Captive breeding, developmental biology and commercial production of Dravidia fasciata- An indigenous ornamental fish of the Western Ghats of India

Ornamental fishes of the Western Ghats of India have great demand in the export market. At present these fishes are collected from the wild and exported. Hence many times, the demand could not be met due to short supply. The only remedial measure for a sustainable supply is to produce the fish in captive conditions. Unfortunately, the breeding technology for the ornamental fishes of the Western Ghats of India has not been attempted seriously till date. The present paper is almost a pioneering attempt to develop captive breeding technology for 12 prioritized species of the indigenous ornamental fishes of the Western Ghats of India. Dravidia fasciata is one of them. It is popularly known as Melon barb. It is a beautiful barb, growing to a maximum size of 80 mm. In the present paper the methodology of captive breeding of this fish is provided with the economics of its production. Melon barbs were collected from the wild and brought to the hatchery of College of Fisheries in oxygen filled plastic bags and gradually acclimatized to the captive conditions. Its size at first maturity, sexual dimorphism, and developmental biology were studied and described with photographs. The total length (TL) at first maturity for males was 50 mm (50-55 mm) and 40 mm for females (40-45 mm). A sexually mature male developed beautiful pinkish red tinge all over the body. The black bands over the body also became deeper in colour during this time. The intensity of the colour reached its maximum during the courtship activities. Male also possessed nuptial tubercles on the operculum which could be identified only by keen observation. But a sexually mature female did not develop any colour change by the onset of sexual maturity. The results of the study clearly demonstrated that D. fasciata could be successfully produced in captivity through scientific management of brooders, eggs, larvae and hatchlings. The successful development of captive breeding technology is likely to pave way towards commercialization of the technology thus leading to the sustainable export of the species

Penetration and infectivity of entomopathogenic nematodes against Lema sp. (Chrysomelidae: Coleoptera) infesting turmeric (Curcuma longa L.) and their multiplication

Penetration and infectivity of eight native isolates of entomopathogenic nematodes (EPNs), Heterorhabditis sp. (IISR-EPN 01); Steinernema sp. (IISR-EPN 02); S. ramanai (IISR-EPN 03); S. carpocapsae (IISR-EPN 06), Oscheius gingeri (IISR-EPN 07) and Oscheius spp. (IISR-EPN 04, 05 and 08) were evaluated against larvae of leaf feeder (LF) Lema sp. infesting turmeric. Among the tested EPNs, Steinernema sp. (IISR-EPN 02) and O. gingeri (IISR-EPN 07) were more pathogenic to LF larva as they brought about 100% mortality to the insect within 48 h post exposure, followed by Heterorhabditis sp. (IISR-EPN 01) and Oscheius sp. (IISR-EPN 08) after 72 h of exposure. S. ramanai (IISR-EPN 03) and Oscheius spp. (IISR-EPN 04 and 05) took 96 and 120 h, respectively, to kill the test insect. Lema sp. larva was the most suitable host for multiplication of infective juveniles (IJs) of O. gingeri (IISR-EPN 07), which yielded 11, 480 IJs larva-1, followed by Steinernema sp. (IISREPN 02) (8, 658 IJs larva-1) and S. carpocapsae (IISR-EPN 06) (6, 810 IJs larva-1), however, Heterorhabditis sp. (IISR-EPN 01) less multiplied. The maximum number of Steinernema sp. (IISREPN 02) IJs penetrated into test larva (17.5 IJs larva-1), followed by S. carpocapsae (IISR-EPN 06) (10.2 IJs larva-1) and the fewest (2.8 IJs larva-1) were of Oscheius sp. (IISR-EPN 08). The infectivity of the above EPNs against LF is being reported for the first time which opens up a new hope of utilizing them in insect pest management in turmeric. &nbsp

Measuring the impact of ambulatory red blood cell transfusion on home functional status: study protocol for a pilot randomized controlled trial

SPIRIT 2013: SPIRIT (Standard Protocol Items: Recommendations for Interventional Trials) Checklist for clinical trial protocols. (DOCX 65 kb

Linking Symptom Inventories using Semantic Textual Similarity

An extensive library of symptom inventories has been developed over time to measure clinical symptoms, but this variety has led to several long standing issues. Most notably, results drawn from different settings and studies are not comparable, which limits reproducibility. Here, we present an artificial intelligence (AI) approach using semantic textual similarity (STS) to link symptoms and scores across previously incongruous symptom inventories. We tested the ability of four pre-trained STS models to screen thousands of symptom description pairs for related content - a challenging task typically requiring expert panels. Models were tasked to predict symptom severity across four different inventories for 6,607 participants drawn from 16 international data sources. The STS approach achieved 74.8% accuracy across five tasks, outperforming other models tested. This work suggests that incorporating contextual, semantic information can assist expert decision-making processes, yielding gains for both general and disease-specific clinical assessment

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

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure fl ux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defi ned as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (inmost higher eukaryotes and some protists such as Dictyostelium ) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the fi eld understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation it is imperative to delete or knock down more than one autophagy-related gene. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways so not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field

Genomic Relationships, Novel Loci, and Pleiotropic Mechanisms across Eight Psychiatric Disorders

Genetic influences on psychiatric disorders transcend diagnostic boundaries, suggesting substantial pleiotropy of contributing loci. However, the nature and mechanisms of these pleiotropic effects remain unclear. We performed analyses of 232,964 cases and 494,162 controls from genome-wide studies of anorexia nervosa, attention-deficit/hyper-activity disorder, autism spectrum disorder, bipolar disorder, major depression, obsessive-compulsive disorder, schizophrenia, and Tourette syndrome. Genetic correlation analyses revealed a meaningful structure within the eight disorders, identifying three groups of inter-related disorders. Meta-analysis across these eight disorders detected 109 loci associated with at least two psychiatric disorders, including 23 loci with pleiotropic effects on four or more disorders and 11 loci with antagonistic effects on multiple disorders. The pleiotropic loci are located within genes that show heightened expression in the brain throughout the lifespan, beginning prenatally in the second trimester, and play prominent roles in neurodevelopmental processes. These findings have important implications for psychiatric nosology, drug development, and risk prediction.Peer reviewe

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 hospitalization2,3,4 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