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In this study, a thermal comfort evaluation of sports buildings in hot and humid climates from the perspective of exercisers and non-exercisers was conducted. The objective was to improve their indoor environment in terms of public use. Thermal environmental indicators, individual data and 294 valid responses form exercisers and non-exercisers to a subjective survey questionnaire were examined. The results indicated that exercisers and non-exercises performed differently in terms of physiological characteristics and subjective perception. The average values of subjective sensation in the thermal environment were different between exercisers and non-exercisers, which corresponded to their subjective preference. However, the average values of their subjective acceptability were generally within the "slightly acceptable". In terms of the relationship between thermal environment and subjective perception, the thermal sensation of exercisers was more hot-oriented than that of non-exercisers at the same operative temperature, while their thermal acceptability was higher than that of non-exercisers since exercisers focused on sports rather than the thermal environment, making them less sensitive and more tolerant than non-exercisers. In addition, affected by the skin wetness from sweating and air velocity generated by exercise, the humidity sensation and draft sensation of exercisers were stronger than those of non-exercisers. Finally, the neutral temperature (28.3 °C and 28.7 °C), satisfactory temperature range (26.3oC–31.2 °C and 26.3oC–32.2 °C), and acceptable temperature range (27.1oC–35.9 °C and 26.3oC–34.1 °C) for exercisers and non-exercisers were derived. This study provides knowledge regarding the thermal comfort of exercisers and non-exercisers in sports buildings as well as guidance to improve the control and regulation of indoor environments. • Thermal comfort between exercisers and non-exercisers was investigated. • Subjective acceptability didn't correspond to subjective sensation and preference. • Exercisers had higher thermal sensation and thermal acceptability than non-exercisers. • Exercisers' subjective sensations were affected by sweating and exercise wind. • Neutral, satisfactory, and acceptable temperatures were analysed. [ABSTRACT FROM AUTHOR]

Cirsii Japonici Herba Carbonisata (Dajitan in Chinese) has been used to treat liver disorders in Asian countries. Pectolinarigenin (PEC), an abundant constituent in Dajitan, has been found to possess a wide range of biological benefits, including hepatoprotective effects. However, the effects of PEC on acetaminophen (APAP)-induced liver injury (AILI) and the underlying mechanisms have not been studied. To explore the role and mechanisms of PEC in protecting against AILI. The hepatoprotective benefits of PEC were studied using a mouse model and HepG2 cells. PEC was tested for its effects by injecting it intraperitoneally before APAP administration. To assess liver damage, histological and biochemical tests were performed. The levels of inflammatory factors in the liver were measured using RT-PCR and ELISA. Western blotting was used to measure the expression of a panel of key proteins involved in APAP metabolism, as well as Nrf2 and PPARα. PEC mechanisms on AILI were investigated using HepG2 cells, while the Nrf2 inhibitor (ML385) and PPARα inhibitor (GW6471) were used to validate the importance of either Nrf2 and PPARα in the hepatoprotective effects of PEC. PEC treatment decreased serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) levels in the liver. PEC pretreatment increased the activity of superoxide dismutase (SOD) and glutathione (GSH) while decreasing malondialdehyde production (MDA). PEC could also up-regulate two important APAP detoxification enzymes (UGT1A1 and SULT1A1). Further research revealed that PEC reduced hepatic oxidative damage and inflammation, and up-regulated APAP detoxification enzymes in hepatocytes by activating the Nrf2 and PPARα signaling pathways. PEC ameliorates AILI by decreasing hepatic oxidative stress and inflammation while increasing phase Ⅱ detoxification enzymes related to APAP harmless metabolism through activation of Nrf2 and PPARα signaling. Hence, PEC may serve as a promising therapeutic drug against AILI. [Display omitted] [ABSTRACT FROM AUTHOR]

To evaluate the safety and effectiveness of transcutaneous electrical acupoint stimulation (TEAS) in postoperative analgesia following pediatric orthopedic surgery with the enhanced recovery after surgery (ERAS) protocol. Prospective randomized controlled trial. The Seventh Medical Center of the Chinese People's Liberation Army General Hospital. Eligible participants were children aged 3–15 years who were scheduled to undergo orthopedic surgery of the lower extremities under general anesthesia. A total of 58 children were randomly allocated into two groups: TEAS (n = 29) and sham-TEAS (n = 29). The ERAS protocol was used in both groups. In the TEAS group, the bilateral Hegu (LI4) and Neiguan (PC6) acupoints were stimulated starting from 10 min before anesthetic induction until the completion of surgery. In the sham-TEAS group, the electric stimulator was also connected to the participants; however, electrical stimulation was not applied. The primary outcome was the severity of pain before leaving the post-anesthesia care unit (PACU) and at postoperative 2 h, 24 h, and 48 h. Pain intensity was measured with the Faces Pain Scale-Revised (FPS-R). None of the participants had any TEAS-related adverse reactions. In comparison with the sham-TEAS group, FPS-R scores in the TEAS group were significantly decreased before leaving the PACU and at postoperative 2 h and 24 h (p < 0.05). The incidence of emergence agitation, intraoperative consumption of remifentanil, and time to extubation were significantly reduced in the TEAS group. Furthermore, the time to first press of the patient-controlled intravenous analgesia (PCIA) pump was significantly longer, the pressing times of the PCIA pump in 48 h after surgery was significantly decreased, and parental satisfaction was significantly improved (all p < 0.05). TEAS may safely and effectively relieve postoperative pain and reduce the consumption of perioperative analgesia in children following orthopedic surgery with the ERAS protocol. Chinese Clinical Trial Registry (ChiCTR2200059577), registered on May 4, 2022. [ABSTRACT FROM AUTHOR]

Long noncoding RNAs (lncRNAs) are a series of RNA molecules without ability to code proteins. LncRNAs have emerged as significant players in almost all aspects of gene function and regulation and play crucial roles in many human diseases. Particular lncRNAs are deemed to be promising molecular biomarkers used for diagnosing diseases and determining patient prognoses and treatment efficacies. LINC00339 is a new budding lncRNA and much of evidence shows that it is abnormally expressed in multifarious diseases, including endometriosis, cardiomyocyte apoptosis, osteoporosis, digestive-system tumors, respiratory-system tumors, nervous-system tumors, and diseases involving other systems. Additionally, LINC00339 is remarkably associated with different clinical features, such as tumor size, TNM stage, and pathological grade. LINC00339 expression has been proved to upregulate in the aforementioned diseases and has been identified to promote disease occurrence and development. It is also reported that LINC00339 is associated with various cellular events, such as tumor cell proliferation, motility and invasiveness, the expression has also been proved that it is closely related to clinical symptoms in cancer patients. This review summarizes the relationships among expression levels, biological features, clinical symptoms, and regulatory mechanisms of LINC00339 in several diseases and discusses the clinical applications of LINC00339 as a cancer diagnostic, prognostic and treatment efficacy biomarker. [ABSTRACT FROM AUTHOR]

Brain-dead (BD) donor is the main source for liver transplantation (LT). We aim to investigate the effect of brain death on donor liver inflammatory activity and its association with ischemia-reperfusion (I/R) injury and biliary tract injury after LT. A brain death model using male Lewis rats was established, in both BD and non-BD groups; livers were harvested for transplantation using a 2-cuff technique. The rats were sacrificed 12 hours (n = 10) or 4 weeks (n = 10) after transplantation. I/R injury and long-term biliary tract injury were observed after transplantation. All rats survived for 4 weeks after transplantation. At 12 hours after BD-donor LT (BDDLT), liver injury worsened; serum transaminases, bilirubin, oxidative stress, inflammatory responses and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining level substantially increased (P <.05). At 4 weeks after BDDLT, serum bilirubin and bile lactate dehydrogenase and γ-glutamyl transpeptidase levels were elevated (P <.05). Biliary fibrosis and epithelial-mesenchymal transition (EMT) were detectable and NDRG1 gene expression was decreased. These results suggested that brain death–induced inflammatory response in donor organs and resulted in a worse I/R injury and biliary tract injury after LT in rats. The brain death–related biliary tract injury may be associated with the regulation of EMT through NDRG1. • Brain death activated liver inflammation in rats. • Brain death was related to ischemia-reperfusion injury after liver transplantation in rats. • Brain death was associated with biliary tract injury after transplantation in rats. • NDRG1 -mediated epithelial-mesenchymal transition in cholangiocytes after brain-dead donor liver transplantation. [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma (HCC) is one of the most common human malignancies and the third most common cause of cancer mortality in the world. In this study, we report that miR-411 expression is markedly upregulated in HCC cells and HCC tissues compared with normal control tissues and cells. Previous studies have shown that miR-411 plays a crucial role in a variety of biological processes in various human cancer cells. However, the specific function of miR-411 in HCC remains unclear. Ectopic expression of miR-411 promoted the proliferation and anchorage-independent growth of HCC cells, whereas inhibition of miR-411 reduced this effect. Bioinformatics analysis further revealed ITCH, a putative tumor suppressor as a potential target of miR-411. Data from luciferase reporter assays showed that miR-411 directly binds to the 3’-untranslated region (3’-UTR) of ITCH mRNA and repressed expression at both transcriptional and translational levels. In functional assays, miR-411 promoted HCC cell proliferation, which could be suppressed by miR-411-in. Taken together, our data provide convincing evidence that miR-411 functions as an onco-miRNA, which was associated with cell proliferation of HCC, and its oncogenic effect is mediated chiefly through direct suppression of ITCH expression. [ABSTRACT FROM AUTHOR]

Abnormal expression of long non-coding RNAs (lncRNAs) plays an essential role in various malignant neoplasia. As a newly identified lncRNA, LINC01234 is abnormally expressed in several types of cancers and promotes the development of cancers. Accumulating evidence indicates that overexpression of LINC01234 is associated with poor clinical outcomes. Moreover, LINC01234 modulates many cellular events as a putative proto-oncogene, including proliferation, migration, invasion, apoptosis, cell cycle progression, and EMT. In terms of molecular mechanism, LINC01234 regulates gene expression by acting as ceRNA, participating in signaling pathways, interacting with proteins and other molecules, and encoding polypeptide. It reveals that LINC01234 may serve as a potential biomarker for cancer diagnosis, treatment, and prognosis. This review summarizes the expression pattern, biological function, and molecular mechanism of LINC01234 in human cancer and discusses its potential clinical utility. [Display omitted] • LINC01234 is abnormally regulated in a variety of cancers. • LINC01234 is associated with cancer prognosis and may be a potential target for cancer therapy. • LINC01234 functions by encoding peptides, interacting with proteins and RNA, and participating in various key signaling pathways. [ABSTRACT FROM AUTHOR]

Long non-coding RNAs (lncRNAs) play important roles in the occurrence and progression of tumors. Extensive research has contributed to the current understanding of the critical roles played by lncRNAs in various cancers. LncRNA MIR4435-2HG has been found to be crucial in many cancers, such as breast, cervical, colorectal, and gastric cancer. Expression of MIR4435-2HG is generally upregulated in cancers and MIR4435-2HG participates in many biological functions through molecular mechanism of competitive endogenous RNA networks. This review profiles recent research findings on the expression, functions, mechanism, and clinical value of MIR4435-2HG in cancer, and serves as a reference for further MIR4435-2HG-related research and clinical trials. [ABSTRACT FROM AUTHOR]

Long non-coding RNAs (lncRNAs), a newly identified class of non-coding RNA (ncRNA), are defined as RNA molecules at least 200 nucleotides in length that are not translated into proteins. LncRNAs contribute to a wide range of biological processes and are master regulators of disease occurrence, development, and response to therapy in human malignancies. The lncRNA prostate cancer‑associated transcript 6 (PCAT6) is upregulated in various human malignancies, including lung cancer, hepatocellular carcinoma, cervical cancer, osteosarcoma, glioblastoma, colorectal cancer, breast cancer, gastric cancer, gastrointestinal stromal tumors, and pancreatic ductal adenocarcinoma. High expression of PCAT6 is closely correlated with aggressive clinicopathological characteristics and poor prognosis in cancer patients, suggesting it is an oncogenic lncRNA. PCAT6 overexpression also facilitates cell proliferation, invasion, and migration while attenuating apoptosis, indicating that it might serve as a new prognostic biomarker and therapeutic target for malignancies. Here, we discuss the molecular mechanisms, regulatory functions, and potential clinical applications of PCAT6 in cancer. [ABSTRACT FROM AUTHOR]

Long non-coding RNAs (lncRNAs) have more than 200 nucleotides and do not encode proteins. Based on numerous studies, lncRNAs have emerged as new and crucial regulators of biological function and have been implicated in the pathogenesis of a variety of diseases, especially cancers. Specific lncRNAs have been identified as novel molecular biomarkers for cancer diagnosis, prognosis, and treatment efficacy. Fetal-lethal non-coding developmental regulatory RNA (FENDRR , also known as FOXF1-AS1) is a novel lncRNA that is located at chr3q13.31 and has four exons and 3099 nucleotides, and its genomic site is located at chr3q13.31. FENDRR is abnormally expressed in a variety of cancers and is significantly associated with different clinical characteristics. In addition, FENDRR has shown potential as a biomarker for cancer diagnosis, prognosis, and treatment. In this review, we summarize the current understanding of FENDRR and its mechanistic role in cancer progression. We also discuss recent insights into the clinical significance of FENDRR for cancer diagnosis, prognosis, and treatment. [ABSTRACT FROM AUTHOR]