26 research outputs found

    Left atrial volumes and associated stroke subtypes.

    Get PDF
    Background: Cardio embolism and cerebrovascular atherosclerosis are two major mechanisms of stroke. Studies investigating associations between advanced echocardiographic parameters and stroke mechanisms are limited. Methods: This study is a standardized review of 633 patients admitted to the stroke service of a tertiary care hospital following a standardized stroke investigation and management pathway. Stroke subtypes were characterized using the Causative Classification System, using the hospitals online radiologic archival system with CCS certified stroke investigators. Patients with two mechanisms were excluded. Results: Patients with cardioembolic stroke had a higher proportion of atrial fibrillation (p \u3c 0.001), acute myocardial infarction (p \u3c 0.001) and ischemic heart disease (p \u3c 0.001). On electrocardiogram (ECG) and transthoracic Echo (TTE), patients with cardioembolic stroke had a greater atrial fibrillation (p \u3c .00), left ventricular thrombus (p \u3c .00), left ventricular ejection fraction \u3c30% (p \u3e\u3c .00) and global hypokinesia (p \u3c .00) Patients with cardioembolic stroke had higher mean left atrial volume indices (LAVi) (p \u3c 0.001), mean left ventricular mass indices (LVMi) (p \u3c 0.05) and mean left atrial diameters (LAD) (p \u3c 0.05). At LAVi of 29–33 ml/m2 , the risk of atherothrombotic stroke increased. The risk of cardioembolic stroke increased with LAVi of 34 ml/m2 and above. Conclusion: Left atrial volume indices may be linked to specific stroke phenotype. At mild increases in left atrial dimensions, the risks of atherosclerotic stroke are high, and probably reflect hypertension as the unifying mechanism. Further increases in left atrial dimensions shifts the risk towards cardioembolic stroke

    Increasing frailty is associated with higher prevalence and reduced recognition of delirium in older hospitalised inpatients: results of a multi-centre study

    Get PDF
    Purpose: Delirium is a neuropsychiatric disorder delineated by an acute change in cognition, attention, and consciousness. It is common, particularly in older adults, but poorly recognised. Frailty is the accumulation of deficits conferring an increased risk of adverse outcomes. We set out to determine how severity of frailty, as measured using the CFS, affected delirium rates, and recognition in hospitalised older people in the United Kingdom. Methods: Adults over 65 years were included in an observational multi-centre audit across UK hospitals, two prospective rounds, and one retrospective note review. Clinical Frailty Scale (CFS), delirium status, and 30-day outcomes were recorded. Results: The overall prevalence of delirium was 16.3% (483). Patients with delirium were more frail than patients without delirium (median CFS 6 vs 4). The risk of delirium was greater with increasing frailty [OR 2.9 (1.8–4.6) in CFS 4 vs 1–3; OR 12.4 (6.2–24.5) in CFS 8 vs 1–3]. Higher CFS was associated with reduced recognition of delirium (OR of 0.7 (0.3–1.9) in CFS 4 compared to 0.2 (0.1–0.7) in CFS 8). These risks were both independent of age and dementia. Conclusion: We have demonstrated an incremental increase in risk of delirium with increasing frailty. This has important clinical implications, suggesting that frailty may provide a more nuanced measure of vulnerability to delirium and poor outcomes. However, the most frail patients are least likely to have their delirium diagnosed and there is a significant lack of research into the underlying pathophysiology of both of these common geriatric syndromes

    Cost & management accounting an introduction

    Get PDF
    Accounting has always concerned itself with information production, processing and reporting while cost and management accounting has sought to provide managers with accounting techniques involved in the production of cost information. Cost and management accounting also describes the application of the techniques to a broad range of managerial decision-making, planning and control activities. The aim of the text is provide a thorough understanding of the basic theory and practice of cost and management accounting. Cost and Management Accounting – An Introduction contains thirteen chapters representing a wide variety of cost and management accounting topics particularly in manufacturing context. The textbook is divided into three parts. Part One (Chapter 1 and 2) gives an overview of cost and management accounting and introduces some cost concepts While Part Two (Chapters 3 to 8) focuses on product cost determination. Part Three (Chapters 9 to 13) discusses the provision of information for management decision-making, planning and control. Each chapter in the book provides learning objectives, content-rich materials and exercises. More examples have been included in the text to provide students with greater exposure in problem solving. This book is specifically written for students on foundation courses in Accounting, Management and Business Studies. The book is also relevant to students preparing themselves for the foundation level of professional examinations such as Association of Certified Chartered Accountants (ACCA) and Chartered Institute of Management Accountants (CIMA) as well as managers and others in industry, commerce, local authorities and similar organizations who wish to gain knowledge of the basic principles and processes of cost and management accounting

    Thyroid Dysfunction and Vitamin D Deficiency among Females of Punjab, Pakistan; A Cross Sectional Analysis

    Get PDF
    Background: Thyroid gland is an important gland which plays a vital role in the stimulation of normal growth and central nervous system (CNS), metabolism regulation, elevated vitamin requirements, metabolism of phosphorus and calcium, promote sexual metabolism, increases mitochondrial metabolism, stimulates the adrenergic activity with myocardial contractility and increase heart rate. In this era, one of the important health issues is vitamin D and calcium deficiency. A large number of populations in all over world are vitamin D or calcium deficient or insufficient. The objective of this study was to evaluate the prevalence of thyroid dysfunction and vitamin D deficiency in females.Methods: A cross sectional study was designed to check the prevalence of thyroid disease and its correlation with vitamin D levels in females. Venous blood was drawn from the female’s patients (11—80 years of age) using gel disposable vials (3.5 ml) in aseptic condition. Samples were centrifuged at four thousand revolutions per minute for five minutes and serums were separated. After the separation of serum, the samples were transferred to the laboratory for the automated estimation of Thyroid Stimulating Hormone (TSH), Triiodothyronine (T3), Thyroxine and Vitamin D.Results: It was observed that out of 79 females who had gone through thyroid profile testing, 70% females had normal thyroid profile. However, hypothyroidism was found in 23% females and 7% females had the condition of hyperthyroidism. Out of 18 (23%) reported cases of hypothyroidism, 8 cases were of mild (subclinical) hypothyroidism, 3 cases indicated non-thyroidal illness; rare pituitary hypothyroidism. Out of 79 female participants, only 20 (25.31%) females had normal serum vitamin D levels. Overall, 59 (74.68%) females had vitamin D deficiency. When the vitamin D deficiency was correlated with thyroid dysfunction, it was observed that vitamin D levels were non-significantly (p = 0.35) associated with hypothyroidism.Conclusion: Hypothyroidism was found prevalent in the tested female population, as 23% of the tested population had hypothyroidism while 9% of them have hyperthyroidism. Moreover, majority of the population had vitamin D deficiency.Keywords: Thyroid Dysfunction; Vitamin D Deficiency; Females

    Prospects for Protective Potential of Moringa oleifera against Kidney Diseases

    No full text
    Kidney diseases are regarded as one of the major public health issues in the world. The objectives of this study were: (i) to investigate the causative factors involved in kidney disease and the therapeutic aspects of Moringa oleifera, as well as (ii) the effectiveness of M. oleifera in the anti-inflammation and antioxidant processes of the kidney while minimizing all potential side effects. In addition, we proposed a hypothesis to improve M. oleifera based drug development. This study was updated by searching the key words M. oleifera on kidney diseases and M. oleifera on oxidative stress, inflammation, and fibrosis in online research databases such as PubMed and Google Scholar. The following validation checking and scrutiny analysis of the recently published articles were used to explore this study. The recent existing research has found that M. oleifera has a plethora of health benefits. Individual medicinal properties of M. oleifera leaf extract, seed powder, stem extract, and the whole extract (ethanol/methanol) can up-increase the activity of antioxidant enzymes like superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH), while decreasing the activity of inflammatory cytokines such as TNF-α, IL-1β, IL-6, and COX-2. In our study, we have investigated the properties of this plant against kidney diseases based on existing knowledge with an updated review of literature. Considering the effectiveness of M. oleifera, this study would be useful for further research into the pharmacological potential and therapeutic insights of M. oleifera, as well as prospects of Moringa-based effective medicine development for human benefits

    Spectrum of neurodevelopmental disease associated with the GNAO1 guanosine triphosphate-binding region

    No full text
    Objective To characterize the phenotypic spectrum associated with GNAO1 variants and establish genotype-protein structure-phenotype relationships. Methods We evaluated the phenotypes of 14 patients with GNAO1 variants, analyzed their variants for potential pathogenicity, and mapped them, along with those in the literature, on a three-dimensional structural protein model. Results The 14 patients in our cohort, including one sibling pair, had 13 distinct, heterozygous GNAO1 variants classified as pathogenic or likely pathogenic. We attributed the same variant in two siblings to parental mosaicism. Patients initially presented with seizures beginning in the first 3 months of life (8/14), developmental delay (4/14), hypotonia (1/14), or movement disorder (1/14). All patients had hypotonia and developmental delay ranging from mild to severe. Nine had epilepsy, and nine had movement disorders, including dystonia, ataxia, chorea, and dyskinesia. The 13 GNAO1 variants in our patients are predicted to result in amino acid substitutions or deletions in the GNAO1 guanosine triphosphate (GTP)-binding region, analogous to those in previous publications. Patients with variants affecting amino acids 207-221 had only movement disorder and hypotonia. Patients with variants affecting the C-terminal region had the mildest phenotypes.

    De Novo Pathogenic Variants in N-cadherin Cause a Syndromic Neurodevelopmental Disorder with Corpus Callosum, Axon, Cardiac, Ocular, and Genital Defects

    No full text
    International audienceCadherins constitute a family of transmembrane proteins that mediate calcium-dependent cell-cell adhesion. The extracellular domain of cadherins consists of extracellular cadherin (EC) domains, separated by calcium binding sites. The EC interacts with other cadherin molecules in cis and in trans to mechanically hold apposing cell surfaces together. CDH2 encodes N-cadherin, whose essential roles in neural development include neuronal migration and axon pathfinding. However, CDH2 has not yet been linked to a Mendelian neurodevelopmental disorder. Here, we report de novo heterozygous pathogenic variants (seven missense, two frameshift) in CDH2 in nine individuals with a syndromic neurodevelopmental disorder characterized by global developmental delay and/or intellectual disability, variable axon pathfinding defects (corpus callosum agenesis or hypoplasia, mirror movements, Duane anomaly), and ocular, cardiac, and genital anomalies. All seven missense variants (c.1057G>A [p.Asp353Asn]; c.1789G>A [p.Asp597Asn]; c.1789G>T [p.Asp597Tyr]; c.1802A>C [p.Asn601Thr]; c.1839C>G [p.Cys613Trp]; c.1880A>G [p.Asp627Gly]; c.2027A>G [p.Tyr676Cys]) result in substitution of highly conserved residues, and six of seven cluster within EC domains 4 and 5. Four of the substitutions affect the calcium-binding site in the EC4-EC5 interdomain. We show that cells expressing these variants in the EC4-EC5 domains have a defect in cell-cell adhesion; this defect includes impaired binding in trans with N-cadherin-WT expressed on apposing cells. The two frameshift variants (c.2563_2564delCT [p.Leu855Valfs∗4]; c.2564_2567dupTGTT [p.Leu856Phefs∗5]) are predicted to lead to a truncated cytoplasmic domain. Our study demonstrates that de novo heterozygous variants in CDH2 impair the adhesive activity of N-cadherin, resulting in a multisystemic developmental disorder, that could be named ACOG syndrome (agenesis of corpus callosum, axon pathfinding, cardiac, ocular, and genital defects)

    Spectrum of neurodevelopmental disease associated with the GNAO1 guanosine triphosphate-binding region

    No full text
    OBJECTIVE: To characterize the phenotypic spectrum associated with GNAO1 variants and establish genotype-protein structure-phenotype relationships. METHODS: We evaluated the phenotypes of 14 patients with GNAO1 variants, analyzed their variants for potential pathogenicity, and mapped them, along with those in the literature, on a three-dimensional structural protein model. RESULTS: The 14 patients in our cohort, including one sibling pair, had 13 distinct, heterozygous GNAO1 variants classified as pathogenic or likely pathogenic. We attributed the same variant in two siblings to parental mosaicism. Patients initially presented with seizures beginning in the first 3 months of life (8/14), developmental delay (4/14), hypotonia (1/14), or movement disorder (1/14). All patients had hypotonia and developmental delay ranging from mild to severe. Nine had epilepsy, and nine had movement disorders, including dystonia, ataxia, chorea, and dyskinesia. The 13 GNAO1 variants in our patients are predicted to result in amino acid substitutions or deletions in the GNAO1 guanosine triphosphate (GTP)-binding region, analogous to those in previous publications. Patients with variants affecting amino acids 207-221 had only movement disorder and hypotonia. Patients with variants affecting the C-terminal region had the mildest phenotypes. SIGNIFICANCE: GNAO1 encephalopathy most frequently presents with seizures beginning in the first 3 months of life. Concurrent movement disorders are also a prominent feature in the spectrum of GNAO1 encephalopathy. All variants affected the GTP-binding domain of GNAO1, highlighting the importance of this region for G-protein signaling and neurodevelopment.status: publishe
    corecore