Huangqin decoction alleviates lipid metabolism disorders and insulin resistance in nonalcoholic fatty liver disease by triggering Sirt1/NF-κB pathway.

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is a clinicopathological entity characterized by intrahepatic ectopic steatosis. As a consequence of increased consumption of high-calorie diet and adoption of a sedentary lifestyle, the incidence of NAFLD has surpassed that of viral hepatitis, making it the most common cause of chronic liver disease globally. Huangqin decoction (HQD), a Chinese medicinal formulation that has been used clinically for thousands of years, has beneficial outcomes in patients with liver diseases, including NAFLD. However, the role and mechanism of action of HQD in lipid metabolism disorders and insulin resistance in NAFLD remain poorly understood. AIM: To evaluate the ameliorative effects of HQD in NAFLD, with a focus on lipid metabolism and insulin resistance, and to elucidate the underlying mechanism of action. METHODS: High-fat diet-induced NAFLD rats and palmitic acid (PA)-stimulated HepG2 cells were used to investigate the effects of HQD and identify its potential mechanism of action. Phytochemicals in HQD were analyzed by high-performance liquid chromatography (HPLC) to identify the key components. RESULTS: Ten primary chemical components of HQD were identified by HPLC analysis. In vivo, HQD effectively prevented rats from gaining body and liver weight, improved the liver index, ameliorated hepatic histological aberrations, decreased transaminase and lipid profile disorders, and reduced the levels of pro-inflammatory factors and insulin resistance. In vitro studies revealed that HQD effectively alleviated PA-induced lipid accumulation, inflammation, and insulin resistance in HepG2 cells. In-depth investigation revealed that HQD triggers Sirt1/NF-κB pathway-modulated lipogenesis and inflammation, contributing to its beneficial actions, which was further corroborated by the addition of the Sirt1 antagonist EX-527 that compromised the favorable effects of HQD. CONCLUSION: In summary, our study confirmed that HQD mitigates lipid metabolism disorders and insulin resistance in NAFLD by triggering the Sirt1/NF-κB pathway.

Phenotypic variation of fluoride responses between inbred strains of mice.

Excessive systemic exposure to fluoride (F) can lead to disturbances in bone homeostasis and dental enamel development. We have previously shown strain-specific responses to F in the development of dental fluorosis (DF) and in bone formation/mineralization. The current study was undertaken to further investigate F responsive variations in bone metabolism and to determine possible relationships with DF susceptibility. Seven-week-old male mice from FVB/NJ, C57BL/6J, C3H/HeJ, A/J, 129S1/SvImJ, AKR/J, DBA/2J, and BALB/cByJ inbred strains were exposed to NaF (0 or 50 ppm as F(-)) in drinking water for 60 days. Sera were collected for F, Ca, Mg, PO(4), iPTH, sRANKL, and ALP levels. Bone marrow cells were subjected to ex vivo cell culture for osteoclast potential and CFU colony assays (CFU-fibroblast, CFU-osteoblast, CFU-erythrocyte/granulocyte/macrophage/megakaryocyte, CFU-granulocyte/macrophage, CFU-macrophage, and CFU-granulocyte). Femurs and vertebrae were subjected to micro-CT analyses, biomechanical testing, and F, Mg, and Ca content assays. DF was evaluated using quantitative fluorescence and clinical criteria. Strain-specific responses to F were observed for DF, serum studies, ex vivo cell culture studies, and bone quality. Among the strains, there were no patterns or significant correlations between DF severity and the actions of F on bone homeostasis (serum studies, ex vivo assays, or bone quality parameters). The genetic background continues to play a role in the actions of F on tooth enamel development and bone homeostasis. F exposure led to variable phenotypic responses between strains involving dental enamel development and bone metabolism.

Librarians' roles in evidence-based dentistry education: a review of literature and a survey in North America.

This study describes the current roles of dental librarians in Evidence-based Dentistry (EBD) education including their perceptions of EBD and barriers to their involvement. A Web-based survey was distributed to the dental librarians in North America, with a 71% response rate. The results showed that the majority of dental librarians are playing multiple and diverse roles in EBD education. The most frequently cited barrier to their involvement is the low level of interest from the dental faculty/student/school. Most dental librarians felt competent in supporting EBD, although continuing education needs in both EBD and teaching skills were pointed out.

[Studies on keratocystic odontogenic tumors].

Keratocystic odontogenic tumors (KCOTs, previously known as odontogenic keratocysts) are aggressive, noninflammatory jaw lesions with a putative high growth potential and a propensity for recurrence. This article puts together a summary of the serial studies related to KCOTs undertaken by the author's research group in recent years. Intraosseous jaw cysts with a solely orthokeratinized lining epithelium have been suggested to differ from the typical KCOTs. We report 20 cases of such cyst type under the term of 'orthokeratinized odontogenic cyst (OOC)'. Apart from the presence of a keratinizing epithelial lining, the OOC lacks the other histological features of KCOT, exhibits little if any tendency to recur, has no apparent association with NBCCS, may be cured by simple enucleation, and may thus constitute its own clinical entity. Mutations in PTCH1 gene are responsible for NBCCS and are related in tumors associated with this syndrome. We have so far detected 26 PTCH1 mutations (2 mutations occurred twice) in 10 out of 34 (29.4%) sporadic and 14 out of 16 (87.5%) NBCCS-associated KCOTs. The 26 mutations consisted of 10 frameshift, 2 nonsense, 3 aberrant splicing, 4 in-frame insertion/deletion/ duplication and 7 missense mutations. Two missense mutations in PTCH2 were also detected in 2 out of 15 NBCCS related KCOT patients. By contrast, no pathogenic mutation was detected in SMO. Thus, our data, together with reports from other groups, indicate that defects of PTCH1 are involved in the pathogenesis of syndromic as well as sporadic KCOTs. The pathogenic role of PTCH2 requires further investigation. A series of in vitro studies on bone resorption of KCOTs and ameloblastomas were undertaken by this group. The results indicate that odontogenic lesions could promote bone resorption in vitro and it is likely to be related to some of the cytokines secreted by the lesions.

[Effects of Ginkgo biloba extract 50 on hypoxia induced endothelial dysfunction].

OBJECTIVE: To preliminarily investigate the influence of hypoxia on human umbilical vein endothelial cells (HUVECs), and the effect of Ginkgo biloba extract 50 (GBE50) on it. METHODS: Flow cytometry, TUNEL, RT-PCR, Western blot, etc. were applied, to study the effect of hypoxia and GBE50 on endothelial cells. RESULTS: After being interfered by hypoxia for 24 h, the levels of reactive oxygen species (ROS) in HUVECs and the apoptotic rate either in the early or in the late stage significantly increased, and accompanied with the increased levels of endothelin-1 mRNA (ET-1) and endothelial oxide synthase (eNOS) protein. However, when HUVECs were pretreated with GBE50 (25 [microg/ml) 4 h before hypoxia, the apoptotic rate in the early or late stage and expression of ET-1 mRNA significantly decreased (P < 0.05), and the heightened ROS level and eNOS expression partially decreased (P > 0.05). CONCLUSION: Hypoxia can induce endothelial dysfunction, which could be partially or significantly reversed by GBE50, it shows a certain protective effect on hypoxia induced endothelial dysfunction.

Electrospun and woven silk fibroin/poly(lactic-co-glycolic acid) nerve guidance conduits for repairing peripheral nerve injury.

We have designed a novel nerve guidance conduit (NGC) made from silk fibroin and poly(lactic-co-glycolic acid) through electrospinning and weaving (ESP-NGCs). Several physical and biological properties of the ESP-NGCs were assessed in order to evaluate their biocompatibility. The physical properties, including thickness, tensile stiffness, infrared spectroscopy, porosity, and water absorption were determined in vitro. To assess the biological properties, Schwann cells were cultured in ESP-NGC extracts and were assessed by morphological observation, the MTT assay, and immunohistochemistry. In addition, ESP-NGCs were subcutaneously implanted in the backs of rabbits to evaluate their biocompatibility in vivo. The results showed that ESP-NGCs have high porosity, strong hydrophilicity, and strong tensile stiffness. Schwann cells cultured in the ESP-NGC extract fluids showed no significant differences compared to control cells in their morphology or viability. Histological evaluation of the ESP-NGCs implanted in vivo indicated a mild inflammatory reaction and high biocompatibility. Together, these data suggest that these novel ESP-NGCs are biocompatible, and may thus provide a reliable scaffold for peripheral nerve repair in clinical application.

A universal microarray for detection of SARS coronavirus.

Severe acute respiratory syndrome (SARS) is caused by the SARS coronavirus (SARS-CoV). There are many point mutations among SARS-CoV genome sequences. Previous studies suggested that the mutations are correlated closely with the SARS epidemic. It was found that the bases of six nucleotide positions (nt9404, nt9479, nt19838, nt21721, nt22222 and nt27827) with high-mutation rate have an important relationship with the SARS epidemic. For viral detection as well as genotyping, a universal microarray system was developed that combines RT-PCR and ligase detection reaction (LDR). The Zip Codes attached covalently to a slide remain constant and their complementary Zip Codes (cZip Codes) can be used for tagging target sequence, making the microarrays universal. The discriminating oligonucleotides contain on the 5' end "cZip Codes" that are used to direct LDR product to specific Zip Codes attached covalently to a slide. Since Zip Codes have no homology to either the target sequence or to other sequences in the genomes of both human host and SARS-CoV, there was no false signal due to mismatch hybridizations. 20 samples assayed with the universal microarray were confirmed by DNA sequencing, demonstrating that this microarray system is a promising diagnostic tool for detection and genotyping of the SARS-CoV.

[Effect of glutathione on blood coagulation function].

The purpose of this study was to investigate the effect of glutathione (GSH) on blood coagulation. The normal plasma samples and mixed plasma samples were taken randomly, and into which the normal dose and different concentration of GSH were added. The prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen (FIB) and thrombin time (TT) were detected by using coagulation method before and after treatment with GSH. The detection results of normal plasma and mixed plasma containing GSH of different concentration were compared and analyzed with linear regression. The results showed that the APTT and FIB values of the plasma containing 2.5 mg/L glutathione or more, PT values of the plasma containing 10 mg/L glutathione or more, and TT values of the plasma containing 1250 mg/L glutathione or more were significantly different from those results of normal plasma or mixed plasma (P < 0.01) . There was a linear relation between all of the detection results of PT,APTT, FIB, TT and glutathione concentrations. The results of TT, APTT, PT and FIB detection in patient plasma were statistically different (P < 0.01) before and after treatment with normal concentration GSH. It is concluded that glutathione can influence detection results of coagulation function.

[Detection of PTCH gene mutations in odontogenic keratocysts by SSCP and DNA sequencing].

OBJECTIVE: To investigate PTCH gene mutations in odontogenic keratocysts (OKC). METHODS: PCR-SSCP and DNA sequencing were used to analyze the PTCH gene mutations in 12 OKCs, including 10 sporadic and 2 nevoid basal cell carcinoma syndrome (NBCCS) associated OKC. RESULTS: Four mutations were identified in 4 cysts, among which two germline mutations were associated with NBCCS and 2 somatic mutations were in 2 unrelated sporadic cases. In addition, eight previously reported polymorphisms in the PTCH gene were also found in 10 cases. CONCLUSION: The present study indicated that both sporadic and NBCCS-related OKCs could carry PTCH gene mutation. Thus, mutational inactivation of PTCH gene may play a significant role in the pathogenesis of OKC.