D. Goyal, Neil, Simmons Sd, F. Mansab, S. Benjamin, Pitfield, S. Boulet, Jaleel A. Miyan
{"title":"Zinc Deficiency in Autism: A Controlled Study","authors":"D. Goyal, Neil, Simmons Sd, F. Mansab, S. Benjamin, Pitfield, S. Boulet, Jaleel A. Miyan","doi":"10.36648/2572-5610.4.3.63","DOIUrl":"https://doi.org/10.36648/2572-5610.4.3.63","url":null,"abstract":"Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder characterised by impaired socialisation and restricted and repetitive patterns of behaviour. Zinc deficiency has previously been reported in patients with ASD. A retrospective controlled trial of serum zinc levels in patients with ASD vs. non-ASD controls was undertaken to explore the potential presence of zinc deficiency in the ASD population. 72 patients with ASD were compared with 234 non-ASD controls. Serum zinc levels were compared between groups and correlations analysed for age, sex, supplement use and diet. Serum chromium and manganese levels were also compared between ASD and control groups to assess general micronutrient status. Further analysis was undertaken in the ASD group investigating potential correlations between serum zinc levels and immune function. 86% of patients with ASD were found to be zinc deficient versus 24% of the non-ASD control group. There was a mean difference of serum zinc levels between the ASD and non-ASD groups of 1·75 μmol/l (P<0·001, CI 1·2-2·1). There was no effect of age or sex on serum zinc levels in either the ASD or control groups. There was no significant difference in chromium or manganese levels between the ASD and control group. These results suggest zinc deficiency is likely to be common in ASD patients and is a potentially modifiable environmental factor associated with the condition. Zinc’s potential role in the aetio-pathogenesis and disease evolution is discussed, and the need to consider zinc status in patients with ASD is highlighted.","PeriodicalId":92214,"journal":{"name":"Insights in biomedicine","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.36648/2572-5610.4.3.63","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69709711","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":"Lobular Breast Cancer and Abdominal Metastasis: What Is The Correct Diagnostic Management?","authors":"A. Invento, R. Emc, Daniela Grigolato, F. Pellini","doi":"10.36648/2572-5610.4.1.52","DOIUrl":"https://doi.org/10.36648/2572-5610.4.1.52","url":null,"abstract":"Invasive lobular breast cancer represents the second most prevalent histological type of breast cancer after invasive ductal cancer (IDC) and its incidence has been constantly growing in the last few years. This trend is largely related to the use of MR as a radiological diagnostic method of second level. We have analyzed our institutional case and the use FDG CT/PET in this case. FDG CT/PET demonstrates lower SUV and less accuracy both in primary as well as in metastastic ILC compared to IDC. Moreover, the patterns of metastatic spread differ between ILC and IDC. We think that for this type of cancer could be use CT-PET with a particular metabolite: 1 [18F]-Fluoroestradiol (18F-FES-PET). 18F-FES-PET has the potential to assess heterogeneity in ER expression that are expressed in lobular breast cancer.","PeriodicalId":92214,"journal":{"name":"Insights in biomedicine","volume":"65 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.36648/2572-5610.4.1.52","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69709011","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}
Insights in biomedicinePub Date : 2017-01-01Epub Date: 2017-06-12DOI: 10.21767/2572-5610.10027
L A Jason, D Ohanian, A Brown, M Sunnquist, S McManimen, L Klebek, P Fox, M Sorenson
{"title":"Differentiating Multiple Sclerosis from Myalgic Encephalomyelitis and Chronic Fatigue Syndrome.","authors":"L A Jason, D Ohanian, A Brown, M Sunnquist, S McManimen, L Klebek, P Fox, M Sorenson","doi":"10.21767/2572-5610.10027","DOIUrl":"https://doi.org/10.21767/2572-5610.10027","url":null,"abstract":"<p><p>Multiple Sclerosis (MS), Myalgic Encephalomyelitis (ME), and Chronic Fatigue syndrome are debilitating chronic illnesses, with some overlapping symptoms. However, few studies have compared and contrasted symptom and disability profiles for these illnesses for the purpose of further differentiating them. The current study was an online self-report survey that compared symptoms from a sample of individuals with MS (N = 120) with a sample of individuals with ME or CFS (N = 269). Respondents completed the self-report DePaul Symptom Questionnaire. Those individuals with ME or CFS reported significantly more functional limitations and significantly more severe symptoms than those with MS. The implications of these findings are discussed.</p>","PeriodicalId":92214,"journal":{"name":"Insights in biomedicine","volume":"2 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.21767/2572-5610.10027","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35820771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Congenital Heart Defects","authors":"Sharma V","doi":"10.36648/2572-5610.4.1.56","DOIUrl":"https://doi.org/10.36648/2572-5610.4.1.56","url":null,"abstract":"A congenital heart defect (CHD) is a structural defect of the heart or the great vessels by birth, which severely affects cardiac function [1]. CHDs are the commonest form of abnormalities seen in newborn babies, affecting 1 in 145 live births (British Heart Foundation). The most common CHD is a ventricular septal defect (VSD), which occurs to varying degrees in around 3570 per million live births (around 3.5/1000). Small VSDs, along with atrial septal defects (ASDs) and small patent ductus arteriosus (PDA) are considered the least severe CHDs, and usually close naturally or do not cause problems to the patient [2]. The most severe CHDs include double outlet right ventricle (DORV), persistent truncus arteriosus (PTA), transposition of the great arteries (TGA), tetralogy of fallot (TOF), atrioventricular septal defects (AVSDs), and large VSDs. These occur collectively at a rate of around 2.5-3 per 1000 live births and cause patients to become seriously ill within the immediate postnatal period, or soon after [2].","PeriodicalId":92214,"journal":{"name":"Insights in biomedicine","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.36648/2572-5610.4.1.56","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69709501","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}
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号
