Notes

Performance of the Home-Based Exercising Treatment in the Health and fitness Report regarding Hispanic Children associated with Breast Cancer.
Locally advanced pheochromocytoma (LAP) behavior remains unknown.

To characterize this population and its recurrence-free survival (RFS).

A retrospective multicentric study run within the ENDOCAN-COMETE network and GTE from 2003 to 2018.

11 French Referral centers.

Patients with LAP as defined by capsular invasion, vascular invasion, adipose tissue invasion and/or positive locoregional lymph nodes at diagnosis without evidence of distant metastasis.

Recurrence was defined as the reappearance of the tumor, including local site and/or distant metastasis. The primary endpoint was RFS analysis. The secondary endpoints were characterization, overall survival (OS) and prognostic factors of recurrence.

Among 950 patients, 90 exhibited LAP criteria (9%). 55 met the inclusion criteria (median age 53 years-old, 61% males, 14% with a germline mutation, 84% with a catecholamine excess). LAP was defined by 31 (56%) capsular invasions, 27 (49%) fat invasions, 6 (11%) positive lymph nodes and 22 (40%) vascular invasions. After a median follow-up of 54 months (range, 6-180), 12 patients (22%) had recurrences and 3 (5%) died of a metastatic disease. Median RFS was 115 months (range, 6-168). The recurrences were local in 2 patients, distant in 2 and both local and distant in 8 patients. Median OS of patients was not reached. Size above 6.5cm (p=0.019) and Ki-67>2% (p=0.028) were identified as independent significant prognostic factors in multivariate analysis.

LAP represents 9% of pheochromocytoma's population and is characterized by a metastatic behavior. This study paved the way of a future pathological TNM classification.
LAP represents 9% of pheochromocytoma's population and is characterized by a metastatic behavior. This study paved the way of a future pathological TNM classification.
Fatigue can be induced after acceleration exposure, however its mechanism is still unclear. The aim of the present study was to examine whether metabolites' changes can decrease cognitive and physical function after acceleration.

Graybiel scale and Fatigue Self-rating scale were used to assess the seasickness and fatigue degrees of 87 male seafarers respectively after sailing. To test the effect of pyruvate on cognitive and physical functions, five different doses of pyruvate were administrated into rats. Insulin can reduce the accumulation of pyruvate. To observe the insulin effect on pyruvate, cognitive and physical functions after acceleration, insulin administration or treatment of promoting insulin secretion was used. Physical and cognitive functions were assessed using open field test (OFT), morris water maze (MWM) and loaded swimming test (LST) in animals.

Physical and cognitive abilities were decreased obviously, and serum pyruvate increased mostly in human and rats after acceleration. Compared with vehicle group, physical and cognitive abilities were significantly decreased after pyruvate administration. Besides, we found a significant decline in adenosine triphosphate (ATP) concentration and pyruvate dehydrogenase (PDH) activity in the hippocampus, prefrontal cortex, liver, and muscle of rats treated with acceleration or pyruvate injection, while insulin administration or treatment of promoting insulin secretion markedly alleviated this decline and the impairment of physical and cognitive abilities, compared with the control group.

Our results indicate that pyruvate has a negative effect on physical and cognitive abilities after acceleration. Insulin can inhibit pyruvate accumulation and cognitive and physical function after acceleration exposure.
Our results indicate that pyruvate has a negative effect on physical and cognitive abilities after acceleration. Insulin can inhibit pyruvate accumulation and cognitive and physical function after acceleration exposure.Hypertension is a complex and multifactorial disorder caused by lifestyle and environmental factors, inflammation and disease-related genetic factors and is a risk factor for stroke, ischemic heart disease and renal failure. Although circulating monocytes and tissue macrophages contribute to the pathogenesis of hypertension, the underlying mechanisms are poorly understood. Cysteine rich protein 1 (CRIP1) is highly expressed in immune cells, and CRIP1 mRNA expression in monocytes associates with blood pressure (BP) and is up-regulated by proinflammatory modulation suggesting a link between CRIP1 and BP regulation through the immune system. To address this functional link, we studied CRIP1 expression in immune cells in relation to BP using a human cohort study and hypertensive mouse models. CRIP1 expression in splenic monocytes/macrophages and in circulating monocytes was significantly affected by angiotensin II (Ang II) in a BP-elevating dose (2 mg/kg/day). GSK J1 mouse In the human cohort study, monocytic CRIP1 expression levels were associated with elevated BP, whereas upon differentiation of monocytes to macrophages this association along with the CRIP1 expression level was diminished. In conclusion, CRIP1-positive circulating and splenic monocytes seem to play an important role in hypertension related inflammatory processes through endogenous hormones such as Ang II. These findings suggest that CRIP1 may affect the interaction between the immune system, in particular monocytes, and the pathogenesis of hypertension.With the recent upswing of infectious disease outbreaks (coronavirus, influenza, Ebola, etc), there is an ever-increasing need for biocontainment animal use protocols to better address the research of emerging diseases and to increase the health of both animals and humans. It is imperative that we as a research community ensure these protocols are conducted with the utmost scrutiny and regulatory compliance for the welfare of the animals as well as the health and safety concerns of the individual conducting these studies. Both the welfare of the animals and the health and safety of the research staff must be balanced with the integrity of the science being studied. Even prior to reviewing biocontainment protocols, the research stakeholders should have professional and collegial interactions across all levels of the proposed project. These stakeholders should include the attending veterinarian, the principal investigator, the sponsor, and any organic institutional health and safety assets (environmental healthintegrity of the science and ultimately the welfare of the animal.New developments in single-cell genomics have transformed developmental biology in recent years by enabling systematic analysis of embryonic cell types and differentiation trajectories. Ongoing efforts in experimental and computational method development aim to reveal gene-regulatory mechanisms and to provide additional spatio-temporal information about developmental cell fate decisions. Here, we discuss recent technological developments as well as biological applications of single-cell genomics, with a particular focus on analysis of developmental cell fate decisions. Although the approaches described here are generally applicable to a broad range of model systems, we focus our discussion on applications in zebrafish, which has proven to be a particularly powerful model organism for establishing novel methods in single-cell genomics.In network and systems medicine, active module identification methods (AMIMs) are widely used for discovering candidate molecular disease mechanisms. To this end, AMIMs combine network analysis algorithms with molecular profiling data, most commonly, by projecting gene expression data onto generic protein-protein interaction (PPI) networks. Although active module identification has led to various novel insights into complex diseases, there is increasing awareness in the field that the combination of gene expression data and PPI network is problematic because up-to-date PPI networks have a very small diameter and are subject to both technical and literature bias. In this paper, we report the results of an extensive study where we analyzed for the first time whether widely used AMIMs really benefit from using PPI networks. Our results clearly show that, except for the recently proposed AMIM DOMINO, the tested AMIMs do not produce biologically more meaningful candidate disease modules on widely used PPI networks than on random networks with the same node degrees. AMIMs hence mainly learn from the node degrees and mostly fail to exploit the biological knowledge encoded in the edges of the PPI networks. This has far-reaching consequences for the field of active module identification. In particular, we suggest that novel algorithms are needed which overcome the degree bias of most existing AMIMs and/or work with customized, context-specific networks instead of generic PPI networks.Cell competition is defined as the context-dependent elimination of cells that is mediated by intercellular communication, such as paracrine or contact-dependent cell signaling, and/or mechanical stresses. It is considered to be a quality control mechanism that facilitates the removal of suboptimal cells from both adult and embryonic tissues. Cell competition, however, can also be hijacked by transformed cells to acquire a 'super-competitor' status and outcompete the normal epithelium to establish a precancerous field. To date, many genetic drivers of cell competition have been identified predominately through studies in Drosophila. Especially during the last couple of years, ethylmethanesulfonate-based genetic screens have been instrumental to our understanding of the molecular regulators behind some of the most common competition mechanisms in Drosophila, namely competition due to impaired ribosomal function (or anabolism) and mechanical sensitivity. Despite recent findings in Drosophila and in mammalian models of cell competition, the drivers of mammalian cell competition remain largely elusive. Since the discovery of CRISPR/Cas9, its use in functional genomics has been indispensable to uncover novel cancer vulnerabilities. We envision that CRISPR/Cas9 screens will enable systematic, genome-scale probing of mammalian cell competition to discover novel mutations that not only trigger cell competition but also identify novel molecular components that are essential for the recognition and elimination of less fit cells. In this review, we summarize recent contributions that further our understanding of the molecular mechanisms of cell competition by genetic screening in Drosophila, and provide our perspective on how similar and novel screening strategies made possible by whole-genome CRISPR/Cas9 screening can advance our understanding of mammalian cell competition in the future.The complex processes necessary for embryogenesis require a gene regulatory network that is complex and systematic. Gene expression regulates development and organogenesis, but this process is altered and fine-tuned by epigenetic regulators that facilitate changes in the chromatin landscape. Epigenetic regulation of embryogenesis adjusts the chromatin structure by modifying both DNA through methylation and nucleosomes through posttranslational modifications of histone tails. The zebrafish is a well-characterized model organism that is a quintessential tool for studying developmental biology. With external fertilization, low cost and high fecundity, the zebrafish are an efficient tool for studying early developmental stages. Genetic manipulation can be performed in vivo resulting in quick identification of gene function. Large-scale genome analyses including RNA sequencing, chromatin immunoprecipitation and chromatin structure all are feasible in the zebrafish. In this review, we highlight the key events in zebrafish development where epigenetic regulation plays a critical role from the early stem cell stages through differentiation and organogenesis.
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