American medical journal最新文献

{"title":"STUDY ON FOLLICLE STIMULATING HORMONE RECEPTOR GENE POLYMORPHISMS IN SOUTH INDIAN WOMEN WITH POLYCYSTIC OVARIAN SYNDROME","authors":"Himavanth Reddy Kambalachenu, S. Paul, S. Nellepalli, P. Venkatachalam","doi":"10.3844/AMJSP.2013.160.167","DOIUrl":"https://doi.org/10.3844/AMJSP.2013.160.167","url":null,"abstract":"Polycystic Ovarian Syndrome (PCOS) is the most common endocrine disorder of women in their reproductive ages. Though PCOS is a complex, heterogeneous disorder, but there is strong evidence for its genetic predisposition. The aim was to study th e association of Follicle Stimulating Hormone Recep tor (FSHR) gene polymorphisms rs1394205, rs6165 and rs6166 in south Indian women with PCOS. The present case control study includes 97 women with P COS and 101 healthy women without any history of infertility. Polymerase chain reaction and Restrict ion fragment length polymorphism based method were applied to identify the genotypes. Distribution of alleles and genotypes did not differ significantly between PCOS and controls (p-value: >0.05). Genotypic association analysis shows a significant association of rs6166 (G/G) genotype with PCOS in recessive gene model (P value: 0.04). Haplotype frequencies and the ir association analysis did not show any significant d ifference between PCOS and controls. No strong linkage is observed between rs6165 and rs6166 in the present study. Our study reveals significant association of FSHR gene polymorphism, rs6166 with PCOS in recessive gene model. When we observe the genotype frequencies, high frequency of heterozygotes in the population s hows that rs6166 (G/A) in heterozygote condition is advantage to the population.","PeriodicalId":89887,"journal":{"name":"American medical journal","volume":"4 1","pages":"160-167"},"PeriodicalIF":0.0,"publicationDate":"2013-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3844/AMJSP.2013.160.167","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70192212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stroke Prevention in Atrial Fibrillation: Pharmacologic Update","authors":"W. Saeed, J. Kusick, M. R. Sardar, E. Gnall, S. Wajihuddin, J. Burke","doi":"10.3844/AMJSP.2013.143.149","DOIUrl":"https://doi.org/10.3844/AMJSP.2013.143.149","url":null,"abstract":"For nearly half a century, the therapeutic options for the risk reduction of stroke in atrial fibrillation have been stagnant with vitamin K antagonists, such as warfarin, being the primary therapy. Although antiplatelet agents have been investigated over this time, they were never shown to reduce the risk of stroke at the level warfarin has. Considering the limited therapeutic options, the main decision facing clinicians was not determining which agent to use, but whether a patient was at high enough risk of stroke to benefit from anticoagulation. The CHADS2 and, more recently, the CHADSVASC risk assessment schemes have been shown to be a simple and predicable tool in determining an individual's risk for stroke. Now, after nearly 50 years with limited alternatives, there has been a surge in therapies in the form of dabigatran, rivaroxaban and apixaban, which have been shown to be non-inferior and in some cases, superior to warfarin in their respective randomized controlled trials. This increase in available options is exciting but at the same time adds another layer of confusion to the process of selecting the appropriate agent for individual patients.","PeriodicalId":89887,"journal":{"name":"American medical journal","volume":"4 1","pages":"143-149"},"PeriodicalIF":0.0,"publicationDate":"2013-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3844/AMJSP.2013.143.149","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70192646","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Review Article; Duodeno-Gastro-Esophageal Reflux Combined and Isolated","authors":"A. Nasr, W. Robb, T. Walsh","doi":"10.3844/AMJSP.2013.127.142","DOIUrl":"https://doi.org/10.3844/AMJSP.2013.127.142","url":null,"abstract":"Barrett’s esophagus is the chief risk factor for esophageal adenocarcinoma. Reflux of gastric acid has long been related to the development of esophagitis and Barrett’s esophagus, but the role of duodenal contents is controversial. We review the literature on the role of duodenal contents in the development of esophagitis, Barrett’s esophagus and adenocarcinoma in addition to the role of acid suppressant therapy in the development or prevention of these changes. A computer-based search of the literature using the terms \"Bilirubin, Barrett, Bile Reflux, duodeno-gastric reflux and oesophagus/esophagus\" was performed. The role of bile and other constituents of duodenal refluxate were examined. Techniques for identifying non-acid reflux were also reviewed, as were the role of pH, medication and surgery in modulating disease severity. Complicated Barrett’s esophagus is associated with increased exposure to gastric and duodenal refluxate. Biological effect of bile acids depends on the conjugation status, the pH of the milieu and the pKa of bile acids. While Proton Pump Inhibitors reduce the levels of DGER, they also produce changes in gastric and lower esophageal pH that activate different bile acids at different pH levels resulting in unexpected injury. Conjugated bile acids are harmful in acidic environment while unconjugated bile acids are harmful at neutral pH environment. An overlap of toxicity among conjugated and unconjugated bile acids occurs between strongly acidic and neutral pH levels. Normalisation of gastric and duodenal refluxate should ideally be the goal of treatment.","PeriodicalId":89887,"journal":{"name":"American medical journal","volume":"4 1","pages":"127-142"},"PeriodicalIF":0.0,"publicationDate":"2013-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3844/AMJSP.2013.127.142","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70192587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Letter: The Idea of Using Botulinum Toxin to Treat Anxiety Disorders","authors":"Taleb Al Abdulmohsen","doi":"10.3844/AMJSP.2013.122.126","DOIUrl":"https://doi.org/10.3844/AMJSP.2013.122.126","url":null,"abstract":"After botulinum toxin was shown to help treat depression, I asked whether it can be therapeutic for anxiety disorders as well. In this brief letter, I go beyond pointing out my pioneering role in the suggesting of this idea and into highlighting some intuitive and counterintuitive aspects of this topic and some misconceptions. For example, if it is true that the effect of botulinum toxin occurs through the interruption of one’s ability to express, and as a result to perceive, sad emotions, then why is it not that common to report a loss of sad feelings after having botulinum toxin injected as a cosmetic in exactly the same way as applied to treat depression?","PeriodicalId":89887,"journal":{"name":"American medical journal","volume":"4 1","pages":"122-126"},"PeriodicalIF":0.0,"publicationDate":"2013-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3844/AMJSP.2013.122.126","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70192576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Current Management of Pleural Disorders","authors":"J. Kastelik","doi":"10.3844/AMJSP.2013.110.121","DOIUrl":"https://doi.org/10.3844/AMJSP.2013.110.121","url":null,"abstract":"A wide range of conditions can present with plural involvement. For this reason patients with pleural disorders may be seen by a number of different specialists. The most common pleural disorders include pleural effusion and pneumothorax. Pleural effusion and pneumothorax are defined as accumulation within the pleural space of fluid and air respectively. The most common disorders responsible for over 90% of pleural effusions include congestive heart failure, malignancy, infection and pulmonary embolism. The pneumothorax can be divided into primary spontaneous, secondary, iatrogenic or traumatic. This review article will discuss our current understanding behind the pathophysiology of pleural effusion. Common causes and less common conditions resulting in pleural effusion will be described. Investigations and management of patients with pleural dsiorders will also be discussed. In addition, recent advances in our understanding of etiology and management of pneumothorax will be covered. Investigations and management of pleural disorders require an understanding of the underlying pathology as well as the expertise in currently available interventional procedures. The main challenge remains to manage patients in accordance to the current guidelines, which is best achieved through specialist services. However, the knowledge related to pleural disorders remains of importance to many specialists.","PeriodicalId":89887,"journal":{"name":"American medical journal","volume":"4 1","pages":"110-121"},"PeriodicalIF":0.0,"publicationDate":"2013-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3844/AMJSP.2013.110.121","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70192495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CHRONIC KIDNEY DISEASE-MINERAL BONE DISODER: FIBROBLAST GROWTH FACTOR-23 AND PHOSPHATE METABOLISM","authors":"W. Cheungpasitporn, Pongsathorn Kue-a-pai, P. Ungprasert, W. Kittanamongkolchai, N. Srivali, Supawat Ratanapo, Teeranun Jirajariyavej, Daych Chongnarungsin, Atipon Kangwanpornsiri","doi":"10.3844/AMJSP.2013.105.109","DOIUrl":"https://doi.org/10.3844/AMJSP.2013.105.109","url":null,"abstract":"Chronic Kidney Disease (CKD) is a growing epidemic in the United States. There are hormonal changes that develop long before the mineral changes in patients with CKD occur. Increased Parathyroid Hormone (PTH) levels first become evident when the estimated Glomerular Filtration Rate (eGFR) is below 60 mL/min/1.73m2. High serum phosphate stimulates the secretion of the Fibroblast Growth Factor 23 (FGF-23) predominantly by bone osteocytes. Recent finding shows that chronically elevated FGF-23 levels in CKD patients are important for the high rates of LVH and the high rates of mortality. Managing phosphorus disorders with phosphate binders and secondary hyperparathyroidism with vitamin D analog and calcimimetics may theoretically reduce cardiovascular morbidity and mortality. We still need more studies on managing phosphorus disorders with phosphate binders, secondary hyperparathyroidism with vitamin D analog and calcimimetics and the outcome data on mortality and fractures in CKD patients.","PeriodicalId":89887,"journal":{"name":"American medical journal","volume":"4 1","pages":"105-109"},"PeriodicalIF":0.0,"publicationDate":"2013-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3844/AMJSP.2013.105.109","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70192453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CRYPTOCOCCAL MENINGITIS IN IMMUNOCOMPETENT PATIENT-CASE REPORT","authors":"Y. B. Bello, Hanna Guapyassu Machado, J. O. Silveira, F. Schettini, Gilberto Canedo Martins Junior, Sergio Dortas Junior, C. Reis, M. Orsini, P. Salem, D. Machado, V. Bastos, Amanda Júlia Ramos Bezerra, F. Catharino, A. Catharino","doi":"10.3844/AMJSP.2013.100.104","DOIUrl":"https://doi.org/10.3844/AMJSP.2013.100.104","url":null,"abstract":"Cryptococcal Meningitis (CM) is a rare infection in immunocompetent patients. A kind of central nervous system infection caused by encapsulated yeast-like fungus Cryptococcus neoformans . A 59-year-old man presented to the Neurology Department of Nova Iguacu General Hospital, complaining has felt “muddled” recently and feeling diaphragmatic spasm without an y apparent cause. In addition, at neurological examination, the patient was slightly confused and during the mini-mental state examination he scored less than 20 points, feeling “slowed down”, no cranial n erve dysfunction, “rigidity of gait as well as of h and movements, more pronounced on the right one, pyramidal signs bilaterally were more intensely noted on the left”. His MRI, lumbar puncture, fungal isolation a nd Nakin Ink were positive to Cryptococcosis while, in turn, HIV tests I and II were both negative. The tr eatment was started with Amphotericin B 50 mg IV, once a day, plus Dexamethashone. From our clinical case, we decided to do a brief review about Cryptococcoa l Meningitis in immunocompetents and Cryptococcoma, researching at MedLine and Pubmed, using terms “Cryptococcal meningitis”, “Cryptococcal meningitis in immunocompetent” and “Cryptococcomas”. It is concluded that CM in immunocompetents is uncommon, but an important cause of non-acute meningitis, that should be included in the range of causes of p reventable blindness. In this sense, this article p urposes advertise clinicians and specialists, to recognize the clinical manifestation and diagnosis of cryptoc occal meningitis in immunocompetents, trying to avoid a l ater diagnosis and the following complications.","PeriodicalId":89887,"journal":{"name":"American medical journal","volume":"4 1","pages":"100-104"},"PeriodicalIF":0.0,"publicationDate":"2013-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3844/AMJSP.2013.100.104","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70192443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"AN OVERVIEW OF MALARIA CONTROL","authors":"E. Chanda, Mulakwa Kamuliwo, R. Steketee, M. Macdonald, O. Babaniyi, V. Mukonka","doi":"10.3844/AMJSP.2013.91.99","DOIUrl":"https://doi.org/10.3844/AMJSP.2013.91.99","url":null,"abstract":"Malaria remains a serious global public health prob lem and a leading cause of morbidity and mortality in sub Saharan Africa. In Zambia the disease is endemic with stable transmission, accounting for 40% of all o ut-patient attendances and is responsible for 20% deaths among children under five. Scaling up of scientifically proven high impact preventive, curative and supportive interven tions and deploying the three-ones strategy: one co ordinating mechanism; one implementation plan and one monitoring plan which is key for increased and successful p ublicprivate sector partner coordination, strengthening and mobilization. There has been marked impact in the reduction of the annual number of malaria deaths by over 60% and malaria cases by 66% (2000-2008), underfive malaria deaths by 41% (2006-2008), parasite pr evalence among children under five from 22 to16% in 2010 and severe anemia rates in children by 56% (2006-2010). Intermittent presumptive treatment in pregnanc y uptake has reached the RBM target at 86%. With these achievements, the country has surpassed targets set by: (i) the Abuja Declaration and (ii) the RBM of reducing the global malaria burden by 50% by 2010. The achievements can be attributed to increased advocacy, communication and behaviour change, efficient partnership coo rdination including strong community engagement, increased financial resources and evidence-based deployment of key technical interventions in accordance with the nati onal malaria control programme policy and strategic direction. Maintaining the momentum and the gains is critical as the programme strives to achieve universal cover age of evidence-based and proven interventions. The country offers some unique models and experiences that could really benefit other programmes in the region. Community-level integrated entomological and active cas e surveillance, prompt effective treatment and sustai ned high levels of contemporary malaria prevention tools is pivotal to the long-term success of malaria control and future malaria elimination. However, there is great need for sustained, predictable, regular resources and broadening the partnership base. To ensure sustain ability, Government needs to remain on the driving seat and committed to malaria control in terms of funding.","PeriodicalId":89887,"journal":{"name":"American medical journal","volume":"4 1","pages":"91-99"},"PeriodicalIF":0.0,"publicationDate":"2013-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3844/AMJSP.2013.91.99","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70192606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In-Depth Review of Human Immunodeficiency Virus-Associated Nephropathy","authors":"N. Permpalung, W. Chaiwatcharayut, Sira Korpaisarn, W. Cheungpasitporn, Daych Chongnarungsin, E. Bischof","doi":"10.3844/AMJSP.2013.82.90","DOIUrl":"https://doi.org/10.3844/AMJSP.2013.82.90","url":null,"abstract":"Human Immunodeficiency Virus (HIV)-Associated Nephropathy (HIVAN) is one of the most important renal complications found in HIV-infected individua ls. Morbidity and mortality in this group of patien ts increases due to End-Stage Renal Disease (ESRD). Classic histological characteristics of HIVAN are collapsing Focal Segmental Glomerulosclerosis (FSGS), microcystic tubular dilation and interstitial inflammation and fibrosis. High prevalence of HIVAN among people of African descent can be explained by host genetic susceptibility, which is associated with several genes on human chromosome 22. HIV can infect renal epithelial cells via uncon ventional mechanisms and cause changes in multiple host cellular pathways, especially in renal tubular cells and podocytes. Accurate diagnosis of HIVAN relies mainly on renal biopsy. Antiretroviral thera py is the mainstay treatment for HIVAN and current standard guidelines recommend the initiation of Hig hly Active Antiretroviral Therapy (HAART) in all HIV-infected individuals with HIVAN, regardless of CD4 level. Other possible treatments for HIVAN including steroids, Angiotensin Converting Enzyme ( ACE) inhibitors, renal replacement therapy and renal transplantation are reviewed in this chapter.","PeriodicalId":89887,"journal":{"name":"American medical journal","volume":"1 1","pages":"82-90"},"PeriodicalIF":0.0,"publicationDate":"2013-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3844/AMJSP.2013.82.90","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70192564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Frequency Distribution of Hemoglobin Variants and Rhesus Blood Groups Among Pregnant Women","authors":"Oyeyemi Ifeoluwa Temitayo, Salawu Oyetunde Timothy","doi":"10.3844/AMJSP.2013.78.81","DOIUrl":"https://doi.org/10.3844/AMJSP.2013.78.81","url":null,"abstract":"Hemoglobin variants, ABO and Rhesus blood groups vary from one population to another. The study was designed to sample pregnant women population from Ayetoro community of Ogun state, Nigeria, for the purpose of updating information on the prevalence of abnormal hemoglobin variants, ABO and Rh blood groups and compare the results with previously published data. Hospital records of recruited pregnant women were sorted out for the determination of the prevalence of hemoglobin variants, ABO and Rh blood groups. Blood group O were the most prevalent (59.1%) followed by groups A (19.1%), B (17.1%) and AB (4.8%). Rhesus D antigen was positive in 97.1% and negative in 2.9% of the study population. Four genotypes; HbAA (70.5%), HbAS (18.1%), HbAC (10.5%) and HbCC (1.0%) were reported in this study. The occurrence of the hemoglobin variants and the different ABO blood groups varied significantly (p","PeriodicalId":89887,"journal":{"name":"American medical journal","volume":"4 1","pages":"78-81"},"PeriodicalIF":0.0,"publicationDate":"2013-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3844/AMJSP.2013.78.81","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70192552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}