复聪香液治疗脑梗死合并高同型半胱氨酸血症32例临床观察

目的观察复聪香液对脑梗死合并高同型半胱氨酸血症患者的临床疗效。方法将本院62例脑梗死合并高同型半胱氨酸血症患者随机分为对照组30例和复聪香液治疗组32例,对照组予以控制血压、血脂、血糖,抗血小板聚集等常规治疗,复聪香液治疗组在对照组治疗方案的基础上加用本院制剂复聪香液治疗,疗程为14d,分别观察2组患者治疗前后神经功能缺损程度评分及血浆同型半胱氨酸水平。结果复聪香液治疗组患者治疗后临床神经功能缺损程度及血浆同型半胱氨酸水平均较治疗前有所改善（P〈0．05）,改善程度优于对照组（P〈0．05）。结论复聪香液能够有效改善脑梗死合并高同型半胱氨酸血症患者的临床神经缺损程度及血浆同型半胱氨酸水平。     

血清同型半胱氨酸和超敏-C反应蛋白测定对急性脑梗死患者的临床意义

目的探讨同型半胱氨酸（Hcy）和超敏-C反应蛋白（hs-CRP）水平与急性脑梗死的关系。方法测定63例急性脑梗死患者和60例健康对照组血清Hcy、hs-CRP含量,并分析其与脑梗死患者临床神经功能缺损评分（NIHSS）的相关性。结果急性脑梗死组Hcy、hs-CRP水平明显高于健康对照组（P〈0.01）,脑梗死不同临床分型组间血清Hcy、hs-CRP水平两两比较差异有统计学意义（P〈0.01）,脑梗死患者血清Hcy、hs-CRP水平与神经功能缺损评分呈正相关（P〈0.01）。结论血清Hcy和hs-CRP是急性脑梗死的一个独立危险因素,且与病变严重程度有关。     

脑梗死患者血清同型半胱氨酸和高敏 C-反应蛋白水平改变及意义

目的：探讨脑梗死患者血清同型半胱氨酸和高敏 C-反应蛋白水平改变及意义。方法2012年4月至2013年6月收治的60例脑梗死患者为试验组,60例健康体检者分为对照组,检测2组患者血清同型半胱氨酸及高敏C-反应蛋白水平。结果试验组患者的血清同型半胱氨酸、高敏 C-反应蛋白含量较对照组明显要高,差异有统计学意义（ P <0.05）。试验组脑梗死患者中血清同型半胱氨酸、高敏 C-反应蛋白伴随着神经功能缺损的加重成递增状态,差异有统计学意义（ P <0.05）。结论血清同型半胱氨酸、高敏 C-反应蛋白的含量与脑梗死有着密切关联,两者同时检查有利于脑梗死的早期诊断和治疗。     

针刺对脑梗死患者高同型半胱氨酸血症干预性作用的临床研究

目的观察针刺疗法对脑梗死患者高同型半胱氨酸血症的影响。方法选择脑梗死合并高同型半胱氨酸血症患者76例,随机分为针刺组41例与西药组35例,分别于治疗前后采用脑卒中患者临床神经缺损程度评分标准评定,并用高效液相色谱结合荧光检测法检测血浆同型半胱氨酸含量。结果针刺组在调节血浆同型半胱氨酸含量上,与西药组比较,差异无显著性意义（P〉0.05）,但是,针刺组在改善神经缺损程度方面明显优于西药组（P〈0.01）。结论针刺疗法能降低脑梗死合并高同型半胱氨酸血症患者的血浆同型半胱氨酸水平,且可提高生活质量。     

血清同型半胱氨酸、高敏C反应蛋白及D-二聚体水平检测急性脑梗死的研究

目的:探究D-二聚体、高敏C反应蛋白及血清同型半胱氨酸水平与急性脑梗死的关系。方法:选取2019年1月~2020年5月某院收治的急性脑梗死患者72例设为研究组,另选取同期健康体检者72例设为对照组,对比两组患者D-二聚体水平、高敏C反应蛋白、血清同型半胱氨酸水平及神经功能缺损程度不同患者D-D、hs-CRP、血清Hcy水平情况。结果:研究组D-二聚体水平、高敏C反应蛋白、血清同型半胱氨酸水平较对照组高,有统计学差异(P<0.05)。结论:急性脑梗死患者神经功能缺损程度与D-二聚体水平、高敏C反应蛋白、血清同型半胱氨酸有关,临床早期诊断、检测D-二聚体水平、高敏C反应蛋白、血清同型半胱氨酸水平对于有效诊断疾病,提高患者预后起到十分重要的作用。     

高尿酸血症与脑梗死相关性的探讨

目的：研究血清尿酸水平与脑梗死的关系。方法：测定106例脑梗死患者和98例健康对照者血清尿酸水平,并根据神经功能缺损程度分析各血清尿酸水平的相关性。结果：急性脑梗死患者血清尿酸水平与健康对照者比较有显著性差异（P〈0.05）。轻型与中型尿酸比较有显著性差异（P〈0.05）,重型与轻型及中型比较有显著性差异（P〈0.05）。结论：血清尿酸水平增高与脑梗死的发生和严重程度有密切关系。     

血浆同型半胱氨酸水平与急性脑梗死的关系

目的探讨高同型半胱氨酸（Hcy）血症与急性脑梗死的关系。方法收集124例脑卒中患者为病例组,选择124例与病例组相匹配的无脑卒中者作为对照组,均采用荧光偏振免疫分析法测定血浆Hcy,按发病〈24h时血浆Hcy水平将患者分为正常Hcy组、高Hcy组,入院时对病例组进行美国国立卫生研究院卒中量表（NIHSS）评分。结果病例组血浆Hcy水平显著高于对照组,差异有统计学意义（P〈0．05）;病例组内高同型半胱氨酸血症（HHe）患者人院时神经功能缺损评分与Hcy水平正常患者相比差异有统计学意义（P〈0．05）。结论高Hcy血症是脑卒中的独立危险因素,并与急性脑梗死严重程度密切相关。     

同型半胱氨酸和超敏C-反应蛋白测定对急性脑梗死患者的临床意义

目的探讨同型半胱氨酸(homocysteine,Hcy)和超敏C-反应蛋白(high-sensitive C-reactive protein,Hs-CRP)水平与急性脑梗死的关系。方法采用酶联免疫吸附法(ELISA)和散射比浊法测定126例急性脑梗死患者和108例健康对照者血清Hcy和Hs-CRP水平,并将脑梗死组按神经功能缺损程度分为A、B、C组,各组进行比较。结果急性脑梗死组Hcy、Hs-CRP明显高于健康对照组(P<0.01),且神经功能缺损程度越重,Hcy及Hs-CRP水平越高,差异有显著性(P<0.05)。结论血清Hcy和Hs-CRP是急性脑梗死的一个独立危险因素,且与病变严重程度有关。     

高同型半胱氨酸血症与脑梗死的相关性研究

目的探讨急性脑梗死与高同型半胱氨酸血症（HHcy）的关系。方法选取本院2009年4月-2011年12月脑梗死患者100例,以及100例健康体格检查人群进行对照研究。分别测定血浆同型半胱氨酸,并进行对比分析。结果（1）研究组的血浆Hcy水平明显高于健康对照组（P〈0．01）。（2）男女患者之间血浆Hcy水平的差异有统计学意义（P〈0．05）。结论脑梗死患者血浆同型半胱氨酸水平明显升高,且男性高于女性。     

脑梗死急性期血浆同型半胱氨酸与TOAST分型关系的临床意义

目的观察不同病因类型脑梗死患者急性期血浆同型半胱氨酸水平,探讨其与急性缺血性脑卒中试验亚型分类标准（TOAST）分型的关系。方法测定2011年1月至2013年12月在山西长平煤业有限责任公司王台医院内科住院的67例发病48 h内脑梗死患者（脑梗死组）和40例健康体检者（对照组）血浆同型半胱氨酸水平,按TOAST分型将67例脑梗死患者分为心源性脑梗死（CE）组（7例）、大动脉粥样硬化性脑梗死（LAA）组（26例）、小动脉闭塞性脑梗死（SAO）组（16例）、其他病因明确性脑梗死（OC）组（2例）、不明病因性脑梗死（UND）组（16例）等5个亚组,并进行统计学分析。结果 LAA、SAO组患者同型半胱氨酸水平明显高于对照组,差异均有统计学意义（t=4.032、3.430,P=0.000、0.001）;其他各脑梗死亚组患者同型半胱氨酸水平与对照组比较,差异均无统计学意义（P〉0.05）。结论同型半胱氨酸水平可能是LAA、SAO的危险因素,且同型半胱氨酸水平对TOAST分型的提示具有一定的临床意义。     

Efficacy of gut lavage,hemodialysis, and hemoperfusion in the therapy of paraquat or diquat intoxication

Clinical and in vitro investigations were carried out to test the efficacy of gut lavage, hemodialysis, and hemoperfusion in the treatment of poisoning with paraquat or diquat. In a patient suffering from diquat intoxication 130 times more diquat was removed by gut lavage 30 h after ingestion than was removed by complete aspiration of the gastric contents.Determination of in vitro clearances for paraquat and diquat by hemodialysis showed that, at serum concentrations of 1–2 ppm, such as are frequently encountered in poisoning in man, toxicologically relevant quantities of herbicide cannot be removed from the body. At a concentration of 20 ppm, on the other hand, hemodialysis proved to be effective, the clearance being 70 ml/min at a blood flow rate of 100 ml/min. The efficacy of hemoperfusion with coated activated charcoal was on the whole better. Especially at concentrations around 1–2 ppm, the clearance values for hemoperfusion were some 5–7 times higher than those for hemodialysis.In a patient suffering from paraquat poisoning, both hemodialysis as well as hemoperfusion were carried out. The in vitro results could be confirmed: At serum concentrations of paraquat less than 1 ppm no clearance could be obtained by hemodialysis while by hemoperfusion with activated charcoal quite high clearance values were measured and the serum level dropped down to zero.

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Zusammenfassung Klinische Untersuchungen und Laboratoriumsversuche wurden durchgeführt, um die Wirksamkeit von Darmspülung, Hämodialyse und Hämoperfusion bei Paraquat- und Deiquat-Vergiftungen zu prüfen.Bei einem Patienten wurde 30 Std nach Deiquat-Aufnahme durch Darmspülung 130mal mehr Deiquat entfernt als durch vollständige Aspiration des Mageninhaltes. In vitro-Versuche ergaben, daß bei Blutserumkonzentrationen von 1–2 ppm, die bei Vergiftungen oft gemessen werden, durch Hämodialyse keine toxikologisch relevanten Paraquat- oder Deiquat-Mengen entfernt werden können. Dagegen erwies sich die Hämodialyse bei 20 ppm und einer Blutumlaufgeschwindigkeit von 100 ml/min mit einer Clearance von 70 ml/min als wirksam. Die Hämoperfusion mit beschicheter Aktivkohle war in diesen Versuchen aber eindeutig überlegen, denn insbesondere bei Konzentrationen um 1–2 ppm waren die Clearance-Werte 5–7mal höher als bei der Hämodialyse.Die in vitro-Ergebnisse wurden bei einem Patienten mit einer Paraquat-Vergiftung bestätigt: Bei Konzentrationen unter 1 ppm war die Hämodialyse wirkungslos, während durch Hämoperfusion relativ hohe Clearance-Werte erreicht wurden, so daß der Serumspiegel rasch unter die Nachweisgrenze abfiel.

     

Aquatic Insects and Trace Metals: Bioavailability,Bioaccumulation, and Toxicity

Abstract

The uptake of metals from food and water sources by insects is thought to be additive. For a given metal, the proportions taken up from water and food will depend both on the bioavailable concentration of the metal associated with each source and the mechanism and rate by which the metal enters the insect. Attempts to correlate insect trace metal concentrations with the trophic level of insects should be made with a knowledge of the feeding relationships of the individual taxa concerned. Pathways for the uptake of essential metals, such as copper and zinc, exist at the cellular level, and other nonessential metals, such as cadmium, also appear to enter via these routes. Within cells, trace metals can be bound to proteins or stored in granules. The internal distribution of metals among body tissues is very heterogeneous, and distribution patterns tend to be both metal and taxon specific. Trace metals associated with insects can be both bound on the surface of their chitinous exoskeleton and incorporated into body tissues. The quantities of trace meals accumulated by an individual reflect the net balance between the rate of metal influx from both dissolved and particulate sources and the rate of metal efflux from the organism. The toxicity of metals has been demonstrated at all levels of biological organization: cell, tissue, individual, population, and community. Much of the literature pertaining to the toxic effects of metals on aquatic insects is based on laboratory observations and, as such, it is difficult to extrapolate the data to insects in nature. The few experimental studies in nature suggest that trace metal contaminants can affect both the distribution and the abundance of aquatic insects. Insects have a largely unexploited potential as biomonitors of metal contamination in nature. A better understanding of the physico-chemical and biological mechanisms mediating trace metal bioavailability and exchange will facilitate the development of general predictive models relating trace metal concentrations in insects to those in their environment. Such models will facilitate the use of insects as contaminant biomonitors.     

Alzheimer’s disease – current trends in basic and clinical research. Highlights from the 16th ECNP

Advances in the molecular biological knowledge of neuronal nicotinic acetylcholine receptors (nAChRs) have led to a growing interest by the pharmaceutical industry in the development of novel compounds that selectively modulate nAChR function. The ability of (-)-nicotine, an activator of nAChRs, to enhance attentional aspects of cognition in animals and humans, to exert neuroprotective and anxiolytic-like effects, and presumably to mediate the negative correlation between smoking and Alzheimer's (and Parkinson's) Disease, has focused interest on the potential therapeutic utility of modulators of nAChR function for treatment of some of the deficits associated with these progressive, neurodegenerative conditions. Numerous compounds are known which activate nAChRs and which might serve as lead compounds toward the development of such agents. The pharmacologic diversity of neuronal nAChR subtypes suggests the possibility of developing selective compounds which would have more favourable side-effect profiles than existing agents. This broader class of agents, collectively called cholinergic channel modulators (ChCMs), is anticipated to encompass compounds which would have more favourable side-effect profiles than existing agents, which generally exhibit low selectivity. This selectivity may be achieved by preferentially activating some subtypes of nAChRs (i.e., Cholinergic Channel Activators, ChCAs) or inhibiting the function of other subtypes (Cholinergic Channel Inhibitors, ChCIs). An overview of the biology of nAChRs and the rationale for the use of ChCMs for the treatment of dementia related to neurodegenerative diseases are presented, followed by a discussion of lead compounds and compounds under consideration for clinical evaluation.     

2-(Acetoxyphenyl)-(Z)-styryl sulfides as cyclooxygenase inhibitors

2-(Acetoxyphenyl)-(Z)-styryl sulfides are described as selective cyclooxygenase-2 (COX-2) inhibitors, useful for treating inflammation and COX-2-mediated disorders including neoplasia. 2-(Acetoxyphenyl)-(Z)-styryl sulfide is claimed to be the most potent COX inhibitor in the series with a COX-2 selectivity ratio of 33. This compound is also claimed to be superior to celecoxib (Celebrex^®, Pfizer) in inhibiting cell growth of colorectal carcinoma cells. In this evaluation, the COX inhibitory activity of this compound is compared to that previously disclosed for diarylheterocycles and 2-(acetoxyphenyl)alkyl sulfides. The validity of the DLD-1 cell line in the growth inhibition studies is questioned based on recent literature reports indicating the lack of COX-2 expression in this cell line.     

Sleep-disordered breathing with chronic opioid use

Chronic opioid use for pain relief or as substitution therapy for illicit drug abuse is prevalent in our societies. In the US, retail distribution of methadone and oxycodone has increased by 824 and 660%, respectively, between 1997 and 2003. μ-Opioids depress respiration and deaths related to illicit and non illicit chronic opioid use are not uncommon. Since 2001 there has been an emerging literature that suggests that chronic opioid use is related to central sleep apnoea of both periodic and non-periodic breathing types, and occurs in ～ 30% of these subjects. The clinical significance of these sleep-related abnormalities are unknown. This review addresses the present knowledge of control of ventilation mechanisms during wakefulness and sleep, the effects of opioids on ventilatory control mechanisms, the sleep-disordered breathing found with chronic opioid use and a discussion regarding the future research directions in this area.     

Drug targets for cognitive enhancement in neuropsychiatric disorders

The investigation of novel drug targets for treating cognitive impairments associated with neurological and psychiatric disorders remains a primary focus of study in central nervous system (CNS) research. Many promising new therapies are progressing through preclinical and clinical development, and offer the potential of improved treatment options for neurodegenerative diseases such as Alzheimer's disease (AD) as well as other disorders that have not been particularly well treated to date like the cognitive impairments associated with schizophrenia (CIAS). Among targets under investigation, cholinergic receptors have received much attention with several nicotinic agonists (α7 and α4β2) actively in clinical trials for the treatment of AD, CIAS and attention deficit hyperactivity disorder (ADHD). Both glutamatergic and serotonergic (5-HT) agonists and antagonists have profound effects on neurotransmission and improve cognitive function in preclinical experiments with animals; some of these compounds are now in proof-of-concept studies in humans. Several histamine H3 receptor antagonists are in clinical development not only for cognitive enhancement, but also for the treatment of narcolepsy and cognitive deficits due to sleep deprivation because of their expression in brain sleep centers. Compounds that dampen inhibitory tone (e.g., GABA_A α5 inverse agonists) or elevate excitatory tone (e.g., glycine transporter inhibitors) offer novel approaches for treating diseases such as schizophrenia, AD and Down syndrome. In addition to cell surface receptors, intracellular drug targets such as the phosphodiesterases (PDEs) are known to impact signaling pathways that affect long-term memory formation and working memory. Overall, there is a genuine need to treat cognitive deficits associated with many neuropsychiatric conditions as well as an increasingly aging population.