高效液相色谱法测定寒痹停片中士的宁含量

目的：建立用ＨＰＬＣ测定寒痹停片中士的含量的方法。方法：氰基柱;流动相－甲醇－水－三乙胺－乙酸（９８００：１５５：１５：３０）;紫外检测波长２５４ｎｍ。结果：在４～２０ｕｇ／ｍｌ范围内,标准曲线回归方程为：Ｙ＝－２８０３＋８９６７ｘ（ｒ＝０．９９９７）,ＲＳＤ＝１．６５％?加样回收率的平均值为９９．８２％。结论：实验表明,这是一个适用于生产控制和产品质量检验的简单、快速、准确的方法。     

Modeling relationships between traditional preadmission measures and clinical skills performance on a medical licensure examination

Medical schools employ a variety of preadmission measures to select students most likely to succeed in the program. The Medical College Admission Test (MCAT) and the undergraduate college grade point average (uGPA) are two academic measures typically used to select students in medical school. The assumption that presently used preadmission measures can predict clinical skill performance on a medical licensure examination was evaluated within a validity argument framework (Kane 1992). A hierarchical generalized linear model tested relationships between the log-odds of failing a high-stakes medical licensure performance examination and matriculant academic and non-academic preadmission measures, controlling for student-and school-variables. Data includes 3,189 matriculants from 22 osteopathic medical schools tested in 2009-2010. Unconditional unit-specific model expected average log-odds of failing the examination across medical schools is -3.05 (se?=?0.11) or 5%. Student-level estimated coefficients for MCAT Verbal Reasoning scores (0.03), Physical Sciences scores (0.05), Biological Sciences scores (0.04), uGPA(science) (0.07), and uGPA(non-science) (0.26) lacked association with the log-odds of failing the COMLEX-USA Level 2-PE, controlling for all other predictors in the model. Evidence from this study shows that present preadmission measures of academic ability are not related to later clinical skill performance. Given that clinical skill performance is an important part of medical practice, selection measures should be developed to identify students who will be successful in communication and be able to demonstrate the ability to systematically collect a medical history, perform a physical examination, and synthesize this information to diagnose and manage patient conditions.     

Preferential expression of insulin-like growth factor binding proteins-1, -3, and -5 during early diabetic renal hypertrophy in rats

The renal insulin-like growth factor-I (IGF-I) system has been implicated in the pathogenesis of renal hypertrophy, altered hemodynamics, and extracellular matrix expansion associated with early diabetes. The relative abundance of IGF binding proteins (IGFBPs) in the renal microenvironment may modulate IGF-I actions. However, the precise IGFBPs expressed in the glomerular and tubulointerstitial compartments during diabetic renal growth have not been characterized. In the present study, in situ hybridization studies were performed to examine the expression of IGFBP-1 to -6 messenger RNAs (mRNAs) 3, 7, and 14 days after streptozotocin (STZ) injection in rats. In control, nondiabetic kidneys, all six IGFBP mRNAs were differentially expressed with a predominance of IGFBP-5. The onset of renal hypertrophy in STZ-induced diabetes was associated with a rapid and site-specific induction of IGFBP-1, -3, and -5 mRNAs. In contrast, basal expression of IGFBP-2, -4, and -6 mRNAs was not altered in diabetic rats. IGFBP-5 mRNA expression increased in diabetic glomeruli, cortical, and inner medullary peritubular interstitial cells at days 3, 7, and 14. Although normal glomeruli failed to express IGFBP-3, it was induced concomitantly with IGFBP-5 in diabetic glomeruli and cortical peritubular interstitial cells. IGFBP-1 mRNA levels also increased in cortical tubular cells at each time point tested. Peak induction of IGFBP-3 and -5 was observed at day 3, whereas IGFBP-1 was delayed until day 7. IGFBP-1, -3, and -5 mRNA levels declined by day 14, but remained persistently elevated above control. By immunoperoxidase staining, similar alterations in the pattern of IGFBP-3 and -5 protein expression were observed at each time point. The preferential and site-specific increase in IGFBP-1, -3, and -5 suggest that these IGFBPs may regulate the local autocrine and/or paracrine actions of IGF-I and contribute to the pathogenesis of the early manifestations of diabetic nephropathy.     

安宫牛黄丸中小檗碱的HPLC法测定

本文报道用HPLC法测定黄连及含黄连中成药安宫牛黄丸中小檗碱型生物碱。实验结果表明选用硅胶柱为固定相,以醋酸乙酯—甲酸—乙醇(15:3:2)为流动相,能使样品中四种小檗碱型的生物碱获得最佳分离。用此法测得不同厂家生产的安宫牛黄丸中盐酸小檗碱的含量为0.331～0.456%,平均回收率为97.23%,变异系数为1.2%。     

Airway inflammation in asthma with incomplete reversibility of airflow obstruction

This study aimed to determine whether there is a persistent or different type of airway inflammation in patients with an incomplete reversibility of airflow obstruction (IRAO) despite optimal treatment and if so, whether it is associated with an accelerated decline of pulmonary function. Fifteen asthmatic patients with IRAO, and 23 with complete reversibility of airflow obstruction (CRAO) had a spirometry and an induced-sputum (IS) analysis. Past FEV1 values were recorded over 2-12 years during periods of stable asthma. Medians (range) for IS cell differentials were: lymphocytes, 0(0-3)/1(0-2)%; neutrophils, 56(13-88)/38(3-84)% and eosinophils, 2.0(0-82)/4.0(0-68)%, (all P>0.05). Among non-smoking patients, those with IRAO had more neutrophils in IS than those with CRAO (P=0.019). Mean (+/-SEM) yearly fall in FEV1 in IRAO or CRAO patients was 54+/-21/84+/-16 ml/year (P>0.05, predicted age-related decline < or = 26 ml/year, P=0.0008). In the whole group of asthmatic patients, decline of FEV1/year was inversely correlated with the % neutrophils in sputum (r(s)=-0.436, P=0.008) and, in IRAO patients, with the duration of asthma (r(s)=-0.559, P=0.037). In conclusion, persistent airway inflammation and increased decline in pulmonary function can be observed in both asthmatic patients with IRAO/CRAO and are of similar magnitude. Non-smoking patients with IRAO had more neutrophils in IS than CRAO.     

Linkage of the MHC to familial multiple sclerosis suggests genetic heterogeneity. The Multiple Sclerosis Genetics Group

Multiple sclerosis (MS) is a demyelinating autoimmune disease of the central nervous system. While its etiology is not well understood, genetic factors are clearly involved. Until recently, most genetic studies in MS have been association studies using the case-control design testing specific candidate genes and studying only sporadic cases. The only consistently replicated finding has been an association with the HLA-DR2 allele within the major histocompatibility complex (MHC) on chromosome 6. Using the genetic linkage design, however, evidence for and against linkage of the MHC to MS has been found, fostering suggestions that sporadic and familial MS have different etiologies. Most recently, two of four genomic screens demonstrated linkage to the MHC, although specific allelic associations were not tested. Here, a dataset of 98 multiplex families was studied to test for an association to the HLA-DR2 allele in familial MS and to determine if genetic linkage to the MHC was due solely to such an association. Three highly polymorphic markers (HLA-DR, D6S273 and TNFbeta) in the MHC demonstrated strong genetic linkage (parametric lod scores of 4.60, 2.20 and 1.24, respectively) and a specific association with the HLA-DR2 allele was confirmed (TDT; P < 0.001). Stratifying the results by HLA-DR2 status showed that the linkage results were limited to families segregating HLA-DR2 alleles. These results demonstrate that genetic linkage to the MHC can be explained by the HLA-DR2 allelic association. They also indicate that sporadic and familial MS share a common genetic susceptibility. In addition, preliminary calculations suggest that the MHC explains between 17 and 62% of the genetic etiology of MS. This heterogeneity is also supported by the minority of families showing no linkage or association with loci within the MHC.      

Preterm neonatal cardiovascular instability: Does understanding the fetus help evaluate the newborn?

相似文献   

Influence of smoking on airway inflammation and remodelling in asthma

Background Although exposure to tobacco smoke has been associated with increased morbidity and mortality, cigarette smoking is still common in the asthmatic population. Induced sputum neutrophilia has been observed in asthmatic smokers, but the effects of regular smoking on their bronchial mucosa morphology remain to be defined. This study documents the inflammatory and remodelling features in bronchial biopsies of smoking compared with non‐smoking asthmatics. Methods We analysed bronchial biopsies from 24 steroid‐naïve young subjects with mild asthma: 12 non‐smoking and 12 currently smoking subjects. In addition to airway morphology assessment, inflammation and remodelling were analysed by immunohistochemistry using antibodies against CD3, CD68, major basic protein, neutrophil elastase, and tryptase. Expression of the cytokines IL‐4, IL‐5, IL‐8, IFN‐γ, transforming growth factor‐β, and TNF was determined by in situ hybridization. Results Compared with non‐smoking asthmatic subjects, smoking asthmatics' bronchial mucosa showed squamous cell metaplasia, in addition to increased expression of subepithelial neutrophil elastase, IFN‐γ, and intraepithelial IL‐8. Conclusions Smoking status modifies morphological and inflammatory processes in young subjects with mild asthma. The changes may possibly affect asthma treatment responses and clinical outcomes.     

Improving knowledge transfer on chronic respiratory diseases: A canadian perspective. How to translate recent advances in respiratory diseases into day-to-day care

Background: Chronic diseases represent an increasing burden for health care systems. Ongoing research efforts provide regularly new scientific evidence on how optimize current medical care. In regard to respiratory diseases, as for other health problems, optimal management of these conditions has been summarized in recent consensus guidelines but implementation of these recommendations is still poor. Not only are the key-messages of such guidelines often unknown to the practitioner and the patient but even when it is, they are often insufficiently integrated into current care, often related to behavioral, organizational and communication barriers.Methods: Literature review on the topic of Clinical Practice Guidelines implementation and reference to recent projects aimed at improving management of asthma in the province of Quebec and elsewhere, as models for such implementation process.Results: The basic principles of an effective translation of current knowledge into day-to-day care are known, but healthcare delivery structures, practice tools and resources, and regional/local leadership should be available to make it happen. Ideally, implementation requires a multidisciplinary effort of care providers, specialists, general practitioners, allied health professionals, patients and their family. The general public, health administrators and policy makers should also be aware of the consequences of poor management of these diseases and be supportive of the proposed initiatives. Finally, these last should be adequately evaluated to ensure their effectiveness and determine if they should be improved. Recently projects performed in Quebec have proposed disease management models to identify asthma care gaps and improve translation of current Guidelines into day-to-day care.Conclusions: Although the human and socio-economical burden of chronic diseases is still increasing, their current management is still often deficient. In the recent decades, Practice Guidelines have been developed to guide Practitioners towards optimal care, but implementation of these Guides is still poor. Recent Canadian and International initiatives have proposed valid models to help address current care gaps.