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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-κB), 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.

This study aimed to investigate the perceived work stress and its influencing factors among hospital staff during the novel coronavirus (COVID‐19) pandemic in Taiwan. A web‐based survey was conducted at one medical center and two regional hospitals in southern Taiwan, targeting physicians, nurses, medical examiners, and administrators. The questionnaire included items on the demographic characteristics of hospital staff and a scale to assess stress among healthcare workers caring for patients with a highly infectious disease. A total of 752 valid questionnaires were collected. The hospital staff reported a moderate level of stress and nurses had a highest level of stress compared to staff in the other three occupational categories. The five highest stress scores were observed for the items “rough and cracked hands due to frequent hand washing and disinfectant use,” “inconvenience in using the toilet at work,” “restrictions on eating and drinking at work,” “fear of transmitting the disease to relatives and friends,” and “fear of being infected with COVID‐19.” Discomfort caused by protective equipment was the major stressor for the participants, followed by burden of caring for patients. Among participants who experienced severe stress (n = 129), work stress was higher among those with rather than without minor children. The present findings may serve as a reference for future monitoring of hospital staff's workload, and may aid the provision of support and interventions.

Since the onset of the coronavirus disease 2019 pandemic, wearing facemasks has become more important for healthcare workers. This study aimed to investigate and compare the influence of wearing N95 respirators and surgical masks for 8 h on physiological and psychological health. Sixty-eight healthcare workers were randomly assigned to the N95 respirator or surgical mask groups. Physiological parameters of participants were measured by Tensor Tip MTX at baseline and at the 2nd, 4th, 6th and 8th h of wearing the facemasks. The symptoms after wearing facemasks were also determined via the questionnaire. There were no significant changes in physiological parameters at most time checkpoints in both groups. Significant differences were observed in terms of heart rate at the 8th h, time trends (adjusted difference of least squares means were −8.53 and −2.01), and interaction of time and mask type between the two groups (p-value for interaction was 0.0146). The values of these physiological parameters were within normal ranges. The N95 respirator group had significantly higher incidences of shortness of breath, headache, dizziness, difficulty talking and fatigue that spontaneously resolved. In conclusion, healthcare workers who wore either N95 respirators or surgical masks during an 8 h shift had no obvious harmful effects on physiological and psychological health. Additionally, the N95 respirator group did not show a higher risk than the surgical mask group.

2-Amino-1-methyl-6-phenylimidazo [4,5-b]pyridine (PhIP) which can be detected in processed meats and red meats, is a potential carcinogen for renal cell carcinoma (RCC). Approximately 30% of patients with metastatic RCC have bone metastases, and the prognosis of RCC with bone metastases is poor. Thus, the aim of the present study was to investigate whether PhIP induced bone metastases and to develop novel therapeutic agents. Our data revealed that PhIP pre-treatment increased the production of parathyroid hormone-related protein (PTHrP) in human 786-O renal cell carcinoma cells. Subsequently, the cultures of human osteoblasts with PhIP-stimulated condition medium of 786-O increased the expression of the macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor kappa-B ligand (RANKL), and decreased the expression of osteoprotegerin (OPG). In addition, PhIP-mediated PTHrP up-regulated as well as increased IL-8 secretion in 786-O cells, and then contributed to 786-O-mediated bone resorption. Furthermore, 6-shogaol, which is an active ingredient in ginger, showed suppressive effects on PhIP-mediated bone resorption. In summary, this is the first study to demonstrate that PhIP pre-treatment increases the stimulatory effect of human renal cell carcinoma 786-O on osteoclastogenesis activity directly by PTHrP. In addition, 6-shogaol treatment reverses PhIP-mediated bone resorption. It suggests that 6-shogaol treatment results in bone resorption activity in the RCC model in vitro.

Hexavalent chromium [Cr(VI)], is a well-known toxic form of the heavy metal chromium in the natural environment. Clinical evidence has indicated that exposure to Cr(VI) can cause severe renal damage. The production of reactive oxygen species (ROS) due to intracellular reduction of Cr(VI) is the main mechanism underlying the induction of cellular dysfunction and apoptosis. The present study aimed to investigate in detail the apoptotic pathways induced by Cr(VI)-exposure in a human immortalized proximal tubular epithelial cell line HK-2, in order to understand the mechanism involved therein. Exposure to 10 µM potassium dichromate (K2Cr2O7), a toxic compound of Cr(VI), significantly decreased cell viability after 24 and 48 h of incubation and induced intracellular ROS generation. The expression levels of markers that activate the apoptotic pathway including cleaved caspase-3 and poly (ADP-ribose) polymerase were significantly upregulated in K2Cr2O7-exposed HK-2 cells. In addition, the induction of intrinsic and extrinsic apoptotic markers was detected in K2Cr2O7-exposed HK-2 cells. In summary, the present study described for the first time the novel apoptotic mechanism of Cr(VI)-toxicity in human renal cells which may be beneficial in designing optimal clinical treatment for renal damage caused by acute Cr(VI) toxicity.

The endoplasmic reticulum (ER) is an organelle involved in various physiological processes such as lipid metabolism, protein synthesis and folding, and cellular calcium storage. In a physiological tumor microenvironment, hypoxia, nutrient deprivation, and calcium dysregulation cause accumulation of unfolded and misfolded proteins. Such accumulation induces ER stress and unfolded protein responses (UPRs). Increased UPR signaling pathways are associated with multiple types of cancer. The influence of ER stress on acyl-CoA metabolic enzymes is not well understood. Evaluation of PRECOG and Kaplan-Meier plotter databases in the present study suggested that high expression of acyl-CoA thioesterase (ACOT)7, ACOT11, ACOT13, soluble carrier family 27 member A4 (SLC27A4) and SLC27A5 was associated with poor clinical outcomes. In addition, expression levels of ACOT7, ACOT11, SLC27A4 and SLC27A5 were not altered after induction of ER stress. By contrast, expression of some enzymes was decreased, such as those of long-chain acyl-CoA synthetase (ACSL)3, ACSL4 and SLC27A2. Fatty acid uptake capacity was suppressed in lung cancer cell lines A549 and CL1-0 after thapsigargin treatment but intracellular reactive oxygen species levels were not suppressed. Gene enrichment and regulatory element analysis were performed; the results provided potential targets for further investigation. On the whole, our findings demonstrate the potential regulatory mechanism of high-expression of acyl-CoA metabolic enzymes, the biological effects of decreased enzyme expression levels, possible regulatory elements, and the interaction network involved in responses to ER stress in lung cancer

Spontaneous pneumocephalus is defined as the presence of air in the absence of intracranial factors. The management of spontaneous pneumocephalus can be conservative or surgical, and surgical intervention could be urgently required if clinical deterioration is rapid. Here, we report a case of pneumocephalus and subdural hemorrhage after sneezing. A 24-year-old male reported to our emergency department with a chief complaint of headache and dizziness. The patient gave a history of onset of headache and dizziness after 2 episodes of heavy sneezing. There was neither a history of recent traumatic episode or previous surgery, nor any signs and symptoms of recent fever or upper respiratory tract infections. Physical examination showed no specific findings. Computed tomography was performed, which showed subdural hemorrhage and PNC in the left occipital lobe, left hemomastoid, and maxillary hemosinus. A neurosurgeon was consulted, who suggested admission in the intensive care unit. An otolaryngologist was then consulted for the left ear otorrhea and hearing impairment. Otoscopic examination showed hemotympanum of the left ear, for which pain control and conservative treatment was suggested. The patient was transferred to general ward 4 days later, since the following brain computed tomography showed resolution of the hemorrhage, and discharged 6 days later because of the improved signs and symptoms. Pneumocephalus and intracranial hemorrhage can occur without a history of trauma or surgery. Special attention is required if headache, dizziness, or other neurologic signs and symptoms occur immediately after sneezing. Intracranial hemorrhage and penumocephalus should be considered in the differential diagnosis.

There were few case reports discuss about iatrogenic chest wall hematoma. Although it is rare life threatening, it still can result in significant morbidity. A 68-year-old woman with histories of end-stage renal disease under regular hemodialysis and congestive heart failure was sent to our emergency department because of progression of ecchymosis over the anterior chest wall a few hours after hemodialysis. The right subclavian hemodialysis catheter was inserted for hemodialysis on the same day. She did not have a history of bleeding disorders and was not taking any antiplatelet or anticoagulant agents. Additionally, she had no recent trauma episodes. Physical examination revealed a large ecchymosis over the anterior right chest wall with swelling and tenderness. Blood examination showed no specific finding. Contrast-enhanced computed tomography of the chest revealed a hyperdense lesion with extravasation over the right chest wall, suggesting the presence of a hematoma with active bleeding. Local compression was applied. However, hematoma expansion was still noted. Therefore, we consulted a thoracic surgeon concerning surgical intervention. During the operation, active bleeding of the intramuscular arterial branch of the right pectoralis major was encountered. After surgical repair, no more bleeding was noted. It is important to confirm the possible cause of chest wall hematoma. Treating the underlying disease and discontinuing anticoagulation and antiplatelet agents should be considered. For iatrogenic chest wall hematoma, bleeding control should be the priority. Contrast-enhanced computed tomography could be arranged if there are no contraindications.

Several of the soluble inflammatory molecules such as cytokines and chemokines are involved in the regulation of cancer behaviors. Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) is a member of the TNF superfamily and is a ligand of fibroblast growth factor inducible 14 (Fn14). TWEAK/Fn14 signaling pathways promote tumor progression in several types of human cancer. In the present study, we investigated the role of TWEAK through bioinformatic assay, in vitro experiments, and serum levels in patients with non-small cell lung cancer (NSCLC). Our results indicated that TWEAK expression in normal tissues was higher than that in lung cancer tissues. In contrast, relatively higher Fn14 expression was detected in lung cancer tissues compared to normal tissues. Recombinant TWEAK treatment did not enhance and inhibit the proliferation and migration of human NSCLC cell lines including A549, H1299, CL1-0 and CL1-5. In addition, the serum concentration of TWEAK in normal controls was significantly higher than that in NSCLC patients. However, the TWEAK levels did not show significant difference in regards to TNM stage, cell type and metastasis status in the sera of NSCLC patients. In summary, the present study suggests that a low serum level of TWEAK may be a feature of NSCLC, and the role of TWEAK-mediated pathways warrant further investigation.

The survival rate in patients with metastatic renal cell carcinoma (RCC) is low. In addition, metastatic RCC resists traditional treatment. Therefore, identification of novel biomarkers, signaling pathways, and therapeutic targets is an important issue. The aim of the present study is to identify novel prognostic markers from the miRNA-mediated network for the regulation of metastasis of RCC. To address this issue, the RNA of human RCC cell lines, 786-O and ACHN, derived from primary and metastatic sites, respectively, were collected and subjected to RNA sequencing and small RNA sequencing. The bioinformatic analysis revealed that the pathways of the genes with different expressions were related to tumor progression, and identified miRNA and miRNA-long non-coding RNA (lncRNA) interactions, and mRNA. The results revealed that the expressions of seven miRNAs were associated with the overall survival rate of patients with RCC. Furthermore, the expressions of two lncRNA and three protein-coding genes (mRNA) were significantly associated with the increased or decreased disease-free survival rate. Although the detailed regulatory mechanism between miRNAs and targeted genes was not fully understood, our findings present novel prognostic markers and novel insight on miRNA-mediated pathways for metastatic RCC.