Multiple classical limits in relativistic and nonrelativistic quantum mechanics

The existence of a classical limit describing interacting particles in a second-quantized theory of identical particles with bosonic symmetry is proved. This limit exists in addition to a previously established classical limit with a classical field behavior, showing that the limit $\hbar \to 0$ of the theory is not unique. An analogous result is valid for a free massive scalar field: two distinct classical limits are proved to exist, describing a system of particles or a classical field. The introduction of local operators in order to represent kinematical properties of interest is shown to break the permutation symmetry under some localizability conditions, allowing the study of individual particle properties.Comment: 13 page

Checkmate to CHK1 in T-cell ALL?

© Impact Journals, LLC.DNA replication ensures accurate duplication of the original genetic information present in a cell in order for it to be properly transmitted to daughter cells. However, replication can be perturbed, for instance in rapidly dividing cancer cells, in a process referred to as replication stress (RS). Checkpoint kinase 1 (CHK1) is an essential component of the ATR-dependent DNA damageresponse pathway that protect cells from RS by preventing replication fork collapse and activating homologous DNA repair. The ATR-CHK1 pathway is triggered upon exposure of single-stranded DNA that arises with the stalling of replication forks, and it is required to reset proper origin firing, and to promote fork stability and checkpoint activation, delaying mitosis until replication is completed and thereby avoiding mitotic catastrophe.info:eu-repo/semantics/publishedVersio

Helminth infections, atopy, asthma and allergic diseases: protocol for a systematic review of observational studies worldwide.

INTRODUCTION: Childhood infections, particularly those caused by helminths are considered to be important environmental exposures influencing the development of allergic diseases. However, epidemiological studies focusing on the relationship between helminth infections and risk of allergic diseases, performed worldwide, show inconsistent findings. Previous systematic reviews of observational studies published 10 or more years ago showed conflicting findings for effects of helminths on allergic diseases. Over the past 10 years there has been growing literature addressing this research area and these need to be considered in order to appreciate the most contemporary evidence. The objective of the current systematic review will be to provide an up-to-date synthesis of findings of observational studies investigating the influence of helminth infections on atopy, and allergic diseases. METHODS AND ANALYSIS: This systematic review protocol was registered at PROSPERO. We will search Cochrane Library, MEDLINE, EMBASE, CINAHL, AMED, ISI Web of Science, WHO Global Health Library, Scielo, IndMed, PakMediNet, KoreaMed, Ichushi for published studies from 1970 to January 2020. Bibliographies of all eligible studies will be reviewed to identify additional studies. Unpublished and ongoing research will also be searched in key databases. There will be no language or geographical restrictions regarding publications. Critical Appraisal Skills Programme quality assessment tool will be used to appraise methodological quality of included studies. A descriptive summary with data tables will be constructed, and if adequate, meta-analysis using random-effects will be performed. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses checklist will be followed for reporting of the systematic review. ETHICS AND DISSEMINATION: Since this systematic review will be only based on published and retrievable literature, no ethics approval will be sought. The multidisciplinary team performing this systematic review will participate in relevant dissemination activities. Findings will be presented at scientific meetings and publish the systematic review in international, peer-reviewed, open-access journals. PROSPERO REGISTRATION NUMBER: CRD42020167249

Hyperuricemia in Chronic Kidney Disease: a Role Yet To Be Explained

The role of uric acid as an independent risk factor for chronic kidney disease development and progression is still a matter of discussion. Several observational studies showed a positive association between hyperuricemia and the progression of kidney dysfunction, but others did not, which probably derived from different biases and studies insufficiencies. Moreover, the results from studies on patients in hemodialysis and peritoneal dialysis are even more controversial, with some evidence pointing towards a protective role of uric acid in hemodialysis patients, but not in peritoneal dialysis. In addition to most evidence suggesting a role of uric acid in chronic kidney disease pathogenesis and progression, pharmacological treatment of asymptomatic hyperuricemia is still not indicated, with no consensus on either the uric acid level at which treatment would be beneficial, or the target-level to achieve. There are several studies on the renal benefits of xanthine oxidase inhibitors allopurinol and febuxostat, with heterogeneous results. Most of them showed a renoprotective effect of both drugs, delaying renal disease progression. However, the different results found in other studies makes it difficult to draw definitive conclusions. Despite recent evidence pointing toward an important role of uric acid in the pathogenesis and progression of kidney disorders, and the benefits of its treatment, there are still several unanswered questions, and well-conducted studies are needed to make valid conclusions.info:eu-repo/semantics/publishedVersio

Multifaceted CK2 in malignant and healthy T cells

Copyright © Ribeiro et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and re-production in any medium, provided the original author and source are credited.Among kinases that support the survival and turnover of tumor cells, the serine/threonine protein kinase CK2 has been shown to be frequently overexpressed or hyperactivated in solid and hematological malignancies. Our previous work on T-cell acute lymphoblastic leukemia (T-ALL) showed that CK2 maintains leukemia cell viability by phosphorylating and thereby inactivating the tumor suppressor PTEN, which results in hyperactivation of PI3K/AKT signaling. We also demonstrated the potential of using the clinical-grade CK2-specific chemical inhibitor, CX-4945 (Silmitasertib), against primary T-ALL cells. We have now extended these findings to the rare (<10% of all cases) form of T-ALL that derives from the transformation of thymocytes belonging to the γδ T-cell lineage.info:eu-repo/semantics/publishedVersio

Olanzapine-Induced Hyperprolactinemia: Two Case Reports

Background: Hyperprolactinemia is a common consequence of treatment with antipsychotics. It is usually defined by a sustained prolactin level above the laboratory upper level of normal in conditions other than that where physiologic hyperprolactinemia is expected. Normal prolactin levels vary significantly among different laboratories and studies. Several studies indicate that olanzapine does not significantly affect serum prolactin levels in the long term, although this statement has been challenged. Aims: Our aim is to report two olanzapine-induced hyperprolactinemia cases observed in psychiatric consultations. Methods: Medical records of the patients who developed this clinical situation observed in psychiatric consultations in the Psychiatry Department of the Prof. Dr. Fernando Fonseca Hospital during the year of 2017 were analyzed, complemented with a non-systematic review of the literature. Results: The case reports consider two women who developed prolactin-related symptoms after the initiation of olanzapine. No baseline prolactinemia was obtained, and prolactin serum levels were only evaluated after prolactin-related symptoms developed: at the time of its measurement, both patients had been taking olanzapine for more than 24 weeks. Hyperprolactinemia was found to be present in Case 2, whereas Case 1 (a 49-year-old woman) had "normal" serum prolactin levels for premenopausal and prolactin levels slightly above the maximum levels for postmenopausal women. Both patients underwent similar pharmacological adjustments, which comprised switches from olanzapine to aripiprazole. After all pharmacological changes, prolactin serum levels decreased to normal range values and prolactin-related symptoms disappeared. Discussion/Conclusions: Laboratorial and literature prolactinemia values variability and discrepancies may make the management of borderline hyperprolactinemia clinical situations difficult. Baseline prolactin levels should have been obtained, as they help in the management of patients who develop neuroleptic-induced hyperprolactinemia. Prolactin-related symptoms can occur with borderline or normal standardized prolactinemia values. Olanzapine-induced hyperprolactinemia is a rare but possible event. Aripiprazole was used as a suitable alternative for olanzapine-induced hyperprolactinemia.info:eu-repo/semantics/publishedVersio

Wernicke-Korsakoff Syndrome: A Case Series in Liaison Psychiatry.

Wernicke-Korsakoff syndrome (WKS) is a life-threatening and underdiagnosed neuropsychiatric condition caused by thiamine deficiency that comprises Wernicke encephalopathy and Korsakoff syndrome. Although mainly associated with chronic alcoholism, WKS can arise from other circumstances. This report describes a series of cases of WKS that were clinically evaluated by liaison psychiatrists on a nonpsychiatric inpatient unit. The cases illustrate a deficit in the recognition and adequate treatment of WKS, demonstrating its clinical complexity and the need to improve physicians' knowledgeinfo:eu-repo/semantics/publishedVersio