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Monkeypox virus (MPV) is a smallpox-like virus belonging to the genus Orthopoxvirus of the family Poxviridae. Unlike smallpox with no animal reservoir identified and patients suffering from milder symptoms with less mortality, several animals were confirmed to serve as natural hosts of MPV. The reemergence of a recently reported monkeypox epidemic outbreak in nonendemic countries has raised concerns about a global outburst. Since the underlying mechanism of animal-to-human transmission remains largely unknown, comprehensive analyses to discover principal differences in gene signatures during disease progression have become ever more critical. In this study, two MPV-infected in vitro models, including human immortal epithelial cancer (HeLa) cells and rhesus monkey ( Macaca mulatta ) kidney epithelial (MK2) cells, were chosen as the two subjects to identify alterations in gene expression profiles, together with co-regulated genes and pathways that are affected during monkeypox disease progression. Using Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and MetaCore analyses, we discovered that elevated expression of genes associated with interleukins (ILs), G protein-coupled receptors (GPCRs), heat shock proteins (HSPs), Toll-like receptors (TLRs), and metabolic-related pathways play major roles in disease progression of both monkeypox-infected monkey MK2 and human HeLa cell lines. Interestingly, our analytical results also revealed that a cluster of differentiation 40 (CD40), plasmin, and histamine served as major regulators in the monkeypox-infected monkey MK2 cell line model, while interferons (IFNs), macrophages, and neutrophil-related signaling pathways dominated the monkeypox-infected human HeLa cell line model. Among immune pathways of interest, apart from traditional monkeypox-regulated signaling pathways such as nuclear factor- (NF- κ B), mitogen-activated protein kinases (MAPKs), and tumor necrosis factors (TNFs), we also identified highly significantly expressed genes in both monkey and human models that played pivotal roles during the progression of monkeypox infection, including CXCL1 , TNFAIP3 , BIRC3 , IL6 , CCL2 , ZC3H12A , IL11 , CSF2 , LIF , PTX3 , IER3 , EGR1 , ADORA2A , and DUOX1 , together with several epigenetic regulators, such as histone cluster family gene members, HIST1H3D , HIST1H2BJ , etc. These findings might contribute to specific underlying mechanisms related to the pathophysiology and provide suggestions regarding modes of transmission, post-infectious sequelae, and vaccine development for monkeypox in the future., Competing Interests: The authors declare that they have no conflicts of interest., (Copyright © 2022 Do Thi Minh Xuan et al.)

Purpose: To assess the reduction of 6 and 12 months postoperatively of Framingham risk score in morbidly obese patients with laparoscopic sleeve gastrectomy (LSG)., Material and Methods: In total, 870 morbid obesity patients received LSG in Taipei Medical University Hospital from June 2007 to June 2014 were retrospectively studied preoperatively, 6 and 12 months after surgery. The coronary heart disease risk was calculated using Framingham risk score., Results: The body mass index in men and women decreased from 43.3 ± 6.9, 39.2 ± 6.0 kg/m 2 preoperatively to 32.9 ± 6.7, 31.0 ± 5.2 kg/m 2 and to 30.4 ± 5.6 , 28.2 ± 4.7 kg/m 2 , respectively, at 6 and 12 months after surgery (P < 0.0001). At 6 and 12 months after LSG, there was a marked improvement on lipid profile as well as a significant decline in the prevalence of diabetes mellitus, systemic hypertension, and smoking. The Framingham risk score in men and women reduced from 3.2 ± 5.7, 6.1 ± 5.7 preoperatively to 1.4 ± 5.9, 3.3 ± 5.9 and 0.1 ± 6.2, 2.8 ± 6.1, respectively, at 6 and 12 months after surgery (P < 0.0001)., Conclusions: Laparoscopic sleeve gastrectomy is efficient not only in the reduction of obesity and its related comorbidities but also in decreasing the long-term coronary event risk. Early intervention for the high-risk group is strongly recommended.

The optic lobe is the largest brain area within the central nervous system of cephalopods and it plays important roles in the processing of visual information, the regulation of body patterning, and locomotive behavior. The oval squid Sepioteuthis lessoniana has relatively large optic lobes that are responsible for visual communication via dynamic body patterning. It has been observed that the visual behaviors of oval squids change as the animals mature, yet little is known about how the structure of the optic lobes changes during development. The aim of the present study was to characterize the ontogenetic changes in neural organization of the optic lobes of S. lessoniana from late embryonic stage to adulthood. Magnetic resonance imaging and micro-CT scans were acquired to reconstruct the 3D-structure of the optic lobes and examine the external morphology at different developmental stages. In addition, optic lobe slices with nuclear staining were used to reveal changes in the internal morphology throughout development. As oval squids mature, the proportion of the brain making up the optic lobes increases continuously, and the optic lobes appear to have a prominent dent on the ventrolateral side. Inside the optic lobe, the cortex and the medulla expand steadily from the late embryonic stage to adulthood, but the cell islands in the tangential zone of the optic lobe decrease continuously in parallel. Interestingly, the size of the nuclei of cells within the medulla of the optic lobe increases throughout development. These findings suggest that the optic lobe undergoes continuous external morphological change and internal neural reorganization throughout the oval squid's development. These morphological changes in the optic lobe are likely to be responsible for changes in the visuomotor behavior of oval squids from hatching to adulthood., (© 2017 Wiley Periodicals, Inc.)

Purpose: This study examined the differences between illness representations of injured patients and those of their caregivers., Design: A comparative descriptive survey was used., Methods: The study setting was the surgical wards of a teaching hospital in Taiwan. Data were collected at 3 to 6 months after hospital discharge. Participants were 127 pairs of injured patients and their caregivers. The participants completed sociodemographic data and completed the Chinese Illness Perception Questionnaire Revised-Trauma, which is composed of eight subscales. Clinical data of the injured patients was obtained from medical records., Results: Injured patients and their caregivers were pessimistic about the injury. Patients perceived significantly more physical symptoms than caregivers did. Caregivers for patients who were severely injured or admitted to an intensive care unit (ICU) had more negative perceptions than did those who were providing care for moderately injured patients or those not admitted to an ICU. Caregivers who did not share their caring responsibilities had more negative perceptions than did those who shared their caring responsibilities with others., Conclusions: This study found that patients and caregivers had negative illness representations several months after injury. Caregivers who provided care for severely injured patients or who did not share caring responsibilities perceived different extents of illness perceptions about the injury. The interventions should highlight the need to assist patients and caregivers after injury., Clinical Relevance: Exploring the discrepancies in illness perceptions between injured patients and their caregivers can help clinicians to provide individualized care, and to design interventions that meet patients' and caregivers' needs., (© 2016 Sigma Theta Tau International.)

Purpose: To fill out the gaps in the existing research on the early recovery experiences of patients who have suffered moderate to severe injuries., Design: Exploratory phenomenology was applied in this study., Methods: Data were collected at a hospital in Taiwan from a purposive sample of 14 participants who were interviewed before hospital discharge. Semi-structured and audio-taped interviews were conducted. Colaizzi's methods were applied to analyze data. Four criteria were applied to establish the rigors of this study., Findings: The patients expressed that during the early stages following their injury, several aspects of the traumatic event caused them concern. Six themes were delineated: "experience of acute pain after the injury," "inability to fulfill daily needs," "concerns with impacts caused by the injury," "perceiving that time is needed to recover," "applying multiple methods to restore one's health," and "perceiving fate as the cause of the accident.", Conclusions: The findings identify that injuries bring several problems for patients. Some culture-related issues such as Chinese diets, Chinese medicine, and karmic causation have emerged. Clinicians should better understand patient care needs in the early stages of recovery after an injury., Clinical Relevance: Findings from this study could lead to new interventions, and finally improve care outcomes for patients with injuries., (© 2014 The Authors. Journal of Nursing Scholarchip published by Wiley Periodicals, Inc. on behalf of sigma Theta Tau International.)

Hepatitis B virus- (HBV-) associated hepatocellular carcinoma (HCC) is the most common type of liver cancer. However, the underlying mechanism of HCC tumorigenesis is very complicated and HBV-encoded X protein (HBx) has been reported to play the most important role in this process. Activation of downstream signal pathways of epidermal growth factor receptor (EGFR) family is known to mediate HBx-dependent HCC tumor progression. Interestingly, HER2 (also known as ErbB2/Neu/EGFR2) is frequently overexpressed in HBx-expressing HCC patients and is associated with their poor prognosis. However, it remains unclear whether and how HBx regulates HER2 expression. In this study, our data showed that HBx expression increased HER2 protein level via enhancing its mRNA stability. The induction of RNA-binding protein HuR expression by HBx mediated the HER2 mRNA stabilization. Finally, the upregulated HER2 expression promoted the migration ability of HBx-expressing HCC cells. These findings deciphered the molecular mechanism of HBx-mediated HER2 upregulation in HBV-associated HCC.

Melatonin protects cells against various types of oxidative stress-induced apoptosis due primarily to its ability to effectively scavenge pathological and disease condition-augmented generation of mitochondrial reactive oxygen species (mROS). Once produced, mROS indiscriminately damage mitochondrial components and more importantly they crucially activate directly the mitochondrial permeability transition (MPT), one of the critical mechanisms for initiating post mitochondrial apoptotic signaling. Whether or not melatonin targets directly the MPT, however, remains inconclusive, particularly during oxidative stress. This study, thus, investigated this possibility of an 'oxidation free Ca(2+) stress' in the presence of vitamin E after ionomycin exposure as a sole Ca(2+)-mediated MPT in order to exclude melatonin's primary antioxidative effects as well as Ca(2+)-mediated oxidative stress. The studies were carried out using cultured rat brain astrocytes RBA-1. With the application of laser scanning multiple fluorescence imaging microscopy, we visualized for the first time multiple mitochondrial protective effects provided by melatonin during Ca(2+) stress. First, melatonin, due to its primary antioxidative actions, completely prevented mCa(2+)-induced mROS formation during ionomycin exposure. Secondly, when melatonin(')s antioxidative effects were prevented due to the addition of vitamin E, melatonin significantly prevented mCa(2+)-mediated MPT and apoptosis suggesting its direct targeting of the MPT. Surprisingly, in the presence of cyclosporin A, a MPT inhibitor, melatonin reduced further mCa(2+)-mediated apoptosis during ionomycin exposure also suggesting its targeting beyond the MPT. As astrocytes are actively involve in regulating synaptic transmission and neurovascular coupling in the CNS, these multiple mitochondrial layers of protection provided by melatonin against mCa(2+)-and/or mROS-mediated apoptosis in astrocytes may be crucial for future therapeutic prevention and treatment of astrocyte-mediated neurodegenerative diseases in the CNS.