecting Aβ_1-42 and tau in CSF. This second round of consensus meetings focused on issues related to clinical use of AD CSF biomarkers.ResultsConsensus was reached that lumbar puncture for AD CSF biomarker analysis be considered as a routine clinical test in patients with early-onset dementia, at the prodromal stage or with atypical AD. Moreover, consensus was reached on which biomarkers to use, how results should be interpreted, and potential confounding factors.ConclusionsChanges in Aβ_1-42, T-tau, and P-tau_181P allow diagnosis of AD in its prodromal stage. Conversely, having all three biomarkers in the normal range rules out AD. Intermediate conditions require further patient follow-up.     

Effects of diazepam on glutamatergic synaptic transmission in the hippocampal CA1 area of rats with traumatic brain injury

The activity of the Schaffer collaterals of hippocampal CA3 neurons and hippocampal CA1 neurons has been shown to increase after fluid percussion injury. Diazepam can inhibit the hyperexcitability of rat hippocampal neurons after injury, but the mechanism by which it affects excitatory synaptic transmission remains poorly understood. Our results showed that diazepam treatment significantly increased the slope of input-output curves in rat neurons after fluid percussion injury. Diazepam significantly decreased the numbers of spikes evoked by super stimuli in the presence of 15 μmol/L bicuculline, indicating the existence of inhibitory pathways in the injured rat hippocampus. Diazepam effectively increased the paired-pulse facilitation ratio in the hippocampal CA1 region following fluid percussion injury, reduced miniature excitatory postsynaptic potentials, decreased action-potential-dependent glutamine release, and reversed spontaneous glutamine release. These data suggest that diazepam could decrease the fluid percussion injury-induced enhancement of excitatory synaptic transmission in the rat hippocampal CA1 area.