Adapting Existing Hospitals for Infectious Disease Prevention and Control

Currently, there isa deficit efficient and contextualized design strategies to aid in infection prevention and save health professionals. Thus, the paper\u27s objective is to validate how the room we enthrall can be made safer from the perspective of architectural design with the aim of creating rules for politicians and highlighting the role of the architect in battling diseases. Two hospitals have been considered to apply these conditions to adapt with new polices of infection control. The modifications have revealed good results that the hospitals have been divided into three sections, triaging, isolated patients, and normal patients

Adapting Existing Hospitals for Infectious Disease Prevention and Control

Currently, there isa deficit efficient and contextualized design strategies to aid in infection prevention and save health professionals. Thus, the paper\u27s objective is to validate how the room we enthrall can be made safer from the perspective of architectural design with the aim of creating rules for politicians and highlighting the role of the architect in battling diseases. Two hospitals have been considered to apply these conditions to adapt with new polices of infection control. The modifications have revealed good results that the hospitals have been divided into three sections, triaging, isolated patients, and normal patients

Is Creutzfeldt-Jakob disease transmitted in blood?

Creutzfeldt-Jakob disease (CJD) has been considered infectious since the mid-1960s, but its transmissibility through the transfusion of blood or blood products is controversial. The causative agent's novel undefined nature and resistance to standard decontamination, the absence of a screening test, and the recognition that even rare cases of transmission may be unacceptable have led to the revision of policies and procedures worldwide affecting all facets of blood product manufacturing from blood collection to transfusion. We reviewed current evidence that CJD is transmitted through blood

التأثير التبادلي بين التصميم وسلوك المستعملين تطبيقا على الفراغات العامة The Complementary Effect between Design and User Behavior in Application to Public Spaces

تكوين بيئة مادية تتماشى مع احتياجات وسلوكيات المستخدمين هو الهدف الاساسي للتصميم والتخطيط للبيئة العمرانية. وقد أوضحت الدراسات أن الفراغات العمرانية التي لا تُشبع متطلبات المستعملين؛ تؤدي إلى تأثيرات سلبية (بيئية/ سلوكية/ اجتماعية/ ثقافية/ ...) على هؤلاء الأفراد. مما قد يؤدي إلى هجر تلك الفراغات العمرانية أو محاولة إدخال تعديلات عليها لتتماشى مع احتياجاتهم، أو اكتساب الأفراد سلوكيات جديدة تساعدهم للتأقلم مع تلك الفراغات. ويتعرض البحث بالدراسة (ما يسمي بسوق الرحاب القديم) ، ويهدف البحث إلى التنسيق بين وظيفة الفراغ العمراني والسلوك الإنساني خلال عنصر الزمن ، بهدف الارتقاء وتطوير وتحسين وضبط السلوك الإنساني داخل الفراغات العمرانية من خلال مرونة التصميم وقابليته للتطوير بالتغذية الراجعة feedback) ). Abstract: Creating a physical environment in line with the needs and behaviors of users is the primary objective of designing and planning the built environment. Studies have shown that urban spaces that do not satisfy the requirements of users; Lead to negative (environmental / behavioral / social / cultural / ...) effects on these individuals. This may lead to the abandonment of these urban spaces or attempts to make modifications to them to meet their needs, or the acquisition of new behaviors by individuals that help them to adapt to those spaces. The research is exposed in the study (the so-called old Rehab market), and the research aims to coordinate between the function of urban space and human behavior during the time element, with the aim of upgrading, developing, improving and controlling human behavior within urban spaces through the flexibility of design and its ability to develop with feedback)

التأثير التبادلي بين التصميم وسلوك المستعملين تطبيقا على الفراغات العامة The Complementary Effect between Design and User Behavior in Application to Public Spaces

تكوين بيئة مادية تتماشى مع احتياجات وسلوكيات المستخدمين هو الهدف الاساسي للتصميم والتخطيط للبيئة العمرانية. وقد أوضحت الدراسات أن الفراغات العمرانية التي لا تُشبع متطلبات المستعملين؛ تؤدي إلى تأثيرات سلبية (بيئية/ سلوكية/ اجتماعية/ ثقافية/ ...) على هؤلاء الأفراد. مما قد يؤدي إلى هجر تلك الفراغات العمرانية أو محاولة إدخال تعديلات عليها لتتماشى مع احتياجاتهم، أو اكتساب الأفراد سلوكيات جديدة تساعدهم للتأقلم مع تلك الفراغات. ويتعرض البحث بالدراسة (ما يسمي بسوق الرحاب القديم) ، ويهدف البحث إلى التنسيق بين وظيفة الفراغ العمراني والسلوك الإنساني خلال عنصر الزمن ، بهدف الارتقاء وتطوير وتحسين وضبط السلوك الإنساني داخل الفراغات العمرانية من خلال مرونة التصميم وقابليته للتطوير بالتغذية الراجعة feedback) ). Abstract: Creating a physical environment in line with the needs and behaviors of users is the primary objective of designing and planning the built environment. Studies have shown that urban spaces that do not satisfy the requirements of users; Lead to negative (environmental / behavioral / social / cultural / ...) effects on these individuals. This may lead to the abandonment of these urban spaces or attempts to make modifications to them to meet their needs, or the acquisition of new behaviors by individuals that help them to adapt to those spaces. The research is exposed in the study (the so-called old Rehab market), and the research aims to coordinate between the function of urban space and human behavior during the time element, with the aim of upgrading, developing, improving and controlling human behavior within urban spaces through the flexibility of design and its ability to develop with feedback)

Human Prion Diseases in the United States

BACKGROUND: Prion diseases are a family of rare, progressive, neurodegenerative disorders that affect humans and animals. The most common form of human prion disease, Creutzfeldt-Jakob disease (CJD), occurs worldwide. Variant CJD (vCJD), a recently emerged human prion disease, is a zoonotic foodborne disorder that occurs almost exclusively in countries with outbreaks of bovine spongiform encephalopathy. This study describes the occurrence and epidemiology of CJD and vCJD in the United States. METHODOLOGY/PRINCIPAL FINDINGS: Analysis of CJD and vCJD deaths using death certificates of US residents for 1979-2006, and those identified through other surveillance mechanisms during 1996-2008. Since CJD is invariably fatal and illness duration is usually less than one year, the CJD incidence is estimated as the death rate. During 1979 through 2006, an estimated 6,917 deaths with CJD as a cause of death were reported in the United States, an annual average of approximately 247 deaths (range 172-304 deaths). The average annual age-adjusted incidence for CJD was 0.97 per 1,000,000 persons. Most (61.8%) of the CJD deaths occurred among persons >or=65 years of age for an average annual incidence of 4.8 per 1,000,000 persons in this population. Most deaths were among whites (94.6%); the age-adjusted incidence for whites was 2.7 times higher than that for blacks (1.04 and 0.40, respectively). Three patients who died since 2004 were reported with vCJD; epidemiologic evidence indicated that their infection was acquired outside of the United States. CONCLUSION/SIGNIFICANCE: Surveillance continues to show an annual CJD incidence rate of about 1 case per 1,000,000 persons and marked differences in CJD rates by age and race in the United States. Ongoing surveillance remains important for monitoring the stability of the CJD incidence rates, and detecting occurrences of vCJD and possibly other novel prion diseases in the United States

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice