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Aim: This article examines India's present radiotherapy (RT) machine status and requirements, geographical distribution, and infrastructure need in six regional areas, which include 31 member states and union territories (UTs). It also considers the influence of the COVID-19 pandemic on India's teletherapy sector. Materials and Methods: Data from reliable resources, including Atomic Energy Regulatory Board, Global Cancer Observatory, and Directory of Radiotherapy Centres databases, were used to analyze the current status of RT machine (RTM) density, regional disparity, and COVID-19 impact on infrastructure growth-rate. Results: In India, the number of functioning RTM and facilities are 823 and 554, respectively, with an average of 1.5 RTM per institute, of which 69.4% have only one RTM. Over the past 22 years, there has been a paradigm shift towards medical linear accelerator (linac) installation instead of telecobalt machines. Presently, there is a teletherapy density of 0.6 RTM per million population, and there is a shortfall of 1209 RTMs. There is a considerable regional disparity in the distribution of RTMs, ranging from (0.08 RTM/million-2.94 RTM/million) across different regions. There is a significant demand for RTMs in the Northern region (480) and the state of Uttar Pradesh (279). The COVID-19 pandemic temporarily impacted India's RT growth rate, reducing it from 5% to 1.9% in 2020-2021. Conclusions: New policies must be established to accelerate the rate of RT installation growth. To better serve local populations and save patient costs, this article proposes that RT facilities be dispersed equitably across states. Keywords: COVID-19, health policy, oncology, particle accelerators, radiotherapy, Author(s): Rohit Singh Chauhan (corresponding author) [1]; Anusheel Munshi [2]; Anirudh Pradhan [3] INTRODUCTION The growing global burden of cancer has become a major concern, with projections indicating a 47% [...]

Author(s): Priya Outtandy [sup.1] [sup.2] , Claire Russell [sup.2] , Robert Kleta [sup.1] , Detlef Bockenhauer [sup.1] Author Affiliations: (Aff1) 0000000121901201, grid.83440.3b, Centre for Nephrology, Royal Free Hospital/Medical School, University [...], Kidney disease is a global problem with around three million people diagnosed in the UK alone and the incidence is rising. Research is critical to develop better treatments. Animal models can help to better understand the pathophysiology behind the various kidney diseases and to screen for therapeutic compounds, but the use especially of mammalian models should be minimised in the interest of animal welfare. Zebrafish are increasingly used, as they are genetically tractable and have a basic renal anatomy comparable to mammalian kidneys with glomerular filtration and tubular filtration processing. Here, we discuss how zebrafish have advanced the study of nephrology and the mechanisms underlying kidney disease.

Byline: Bharath. Pandu, D. Khanna, P. Mohandass, Hima. Ninan, Rajadurai. Elavarasan, Saro. Jacob, Goutham. Sunny Purpose: The aim of the current study is to commission compensator-based total body irradiation (TBI) [...]

Introduction The World Health Organization reports that globally, one of the top five risk factors for disease, disability, and mortality is harmful alcohol (ethanol, ethyl alcohol) use (WHO 2014). Although [...], The term fetal alcohol spectrum disorder (FASD) refers to the entire suite of deleterious outcomes resulting from embryonic exposure to alcohol. Along with other reviews in this special issue, we provide insight into how animal models, specifically the zebrafish, have informed our understanding of FASD. We first provide a brief introduction to FASD. We discuss the zebrafish as a model organism and its strengths for alcohol research. We detail how zebrafish has been used to model some of the major defects present in FASD. These include behavioral defects, such as social behavior as well as learning and memory, and structural defects, disrupting organs such as the brain, sensory organs, heart, and craniofacial skeleton. We provide insights into how zebrafish research has aided in our understanding of the mechanisms of ethanol teratogenesis. We end by providing some relatively recent advances that zebrafish has provided in characterizing gene-ethanol interactions that may underlie FASD. Key words: zebrafish, fetal alcohol spectrum disorder, genetics, environment, brain and behavior. Le trouble du spectre de l'alcoolisation foetale (TSAF) referent a tout un ensemble de consequences deleteres resultant d'une exposition de l'embryon a l'alcool. Parallelement aux autres syntheses comprises dans ce numero, les auteurs presentent comment les modeles animaux, plus specifiquement le poisson-zebre, ont contribue a mieux comprendre les TSAF. Ils presentent d'abord une breve introduction sur les TSAF. Ils discutent du poisson-zebre comme organisme modele et de ses atouts dans la recherche sur l'alcool. Ils passent en detail comment le poisson-zebre a ete utilise comme modele de certains des deficits majeurs presents dans les TSAF. Ceux-ci comprennent des deficits comportementaux sur les plans social, de l'apprentissage et de la memoire, et des deficits structuraux qui affectent des organes comme le cerveau, les organes sensoriels, le coeur les le squelette cranio-facial. Ils presentent comment le poisson-zebre a contribue a la comprehension des mecanismes de la teratogenese par l'ethanol. Ils concluent en presentant certaines des percees les plus recentes que le poisson-zebre a permis de realiser dans la caracterisation des interactions gene-ethanol qui pourraient sous-tendre les TSAF. [Traduit par la Redaction] Mots-cles : poisson-zebre, trouble du spectre de l'alcoolisation foetale, genetique, environnement, cerveau et comportement.

Primary cilia dysfunction in BBS Primary cilia are short membrane protrusions, emanating from the surface of most vertebrate cells. They function as cellular antennae, receiving information from the environment and [...], Bardet-Biedl syndrome (BBS) is a syndromic ciliopathy that has obesity as a cardinal feature. BBS is caused by mutations in BBS genes. BBS proteins control primary cilia function, and BBS mutations therefore lead to dysfunctional primary cilia. Obesity in patients with BBS is mainly caused by hyperphagia due to dysregulated neuronal function in the brain, in particular in the hypothalamus. However, the mechanism by which mutations in BBS genes result in dysfunction in hypothalamic neurons is not well understood. In this issue of the JCI, Wang et al. used BBS and non-BBS patient-derived induced pluripotent stem cells to generate neurons and hypothalamic neurons. Using this human model system, the authors demonstrated that mutations in BBS genes affected primary cilia function, neuronal morphology, and signaling pathways regulating the function of hypothalamic neurons, which control energy homeostasis. This study provides important insights into the mechanisms of BBS-induced obesity.

Introduction Epithelial cell polarity is an important process involved in renal tubule formation presenting itself in two dimensions: apical-basolateral polarity, established at the point the cell membrane differentiates into an [...], Epithelial cell polarity is essential for organ development; aberrations in this process have been implicated in various diseases, including polycystic kidney disease. Establishment and maintenance of cell polarity is governed by a number of molecular processes and how these processes operate remains an interesting question. Conserved protein complexes guide both apical-basolateral polarity and planar cell polarity. In this review we discuss the recent findings that provide insights into polarity mechanisms and the intriguing crosstalk between apical-basolateral polarity and planar cell polarity, and their relationship to cystic kidney disease. Keywords Cystic kidney disease * Cell polarity * Planar polarity * Apical junction

Introduction Ciliopathies comprise a group of disorders associated with genetic mutations encoding defective proteins, which result in abnormal formation or function of cilia. As cilia are a component of almost [...], Ciliopathies comprise a group of disorders associated with genetic mutations encoding defective proteins, which result in either abnormal formation or function of cilia. As cilia are a component of almost all vertebrate cells, cilia dysfunction can manifest as a constellation of features that include characteristically, retinal degeneration, renal disease and cerebral anomalies. Additional manifestations include congenital fibrocystic diseases of the liver, diabetes, obesity and skeletal dysplasias. Ciliopathic features have been associated with mutations in over 40 genes to date. However, with over 1,000 polypeptides currently identified within the ciliary proteome, several other disorders associated with this constellation of clinical features will likely be ascribed to mutations in other ciliary genes. The mechanisms underlying many of the disease phenotypes associated with ciliary dysfunction have yet to be fully elucidated. Several elegant studies have crucially demonstrated the dynamic ciliary localisation of components of the Hedgehog and Wnt signalling pathways during signal transduction. Given the critical role of the cilium in transducing 'outside-in' signals, it is not surprising therefore, that the disease phenotypes consequent to ciliary dysfunction are a manifestation of aberrant signal transduction. Further investigation is now needed to explore the developmental and physiological roles of aberrant signal transduction in the manifestation of ciliopathy phenotypes. Utilisation of conditional and inducible murine models to delete or over express individual ciliary genes in a spatiotemporal and organ/cell-specific manner should help clarify some of the functional roles of ciliary proteins in the manifestation of phenotypic features. Keywords Ciliopathy * Renal disease * Retinal disease * Heterogeneous

Bardet-Biedl syndrome (BBS) is a multisystemic disorder typified by developmental and progressive degenerative defects. A combination of genetic, in vitro, and in vivo studies have highlighted ciliary dysfunction as a primary cause of BBS pathology, which has in turn contributed to the improved understanding of the functions of the primary cilium in humans and other vertebrates. Here we discuss the evidence linking the clinical BBS phenotype to ciliary defects, highlight how the genetic and cellular characteristics of BBS overlap with and inform other ciliary disorders, and explore the possible mechanistic underpinnings of ciliary dysfunction., Bardet-Biedl syndrome (BBS; MIM 209900) is a genetic disorder characterized by defects in multiple organ systems, and the estimated prevalence ranges from one in 160,000 in northern European populations (1), [...]

Abstract: To study genes that are specifically expressed in the eyes, we employed microarray and in situ hybridization analyses to identify and characterize differentially expressed ocular genes in eyeless masterblind [...]

Abstract: The development of a metazoan from a single-celled zygote to a complex multicellular organism requires elaborate and carefully regulated programs of gene expression. However, the tight packaging of genomic [...]

INTRODUCTION The formation of red blood cells (erythropoiesis) in the developing vertebrate embryo assumes vital importance as circulation is established and diffusion alone can no longer supply increasing oxygenation demands. [...]

THE HOMEOBOX GENE FAMILY The homeobox gene family plays a fundamental role in the developmental control of metazoan organisms. In this article, we review the distribution of this gene family [...]

Author(s): Janelle A. Jiminez[sup.1,2] , Trina C. Uwiera[sup.3] , G. Douglas Inglis[sup.1] and Richard R. E. Uwiera[sup.2] Background Diseases are often categorized by the organs affected and the resulting clinical [...], Acute and chronic inflammatory diseases of the intestine impart a significant and negative impact on the health and well-being of human and non-human mammalian animals. Understanding the underlying mechanisms of inflammatory disease is mandatory to develop effective treatment and prevention strategies. As inflammatory disease etiologies are multifactorial, the use of appropriate animal models and associated metrics of disease are essential. In this regard, animal models used alone or in combination to study acute and chronic inflammatory disease of the mammalian intestine paired with commonly used inflammation-inducing agents are reviewed. This includes both chemical and biological incitants of inflammation, and both non-mammalian (i.e. nematodes, insects, and fish) and mammalian (i.e. rodents, rabbits, pigs, ruminants, dogs, and non-human primates) models of intestinal inflammation including germ-free, gnotobiotic, as well as surgical, and genetically modified animals. Importantly, chemical and biological incitants induce inflammation via a multitude of mechanisms, and intestinal inflammation and injury can vary greatly according to the incitant and animal model used, allowing studies to ascertain both long-term and short-term effects of inflammation. Thus, researchers and clinicians should be aware of the relative strengths and limitations of the various animal models used to study acute and chronic inflammatory diseases of the mammalian intestine, and the scope and relevance of outcomes achievable based on this knowledge. The ability to induce inflammation to mimic common human diseases is an important factor of a successful animal model, however other mechanisms of disease such as the amount of infective agent to induce disease, invasion mechanisms, and the effect various physiologic changes can have on inducing damage are also important features. In many cases, the use of multiple animal models in combination with both chemical and biological incitants is necessary to answer the specific question being addressed regarding intestinal disease. Some incitants can induce acute responses in certain animal models while others can be used to induce chronic responses; this review aims to illustrate the strengths and weaknesses in each animal model and to guide the choice of an appropriate acute or chronic incitant to facilitate intestinal disease. Keywords: Intestine, Inflammation, Acute, Chronic, Animal models, Incitants, Chemical, Biological

INTRODUCTION Many tumor viruses stimulate the proliferation of their host cells. The analysis of vital transforming proteins has revealed several strategies by which viruses achieve this end. In some cases, [...]