Visceral adiposity indicators and anthropometric indices as screening tools of metabolic syndrome among chinese athletic patients

Aim: More alarming is the increase in the metabolic syndrome (MetS) prevalence in athletic patients suffering adult growth hormone deficiency (AGHD). Chinese visceral adipose index (CVAI) serves for measuring visceral adiposity as well as predicting Chinese people’s MetS, while studies have not confirmed its predictive ability for AGHD athletic patients. The study aims at proving such predictive ability by directly comparing the screening abilities exhibited by CVAI, VAI, LAP, WHR, WHtR and WC for identifying MetS of AGHD athletic patients in China. Materials and methods: The study involved 113 AGHD athletic patients together with 113 healthy controls, calculating the CVAI, LAP, VAI, BMI, WHtR, WHR, and HOMA-IR. The definition of MetS followed the Joint Interim Statement criteria. The ROC assisted in comparing the AUC regarding each index, obtaining their cut-off points for the prediction of MetS. Results: The WC, WHR, WHtR, VAI, LAP and CVAI were in a higher level in AGHD patients. AGHD patients had a MetS prevalence of 41.3 %. AGHD athletic patients suffering MetS exhibited remarkably larger WC, WHR, WHtR, VAI, LAP, CVAI but lower IGF-1, relative to those without MetS. The CVAI was taken into account to divide AGHD patients to four quartiles. With the increase in CVAI, HDL-C, IGF-1 declined, while other related indicators were on the rise. Pearson analysis revealed the obvious association between CVAI, VAI and LAP with MetS, regardless of gender and age. According to the ROC curve of VAI and the anthropometric indicators (ATI) diagnosing metabolic syndrome, CVAI presented the maximum AUC value (85.80 and 84.45 for males and females, respectively) for AGHD patients (AU)

Inkjet-Printed Quantum Dot Fluorescent Security Labels with Triple-Level Optical Encryption.

Optical security labels play a significant role in protecting both our wealth and health. However, simultaneously meeting the requirements including low-cost fabrication, easy detection, and high-level security is still challenging for security labels. Here, we design an unclonable anti-counterfeiting system with triple-level security by using the inkjet printing technique, which can be authenticated by naked eyes, a portable microscope, and a fluorescence microscope. These labels are achieved by printing microscale quantum dot (QD) ink droplets on premodified substrates with random-distributed glass microspheres. Due to the unique capillary action induced by the glass microspheres, QDs in the ink droplets are deposited around the microspheres, forming microscale multicircular patterns. Multiple pinning of QDs at the three-phase contact lines appears during the evaporation of the droplet, resulting in the formation of a nanoscale labyrinthine pattern around the microspheres. The nanoscale labyrinth pattern and the microscale multicircular microsphere array, together with the printed macroscopic image, constitute a triple-level progressive anti-counterfeiting system. Moreover, the system is compatible with an artificial intelligence-based identification strategy that allows rapid identification and verification of the unclonable security labels.

Glaucocalyxin B induces apoptosis and autophagy in human cervical cancer cells.

Glaucocalyxin (Gln), an ent­kaurane diterpenoid isolated from the Chinese traditional medicine, Rabdosia japonica, represents a novel class of anticancer drugs. GlnA is one of the three major forms of Gln and has demonstrated potent anticancer effects in a variety of cancer types. GlnB has only one structural difference from GlnA, an acetylated hydroxyl group at C14. This acetyl group results in high liposolubility and may enhance the antitumor activity of ent­kaurane diterpenoid GlnB. However, few studies have reported the role of GlnB in cancer. The present study investigated the effect of GlnB in cervical cancer proliferation and cell death. Treatment with GlnB inhibits the proliferation of HeLa and SiHa cervical cancer cell lines in a dose­dependent manner, as assessed by 3­(4,5­dimethylthiazol-2­yl)-2,5 diphenyl tetrazolium bromide assays. In addition, GlnB increases the apoptotic cell population of HeLa and SiHa cells, as determined by fluorescence­activated cell sorting analysis and enhanced poly (ADP­ribose) polymerase 1 cleavage by western blotting. GlnB also induces increased light chain 3 II/I protein cleavage in both cells, indicating the induction of autophagy. Furthermore, GlnB treatment increased the expression of phosphatase and tensin homolog and decreased the expression of phosphorylated­protein kinase B (Akt) in HeLa and SiHa cells, as assessed by western blotting. Taken together, the present results demonstrated that GlnB inhibited the proliferation of human cervical cancer cells in vitro through the induction of apoptosis and autophagy, which may be mediated by the phosphatidylinositol­4,5­bisphosphate 3­kinase/Akt signaling pathway.

[Overexpression of Sox9 gene by the lentiviral vector in rabbit bone marrow mesenchymal stem cells for promoting the repair of cartilage defect].

OBJECTIVE: To study the overexpression of Sox9 gene on rabbit bone marrow mesenchymal stem cells for repairing articular cartilage injury in vivo. METHODS: Rabbit bone marrow mesenchymal stem cells (BMSCs) were transduced with lentivirus vector containing Sox9 gene and then cartilage specific molecule was detected by RT-PCR in vitro. Total 48 knee joints of 24 mature New Zealand white rabbits were randomly divided into 3 groups according to different defect treatment. After animals anesthesia,a full-thickness cylindrical cartilage defect of 4 mm diameter and 3 mm deep was created in the patellar groove using a stainlesssteel punch. Meanwhile, the transfected cells were implanted to repair the rabbit model with full-thickness cartilage defects. Cartilage defects tissue was observed with light microscope, electron microscope, HE and immunohistochemistry staining to assess the repair of defects by the complex at 6 weeks or 12 weeks after the implantation. RESULTS: At 3 days after the transfection, Sox9 gene expression was highest and Sox9 gene expression decreased with the increase of time. At 3 days after the transfection, the expression of collagen type II began and reached the peak at 14 days. It showed that the bone marrow mesenchymal stem cells went into chondrogenic differentiation after transfected by Sox9 gene. Histological observation showed that at 6 weeks after the operation, the defects in the experimental group was filled with hyaline like cartilage tissue, 12 weeks after operation,the defects of cartilage and subchondral bone had satisfactory healing. Both at 6 and 12 weeks postoperatively, the defects were filled with fibrous tissues in control groups. Meanwhile, immunohistochemical staining of sections with type II collagen antibodies showed the proteins in the regenerated tissue stained positive for type II collagen and stronger than the control groups. The histological scoring system indicated that the cartilage repair of experiment groups were better than the two control groups with statistical significances. CONCLUSION: Overexpression of Sox9 gene on rabbit bone marrow mesenchymal stem cells (BMSCs) promote the repair of cartilage defect.

[Gene expression of bone mesenchymal stem cells transduced by the lentiviral vector of SOX9 gene].

OBJECTIVE: To construct one lentiviral vector containing mouse SRY-related high mobility group-box gene 9 (SOX9) and transfect the murine bone mesenchymal stem cells (mBMSCs) in vitro and observe the expression of target gene. METHODS: RNA from the vectors containing mouse SOX9 gene were extracted and SOX9 genes were amplified by reverse transcription-Polymerase Chain Reaction (RT-PCR). The SOX9 genes were connected into lentiviral vectors pGC-FU. Then pGC-FU-SOX9 transduced into 293T cells to produce recombinant lentivirus called as Lenti-SOX9-EGFP. mBMSCs were transfected. The expression of target gene was detected by immunofluorescence, RT-PCR and Western Blot. RESULTS: Lenti-SOX9-EGFP was recombined successfully and transduced efficiently into mBMSCs. The expression of SOX9 gene was confirmed by RT-PCR and Western Blot. CONCLUSION: Lentiviral vector of mouse SOX9 gene can transfect successfully into mBMSCs. Meanwhile, SOX9 gene may be expressed in mBMSCs. This will provide the target cells for the following study about SOX9 gene repairing cartilage injury.

[Gene expression of bone mesenehymal stem cells transduced by the lentiviral vector of SOX9 gene knockdown].

OBJECTIVE: To construct one lentiviral vector containing mouse SRY-related silencing group--box gene 9 (SOX9) and to transfect murine bone mesenehymal stem cells (mBMSCs) in vitro and observe the expression of target gene. METHODS: RNA inteference target sequence was designed in connectin with mice SOX9 gene sequence. The double strands DNAoligo containing interference sequence were synthesized and cloned into lentivirus vector. The siRNA lentiviral vector with SOX9 gene silencing was constructed and identified, which was transfected into rat bone mesenehymal stem cells. The expression of target gene was detected by immunofluorescence, RT-PCR and Western blot. RESULTS: Lenti-SOX9-siRNA-EGFP was recombined successfully and transduced efficiently into mBMSCs. The expression of SOX9 gene silencing was confirmed by RT-PCR and Western blot. CONCLUSION: Mouse SOX9 gene silencing by RNA interference and Lentiviral vector can transfected successfully into mBMSCs. Meanwhile,SOX9 gene may be silenced in SOX9 transduced mBMSCs. This will provide target cells for the following study about SOX9 gene respairing cartilage injury.