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Normal weight obesity (NWO) is defined as having a normal body mass index (BMI), but a high body fat mass. There is growing interest in individuals with NWO, which is an underdiagnosed and understudied group, because of their increased risk for cardiometabolic morbidity and mortality. In this review, we summarized the definition, prevalence, etiology, pathophysiology, and cardiovascular outcomes seen in NWO. We have also summarized the available literature on interventions for NWO. There is a wide variation in the body fat percent cutoffs used to diagnose excess body fat. Hence, the prevalence rates of NWO vary between different populations and studies. It is estimated that about 30 million Americans have NWO and the worldwide prevalence ranges from 4.5% to 22%. Genetics, diet, and physical activity are related to NWO. However, etiological factors are not clear. Changes in body composition, inflammation, oxidative stress are present in NWO in comparison to normal weight lean (NWL) who have a normal BMI and normal body fat amount. Furthermore, cardiometabolic changes are observed and some are subclinical. Thus, screening for NWO will enhance the primary prevention of cardiovascular disease. Due to the use of various body fat percent cutoffs and methods to measure body fat, it is challenging to compare between studies. Researchers working in this field should ideally work towards developing standard body fat percent cutoffs for diagnosing NWO. There are many gaps in the literature on NWO unlike for overt obesity and future studies should explore the etiology, molecular mechanisms, and adipose tissue changes of NWO as well as conduct well planned and executed randomized controlled trials testing dietary, physical, and behavioral interventions for NWO in both males and females of different racial and age groups.

To examine whether leisure time physical activity changes predict subsequent body mass index (BMI) changes, and conversely, whether BMI changes predict subsequent leisure time physical activity changes.

This prospective cohort study included adults attending ≥3 consecutive Tromsø Study surveys (time T1, T2, T3) during 1974-2016 (n = 10779). If participants attended >3 surveys, we used the three most recent surveys. We computed physical activity change (assessed by the Saltin-Grimby Physical Activity Level Scale) from T1 to T2, categorized as Persistently Inactive (n = 992), Persistently Active (n = 7314), Active to Inactive (n = 1167) and Inactive to Active (n = 1306). We computed BMI change from T2 to T3, which regressed on preceding physical activity changes using analyses of covariance. The reverse association (BMI change from T1 to T2 and physical activity change from T2 to T3; n = 4385) was assessed using multinomial regression.

Average BMI increase was 0.86 kg/m

(95% CI 0.82-0.90) from T2 to anges, whereas BMI change predicted subsequent physical activity change. These findings indicate that BMI change predicts subsequent physical activity change at population level and not vice versa.Encapsulated papillary carcinoma (EPC) of the breast is a rare subtype of tumor. To date, the genetic abnormalities underlying EPC remain elusive. The purpose of this study was to gain further insight into EPC mutation profile. Forty-one EPCs diagnosed from 2015 to 2018 were included. Twenty-six EPCs were submitted to whole-exome sequencing (WES), and a 185 gene-targeted sequencing panel was designed to validate the results of the 26 EPCs that underwent WES and 15 additional cases. Recurrently mutated genes were further confirmed by Sanger sequencing. Selleck NVP-ADW742 Our study revealed multiple recurrently mutated genes including PI3K-AKT-mTOR pathway genes (PIK3CA, AKT1, ULK1, MAP3K1, MAP2K4, RHOA, and PTEN) (27/41, 65.8%) and chromatin modification genes (ZFPM1, GATA3, CTCF, and KMT2C) (21/41, 51.2%) in EPC. Importantly, somatic ZFPM1 mutations existed in 9/41 (21.9%) of the EPCs. The frequency of ZFPM1 mutations in the EPCs was significantly higher than that of other tumor types. Of the nine ZFPM1 mutations, seven were frameshift mutations, and the remaining two were nonsense mutations. Moreover, a significant concurrence of ZFPM1 and PI3K-AKT-mTOR mutations were revealed in the EPCs. Of note, no TP53 mutations were detected in our EPCs, whereas it was detected in a considerable proportion of the luminal A invasive ductal carcinomas of no special type (IDC-NSTs) from TCGA. We reveal that recurrent somatic ZFPM1 mutation is characteristic of EPC and concurred with mutations in the PI3K-AKT-mTOR pathway. The distinctive genetic features of EPC might underlie its special histological structures and indolent behavior.Pigeon pea, a grain legume of the semiarid tropics, is a rich source of high-quality protein. The productivity of this pulse is seriously affected by lepidopteron insect pests. To generate a sustainable insect-resistant plant, synthetically prepared bioactive key constituents of a crystal protein (Syn Cry1Ab) of Bacillus thuringiensis were expressed in pigeon pea under the guidance of a tissue-specific promoter of the RuBP carboxylase/oxygenase small subunit (rbcS) gene. Regenerated transgenic plants with the cry1Ab expression cassette (cry1Ab-lox-bar-lox) showed the optimum insect motility rate (90%) in an in vitro insect bioassay with second instar larvae, signifying the insecticidal potency of Syn Cry1Ab. In parallel, another plant line was also generated with a chimaeric vector harbouring a cre recombinase gene under the control of the CaMV 2 × 35S promoter. Crossing between T1 plants with a single insertion of cry1Ab-lox-bar-lox T-DNA and T1 plants with moderate expression of a cre gene with a linked hygromycin resistance (hptII) gene was performed to exclude the bialaphos resistance (bar) marker gene. Excision of the bar gene was achieved in T1F1 hybrids, with up to 35.71% recombination frequency. Insect-resistant pigeon pea plants devoid of selectable marker genes (syn Cry1Ab- bar and cre-hptII) were established in a consecutive generation (T1F2) through genetic segregation.A Correction to this paper has been published https//doi.org/10.1038/s41586-021-03367-9.

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