亚健康的状态指徵（自我对照具备三项者应及时就医）

1、“将军肚”早现。30-50岁的人，大腹便便，是成熟的标志，也是高血脂、脂肪肝、高血压、冠心病的伴侣。2、脱发、斑秃、早秃。每次洗发都有一大堆头发脱落。3、频频去洗手间。排泄次数超过正常人，说明消化系统和泌尿系统开始衰退。4、做事经常後悔、易怒、烦躁、悲观，难以控制自己的情绪。5、记忆力减退，     

食物调理防脱发

推荐食物：黑芝麻、黑豆、核桃仁、桂圆肉、栗子、黑枣、枸杞莱、桑椹子、羊肉、狗肉等。 推荐药膳：核桃芝麻粥。取核桃仁200克，芝麻、粳米各100克。将核桃仁及芝麻各研末，备用。粳米加水煮粥至三成熟，再加入核桃仁、芝麻各30克，煮熟即可。每日分1至2次食用。     

有益肝脏的6种美味

虾，营养丰富。含有蛋白质、脂肪、碳水化合物、钙、磷、铁、维生素A、硫胺素、核黄素、尼克酸。其中谷氮酸含量最多，鲜味即由此而米。此外还有微量元素硒。能预防癌症。     

板蓝根药理作用研究进展

板蓝根为十字花科菘蓝属植物菘蓝Isantis indigotica Fort．的干燥根，原产我国，分布于江苏、浙江、福建、河南、广西、台湾等地，全国各地均有栽培。本品味苦性寒，归心、肝、胃经。具有清热、解毒、凉血、利咽之功效。临床上常用于治疗瘟毒发斑、高热头痛、大头瘟疫、烂喉丹疹、疼腮、喉痹、疮肿、水痘、麻疹、肝炎、流行性感冒等病症。     

丹参对心血管系统作用的研究

丹参又名紫丹参、红丹参、红根、红大袍、活血参、血参根、血山根。为唇形科植物丹参Salvia miltiorrhiza Bge的根。全国大部分地区均有生产。生用或酒炒用。主要归心、心包、肝经。有活     

现任《海峡药学》主编

张炳祥，男，1953年8月出生，福州市人，福建省食品药品监督管理局副局长。1972年12月入伍，历任战士、文书、班长、副排长、营部行政书记、干事、科长、团政委、师政治部副主任等职。1993年8月转业地方。历任福建省医药局办公室副主任、主任、省医药公司总经理、省医药集团董事长。2002年任省药学会法人代表，常务副理事长。《海峡药学》主编。2007年当选为福建省科学技术协会委员。     

罗布麻（2011年第11期封面药用植物）

【科属】夹竹桃科。 【别名】吉吉麻,泽漆麻,红花草,野茶等。 【分布】生长于河岸、山沟、山坡的砂质地。分布于辽宁、吉林、内蒙古、甘肃、新疆、陕西、山西、山东、河南、河北、江苏、安徽等地。     

06年12月美FDA批准的ANDA

美国FDA于2006年12月份批准了63件ANDA。其中12件是第一时间提出的申请（见下表带＊者）。这个月份获准销售辛伐他汀的公司有6家，即Cobalt、Aurobindo、Dr Reddy、Sandoz、Zydus和Perrigo公司。获准销售昂丹司琼注射剂和昂丹司琼注射剂（不含防腐剂）的公司分别有11和10家。前者有Mayne、Hikma（葡萄牙）、Bedford、Abraxis、Sun、Baxter Healthcare、Apotex、Hospira、Pfiva、Wockhardt和PharmaForce公司。后者有Mayne、Hikma（葡萄牙）、Abraxis、Bedford、Sun、Aptex、PharmaForoe、Baxter Healatheare、Hospira和Wockhardt公司。     

欢迎订阅2013年《安徽医学》

《安徽医学》是由安徽省卫生厅主管,安徽省医学情报研究所主办的综合性医学期刊。本刊设有栏目:论著、综述、评论、经验交流、笔谈、讲座、病理分析、教学与论坛、医学与法律、医院管理、新理论、新技术、医事案例点评、病例报告、读片窗等。内容丰富,编辑规范。读者对象全国各地医院、医学院校、科研院所及有关单位。     

生命力旺盛的鱼腥草

鱼腥草,味辛,性微寒。入肝、肺经。功能清热解毒、排痈疗疮、利水消肿、健胃消食。用治实热、热毒、湿邪、疾热为患的肺炎、肺脓肿、痰热咳嗽、肾炎水肿、白带异常、尿路感染、淋病、热痢、疟疾、脾胃积热、痔疮便血、脱肛、痈疖、湿疹、疮疡肿毒、秃疮、疥癣等。     

盐酸美金刚与多奈哌齐治疗阿尔茨海默病的对照研究

目的探讨盐酸美金刚与多奈哌齐治疗阿尔茨海默病（AD）的临床疗效及安全性。方法将96例AD患者随机分为盐酸美金刚组和多奈哌齐组,在治疗前、治疗后2周、4周、8周、16周、24周末分别进行简易智能状态检查（MMSE）评分和临床疗效评估。结果在治疗2、4、8周末评估两组相仿,第16、24用末多奈哌齐组优于盐酸美金刚组。结论盐酸美金刚与多奈哌齐短期疗效相仿,多奈哌齐组远期疗效优干盐酸美金刚组,两组均有良好的安全性。     

Memantine对新生大鼠缺氧缺血性脑损伤的影响

目的：研究美金胺(Memantine)对新生大鼠缺氧、缺血性脑损伤(HIBD)脑保护作用及机制。方法：应用新生7日龄Wistar大鼠随机分为假手术组、HIBD组、Memantine治疗组,采用结扎左侧颈总动脉并吸入8％O2 92％N2混合气体制成新生大鼠HIBD动物模型。于HIBD后即刻腹腔注射Memantine 20mg/kg或等量生理盐水,48h后处死,用放射免疫法测血清NSE水平,用硝酸还原酶法测血清NO水平．用H-E染色观察脑组织病理变化。结果：Memantine可使脑组织病理改变明显减轻,可降低血清中NSE浓度．可降低血清中NO浓度。结论：Memantine对脑缺氧缺血损伤具有脑保护作用;Memantine通过阻断NMDA受体减少毒性NO的生成,是其脑保护作用可能机制之一。     

盐酸美金刚口腔崩解片的制备

目的制备盐酸美金刚口腔崩解片,优化其制备处方。方法通过处方筛选,考察各处方制得的盐酸美金刚口腔崩解片的外观、崩解时限、口感等,确定最佳处方,并进行了稳定性加速试验。结果与结论最佳处方制备得到的盐酸美金刚口腔崩解片的外观、崩解时限、溶出度、片重差异等均符合规定,且质量稳定。     

Anti-Amnesic and Neuroprotective Effects of Fluoroethylnormemantine in a Pharmacological Mouse Model of Alzheimer’s Disease

BackgroundCurrent therapies in Alzheimer’s disease (AD), including Memantine, have proven to be only symptomatic but not curative or disease modifying. Fluoroethylnormemantine (FENM) is a structural analogue of Memantine, functionalized with a fluorine group that allowed its use as a positron emission tomography tracer. We here analyzed FENM neuroprotective potential in a pharmacological model of AD compared with Memantine.MethodsSwiss mice were treated intracerebroventricularly with aggregated Aβ _25–35 peptide and examined after 1 week in a battery of memory tests (spontaneous alternation, passive avoidance, object recognition, place learning in the water-maze, topographic memory in the Hamlet). Toxicity induced in the mouse hippocampus or cortex was analyzed biochemically or morphologically.ResultsBoth Memantine and FENM showed symptomatic anti-amnesic effects in Aβ _25-35-treated mice. Interestingly, FENM was not amnesic when tested alone at 10 mg/kg, contrarily to Memantine. Drugs injected once per day prevented Aβ _25-35-induced memory deficits, oxidative stress (lipid peroxidation, cytochrome c release), inflammation (interleukin-6, tumor necrosis factor-α increases; glial fibrillary acidic protein and Iba1 immunoreactivity in the hippocampus and cortex), and apoptosis and cell loss (Bcl-2–associated X/B-cell lymphoma 2 ratio; cell loss in the hippocampus CA1 area). However, FENM effects were more robust than observed with Memantine, with significant attenuations vs the Aβ _25-35-treated group.ConclusionsFENM therefore appeared as a potent neuroprotective drug in an AD model, with a superior efficacy compared with Memantine and an absence of direct amnesic effect at higher doses. These results open the possibility to use the compound at more relevant dosages than those actually proposed in Memantine treatment for AD.     

Acute effects of memantine in combination with alcohol in moderate drinkers

Rationale Alcohol effects in humans involve N-methyl-d-aspartate (NMDA) receptor-mediated glutamatergic neurotransmission. It has been proposed that NMDA receptor antagonists may be effective in the treatment of alcohol dependence.Objective This study evaluated the acute effects of memantine, an NMDA receptor antagonist, on the subjective, physiological, and performance effects of alcohol in moderate (10–30 drinks per week) alcohol drinkers.Methods Eighteen volunteers without alcohol dependence were tested using a double-blind design with three 3-day long inpatient phases separated by at least a 2-week wash-out period. Memantine (0, 15, and 30 mg) was administered 4 h before alcohol (1.5 g/l body water), which was given in four divided doses every 20 min.Results Pretreatment with memantine attenuated the craving for alcohol before alcohol administration, but not after alcohol was given. Memantine increased the dissociative effects of alcohol, without altering its sedative, stimulant, and overall intoxicating effects. Memantine also did not affect alcohol-induced impairment in performance, physiological changes, or pharmacokinetics. Memantine increased subjective reports of dissociation, confusion, and stimulation, and impaired motor coordination on the balance task.Conclusions Memantine was well tolerated in combination with alcohol. The findings suggest that NMDA receptor neurotransmission may be involved in alcohol craving and alcohol-induced subjective dissociative effects.     

Memantine

Memantine, an uncompetitive antagonist with moderate affinity for NMDA receptors, demonstrates voltage-dependency and relatively fast on/off receptor kinetics. Memantine 20 mg/day significantly slowed the rate of deterioration in outpatients with moderate to severe Alzheimer's disease in a 28-week US randomised, double-blind, placebo-controlled, multicentre study. Memantine 10 mg/day improved measures of dementia in care-dependent inpatients with Alzheimer's disease or vascular dementia in a 12-week randomised, double-blind study. Significantly more memantine than placebo recipients were responders according to Clinical Global Impression of Change scores and the Behavioural Rating Scale for Geriatric Patients Care Dependence subscale. Memantine 20 mg/day significantly improved cognition-related outcomes (cognitive subscale of the Alzheimer's Disease Assessment Scale) in patients with vascular dementia in two 28-week randomised, double-blind, placebo-controlled, multicentre trials. No statistically significant between-group difference was seen in other primary endpoints. Adverse events (incidence in memantine recipients greater than in placebo recipients) occurring in patients with moderately severe to severe dementia included diarrhoea, insomnia, dizziness, headache and hallucination.     

Evaluation of memantine for neuroprotection in dementia

Memantine, a non-competitive NMDA antagonist, has been approved for use in the treatment of dementia in Germany for over ten years. The rationale for use is excitotoxicity as a pathomechanism of neurodegenerative disorders. Memantine acts as a neuroprotective agent against this pathomechanism, which is also implicated in vascular dementia. HIV-1 proteins Tat and gp120 have been implicated in the pathogenesis of dementia associated with HIV infection and the neurotoxicity caused by HIV-1 proteins can be blocked completely by memantine. Memantine has been investigated extensively in animal studies and following this, its efficacy and safety has been established and confirmed by clinical experience in humans. It exhibits none of the undesirable effects associated with competitive NMDA antagonists such as dizocilpine. The efficacy of memantine in a variety of dementias has been shown in clinical trials. Memantine is considered to be a promising neuroprotective drug for the treatment of dementias, particularly Alzheimer’s disease for which there is no neuroprotective therapy available currently. It can be combined with acetylcholinesterase inhibitors which are the mainstay of current symptomatic treatment of Alzheimer’s disease. Memantine has a therapeutic potential in numerous CNS disorders besides dementias which include stroke, CNS trauma, Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), epilepsy, drug dependence and chronic pain. If memantine is approved by the FDA for some of these indications by the year 2005, it can become a blockbuster drug by crossing the US$1 billion mark in annual sales.     

Memantine: a review of its use in Alzheimer's disease

Memantine (Ebixa, Axura, Namenda, Akatinol) is a moderate-affinity, uncompetitive, voltage-dependent, NMDA-receptor antagonist with fast on/off kinetics that inhibits excessive calcium influx induced by chronic overstimulation of the NMDA receptor. Memantine is approved in the US and the EU for the treatment of patients with moderate to severe dementia of the Alzheimer's type. In well designed clinical trials, oral memantine, as monotherapy or in addition to a stable dose of acetylcholinesterase inhibitors, was well tolerated during the treatment of mild to severe Alzheimer's disease for up to 52 weeks. Memantine generally modified the progressive symptomatic decline in global status, cognition, function and behaviour exhibited by patients with moderate to severe Alzheimer's disease in four 12- to 28-week trials. In patients with mild to moderate Alzheimer's disease, data from three 24-week trials are equivocal, although meta-analyses indicate beneficial effects on global status and cognition. Memantine is an effective pharmacotherapeutic agent, and currently the only approved option, for the treatment of moderate to severe Alzheimer's disease.     

石杉碱甲联合美金刚治疗老年性痴呆的临床观察

目的：探讨石杉碱甲联合美金刚治疗老年性痴呆（AD）临床疗效。方法：随机抽取某院门诊及住院老年性痴呆患者42例（年龄69±4.5岁）,分为对照组（20例）,给予石杉碱甲（商品名：哈伯因）及一般常规治疗;试验组（22例）给予石杉碱甲联合美金刚治疗,并给予所有患者简易精神量表（MMSE）、日常生活功能量表（ADL）及神经精神科问卷（NPI）评分,治疗18周后再复查量表评分,用统计学分析方法对终点时两组量表分值作组间对照分析。结果：经组间对照t检验分析结果显示,对照组和试验组MMSE、ADL、NPI有显著性差异（P〈0.05）。结论：石杉碱甲联合美金刚治疗老年性痴呆治疗显效,较单纯应用石杉碱甲对患者的认知功能、日常生活能力及精神行为异常疗效有明显提高。     

Evaluation of memantine for neuroprotection in dementia

Memantine, a non-competitive NMDA antagonist, has been approved for use in the treatment of dementia in Germany for over ten years. The rationale for use is excitotoxicity as a pathomechanism of neurodegenerative disorders. Memantine acts as a neuroprotective agent against this pathomechanism, which is also implicated in vascular dementia. HIV-1 proteins Tat and gp120 have been implicated in the pathogenesis of dementia associated with HIV infection and the neurotoxicity caused by HIV-1 proteins can be blocked completely by memantine. Memantine has been investigated extensively in animal studies and following this, its efficacy and safety has been established and confirmed by clinical experience in humans. It exhibits none of the undesirable effects associated with competitive NMDA antagonists such as dizocilpine. The efficacy of memantine in a variety of dementias has been shown in clinical trials. Memantine is considered to be a promising neuroprotective drug for the treatment of dementias, particularly Alzheimer's disease for which there is no neuroprotective therapy available currently. It can be combined with acetylcholinesterase inhibitors which are the mainstay of current symptomatic treatment of Alzheimer's disease. Memantine has a therapeutic potential in numerous CNS disorders besides dementias which include stroke, CNS trauma, Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), epilepsy, drug dependence and chronic pain. If memantine is approved by the FDA for some of these indications by the year 2005, it can become a blockbuster drug by crossing the US$1 billion mark in annual sales.