Objective To analyse the distribution and evolution law of TCM syndrome for elderly hypertension (EH), to provide evidence for syndrome standardization study. Methods Case history of 2 029 EH patients during recent ten years were investigated in the way of epidemiology. The main and complicated syndrome types were studied. Results The main syndrome types of EH were yin deficiency of liver and kidney (40.0%), kidney qi deficiency (28.4%), hyperactivity of liver-yang (9.7%), excessive accumulation of phlegm-dampness (7.4%), collateral obstruction by blood stasis (6.6%), phlegm and blood stasis (5.7%), liver-fire hyperactivity (1.1%). The complicated syndrome types were liver-fire hyperactivity (26.5%), excessive accumulation of phlegm-dampness (9.6%), collateral obstruction by blood stasis (7.2%), phlegm and blood stasis (5.5%), kidney yin deficiency (3.7%). Conclusion The distribution of EH TCM syndrome is mainly about deficiency syndromes, in which kidney qi deficiency syndrome is very common, and mostly complicated with phlegm and blood.

OBJECTIVE: To investigate if the OTOF gene contributes to the non-syndromic hearing loss of a Chinese pedigree with dominantly inherited auditory neuropathy (AN). METHOD: The subjects included were 9 live individuals in an autosomal dominant AN pedigree, 3 sporadic AN patients and 3 normal-hearing controls. Genomic DNA was isolated from the peripheral leukocytes of the subjects using the Pure gene DNA Isolation Kits. Firstly, the whole coding sequence of OTOF gene of one family patient were PCR amplified using specific primers. Each fragment was purified and subsequently analyzed by direct sequencing in an Applied Biosystems 3 730 automated DNA sequencer. The resultant sequence data were compared with the standard sequence to identify deafness-associated mutations. Other DNA samples were then screened for these mutations by PCR amplification and sequence analysis. RESULT: PCR amplifications were successfully conducted in all the subjects. Comparison of the resultant OTOF sequence in one family patient with the standard sequence identified 10 nucleotide variants which do not lead to amino acid change. These mutations were also detectable in other family individuals, 3 sporadic AN patients and 3 normal-hearing controls. CONCLUSION The OTOF does not seem to contribute to the pathogenesis of this Chinese AN family, which suggest new gene(s) involvement.
Asian Continental Ancestry Group ; genetics ; Base Sequence ; Case-Control Studies ; Chromosome Disorders ; ethnology ; genetics ; DNA Mutational Analysis ; Female ; Genetic Testing ; Hearing Loss ; genetics ; Humans ; Male ; Membrane Proteins ; genetics ; Mutation ; Pedigree ; Sequence Analysis ; Vestibulocochlear Nerve Diseases ; ethnology ; genetics

Objective To investigate the predictors of long-term remission of type 2 diabetes induced by short-term intensive insulin treatment.Methods Fifty-four cases of diabetes mellitus with the duration of illness less than 5 years received an intensive insulin treatment for 2 weeks.The standard meal test and intravenous glucose tolerance test were performed at the baseline and 24 h after treatment completion respectively.Long-term remission meant that the diabetic patients should maintain the target glyeaemic control without any hypoglyeaemie agent within one year.Results The remission rate was 57.4% (31/54) overall,and even reached to 80.6% (29/36) in patients with the duration of illness less than 6 months,whereas,the remission rate was only 11.1% (2/18) in those with the duration of illness more than 12 months.In another view,the remission rate was significantly higher in the patients with fasting plasma glucose (FPG) level of less than 7 mmol/L (78.8%,26/ 33) 24 h after intensive treatment than those with FPG level of more than 7 mmol/L (23.8%,5/21,P

OBJECTIVE: To investigate if the DFNB59 gene contributes to the hearing loss of a Chinese pedigree with dominantly inherited auditory neuropathy (AN). METHOD: Nine members in four generations of the family were selected for this study. Genomic DNA was isolated from the peripheral leukocytes of the patients using the pure gene DNA isolation kits. Firstly, the subjects DNA fragment was PCR amplified using specific primers corresponding to exon 2 and 4 of the DFNB59 gene. Each fragment was purified and subsequently analyzed by direct sequencing in an applied biosystems 3730 automated DNA sequencer. The whole coding sequence of DFNB59 gene of one family patient were then PCR amplified and submitted for sequence analysis as described above. The resultant sequence data were compared with the standard sequence to identify deafness-associated mutations. RESULT: PCR amplifications were successfully conducted in all the subjects. We failed to detect the presence either of mutations T54I and R183W in the exon 2 and exon 4 that have been reported, or any other deafness-associated mutations in the whole DFNB59 gene, by sequence analysis. CONCLUSION The DFNB59 gene seems not contribute to the pathogenesis of this Chinese AN family, which suggesting new gene(s) involvement.
Asian Continental Ancestry Group ; genetics ; Base Sequence ; DNA Primers ; Female ; Humans ; Male ; Mutation ; Nerve Tissue Proteins ; genetics ; Pedigree ; Sequence Analysis, DNA ; Vestibulocochlear Nerve Diseases ; genetics

Aim To investigate the effect of miR-199a-5p on the proliferation and migration of human glioma cells. Methods U251 cells were selected as experimental subjects to construct a U251 cell line overexpressing miR-199a-5p. The experiment was divided into; control group (U251 cells without transfection, Control), negative control group (transfected with empty vector plasmid U251 cells, NC) and experimental group (transfected with miR-199a-5p mature mimics, mimics). Real-time fluorescent quantitative PCR was used to detect the expression of miR-199a-5p in each group; CCK-8 was used to detect the proliferation of cells transfected with miR-199a-5p; the cell scratch test and Transwell migration test were used to detect the migration of U251 in each group; Western blot was applied to detect DDR1 expression; a U251 cell line overexpressing DDR1 was constructed to detect the effect of overexpression of DDR1 on the proliferation and migration of U251 cells transfected with miR-199a-5p. Results The level of miR-199a-5p in mimics group was significantly higher than that in control group (P < 0.01), the cell viability was reduced (P < 0.01), and the proliferation ability was weakened (P <0. 01). The expression of DDR1 in miR-199a-5p group cells was significantly reduced (P < 0. 01). Compared with mimincs group, the pcDNA3. 1-DDR1 transfected group could up-regulate DDR1 (P < 0. 01), increase cell viability, and promote cell proliferation (P < 0. 05 or P < 0. 01). Conclusions miR-199a-5p can down-regulate the expression of DDR1 and inhibit the proliferation and migration of human glioma cells.

Rabies remains an important worldwide health problem. Newcastle disease virus (NDV) was developed as a vaccine vector in animals by using a reverse genetics approach. Previously, our group generated a recombinant NDV (LaSota strain) expressing the complete rabies virus G protein (RVG), named rL-RVG. In this study, we constructed the variant rL-RVGTM, which expresses a chimeric rabies virus G protein (RVGTM) containing the ectodomain of RVG and the transmembrane domain (TM) and a cytoplasmic tail (CT) from the NDV fusion glycoprotein to study the function of RVG's TM and CT. The RVGTM did not detectably incorporate into NDV virions, though it was abundantly expressed at the surface of infected BHK-21 cells. Both rL-RVG and rL-RVGTM induced similar levels of NDV virus-neutralizing antibody (VNA) after initial and secondary vaccination in mice, whereas rabies VNA induction by rL-RVGTM was markedly lower than that induced by rL-RVG. Though rL-RVG could spread from cell to cell like that in rabies virus, rL-RVGTM lost this ability and spread in a manner similar to the parental NDV. Our data suggest that the TM and CT of RVG are essential for its incorporation into NDV virions and for spreading of the recombinant virus from the initially infected cells to surrounding cells.
Animals ; Antibody Formation ; Cytoplasm* ; Glycoproteins* ; GTP-Binding Proteins ; Humans ; Mice ; Newcastle disease virus* ; Newcastle Disease* ; Parents ; Rabies virus ; Rabies* ; Reverse Genetics ; Tail* ; Vaccination ; Virion*

Adaptation, Physiological ; Adenosine Monophosphate ; administration & dosage ; analogs & derivatives ; pharmacology ; therapeutic use ; Administration, Intranasal ; Alanine ; administration & dosage ; analogs & derivatives ; pharmacology ; therapeutic use ; Animals ; Betacoronavirus ; genetics ; physiology ; Chlorocebus aethiops ; Coronavirus Infections ; drug therapy ; virology ; Disease Models, Animal ; Female ; Host Specificity ; genetics ; Lung ; pathology ; virology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mutation, Missense ; Nasal Mucosa ; virology ; Pandemics ; Pneumonia, Viral ; drug therapy ; virology ; RNA, Viral ; administration & dosage ; genetics ; Turbinates ; virology ; Vero Cells ; Viral Load ; Virus Replication

The objective of this study was to investigate the expression profile of the myozenin2 (MYOZ2) gene and elucidate its effect on adipogenic differentiation of C3H10T1 / 2 cells and its possible mechanism∙ The longissimus dorsi‚ subcutaneous fat and liver tissue was collected from 180-day-old Mashen pigs‚ 60-day-old ICR mice‚ 35-day-old Ross broiler and 12-month-old Small tail han sheep‚ and the expression profile of the MYOZ2 gene mRNA was detected∙ The results showed that the MYOZ2 gene has similar patterns of tissue expression in examined species‚ with the highest expression level in longissimus dorsi‚ and a small amount of expression in the subcutaneous fat and liver tissue∙ After the MYOZ2 gene was silenced in C3H10T1 / 2 cells‚ qRT-PCR results showed that the expression levels of key adipogenic genes PPARγ and FABP4 were significantly down-regulated compared with the control group (P < 0∙ 01) ; Western Blotting results showed that the PPARγ protein content was significantly decreased (P < 0∙ 05) ; Oil red O staining showed that the number of lipid droplets and the content of triglyceride were significantly decreased after silencing MYOZ2 (P < 0∙ 05) ∙ The expression of fatty acid metabolism related genes SCD‚ FASN‚ SREBP1‚ NR1H3‚ DGAT1‚ PNPLA2‚ HSL‚ CES1‚ CPT1 after MYOZ2 silencing were detected by qRT-PCR∙ The results showed that SCD‚ FASN‚ SREBP1‚ PNPLA2 and HSL were significantly down-regulated (P < 0∙ 01) ‚ NR1H3 was significantly reduced (P < 0∙ 05) ‚ DGAT1 expression was down-regulated but the difference was not significant‚ CES1 and CPT1 were significantly up-regulated (P < 0∙ 05) ∙ The STRING database was used to construct a MYOZ2-related protein interaction network map‚ and it was found that MYOZ2 may affect the adipogenic differentiation through the interaction of titin-cap (TCAP) and PPARγ∙ After silencing TCAP‚ qRT-PCR results showed that compared with the control group‚ the expression of key adipogenic genes PPARγ and FABP4 were significantly up-regulated (P < 0∙ 01) ; Western Blotting results showed that PPARγ protein was significantly increased (P< 0∙ 05) ; Oil red O staining showed that the number of lipid droplets and the content of triglyceride were significantly increased after TCAP silencing (P < 0∙ 05) ∙ qRT-PCR was used to detect the expression of TCAP after silencing MYOZ2‚ and the results showed that the expression of TCAP was significantly increased (P<0∙ 01) ∙ In summary‚ MYOZ2 was highly expressed in longissimus dorsi and lower expressed in subcutaneous fat and liver tissues∙ In addition‚ MYOZ2 may regulate the expression of key adipogenic genes PPARγ and FABP4 through the interaction of MYOZ2-TCAP -PPARγ‚ and to further regulate the expression of fatty acid metabolism related genes SCD‚ FASN‚ SREBP1‚ NR1H3‚ DGAT1‚ PNPLA2‚ HSL‚ CES1 and CPT1‚ thus playing an important role in the process of adipogenic differentiation∙

The mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway is widely activated by a variety of extracellular stimuli, and its dysregulation is associated with the proliferation, invasion, and migration of cancer cells. ERK1/2 is located at the distal end of this pathway and rarely undergoes mutations, making it an attractive target for anticancer drug development. Currently, an increasing number of ERK1/2 inhibitors have been designed and synthesized for antitumor therapy, among which representative compounds have entered clinical trials. When ERK1/2 signal transduction is eliminated, ERK5 may provide a bypass route to rescue proliferation, and weaken the potency of ERK1/2 inhibitors. Therefore, drug research targeting ERK5 or based on the compensatory mechanism of ERK5 for ERK1/2 opens up a new way for oncotherapy. This review provides an overview of the physiological and biological functions of ERKs, focuses on the structure-activity relationships of small molecule inhibitors targeting ERKs, with a view to providing guidance for future drug design and optimization, and discusses the potential therapeutic strategies to overcome drug resistance.