PAAD: Panelization algorithm for architectural designs.

Due to the competitive nature of the construction industry, the efficiency of requirement analysis is important in enhancing client satisfaction and a company's reputation. For example, determining the optimal configuration of panels (generally called panelization) that form the structure of a building is one aspect of cost estimation. However, existing methods typically rely on rule-based approaches that may lead to suboptimal material usage, particularly in complex designs featuring angled walls and openings. Such inefficiency can increase costs and environmental impact due to unnecessary material waste. To address these challenges, this research proposes a Panelization Algorithm for Architectural Designs, referred to as PAAD, which utilizes a genetic evolutionary strategy built on the 2D bin packing problem. This method is designed to balance between strict adherence to manufacturing constraints and the objective of optimizing material usage. PAAD starts with multiple potential solutions within the predefined problem space, facilitating dynamic exploration of panel configurations. It approaches structural rules as flexible constraints, making necessary corrections in post-processing, and through iterative developments, the algorithm refines panel sets to minimize material use. The methodology is validated through an analysis against an industry implementation and expert-derived solutions, highlighting PAAD's ability to surpass existing results and reduce the need for manual corrections. Additionally, to motivate future research, a synthetic data generator, the architectural drawing encodings used, and a preliminary interface are also introduced. This not only highlights the algorithm's practical applicability but also encourages its use in real-world scenarios.

Early Growth Response-1: Friend or Foe in the Heart?

Cardiovascular disease is a major cause of mortality and morbidity worldwide. Early growth response-1 (Egr-1) plays a critical regulatory role in a range of experimental models of cardiovascular diseases. Egr-1 is an immediate-early gene and is upregulated by various stimuli including shear stress, oxygen deprivation, oxidative stress and nutrient deprivation. However, recent research suggests a new, underexplored cardioprotective side of Egr-1. The main purpose of this review is to explore and summarise the dual nature of Egr-1 in cardiovascular pathobiology.

COVID-19 vaccines: their effectiveness against the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and its emerging variants.

Background: The world has been suffering from the COVID-19 pandemic (officially declared by WHO in March 2020), caused by the severe acute respiratory ß-coronavirus 2 (SARS-CoV-2) since the last week of December 2019. The disease was initially designated as a Public Health Emergency of International Concern on January 30, 2020. In order to protect the health of mass public, an array of research on drugs and vaccines against SARS-CoV-2 has been conducted globally. However, the emerging variants of SARS-CoV-2, i.e., Alpha (B.1.1.7), Beta (B.1.351), Gamma (P.1), and Delta (B.1.617.2) variants which evolved in late 2020 and the Omicron variant (B.1.1.529) which emerged in November 2021 along with its subvariant BA.2 which was first identified in India and South Africa in late December 2021, have raised the doubt about the efficiency of the currently used vaccines especially in terms of the consistent potential to produce neutralizing antibodies targeting the viral spike (S) protein. Main body of the abstract: The present review discussed the functional details of major vaccines regarding their efficiency against such variants during the pandemic. Overall, the mRNA vaccines have shown around 94% effectiveness; the adenovector vaccine showed approximately 70% efficacy, whereas Sputnik V vaccines showed around 92% effectiveness; the inactivated whole-virus vaccine CoronaVac/PiCoVacc and BBIBP-CorV showed a varying effectiveness of 65-86% according to the geographic locations; the subunit vaccine NVX-CoV2373 has shown 60-89% effectiveness along with the global regions against the wild-type SARS-CoV-2 strain. However, reduced effectiveness of these vaccines against the SARS-CoV-2 variants was noticed which is suggestive for the further administration of booster dose. Short conclusion: Maximum variants of SARS-CoV-2 emerged during the second wave of COVID-19; and extensive studies on the viral genomic sequences from all geographical locations around the world have been conducted by an array of groups to assess the possible occurrence of mutations(s) specially within the receptor binding domain of the viral spike (S) protein. Mutational similarities and the new or critical mutations within all variants have been clearly identified so far. The study of effectiveness of the currently used vaccines is also ongoing. The persistence of memory B cell action and the other immune components as well as the administration of booster dose is expected to mitigate the disease.

Microorganisms and cardiovascular diseases: importance of gut bacteria.

Cardiovascular diseases including myocardial infarctions, myocarditis, strokes, coronary artery disease, chronic granulomatous disease, atherosclerotic cardiovascular disease, etc. can be regarded as the severe health trouble round the globe. The reasons behind the heart related complications have been well chalked our so far. Interestingly, along with the non-infectious reasons, an array of bacteria, fungi, parasites and viruses is known to cause different types of heart complications. Unfortunately, the role of microorganisms in inducing heart diseases is not that much known by the mass community in the underdeveloped and even in the developing countries over the world. However, among the microorganisms causing heart diseases, the multifaceted bionetwork by the gut microorganisms especially drew the interests of microbiologists. The impairment of cardiac membrane, the metabolic malfunction of heart, and imbalance in the functionality of the immune cells by the alternation in the composition of gut microorganisms are currently not unknown. Present review outlined the onset of heart diseases caused by the gut microflora in a simple way which would be important in public health regard.

Recruitment and maturation of the coronary collateral circulation: Current understanding and perspectives in arteriogenesis.

The coronary collateral circulation is a rich anastomotic network of primitive vessels which have the ability to augment in size and function through the process of arteriogenesis. In this review, we evaluate the current understandings of the molecular and cellular mechanisms by which this process occurs, specifically focussing on elevated fluid shear stress (FSS), inflammation, the redox state and gene expression along with the integrative, parallel and simultaneous process by which this occurs. The initiating step of arteriogenesis occurs following occlusion of an epicardial coronary artery, with an increase in FSS detected by mechanoreceptors within the endothelium. This must occur within a 'redox window' where an equilibrium of oxidative and reductive factors are present. These factors initially result in an inflammatory milieu, mediated by neutrophils as well as lymphocytes, with resultant activation of a number of downstream molecular pathways resulting in increased expression of proteins involved in monocyte attraction and adherence; namely vascular cell adhesion molecule 1 (VCAM-1), monocyte chemoattractant protein 1 (MCP-1) and transforming growth factor beta (TGF-ß). Once monocytes and other inflammatory cells adhere to the endothelium they enter the extracellular matrix and differentiate into macrophages in an effort to create a favourable environment for vessel growth and development. Activated macrophages secrete inflammatory cytokines such as tumour necrosis factor-α (TNF-α), growth factors such as fibroblast growth factor-2 (FGF-2) and matrix metalloproteinases. Finally, vascular smooth muscle cells proliferate and switch to a contractile phenotype, resulting in an increased diameter and functionality of the collateral vessel, thereby allowing improved perfusion of the distal myocardium subtended by the occluded vessel. This simultaneously reduces FSS within the collateral vessel, inhibiting further vessel growth.

Mobile consulting (mConsulting) and its potential for providing access to quality healthcare for populations living in low-resource settings of low- and middle-income countries.

OBJECTIVE: The poorest populations of the world lack access to quality healthcare. We defined the key components of consulting via mobile technology (mConsulting), explored whether mConsulting can fill gaps in access to quality healthcare for poor and spatially marginalised populations (specifically rural and slum populations) of low- and middle-income countries, and considered the implications of its take-up. METHODS: We utilised realist methodology. First, we undertook a scoping review of mobile health literature and searched for examples of mConsulting. Second, we formed our programme theories and identified potential benefits and hazards for deployment of mConsulting for poor and spatially marginalised populations. Finally, we tested our programme theories against existing frameworks and identified published evidence on how and why these benefits/hazards are likely to accrue. RESULTS: We identified the components of mConsulting, including their characteristics and range. We discuss the implications of mConsulting for poor and spatially marginalised populations in terms of competent care, user experience, cost, workforce, technology, and the wider health system. CONCLUSIONS: For the many dimensions of mConsulting, how it is structured and deployed will make a difference to the benefits and hazards of its use. There is a lack of evidence of the impact of mConsulting in populations that are poor and spatially marginalised, as most research on mConsulting has been undertaken where quality healthcare exists. We suggest that mConsulting could improve access to quality healthcare for these populations and, with attention to how it is deployed, potential hazards for the populations and wider health system could be mitigated.

Remote Ischemic Preconditioning induces Cardioprotective Autophagy and Signals through the IL-6-Dependent JAK-STAT Pathway.

: Autophagy is a cellular process by which mammalian cells degrade and assist in recycling damaged organelles and proteins. This study aimed to ascertain the role of autophagy in remote ischemic preconditioning (RIPC)-induced cardioprotection. Sprague Dawley rats were subjected to RIPC at the hindlimb followed by a 30-min transient blockade of the left coronary artery to simulate ischemia reperfusion (I/R) injury. Hindlimb muscle and the heart were excised 24 h post reperfusion. RIPC prior to I/R upregulated autophagy in the rat heart at 24 h post reperfusion. In vitro, autophagy inhibition or stimulation prior to RIPC, respectively, either ameliorated or stimulated the cardioprotective effect, measured as improved cell viability to mimic the preconditioning effect. Recombinant interleukin-6 (IL-6) treatment prior to I/R increased in vitro autophagy in a dose-dependent manner, activating the Janus kinase/signal transducers and activators of transcription (JAK-STAT) pathway without affecting the other kinase pathways, such as p38 mitogen-activated protein kinases (MAPK), and glycogen synthase kinase 3 Beta (GSK-3ß) pathways. Prior to I/R, in vitro inhibition of the JAK-STAT pathway reduced autophagy upregulation despite recombinant IL-6 pre-treatment. Autophagy is an essential component of RIPC-induced cardioprotection that may upregulate autophagy through an IL-6/JAK-STAT-dependent mechanism, thus identifying a potentially new therapeutic option for the treatment of ischemic heart disease.

Circulating mediators of remote ischemic preconditioning: search for the missing link between non-lethal ischemia and cardioprotection.

Acute myocardial infarction (AMI) is one of the leading causes of mortality and morbidity worldwide. There has been an extensive search for cardioprotective therapies to reduce myocardial ischemia-reperfusion (I/R) injury. Remote ischemic preconditioning (RIPC) is a phenomenon that relies on the body's endogenous protective modalities against I/R injury. In RIPC, non-lethal brief I/R of one organ or tissue confers protection against subsequent lethal I/R injury in an organ remote to the briefly ischemic organ or tissue. Initially it was believed to be limited to direct myocardial protection, however it soon became apparent that RIPC applied to other organs such as kidney, liver, intestine, skeletal muscle can reduce myocardial infarct size. Intriguing discoveries have been made in extending the concept of RIPC to other organs than the heart. Over the years, the underlying mechanisms of RIPC have been widely sought and discussed. The involvement of blood-borne factors as mediators of RIPC has been suggested by a number of research groups. The main purpose of this review article is to summarize the possible circulating mediators of RIPC, and recent studies to establish the clinical efficacy of these mediators in cardioprotection from lethal I/R injury.