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The degree of withering significantly affected the formation of tea quality. This study analyzed the effects of light withering (LW), moderate withering (MW) and heavy withering (HW) on tea quality jointly by transcriptome and metabolomics. It was found that LW was more beneficial in increasing gene expression of the ko00500, ko00511, ko00940, ko00944, ko00941, ko00740 and ko02010 pathways in tea leaves, thereby increasing the content of quinones, phenolic acids, lignans and coumarins, and flavonoids; MW was more beneficial in increasing gene expression of ko00500, ko00511, ko00130, ko00380 and ko00520 pathways, thereby increasing the content of terpenoids, organic acids and lipids. The aroma intensity was highest in moderately withering tea leaves and bitterness intensity was highest in lightly withering tea leaves, while the intensity of mellowness, fresh and brisk taste was significantly higher in MW and LW than in HW. This study provides an important basis for guiding the processing of Wuyi rock tea with different flavors. • The degree of withering can significantly change the taste of tea. • Light withering mainly enhanced gene expression of 7 metabolic pathways. • Light withering mainly increased the content of 4 categories metabolites. • Aroma intensity was strongest in tea leaves with moderate withering. • Bitterness intensity was strongest in tea leaves with light withering. [ABSTRACT FROM AUTHOR]

Abstract: Adenosquamous carcinoma (ADSQ) is uncommon in non-small cell lung cancer (NSCLC). The frequency rate of ADSQ was 9.7% of 6990 primary lung cancers resected in our department. Many researches have analyzed genetic and molecular alterations in adenocarcinoma (AD) and squamous cell carcinoma (SQ), but few molecular studies have been conducted on heterogeneous ADSQ. The current study was to investigate gene mutations of epidermal growth factor receptor (EGFR) and Kirsten rat sarcoma viral oncogene (KRAS) and their correlation with clinical variables in Chinese patients with ADSQ. Histologic features were reviewed, and immunohistochemical (IHC) and molecular (EGFR and KRAS) studies were done in 55 Chinese patients with ADSQ. Microscopically, all the tumors demonstrated dual differentiation with varying proportions of AD and SQ. Based on morphological diagnosis, a combination of multiple IHC markers is helpful for accurately discriminating two undifferentiated histologic subtypes of ADSQ. EGFR mutations were identified in 21 (38.2%) patients: 11 mutations were in exon 19, 1 in exon 20, 7 in exon 21 and double mutations were found in two patients. We also found two new mutations, namely, L747-E749del K754A within exon 19 and H850R within exon 21. Moreover, 16 (29.1%) silent mutations Q787Q in exon 20 were found in the series, five of which coexisted with other mutations. EGFR mutations were more frequently found in patients with size of the tumors ≥3cm [19/35 (54.3%); 2/20 (10%); P =0.001] or coexistent double cancer. However, the EGFR mutation was not associated with gender, age, lymph node status, tumor stage and smoking history. KRAS mutations were present in 2 (3.64%) male patients in codon12 (G12C) and none of them showed EGFR mutation. Moreover, identical EGFR and KRAS mutations in both components of ADSQ were further confirmed by microdissection techniques. The data indicated that the incidence of EGFR and KRAS mutations in Chinese patients with ADSQ were similar to those of Asian patients with AD. Furthermore, EGFR silent mutations accounted for a large proportion in ADSQ. Additional prospective studies are needed in order to define the clinical relevance of new and silent mutation variants. [Copyright &y& Elsevier]

High sucrose can induce tau hyperphosphorylation and cognitive dysfunction/memory impairment as observed in Alzheimer's disease (AD). Rutaecarpine, a specific (transient receptor potential vanilloid 1 [TRPV1]) agonist, is neuroprotective against high sucrose diet-induced impairment, but detailed mechanisms are still elusive. In this study, we investigated whether rutaecarpine mitigates high sucrose diet-induced pathological alterations and cognitive in AD-like mice. Mice were administered fodder containing 0.01% rutaecarpine and 20% sucrose solution. Our results showed that rutaecarpine significantly attenuated high sucrose diet-induced spatial memory impairment and enhanced synaptic plasticity; rutaecarpine prevented high sucrose diet-induced tau hyperphosphorylation by decreasing glycogen synthase kinase-3β (GSK-3β) activity; activation of GSK-3β reversed the protective effect of rutaecarpine on learning and memory deficits, synaptic plasticity, and tau hyperphosphorylation induced by high-glucose diet significantly, suggesting that GSK-3β activation is required for high glucose-induced tau hyperphosphorylation. These results demonstrated that rutaecarpine can mitigate high sucrose diet-induced hyperphosphorylation of AD-associated tau protein and cognitive impairment by inhibiting GSK-3β, which supported that dietary rutaecarpine might have a promising use for therapeutic intervention of AD. [ABSTRACT FROM AUTHOR]

Background and aim: The doctor–patient relationship has been a major focus of society. Hospitals’ efforts to improve the quality of their medical services have been to reduce the probability of doctor–patient conflicts. In this study, we aimed to determine the gap between expectations and perceptions of service quality according to patients to provide reference data for creating strategies to improve health care quality. Methods: Twenty–seven hospitals in 15 provinces (municipalities directly beneath the central government) were selected for our survey; we sent out 1,589 questionnaires, of which 1,520 were collected (response rate 95.65%) and 1,303 were valid (85.72% effective recovery rate). Paired t-tests were used to analyze whether there were significant differences between patients' expectations and perceived service quality. A binary logistic regression analysis was used to determine whether there were significant differences in the gap between expectation and perception of service quality according to patients' demographic characteristics. Results: There was a significant difference between the expected and perceived service quality (p < 0.05) according to patients both before and after receiving medical services. Furthermore, the service quality gap of each service dimension was negative. Specifically, the gaps in service quality were as follows: economy, responsiveness, empathy, assurance, reliability, and tangibles. Overall, we can conclude that patients’ perceptions of service quality are lower than their expectations. Conclusions: According to the study results, the quality of health care services as perceived by patients was lower than expected. Hospitals should make adjustments according to the actual situation and should strive to constantly improve the quality of medical services for patients. [ABSTRACT FROM AUTHOR]

[Display omitted] Traumatic brain injury (TBI) is a brain injury resulting from blunt mechanical external forces, which is a crucial public health and socioeconomic problem worldwide. TBI is one of the leading causes of death or disability. The primary injury of TBI is generally irreversible. Secondary injury caused by neuroinflammation could result in exacerbation of patients, which indicated that anti-inflammation and immunomodulatory were necessary for the treatment of TBI. Accumulated evidence reveals that the transplantation of umbilical cord mesenchymal stem cells (UCMSCs) could regulate the microenvironment in vivo and keep a balance of helper T 17(Th17)/ regulatory T cell (Treg). Therefore, it is reasonable to hypothesize that the UCMSCs could repair neurological impairment by maintaining the balance of Th17/Treg after TBI. In the study, we observed the phenomenon of trans-differentiation of T lymphocytes into Th17 cells after TBI. Rats were divided into Sham, TBI, and TBI + UCMSCs groups to explore the effects of the UCMSCs. The results manifested that trans-differentiation of Th17 into Treg was facilitated by UCMSCs, which was followed by promotion of neurological recovery and improvement of learning and memory in TBI rats. Furthermore, UCMSCs decreased the phosphorylation of nuclear factor-kappa B (NF-κB) and increased the expression of mothers against decapentaplegic homolog 3 (Smad3) in vivo and vitro experiments. In conclusion, UCMSCs maintained Th17/Treg balance via the transforming growth factor-β (TGF-β)/ Smad3/ NF-κB signaling pathway. [ABSTRACT FROM AUTHOR]

Background. Breast carcinoma is one of most prevalent malignant tumors occurring in women. Short of prevention, detection of breast carcinoma at an early, still curable stage would offer the best route to decrease its mortality rates. This highlights the urgent need for suitable biomarkers for early diagnosis and a better understanding of the disease pathogenesis. Material and methods. NMPs were extracted from normal human breast tissue (Group I), from hyperplastic mammary tissue specimens (Group II), from atypical epithelial hyperplasia specimens (Group III), and from breast carcinoma (Group IV) tissue. Differential proteome profiles were established and analyzed by means of immobilized pH gradient-based two-dimensional polyacrylamide gel electrophoresis (2D-PAGE) and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS). The different NMPs were analyzed in the National Center for Biotechnology Information (NCBI) database with Mascot software. Results. Well-resolved, reproducible 2-DE profiles of human breast tissues were obtained. Average protein spots were 904 ± 58, 912 ± 51, 931 ± 63, 944 ± 70 in Group I, Group II, Group III, and Group IV, respectively. Several different proteins were analyzed using mass spectrometry and bioinformation. Of these, 12 were well characterized. Compared to Group I, three proteins were up-regulated in Groups II, III, and IV, including Hsp27, prohibitin, and laminA/C. Upregulation was confirmed using Western blotting and immunohistochemical analysis. The correlation of prohibitin expression with clinicopathological features was also investigated. Discussion. The proteins identified in this study may potentially prove to be useful markers for breast carcinoma diagnosis. [ABSTRACT FROM AUTHOR]

To investigate the cardioprotective effects of hypothermic (25 °C) reperfusion on ischemia/reperfusion injury and the role of transient potential channel M8 (TRPM8) in this process. Western blot and real-time PCR were used to monitor the expression of TRPM8 in myocardium. Myocardial ischemia/reperfusion injury was induced by 30 min of global ischemia followed by 120 min of reperfusion in Langendorff-perfused hearts from Sprague-Dawley rats. The reperfusion was either normothermic (37 °C) or hypothermic (25 °C). Infarct size and left ventricular function were assessed, and lactate dehydrogenase (LDH), superoxide dismutase (SOD), and malondialdehyde (MDA) in the coronary effluent were measured spectrophotometrically, and cardiomyocyte apoptosis was detected by TUNEL assay. The expression of TRPM8, Bcl-2, Bax, cleaved capspase-3, RhoA, and ROCK2 was quantified. TRPM8 protein and mRNA were expressed in rat myocardium. Hypothermic reperfusion decreased the infarct size, LDH activity, MDA content, apoptosis, and expression of Bax, cleaved caspase-3, RhoA, and ROCK2 compared with normothermic reperfusion. These effects were associated with improved recovery of left ventricular contractility, and were reduced by BCTC, a TRPM8 antagonist. Ischemia/reperfusion injury and the increased expression of Bax, caspase-3, RhoA, and ROCK2 induced by normothermic reperfusion were reduced by Icilin, a TRPM8 agonist. Hypothermic reperfusion at 25 °C has cardioprotective effects against ischemia/reperfusion injury via activation of TRPM8 to inhibit the oxidative stress-related RhoA/ROCK2 signal pathway. [ABSTRACT FROM AUTHOR]