CHARACTERISTICS OF DEVELOPMENT OF EMOTIONAL BURNOUT SYNDROME IN FAMILY DOCTORS AND THEIR CORRECTION METHODS.

Objective: The aim: Among the adverse psychological changes associated with medical work, a significant place belongs to the emotional burnout syndrome, which significantly affects a doctor's social functioning. The purpose of the study was to determine the behavioural activity types and to study the muscular sensitivity threshold of family doctors with the formed emotional burnout syndrome.

Patients And Methods: Materials and methods: We examined 83 female family doctors with diagnosed emotional burnout syndrome.

PHENSIM: Phenotype Simulator.

Despite the unprecedented growth in our understanding of cell biology, it still remains challenging to connect it to experimental data obtained with cells and tissues' physiopathological status under precise circumstances. This knowledge gap often results in difficulties in designing validation experiments, which are usually labor-intensive, expensive to perform, and hard to interpret. Here we propose PHENSIM, a computational tool using a systems biology approach to simulate how cell phenotypes are affected by the activation/inhibition of one or multiple biomolecules, and it does so by exploiting signaling pathways.

A phase I delayed-start, randomized and pharmacodynamic study of metformin and chemotherapy in patients with solid tumors.

Purpose: Metformin activates AMP-related pathways leading to inactivation of mammalian target of rapamycin (mTOR) and suppression of its downstream effectors, crucial for cancer growth. Epidemiologic studies showed a reduced incidence and improved survival in cancer patients. We conducted a prospective phase I study to assess the safety of metformin in combination with chemotherapy in patients with solid tumors.

The combination of knockdown and TNFα causes synthetic lethality via caspase-8 activation in human carcinoma cell lines.

Most normal and tumor cells are protected from tumor necrosis factor α (TNFα)-induced apoptosis. Here, we identify the MAP3 kinase tumor progression locus-2 (TPL2) as a player contributing to the protection of a subset of tumor cell lines. The combination of knockdown and TNFα gives rise to a synthetic lethality phenotype via receptor-interacting serine/threonine-protein kinase 1 (RIPK1)-dependent and -independent mechanisms.

Health-related behaviour in adolescents who have received basic instruction in health promotion.

Objective: Introduction: Both positive and risky health behaviours among adolescents are of paramount importance as they often pathway further lifestyles and determine future health outcomes. The paper focuses on the trends of health promotion activities and health risks among adolescents who have been instructed on these topics at secondary schools. The aim: to detect trends in pro-active health behaviour and risk taking activities of Ukrainian adolescents in the last 14 years.

Computer-tomographic characteristics of root length incisors and canines of the upper and lower jaws in boys and girls with different craniotypes and physiological bite.

Introduction: In recent years, in world literature appeared research, which focuses on the study of relationships craniotypes with odonto-metric indicators, size, shape of the dental arches and occlusion. However, most of the experts focus on the study of individual features of the structure of the teeth-jaw system in people with different types of faces and aspects of sexual dimorphism and ethnic characteristics. Studies containing information about cranio-typological variability of the roots of teeth we did not encounter.

MicroRNA214 Is Associated With Progression of Ulcerative Colitis, and Inhibition Reduces Development of Colitis and Colitis-Associated Cancer in Mice.

Background & Aims: Persistent activation of the inflammatory response contributes to the development of inflammatory bowel diseases, which increase the risk of colorectal cancer. We aimed to identify microRNAs that regulate inflammation during the development of ulcerative colitis (UC) and progression to colitis-associated colon cancer (CAC).

Methods: We performed a quantitative polymerase chain reaction analysis to measure microRNAs in 401 colon specimens from patients with UC, Crohn's disease, irritable bowel syndrome, sporadic colorectal cancer, or CAC, as well as subjects without these disorders (controls); levels were correlated with clinical features and disease activity of patients.

Tpl2 ablation promotes intestinal inflammation and tumorigenesis in Apcmin mice by inhibiting IL-10 secretion and regulatory T-cell generation.

To address the role of Tpl2, a MAP3K8 that regulates innate/adaptive immunity and inflammation, in intestinal tumorigenesis, we crossed a Tpl2 KO allele into the Apc(min/+) genetic background. Here, we show that Apc(min/+)/Tpl2(-/-) mice exhibit a fivefold increase in the number of intestinal adenomas. Bone marrow transplantation experiments revealed that the enhancement of polyposis was partially hematopoietic cell-driven.

Tumor progression locus 2 mediates signal-induced increases in cytoplasmic calcium and cell migration.

The mitogen-activated protein kinase kinase kinase (MAPKKK or MAP3K) tumor progression locus 2 (Tpl2) is required for the transduction of signals initiated by the thrombin-activated G protein-coupled receptor (GPCR) protease-activated receptor-1 (PAR1), which promote reorganization of the actin cytoskeleton and cell migration. Here, we show that Tpl2 is activated through Gα(i2)-transduced GPCR signals. Activated Tpl2 promoted the phosphorylation and activation of phospholipase C-β3 (PLCβ(3)); consequently, Tpl2 was required for thrombin-dependent production of inositol 1,4,5-trisphosphate (IP(3)), IP(3)-mediated cytoplasmic calcium ion (Ca(2+)) signals, and the activation of classical and novel members of the protein kinase C (PKC) family.

Members of a family of JmjC domain-containing oncoproteins immortalize embryonic fibroblasts via a JmjC domain-dependent process.

A common integration site, cloned from MoMuLV-induced rat T cell lymphomas, was mapped immediately upstream of Not dead yet-1 (Ndy1)/KDM2B, a gene expressed primarily in testis, spleen, and thymus, that is also known as FBXL10 or JHDM1B. Ndy1 encodes a nuclear, chromatin-associated protein that harbors Jumonji C (JmjC), CXXC, PHD, proline-rich, F-box, and leucine-rich repeat domains. Ndy1 and its homolog Ndy2/KDM2A (FBXL11 or JHDM1A), which is also a target of provirus integration in retrovirus-induced lymphomas, encode proteins that were recently shown to possess Jumonji C-dependent histone H3 K36 dimethyl-demethylase or histone H3 K4 trimethyl-demethylase activities.