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There was no decrease in the size of the stria vascularis from the age of 5-7 months in C57BL/6J mice. The present model failed to reveal the effect of NYT on atrophy of the stria vascularis of the cochlear duct. In conclusion, NYT appears to have a protective effect on the auditory nerve and suppress the progression of age-related hearing loss by reducing age-related auditory nerve degeneration.Background As the population ages, the rate of hip fractures and the need for rehabilitation increases. Home-based rehabilitation (HBR) is an alternative to classic inpatient rehabilitation (IR), which is an expensive framework with non-negligible risks. Methods A retrospective study of patients 65 years and above following surgery to repair a hip fracture who underwent HBR or IR between 2016 and 2019. The two rehabilitation frameworks were compared for rehabilitation outcome and factors predicting successful rehabilitation. The outcome was determined with the Montebello Rehabilitation Factor Score-Revised (MRFS-R). Results Data were collected for 235 patients over 3 years. The mean age was 81.3 ± 8.0 and 172 (73.3%) were women. Of these, 138 underwent IR and 97 HBR. The HBR group had better family support and fewer lived alone. There were also differences in the type of fracture and surgery. The medical condition of the IR group was more complex, as reflected in a higher Charlson's comorbidity scores, higher rates for delirium and more infectious complications, a lower Norton score, lower serum hemoglobin, and albumin levels, and higher serum creatinine and urea levels. It also had a more significant functional decline after surgery and required a longer rehabilitation period. However, no difference was found in the rehabilitation outcomes between the two groups (MRFS-R ≥ 50). The independent predictors for rehabilitation in the IR group were serum albumin level, comorbidity, and cognitive state. There were no independent predictors in the HBR group. Conclusions In this retrospective study, there was no significant difference in short-term rehabilitation outcomes between the HBR and IR groups event though the patients in the IR group were medically more complex. This result should be taken into account when planning rehabilitation services after hip fracture and tailoring rehabilitation frameworks to patients.Introduction Despite improved therapies and management, patients with systemic lupus erythematosus (SLE) still have increased risks of cerebrovascular and cardiovascular disease. High-frequency ultrasound (US) provides an opportunity to distinguish atherosclerosis from inflammation in the vessels. We hypothesized that an extended US protocol may add information regarding vascular affection in SLE. Methods Sixty patients (52 women, 8 men; mean age 43.2 ± 11.3 years) with SLE characterized by either lupus nephritis (LN; n = 20), antiphospholipid syndrome (APS; n = 20), or skin and joint involvement (n = 20) as well as matched healthy controls (n = 60) were included. Intima-media thickness (IMT), assessment of vessel walls, and plaque occurrence were recorded using high-frequency US (GE Logic E9) in common carotid, internal carotid, brachiocephalic, subclavian, axillary, common femoral, and proximal superficial femoral arteries as well as in the aortic arch. Results For the entire SLE group, IMT was increased inmong SLE patients without presence of plaques, an extended US protocol revealed increased wall thickness with predominantly medium echogenic appearance highlighting possibly inflammation or early atherosclerosis. The appearance of vessel walls has not previously been studied in detail. An increased number of plaques were found in SLE compared to age- and sex-matched healthy controls. We found similar risk factors for increased IMT and occurrence of plaques, possibly indicating atherosclerotic mechanisms rather than inflammation.Providing routine healthcare to patients with serious health illnesses represents a challenge to healthcare providers amid the SARS-CoV-2 pandemic. Treating cancer patients during this pandemic is even more complex due to their heightened vulnerability, as both cancer and cancer treatment weaken the immune system leading to a higher risk of both infections and severe complications. Tefinostat mw In addition to the need to protect cancer patients from unnecessary exposure to SARS-CoV-2 infection during their routine care, interruption, and discontinuation of cancer treatment can result in negative consequences on patients' health, in addition to the ghost of rationing healthcare resources in high demand during a global health crisis. This article aims to explore the ethical dilemmas faced by decision-makers and healthcare providers caring for cancer patients during the SARS-CoV-2 pandemic. This includes setting triage criteria for non-infected cancer patients, fairly allocating limited healthcare resources between cancer patients and SARS-CoV-2 patients, prioritizing SARS-CoV-2 treatment or vaccine, once developed, for cancer patients and non-cancer patients, patient-physician communication on matters such as end-of-life and do-not-resuscitate (DNR), and lastly, shifting physicians' priorities from treating their own cancer patients to treating critically ill SARS-CoV-2 infected patients. Ultimately, no straightforward decision can be easily made at such exceptionally difficult times. Applying different ethical principles can result in very different scenarios and consequences. In the end, we will briefly share the experience of the King Hussein Cancer Center (KHCC), the only standalone comprehensive cancer center in the region.During oogenesis and fertilization, histone lysine methyltransferases (KMTs) and histone lysine demethylases (KDMs) tightly regulate the methylation of histone H3 on lysine-4 (H3K4me) by adding and removing methyl groups, respectively. Female germline-specific conditional knockout approaches that abolish the maternal store of target mRNAs and proteins are used to examine the functions of H3K4 KMTs and KDMs during oogenesis and early embryogenesis. In this review, we discuss the recent advances in information regarding the deposition and removal of histone H3K4 methylations, as well as their functional roles in sculpting and poising the oocytic and zygotic genomes. We start by describing the role of KMTs in establishing H3K4 methylation patterns in oocytes and the impact of H3K4 methylation on oocyte maturation and competence to undergo MZT. We then introduce the latest information regarding H3K4 demethylases that account for the dynamic changes in H3K4 modification levels during development and finish the review by specifying important unanswered questions in this research field along with promising future directions for H3K4-related epigenetic studies.Actin is the major protein constituent of the cytoskeleton that performs wide range of cellular functions. It exists in monomeric and filamentous forms, dynamics of which is regulated by a large repertoire of actin binding proteins. However, not much was known about existence of these proteins in trypanosomatids, till the genome sequence data of three important organisms of this class, viz. Trypanosoma brucei, Trypanosoma cruzi and Leishmania major, became available. Here, we have reviewed most of the findings reported to date on the intracellular distribution, structure and functions of these proteins and based on them, we have hypothesized some of their functions. The major findings are as follows (1) All the three organisms encode at least a set of ten actin binding proteins (profilin, twinfilin, ADF/cofilin, CAP/srv2, CAPz, coronin, two myosins, two formins) and one isoform of actin, except that T. cruzi encodes for three formins and several myosins along with four actins. (2) Actin 1 and a few actin bindinates karyokinesis by effecting splindle elongation and DNA synthesis. (10) Leishmania coronin binds and promotes actin filament formation and exists in tetrameric form rather than trimeric form, like other coronins. (11) Trypanosomatid profilins are essential for survival of all the three parasites.Owing to its pronounced regenerative capacity in many tissues and organs, the zebrafish brain represents an ideal platform to understand the endogenous regeneration mechanisms that restore tissue integrity and function upon injury or disease. Although radial glial and neuronal cell populations have been characterized with respect to specific marker genes, comprehensive transcriptomic profiling of the regenerating telencephalon has not been conducted so far. Here, by processing the lesioned and unlesioned hemispheres of the telencephalon separately, we reveal the differentially expressed genes (DEGs) at the early wound healing and early proliferative stages of regeneration, i.e., 20 h post-lesion (hpl) and 3 days post-lesion (dpl), respectively. At 20 hpl, we detect a far higher number of DEGs in the lesioned hemisphere than in the unlesioned half and only 7% of all DEGs in both halves. However, this difference disappears at 3 dpl, where the lesioned and unlesioned hemispheres share 40% of all DEGs. By performing an extensive comparison of the gene expression profiles in these stages, we unravel that the lesioned hemispheres at 20 hpl and 3 dpl exhibit distinct transcriptional profiles. We further unveil a prominent activation of Wnt/β-catenin signaling at 20 hpl, returning to control level in the lesioned site at 3 dpl. Wnt/β-catenin signaling indeed appears to control a large number of genes associated primarily with the p53, apoptosis, forkhead box O (FoxO), mitogen-activated protein kinase (MAPK), and mammalian target of rapamycin (mTOR) signaling pathways specifically at 20 hpl. Based on these results, we propose that the lesioned and unlesioned hemispheres react to injury dynamically during telencephalon regeneration and that the activation of Wnt/β-catenin signaling at the early wound healing stage plays a key role in the regulation of cellular and molecular events.Epigenetic modulation, including acetylation, methylation, phosphorylation, and ubiquitination, plays a pivotal role in regulation of gene expression. Histone acetylation-a balance between the activities of histone acetyltransferases (HATs) and histone deacetylases (HDACs)-is one of the key epigenetic events. Our understanding of the role of HDACs in cancer is evolving. A number of HDAC isoenzymes are overexpressed in a variety of malignancies. Aberrant histone acetylation is associated with dysregulation of tumor suppressor genes leading to development of several solid tumors and hematologic malignancies. Pre-clinical studies have demonstrated that HDAC-1 gene expression is associated with lung cancer progression. Histone hypoacetylation is associated with more aggressive phenotype in adenocarcinoma of the lung. HDAC inhibitors (HDACi) have pleiotropic cellular effects and induce the expression of pro-apoptotic genes/proteins, cause cellular differentiation and/or cell cycle arrest, inhibit angiogenesis, and inhibit transition to a mesenchymal phenotype. Consequently, treatment with HDACi has shown anti-proliferative activity in non-small cell lung cancer (NSCLC) cell lines. Despite promising results in pre-clinical studies, HDACi have shown only modest single agent activity in lung cancer clinical trials. HDAC activation has been implicated as one of the mechanisms causing resistance to chemotherapy, molecularly targeted therapy, and immune checkpoint inhibition. Therefore, there is a growing interest in combining HDACi with these agents to enhance their efficacy or reverse resistance. In this paper, we review the available preclinical and clinical evidence for the use of HDACi in NSCLC. We also review the challenges precluding widespread clinical utility of HDACi as a cancer therapy and future directions.
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