Adenomyosis

Adenomyosis is a benign uterus disease in which the invasion of the endometrial glands and/or stroma within myometrium is found and usually appears between the ages of 40 and 50 years in women. There are several differences in their pathogenesis. The secondary dysmenorrhea and menorrhagia are the common symptoms. Ultrasound sonography, MRI, CA125, and histological examination can be helpful for the diagnosis of adenomyosis. The treatment of adenomyosis depends on the patient’s age, symptoms, and desire for future fertility, including medical treatment and surgical treatment

Hygienismus a Socialismus v diskursivní reprezentaci Cité-jardin (1919-1950): diplomní práce na Institutu urbanismu pařížské University

Hygienismus a Socialismus v diskursivní reprezentaci cité-jardin (1919-1950): diplomní práce na Institutu urbanismu pařížské University Boya Wei Abstrakt Tato studie sleduje historii sociálního bydlení ve Francii 1919-1950, se zaměřením na tvorbu cité- jardin (zahradních měst) v okolí Paříže. V návaznosti na pojetí diskurzu a moci u Michela Foucaulta, a pojmu sociálního prostoru podle Henriho Lefèbvra, se tato studie zabývala reprezentacemi zahradních měst v textech studentských prací na Institut d'urbanisme de l'Université de Paris. V centru pozornosti byl výzkum způsobu, jakým elitní urbanistické prostředí při práci s konceptem cité-jardin odhalovalo aplikaci dvou diskurzů zásadního významu: "hygienistického" a "socialistického". Klíčová slova: Sociální bydlení, Paříž, cité-jardin, zahradní město, Michel Foucault, formování diskurzu Powered by TCPDF (www.tcpdf.org)Discursive Representations of cité-jardin through Hygienism and Socialism (1919-1950): Student Theses at Institut d'urbanisme de l'Université de Paris Boya Wei Abstract This study will trace the social housing history in France from 1919 to 1950, with a focus on the creation of cités-jardins in Paris region. Drawing on Michel Foucault's notion of discourse and power, and Henri Lefebvre's notion of social space, this study will look into the representations of cité-jardin in the writings of student thesis at the Institut d'Urbanisme de l'Université de Paris, while examining the ways in which elite discourses on cité-jardin provided a window into the re-appropriations of hygienist and socialist discourses. Keywords: Social housing, Paris, cité-jardin, garden city, Michel Foucault, discursive formation Powered by TCPDF (www.tcpdf.org)Institute of General HistoryÚstav světových dějinFilozofická fakultaFaculty of Art

The Prospects for Immigration Amendments

Obg proteins are a family of P-loop GTPases, conserved from bacteria to human. The Obg protein in Escherichia coli (ObgE) has been implicated in many diverse cellular functions, with proposed molecular roles in two global processes, ribosome assembly and stringent response. Here, using pre-steady state fast kinetics we demonstrate that ObgE is an anti-association factor, which prevents ribosomal subunit association and downstream steps in translation by binding to the 50S subunit. ObgE is a ribosome dependent GTPase; however, upon binding to guanosine tetraphosphate (ppGpp), the global regulator of stringent response, ObgE exhibits an enhanced interaction with the 50S subunit, resulting in increased equilibrium dissociation of the 70S ribosome into subunits. Furthermore, our cryo-electron microscopy (cryo-EM) structure of the 50S? ObgE? GMPPNP complex indicates that the evolutionarily conserved N-terminal domain (NTD) of ObgE is a tRNA structural mimic, with specific interactions with peptidyl-transferase center, displaying a marked resemblance to Class I release factors. These structural data might define ObgE as a specialized translation factor related to stress responses, and provide a framework towards future elucidation of functional interplay between ObgE and ribosome-associated (p) ppGpp regulators. Together with published data, our results suggest that ObgE might act as a checkpoint in final stages of the 50S subunit assembly under normal growth conditions. And more importantly, ObgE, as a (p) ppGpp effector, might also have a regulatory role in the production of the 50S subunit and its participation in translation under certain stressed conditions. Thus, our findings might have uncovered an under-recognized mechanism of translation control by environmental cues

Inhibition of the m6A reader IGF2BP2 as a strategy against T-cell acute lymphoblastic leukemia

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignant leukemia with extremely limited treatment for relapsed patients. N6‐methyladenosine (m6A) reader insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) participates in the initiation and growth of cancers by communicating with various targets. Here, we found IGF2BP2 was highly expressed in T-ALL. Gain and loss of IGF2BP2 demonstrated IGF2BP2 was essential for T-ALL cell proliferation in vitro and loss of IGF2BP2 prolonged animal survival in a human T-ALL xenograft model. Mechanistically, IGF2BP2 directly bound to T-ALL oncogene NOTCH1 via an m6A dependent manner. Furthermore, we identified a small-molecule IGF2BP2 inhibitor JX5 and treatment of T-ALL with JX5 showed similar functions as knockdown of IGF2BP2. These findings not only shed light on the role of IGF2BP2 in T-ALL, but also provide an alternative γ‑Secretase inhibitors (GSI) therapy to treat T-ALL.Inhibition of the m6A reader IGF2BP2 as a strategy against T-cell acute lymphoblastic leukemiapublishedVersio

Deacetylation of HSD17B10 by SIRT3 regulates cell growth and cell resistance under oxidative and starvation stresses.

17-beta-hydroxysteroid dehydrogenase 10 (HSD17B10) plays an important role in mitochondrial fatty acid metabolism and is also involved in mitochondrial tRNA maturation. HSD17B10 missense mutations cause HSD10 mitochondrial disease (HSD10MD). HSD17B10 with mutations identified from cases of HSD10MD show loss of function in dehydrogenase activity and mitochondrial tRNA maturation, resulting in mitochondrial dysfunction. It has also been implicated to play roles in the development of Alzheimer disease (AD) and tumorigenesis. Here, we found that HSD17B10 is a new substrate of NAD-dependent deacetylase Sirtuin 3 (SIRT3). HSD17B10 is acetylated at lysine residues K79, K99 and K105 by the acetyltransferase CBP, and the acetylation is reversed by SIRT3. HSD17B10 acetylation regulates its enzymatic activity and the formation of mitochondrial RNase P. Furthermore, HSD17B10 acetylation regulates the intracellular functions, affecting cell growth and cell resistance in response to stresses. Our results demonstrated that acetylation is an important regulation mechanism for HSD17B10 and may provide insight into interrupting the development of AD

A geometric approach to time evolution operators of Lie quantum systems

Lie systems in Quantum Mechanics are studied from a geometric point of view. In particular, we develop methods to obtain time evolution operators of time-dependent Schrodinger equations of Lie type and we show how these methods explain certain ad hoc methods used in previous papers in order to obtain exact solutions. Finally, several instances of time-dependent quadratic Hamiltonian are solved.Comment: Accepted for publication in the International Journal of Theoretical Physic

Elevated p62/SQSTM1 determines the fate of autophagy-deficient neural stem cells by increasing superoxide

Autophagy plays important roles in many biological processes, but our understanding of the mechanisms regulating stem cells by autophagy is limited. Interpretations of earlier studies of autophagy using knockouts of single genes are confounded by accumulating evidence for other functions of many autophagy genes. Here, we show that, in contrast to Fip200 deletion, inhibition of autophagy by deletion of Atg5, Atg16L1, or Atg7 does not impair the maintenance and differentiation of postnatal neural stem cells (NSCs). Only Fip200 deletion, but not Atg5, Atg16L1, or Atg7 deletion, caused p62/sequestome1 aggregates to accumulate in NSCs. Fip200 and p62 double conditional knockout mice demonstrated that p62 aggregate formation triggers aberrant superoxide increases by impairing superoxide dismutase functions. By comparing the inhibition of autophagy by deletion of Atg5, Atg16L1, or Atg7 with Fip200 deletion, we revealed a critical role of increased p62 in determining the fate of autophagy-deficient NSCs through intracellular superoxide control

Simultaneous Induction of Non-Canonical Autophagy and Apoptosis in Cancer Cells by ROS-Dependent ERK and JNK Activation

Background: Chemotherapy-induced reduction in tumor load is a function of apoptotic cell death, orchestrated by intracellular caspases. However, the effectiveness of these therapies is compromised by mutations affecting specific genes, controlling and/or regulating apoptotic signaling. Therefore, it is desirable to identify novel pathways of cell death, which could function in tandem with or in the absence of efficient apoptotic machinery. In this regard, recent evidence supports the existence of a novel cell death pathway termed autophagy, which is activated upon growth factor deprivation or exposure to genotoxic compounds. The functional relevance of this pathway in terms of its ability to serve as a stress response or a truly death effector mechanism is still in question; however, reports indicate that autophagy is a specialized form of cell death under certain conditions. Methodology/Principal Findings: We report here the simultaneous induction of non-canonical autophagy and apoptosis in human cancer cells upon exposure to a small molecule compound that triggers intracellular hydrogen peroxide (H2O2) production. Whereas, silencing of beclin1 neither inhibited the hallmarks of autophagy nor the induction of cell death, Atg 7 or Ulk1 knockdown significantly abrogated drug-induced H2O2-mediated autophagy. Furthermore, we provide evidence that activated extracellular regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) are upstream effectors controlling both autophagy and apoptosis in response to elevated intracellular H2O2. Interestingly, inhibition of JNK activity reversed the increase in Atg7 expression in this system, thus indicating that JNK may regulate autophagy by activating Atg7. Of note, the small molecule compound triggered autophagy and apoptosis in primary cells derived from patients with lymphoma, but not in non-transformed cells. Conclusions/Significance: Considering that loss of tumor suppressor beclin 1 is associated with neoplasia, the ability of this small molecule compound to engage both autophagic and apoptotic machineries via ROS production and subsequent activation of ERK and JNK could have potential translational implications.Singapore. Biomedical Research CouncilSingapore. Ministry of Educatio