Gemfibrozil in the treatment of hyperlipidemia

An elevated serum cholesterol level is a well known major risk factor for developing atherosclerosis in general, and for coronary heart disease in particular. There are many lipid lowering agents currently available. We used gemfibrozil in twenty hyperlipidemic cases who failed to response to diet control for three months. They were thirteen males and seven females with their ages ranging from thirty to eighty-one year-old. They included ten diabetes, one nephrotic syndrome and nine pure hyperlipidemic patients. All cases received gemfibrozil 600mg twice daily for 4-12 weeks. Gemfibrozil caused an increase in HDL cholesterol. The reductions in serum level of total cholesterol, total cholesterol/HDL cholesterol, and triglyceride were found. Only one case developed mild gastrointestinal side effect. There was no other major side effects.     

Fall prevention exercise program for fall risk factor reduction of the community-dwelling elderly in Korea

A randomized comparison of pre-and post-experimental design was used to examine the effects of a fall prevention exercise program (FPEP) on muscle strength, ankle flexibility, balance, instrumental activities of daily living (IADLs), and depression for the community-dwelling elderly in Korea. Twenty-two subjects were assigned to an experimental group and twenty-three to a control group. The experimental group participated in a 4-day-per week FPEP of 8 weeks duration, twice a week by direct instruction and twice a week with videotaped instruction by the program instructor at each senior center. The eight-week FPEP turned out to be significantly effective in enhancing muscle strength, ankle flexibility and balance, and in reducing depression, after intervention among community-dwelling elderly in Korea. IADLs, however, was not changed by the intervention. Further research with a larger sample and longer follow up period is needed to expand our understanding about the effects of FPEP. Future study is also recommended to differentiate between the effects of FPEP by direct instruction and by videotaped.     

Rat sponge implant model: a new system for evaluating angiogenic gene transfer

Therapeutic angiogenesis, either by protein injection or gene therapy, holds considerable promise for the treatment of coronary and peripheral artery diseases. Given the large number of angiogenic genes available, a simple, well defined, standard system to compare the relative angiogenic efficacy of such genes would be valuable. We have employed a replication-deficient adenovirus vector (complete E1a-, partial E1b- and partial E3-) to deliver the beta-galactosidase (beta-gal, AdLacZ) reporter gene or the human VEGF121 gene (AdGV VEGF121.10) to a rat sponge implant model of angiogenesis. beta-gal staining results reveal a transfection efficiency as high as 60% 24 h after 2x1010 particle units AdLacZ injection. Our results also indicate that a single injection of 2x1010 particle units of AdGVVEGF121.10 in the sponge results in >10, 000 pg VEGF protein expression per milligram of sponge tissue 24 h later. VEGF121 protein concentrations decreased 10-fold within 3 days and 100-fold within 7 days after injection. Significant VEGF121 protein levels were still detectable 14 days after initial virus injection. The high level of gene transfection efficiency was accompanied by enhanced angiogenesis in the sponge, a tissue devoid of any vessels before implantation. Compared to control (AdNull: adenovirus vector without the VEGF gene), AdGVVEGF121.10 induced a 2- to 3-fold up-regulation of angiogenesis at 7 and 14 days post vector injection as determined by both increased capillary number and increased tissue ingrowth. The angiogenic effects of AdGVVEGF121. 10 were dose-related in this model system. These findings demonstrate a dose-related angiogenic response to adenovirus-mediated gene therapy in this model.     

培养细胞整装内质网三维结构的多态性

用高锰酸钾－锇酸固定法制备了５种培养细胞整装内质网标本，并在扫描电镜下对其三维结构进行了观察。观察结果表明内质网是由膜性小管构成的贯穿整个细胞质的管囊网络样膜性区室，并以多种形态深入到细胞伪足及突起中；细胞质中内质网则表现为簇状网络（见于ＧＣＭ３Ｔ３细胞）、多态性多孔扁囊样网络、筛网状网络、条索状网络、大孔条索网状和细孔扁囊样分区网络、不规则管网状和多孔管囊分区网络（见于ＣＶ－１细胞）、细管网络（见于ＣＣＬ１８７和ＣＣＬ２２９细胞）、球囊网络（见于ＣＣＬ１８７和Ａ４３１细胞）和不规则管网状网络（见于Ａ４３１细胞）等。内质网的这种多态性提示它是一种高度可变的结构，其可变性可能与细胞特性、分化程度、细胞功能状态及细胞骨架系统的分布变化等因素有关。     

抗体包被对红细胞变形性影响的研究

作者对抗体包被的红为性进行研究，发现抗体包被改变了红细胞的变形性，在我们研究的抗体量范围内，抗体量越多，红细胞的变形性越小，作者从血液流变学的角度对上述结果作了讨论，并提出了通过测定其对红细胞变形性的影响来比较准确地标定抗体效价的可能性。     

Hybridization studies of cultured human pituitary prl and gh producing adenoma cells: Effects of thyrotropin-releasing hormone,somatostatin, and phorbol ester

The effects of the hypothalamic hormones, thyrotropin-releasing hormone (TRH), and somatostatin (SRIH), and of phorbol 12-myristate 13-acetate (PMA) on PRL and GH secretion and messenger RNA (mRNA) levels were analyzed in 10 GH and/or PRL producing adenomas after culturing the tumor cells in the presence of these secretagogues for 7 days. The expression of chromogranin A and B mRNAs was also examined. All four of the clinically diagnosed GH adenomas expressed or secreted both GH and PRL while four of six clinically diagnosed prolactinomas produced or secreted both PRL and GH. Prolactinomas had less than 10% of tumor cells expressing chromogranin A mRNA while more than 40% of the adenoma cells expressed chromogranin B mRNA. TRH stimulated PRL secretion and increased PRL mRNA levels while SRIH decreased GH secretion and mRNA expression in some cases. Unexpectedly, PMA stimulated PRL mRNA levels four- to sevenfold above control levels in two adenomas and generally stimulated chromogranin A and B mRNA expression but not GH mRNA, as determined by Northern hybridization and in situ hybridization analyses. These results indicate that cultured prolactinoma cells express significantly more chromogranin B mRNA than chromogranin A mRNA, and that PMA increases PRL mRNA expression in some prolactinomas, although the effect of PMA on various adenomas reflects the heterogeneity of these tumors with respect to protein kinase C stimulation.     

“Smart” Materials for Biosensing Devices: Cell-Mimicking Supramolecular Assemblies and Colorimetric Detection of Pathogenic Agents

Mimicking cell membrane and the biomolecular recognition associated with membranes represents a great technical challenge, yet it has opened doors to innovative diagnostic and therapeutic methods. Our work has focused on design and synthesis of a class of smart materials exploiting biological principals for use in biosensors: these materials are functional polymeric assemblies that mimic the cell membrane and conveniently report the presence of pathogens with a color change. Biologically active cell membrane components are incorporated into conjugated polymers with desirable optical properties and the binding of the target molecules onto the material triggers conformational and electronic shifts that are reflected in a chromatic change (a so-called biochromic shift) that is conveniently observed and recorded. Langmuir–Blodgett thin films and vesicle bilayers provide ideal configurations for precise delivery of the biological binding entity to the sensing interface, and for control of molecular orientation for effective biomolecular interaction. Polydiacetylenic membrane-mimicking materials containing cell surface receptor gangliosides and sialic acid residues, respectively were formulated into these architectures and used for colorimetric detection of bacterial toxins and influenza virus. One advantage of these biochromic conjugated polymer (BCP) sensors is that their molecular recognition and signal transduction functionalities are resident in a single functional unit, making them amenable to convenient microfabrication and use.     

Application of monoclonal antibodies to detect intraocular mycoplasma antigens in Mycoplasma arthritidis-infected Sprague-Dawley rats.

Sprague-Dawley rats infected with Mycoplasma arthritidis by tail vein inoculation develop extensive disseminated joint inflammation, frequently accompanied by conjunctivitis and anterior uveitis. The intraocular inflammation is apparently directed at mycoplasmas localized within the stroma of the ciliary body, which have been detected with monoclonal antibodies by indirect immunofluorescence. The monoclonal antibodies are directed against an antigenic determinant on the enzyme arginine deiminase isolated from M. arthritidis, but they do not react with the same enzyme derived from Mycoplasma hominis. The antigen bound by the monoclonal antibodies can also be detected by immunofluorescence in M. arthritidis-infected tissue cultures and is not lost after glutaraldehyde fixation or paraffin-embedding procedures. The value in the application of monoclonal antibodies reactive with arginine deiminase lies in the fact that although this enzyme may be found in mycoplasmas and several other species of bacteria it is not a normal constituent of mammalian tissues.     

Roles of sortase in surface expression of the major protein adhesin P1, saliva-induced aggregation and adherence,and cariogenicity of Streptococcus mutans

Sortase is a newly discovered transpeptidase that covalently links LPXTGX-containing surface proteins to the gram-positive bacterial cell wall. In this study, the sortase gene (srtA) was isolated from Streptococcus mutans NG8 by PCR. The gene encoded a 246-amino-acid protein, including a 40-amino-acid signal peptide. The srtA gene was insertionally inactivated by a tetracycline resistance cassette. P1, a major surface protein adhesin previously shown to anchor to the peptidoglycan by the LPXTGX motif, was secreted into the culture medium by the srtA mutant. In contrast, the wild-type P1 remained cell wall associated. Complementation of the mutant with srtA restored the P1 surface expression phenotype. P1 produced by the mutant, but not that produced by the wild type and the srtA-complemented mutant, was recognized by an antibody raised against the hydrophobic domain and charged tail C terminal to the LPXTGX motif. These results suggest that the failure to anchor P1 to the cell wall is due to the lack of cleavage of P1 at the LPXTGX motif. The srtA mutant was markedly less hydrophobic than the wild type and the complemented mutant. The srtA mutant failed to aggregate in the presence of saliva or salivary agglutinin and adhered poorly to saliva- or salivary agglutinin-coated hydroxylapatite. In rats, the srtA mutant colonized the teeth poorly when sucrose was absent. When sucrose was present, the srtA mutant colonized the teeth but less effectively and induced significantly less caries (P < 0.05) than the wild-type strain. In conclusion, the sortase enzyme in S. mutans is responsible for anchoring P1 to the cell surface and plays a role in modulating the surface properties and cariogenicity of S. mutans.