海州香薷与石香薷的栽培品江香薷挥发油的气相色谱—质谱分析比较

采用石英毛细管气相色谱—质谱—计算机联用法,比较了海州香蕉(Elsholtzia splendensNakai ex F.Maekawa)与石香蕉的栽培品江香薷(Mosla chinensis Maxim.)药材挥发油中的化学成分,初步鉴定了93个组分中的68个化合物。自海州香薷挥发油中分离并鉴定了以香薷酮(elsholtzia ketone)(80.81％)、反式-石竹烯(trans-caryophyllene)(2.14％)、葎草烯(humulene)(1.45％)、芳樟醇(linalool)(0.72％)等为主的43个成分,占挥发油总量的％.61％。自石香薷的栽培品江香薷挥发油中分离并鉴定了以香荆芥酚(carvacrol)(51.11％)、百里香酚(thymol)(22.00％)、对-聚伞花素(p-cymene)(5.58％)、γ-松油烯(γ-terpinene)(2.57％)等为主的50个成分,占挥发油总量的93.91％。     

海州香薷与石香薷的栽培品江香薷挥发油的气相色谱—质谱分析比较

采用石英毛细管气相色谱—质谱—计算机联用法,比较了海州香蕉(Elsholtzia splendens Nakai ex F.Maekawa)与石香蕉的栽培品江香薷(Mosla chinensis Maxim.)药材挥发油中的化学成分,初步鉴定了93个组分中的68个化合物。自海州香薷挥发油中分离并鉴定了以香薷酮(elsholtzia ketone)(80.81%)、反式-石竹烯(trans-caryophyllene)(2.14%)、葎草烯(humulene)(1.45%)、芳樟醇(linalool)(0.72%)等为主的43个成分,占挥发油总量的%.61%。自石香薷的栽培品江香薷挥发油中分离并鉴定了以香荆芥酚(carvacrol)(51.11%)、百里香酚(thymol)(22.00%)、对-聚伞花素(p-cymene)(5.58%)、γ-松油烯(γ-terpinene)(2.57%)等为主的50个成分,占挥发油总量的93.91%。     

3种疗法对人卵巢癌细胞的联合应用实验研究

为了观察低剂量率放疗、热疗和顺铂联合应用对人卵巢癌细胞的疗效,对１ 对人卵巢癌细胞系Ａ２７８０Ｓ（ 对辐射和顺铂敏感）和Ａ２７８０ＣＰ（抗辐射和顺铂） ,采用低剂量率（０．８８ｃＧｙ／ｍｉｎ） 放疗、热疗（４０ ℃）和顺铂（０ ．５～３．０ μｇ／ｍｌ）同时处理,观察３者联合应用的效果。结果Ａ２７８０ＣＰ对放疗和对顺铂均有较强的抵抗力,细胞存活率为６ ．０％ （１０ Ｇｙ） 和４５．０ ％（１．０ μｇ／ｍｌ,８ ｈ） ,但对热疗则比Ａ２７８０Ｓ稍敏感。如果３ 种处理方法同时应用,结果显示为很明显的协同作用。这一效果在Ａ２７８０ＣＰ更为明显,Ａ２７８０ＣＰ的存活率为３．８ ％（８ Ｇｙ,４０ ℃,１．０ μｇ／ｍｌ） 。结果显示,热疗、顺铂和低剂量率放疗３ 者联合应用有很好的临床应用前景,值得进一步深入研究。     

Ischemic and pharmacological preconditioning induces further delayed protection in transgenic mouse cardiac myocytes over-expressing adenosine A<Subscript>1</Subscript> receptors (A<Subscript>1</Subscript>AR): role of A<Subscript>1</Subscript>AR,iNOS and K<Subscript>ATP</Subscript> channels

In this study we examined the hypotheses that over-expression of the adenosine A(1) receptor (A(1)AR) in transgenic mouse cardiac myocytes (A(1)AR-tgm) induces cellular protection against subsequent sustained simulated ischemia (SI); that the cellular protection induced by over-expression of A(1)AR in A(1)AR-tgm is mediated through inducible nitric oxide synthase (iNOS) and K(ATP) channels. Sub-lethal simulated ischemia (SSI) and the A(1)AR agonists chloro- N(6)-cyclopentyl adenosine (CCPA) or (2 S)- N(6)-[2-endo-norbornyl]adenosine (S-ENBA) induce further, delayed cytoprotection, additional to the existing protection in A(1)AR-tgm. Cellular injury and cell viability was measured by the release of lactate dehydrogenase (LDH) or creatine kinase (CK) into the medium and the amount remaining in the cells. The cellular resistance acquired by cardiac myocytes due to the over-expression of A(1)AR was reflected by the reduced release of LDH (in units/liter) from 44.94+/-1.46 (wild-type mouse cardiac myocytes, wt) to 29.59+/-2.83 (A(1)AR-tgm, P<0.001). Conversely, LDH release from A(1)AR-tgm increased to 42.53+/-2.23 ( P<0.01) on exposure to 5-hydroxydecanoate (a mitochondrial K(ATP) channel blocker), to 45.93+/-2.90 ( P<0.01) on exposure to S-methylthiourea (an iNOS inhibitor) and to 56.04+/-3.00 ( P<0.01) on exposure to glibenclamide (a K(ATP) channel blocker). Treatment of A(1)AR-tgm is with SSI and the A(1)AR agonists chloro- N(6)-cyclopentyl adenosine (CCPA) or (2 S)- N(6)-[2-endo-norbornyl]adenosine (S-ENBA) decreased the release of LDH from 46.44+/-0.57 (A(1)AR-tgm) to 42.08+/-0.48 (A(1)AR-tgm plus SSI, P<0.05), 38.03+/-1.16 (A(1)AR-tgm plus CCPA, P<0.001) and 32.77+/-0.58 (A(1)AR-tgm plus S-ENBA, P<0.001). Our data suggest that the A(1)AR has a cytoprotective effect against subsequent sustained SI in A(1)AR-tgm and that the cellular protection induced by over-expression of A(1)AR in A(1)AR-tgm depends on iNOS and K(ATP) channels. Further, SSI and the A(1)AR agonists CCPA or S-ENBA induce further, delayed cytoprotection in A(1)AR-tgm.     

Pertussis toxin sensitive and insensitive effects of adenosine and carbachol in murine atria overexpressing A(1)-adenosine receptors

1 It was investigated how A(1)-adenosine receptor overexpression alters the effects of carbachol on force of contraction and beating rate in isolated murine atria. Moreover, the influence of pertussis toxin on the inotropic and chronotropic effects of adenosine and carbachol in A(1)-adenosine receptor overexpressing atria was studied. 2 Adenosine and carbachol alone exerted negative inotropic and chronotropic effects in electrically driven left atrium or spontaneously beating right atrium of wild-type mice. 3 These effects were abolished or reversed by pre-treatment of animals with pertussis toxin which can interfere with signal transduction through G-proteins. 4 Adenosine and carbachol exerted positive inotropic but negative chronotropic effects in atrium overexpressing A(1)-adenosine receptors from transgenic mice. 5 The positive inotropic effects of adenosine and carbachol were qualitatively unaltered whereas the negative chronotropic effects were abolished or reversed in atrium overexpressing A(1)-adenosine receptors after pre-treatment by pertussis toxin. 6 Qualitatively similar effects for adenosine and carbachol were noted in the presence of isoprenaline, beta-adrenoceptor agonist. 7 It is concluded that overexpression of A(1)-adenosine receptors also affects the signal transduction of other heptahelical, G-protein coupled receptors like the M-cholinoceptor in the heart. The chronotropic but not the inotropic effects of adenosine and carbachol in transgenic atrium were mediated via pertussis toxin sensitive G-proteins.     

Relationship between biomarkers and subsequent clinical and angiographic restenosis after paclitaxel-eluting stents for treatment of STEMI: a HORIZONS-AMI substudy

Drug-eluting stents (DES) reduce the incidence of in-stent restenosis (ISR) after primary percutaneous coronary intervention (PCI) for ST-elevation myocardial infarction (STEMI). Whether the use of biomarkers might be of utility to identify patients who remain at risk for DES ISR after primary PCI has never been examined. A total of 26 biomarkers were measured at enrollment and 30 days and analyzed at a central core laboratory in 501 STEMI patients from the HORIZONS-AMI trial. All patients underwent primary PCI with the TAXUS paclitaxel-eluting stent (PES), were scheduled for routine angiographic follow-up at 13 months, and were followed for 3 years. Mean in-stent late-loss was 0.28 ± 0.57 mm, and target lesion revascularization (TLR) at 3 years occurred in 9.1 % of patients. Low levels of interleukin-6 (IL-6) and placental growth factor (PLGF) at admission were associated with both higher in-stent late loss and ischemia-driven TLR. Additionally, low admission levels of cardiotrophin-1 (CT-1) were associated with higher rates of ischemia-driven TLR. At 30-day follow-up lower values of IL-1ra (IL-1ra), matrix metalloproteinase 9 (MMP9), and myeloperoxidase (MPO), and a decline relative to admission in IL-1ra, monocyte chemotactic protein-1 (MCP-1), and MMP9 were associated with higher in-stent late loss. Low values of IL-6 at 30 days were also associated with ischemia-driven TLR. After multivariate adjustment, only MPO at 30 days and a decline of MCP-1 between admission and 30 days were associated with in-stent late loss, and only CT-1 was associated with TLR. MPO at 30 days and a decline of MCP-1 between admission and 30 days were independently associated with in-stent late loss, and CT-1 was associated with TLR. Additional studies to confirm and validate the utility of these biomarkers are warranted.     

Capecitabine-induced systemic lupus erythematosus and palmoplantar erythrodysesthesia

Capecitabine is emerging as an important drug in the treatment of metastatic breast and colorectal cancers. Marketed as Xeloda ?, this prodrug is taken orally and readily absorbed. It is novel in its increased convenience for patients, similar efficacy to the intravenous form of its active metabolite and its increased tolerability.1 We present a woman with metastatic breast cancer who presented with cutaneous abnormalities two months after starting treatment with capecitabine. Various dermatologic side effects have been attributed to capecitabine, often requiring cessation of the offending drug. We describe an unreported dermatological side effect of capecitabine therapy, systemic lupus erythematosus concurrent with palmoplantar erythrodysesthesia. As the use of this chemotherapeutic agent becomes more prevalent, it is important to recognize the range of its cutaneous side effects.     

Developing best practice for fungal specimen management: audit of UK microbiology laboratories

This study represents an audit of microbiology laboratories in the UK to ascertain whether they are aware of, or follow, the Health Protection Agency (HPA) National Standard Methods Standard Operating Procedure (NSM SOP) for the investigation of dermatological specimens for superficial mycoses, or use a locally adapted version. A questionnaire audit was distributed to 179 NHS microbiology laboratories throughout England, Wales, Scotland and Northern Ireland. The NSM SOP was followed by 92% of laboratories for the microscopy of dermatological samples; light microscopy/ KOH digestion was used by 63% and fluorescence microscopy/KOH digestion by 29% of laboratories. Preliminary reports post-microscopy were issued by 98% of laboratories, with 93% issuing reports within 48 hours. Adherence to the NSM SOP guidelines for culture was low; only 34% of laboratories incubated microscopy-negative specimens for the recommended 14 days, while approximately 60% incubated microscopy-positive specimens for 21 days. The culture medium recommended by the NSM SOP was used in 82% of laboratories. Comments were added to culture reports by 51% of laboratories; most were added manually and comments varied between laboratories. Nail samples were the most common sample received from primary care, followed by skin and hair. These results show no significant difference in the rate of microscopy positives versus culture positives. Microscopy and culture are the easiest and cheapest methods available to UK laboratories for the investigation of suspected superficial fungal infections. Although most laboratories included in this audit claimed to follow the NSM SOP for microscopy and culture, these results show that the techniques used vary throughout the UK. To maximise the service provided to primary care, UK laboratories should use standardise methods based on the NSM SOP.