Objective To investigate the effects of telmisartan on the blood glucose, blood lipid, blood insulin, and insulin resistance in the hypertensive patients with dyslipidemia, and also its effect on controlling blood pressure. Patients and Methods A total of 96hypertensive patients (34 females, 62 males) with dyslipidemia were included (mean age 51.2±9.6, range 42-65 years). Patients were randomized to receive either telmisartan 80 mg/day (n=46) or enalapril 10 mg/day (n=50) for 6 months. The levels of blood pressure (BP), heart rate (HR), and biochemical data were measured before therapy and at the end of the 3-month treatment and 6-month treatment, respectively. Meanwhile, insulin resistance was evaluated by using a homeostasis model assessment of insulin resistance (HOMA-IR) and insulin sensitivity (HOMA-IS). Results In the telmisartan group, the mean blood pressure was obviously lower than that of pre-therapy (P＜0.05), and the levels of triglyceride (TG), HOMA-IR, and HOMA-IS were all obviously lower than those of pre-therapy and of the enalapril group at the end of the 3-month-treatment period (P＜0.05). After 6 months of treatment, the levels of TG, HOMA-IR, and HOMA-IS in the telmisartan group were significantly lower in comparison with those of pre-therapy, the enalapril group (P＜0.01), and 3-month-treatment (P＜0.05). Post-prandial12 hour blood glucose (P2HBG) in the telmisartan group decreased significantly after 6-month treatment compared with that of pre-therapy and the enalapril group (P＜0.05). The level of high density lipoprotein (HDL) cholesterol was significantly higher after 6-month treatment in the telmisartan group than with pre-therapy and the enalapril group(P＜0.05). Conclusions Telmisartan could not only control blood pressure steadily and effectively, but also decrease blood TG, increase HDL cholesterol and insulin sensitivity, and lower insulin resistance.

The nucleocapsid protein (N) is a major structural protein of coronaviruses. The N protein of bat SARS-like coronavirus (SL-CoV) has a high similarity with that of SARS-CoV. In this study, the SL-CoV N protein was expressed in Escherichia coli, purified and used as antigen. An Indirect Enzyme-Linked Immunosorbent Assay (indirect ELISA) was developed for detection of SARS- or SL-CoV infections in bat populations. The detection of 573 bat sera with this indirect ELISA demonstrated that SL-CoVs consistently circulate in Rhinilophus species, further supporting the proposal that bats are natural reservoirs of SL-CoVs. This method uses 1-2 μl of serum sample and can be used for preliminary screening of infections by SARS- or SL-CoV with a small amount of serum sample.

Objective To explore the effects and mechanism in patients with ulcerative colitis (UC) treated by Yin Yang equilibrated preparation. Method 82 patients with UC as treatment group and 35 health parsons as control group underwent the testing. The serum and mucosal of all testing persons were taken pre and post treatment to detect CD+4 CD+25 regulatory T cells(Tregs) by flow cytometry at the end of one month,treating with SASP and Yin Yang equilibrated preparation. Result Compared with normal control group,the proportion of CD+4 CD+25 Tregs was markedly decreased in PB and mucesal of group A and B(P <0.01). But it was significanfly increased in therapeutic groups of SASP and Yin Yang equilibrated preparation, and their CD+4 CD+25 Tregs in PB and mucosal were much more than the control group at the end of one month after treating with SASP and Yin Yang equilibrated preparation(P <0.01 or P< 0.05). Conclusion CD+4 CD+25 Tregs with strong immune suppression play a central role in the initia-tion and development of UC,and the Yin Yang equilibrated preparation might exert its therapeutic effects on UC by the regulation of number and function of CD+4 CD+25 Tregs.

Objective To investigate low density lipoprotein receptor (LDLR)gene mutation in familial hypercholesterolemia (FH) patients. Methods The proband was given clinical diagnosis of homozygous FH based on marked features and blood lipid tests results. After apoB100R3500Q mutation was excluded, the promoter region and all of the 18 exons of LDLR gene were amplified by touch-downpolymerase chain reaction (PCR). The PCR products were analyzed by single-strand conformationalpolymorphism (SSCP). The PCR products with abnormal single strands were sequenced directly. Thesecondary structures of the mutational and wild type proteins were analyzed and compared byANTHEPROT5.0, and then the tertiary structures of the mutant and wild type LDLR were predicted atSWISS MODEL homepage online. Results A homozygous mutation A606T at exon 13 of the patients wasfound by SSCP and confirmed by DNA sequencing. GOR Ⅰ method in ANTHEPROT5.0 indicates that therandom coils and turns would replace some helixes at the mutation site. The online prediction from theSWISS MODEL homepage indicates the backbone structure of the mutant LDLR has no difference from thewild type one. Conclusion The results suggest the A606T mutation of LDLR gene is the cause of the FH inthis pedigree.

To adapt to the system reformation of medical laboratory science from five academic years to four academic years and to meet the new professional technology-oriented requirements, the medical laboratory science institute of Guangdong Medical College has carried out a comprehensive reform of curriculum system. This paper has analyzed the current problems in the school medical ex-amination and explored the curriculum system reform from three respects such as adjusting curriculum by restructuring and integrating programs, implementing modular teaching to build its characteristics and strengthening practice teaching.And it has also explored the full assessment mode by optimizing the traditional one-stop assessment.

OBJECTIVETo screen the mutations of the low density lipoprotein receptor (LDLR) gene in a familial hypercholesterolemia (FH) family, and analyze the LDL-uptaking function of LDLR on lymphocytes of patients.

METHODSGenomic DNA was extracted from four affected members in a Chinese FH family. The presence of apoB100 gene R3500Q mutation which results in familial defective apolipoprotein B100 (FDB) was excluded first. Fragments of the LDLR gene were amplified by touch-down polymerase chain reaction (Touch-down PCR) and analyzed by single-strand conformational polymorphism (SSCP). The suspect fragments of the LDLR gene were cloned and sequenced. Furthermore, the lymphocytes bounded with fluorescent-labeled LDL (DiI-LDL) were measured by fluorescence flow cytometry.

RESULTSA nonsense mutation was identified in exon 10 of LDLR gene. This mutation gave rise to a premature stop codon (W462X), resulting in the absence of most of the LDLR domains. It was detected in all the affected members of the FH family. The ratios of functional LDLR in lymphocytes from patients and normal controls were 63.7% and 77.3% respectively. As a result, the activity of the functional LDLR in patients was just 82.4% of that in the normal controls.

CONCLUSIONIt is possible that the W462X mutation of LDLR gene is the main cause for the disease in this family.

Adult ; Apolipoprotein B-100 ; genetics ; Base Sequence ; Case-Control Studies ; DNA Mutational Analysis ; Deoxyribonuclease I ; metabolism ; Exons ; genetics ; Female ; Flow Cytometry ; Humans ; Hyperlipoproteinemia Type II ; genetics ; metabolism ; pathology ; Lipoproteins, LDL ; metabolism ; Lymphocytes ; metabolism ; Male ; Middle Aged ; Mutation ; Pedigree ; Receptors, LDL ; genetics ; metabolism

Objective To explore the expression of triggering receptor expressed on myeloid cells 2(TREM2)in high-glucose microglia and to investigate the role of TREM2 in the proliferation,migration and phagocytosis of high-glucose microglia.Methods Microglia cells were divided into control group and high-glucose treatment group(67.5 mmol/L glucose,24 h).The microglia cells were counted and the expression of Iba1 and TREM2 was de-tected.TREM2 siRNA was transfected to detect the proliferation and migration of microglia.The amyloid β-peptide(Aβ)with a fluorescent tag was added to observe the phagocytosis of Aβ by microglia.Results Compared to normal microglia,the number of microglia significantly decreased after high-glucose treatment(P＜0.001),while the ex-pression of TREM2 and Iba1 markedly increased(P＜0.001).High glucose and TREM2 did not affect the prolifer-ation of microglia.Compared to the normal group,the migration of microglia significantly decreased after high-glu-cose treatment(P＜0.05)and TREM2 did not affect the migration ability of high-glucose microglia.Compared to the normal group,the phagocytosis of Aβ by microglia significantly decreased in the high-glucose treated group(P＜0.001).Furthermore,TREM2 knockdown further decreased the phagocytosis of Aβ by high-glucose microglia(P＜0.001).Conclusions The expression of TREM2 in microglia significantly increases after high-glucose treat-ment,which significantly affects phagocytosis of Aβ by microglia.

Bilirubin has good anti-inflammatory， antioxidant and immunomodulatory effects， but its poor water solubility and low bioavailability greatly limit its clinical application. Researchers have developed bilirubin into various nanoparticles， which effectively eliminate the limitation of low solubility of bilirubin with the advantage of dosage form， so that they can maximize its pharmacological activities such as anti-inflammatory， anti-oxidation and immune regulation. Bilirubin nanoparticles have great application potential in a variety of gastrointestinal diseases， liver and kidney diseases， skin diseases， autoimmune diseases， islet transplantation and targeted therapy of tumors （both as a direct anti-tumor drug and as a drug delivery system）. The study of bilirubin nanoparticles will promote the clinical application of bilirubin and the development of related new drugs.