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Biomedical subjects

H Lin

Publications and source records attributed to H Lin.

At least 415 records · Page 23Linked to original sources
PubMed1992

Characterization of the rRNA-encoding genes and transcripts, and a group-I self-splicing intron in Pneumocystis carinii.

Although Pneumocystis carinii is the most common opportunistic pathogen infecting individuals with AIDS, very little is known of the basic biology of the organism. We have examined the ribosomal RNA (rRNA) and the DNA encoding it (rDNA) in P. carinii in an attempt to clarify its taxonomic position and to begin to study its genetic processes. Electrophoretic analysis showed that the sizes of the P. carinii rRNAs are quite similar to the sizes of the corresponding rRNAs from Saccharomyces cerevisiae. Direct sequence analysis of approx. 60% of the 18S small subunit-rRNA (Ss-rRNA) confirmed that its sequence is similar to that of yeast-like fungi and that a putative group-I intron previously observed in the 18S rDNA is, in fact, excised from the mature rRNA. PCR analysis of the intron in P. carinii genomic DNA showed that each of the multiple rDNA genes bears the group-I intron and in vitro transcripts of the intron autocatalytically excise from the rRNA primary transcript in the presence of GTP. Finally, analogues of GTP inhibit the self-splicing reaction, indicating that the guanosine-binding site of the intron closely resembles that of other well-characterized group-I introns. Since no group-I introns have been found in higher eukaryotes, this self-splicing process represents a viable target for chemotherapy of P. carinii pneumonia (PCP).

Antifungal Agents↗
PubMed1992

Identification of MRF4, myogenin, and E12 oligomer complexes by chemical cross-linking and two-dimensional gel electrophoresis.

The muscle-specific regulatory factors MRF4 and myogenin, as well as the ubiquitous factor E12, belong to a protein family which shares a common structural motif referred to as the basic helix-loop-helix domain. Recent studies have demonstrated that MRF4 and myogenin, in the presence of E12, bind efficiently to enhancer regions of muscle-specific genes, thereby activating their transcription. Although several lines of evidence suggest that MRF4 and E12 or myogenin and E12 hetero-oligomers exist, direct studies revealing the composition of these protein complexes have not been reported. Here, we demonstrate that MRF4 and myogenin preferentially form heterodimers with E12 in solution and that heterodimer formation in vitro is greatly enhanced when the two proteins are co-synthesized. Utilizing a novel two-dimensional gel electrophoresis system, we have found that MRF4 and myogenin, when complexed with E12, bind as heterodimers to the E-box consensus sequences associated with the troponin I, M-creatine kinase, and myosin light chain gene enhancers. In all cases, higher order oligomer structures were not detected, demonstrating that in vitro DNA binding abilities of these basic helix-loop-helix proteins require heterodimer formation.

Base Sequence↗
PubMed1992

Permucosal implantation pilot study with HA-coated dental implant in dogs.

The histological response of transmucosal one-stage titanium dental implants coated with hydroxyapatite is described. The gingival adhesion to the implant was examined with regard to coated, partially coated or non-coated surfaces in the cervical region. From each coating type, 9 implants were inserted into dogs. Six months after the insertion, 19 implants could be evaluated, but 8 implants were lost. From these 19 implants, 6 implants showed severe pockets with inflammation up to the bony tissue. The 13 successful implants showed direct bone bonding with the hydroxyapatite coating and adhesion of submucosal connective tissue to the implant surface, with inflammation. The marginal gingiva showed slight inflammation. A totally coated implant will probably introduce inflammation by debris formation against the rough implant surface more easily. The hydroxyapatite coating often disappeared in the soft tissue or in the oral cavity. Bone which directly adapted to the coating seemed to prevent it from resorption.

Animals↗
PubMed1992

Prolongation of cardiac allograft survival in rats by anti-TNF and cyclosporine combination therapy.

Cyclosporine is well known to have many adverse side effects. However, while decreasing the dosage of CsA can reduce its toxicity, this also lowers its immunosuppressive effectiveness. Additionally, anti-tumor necrosis factor has been demonstrated to have immunosuppressive activity and been shown to prolong cardiac allograft survival. This current study therefore investigated the efficacy of a combined therapy of anti-TNF with low-dose CsA in a rat heterotopic cardiac transplant model utilizing Brown-Norway donors and Lewis recipients. Control transplant recipients received no immunotherapy. Experimental animals received single-dose anti-TNF intraperitoneally on posttransplant days 0, 3, or 5 and/or low-dose CsA (1.5 mg/kg/day) intramuscularly from days 0 to 14 after transplantation. Rejection was determined by the lack of contractions in the transplanted heart. No animal received any other form of immunosuppression. Graft survival was significantly prolonged with combination CsA and anti-TNF therapy, suggesting a synergistic effect against acute cardiac allograft rejection, possibly from CsA and anti-TNF interacting at different levels of the recipient immune response. This form of combination therapy may hold promise for future immunosuppressive techniques.

Animals↗
PubMed1992

[ELISA for detection of anti-filamin antibody in sera from patient with myasthenia gravis].

The activity of anti-filamin antibody was determined in sera from 128 patients with myasthenia gravis (MG) by enzyme-linked immunosorbent assay (ELISA). The positive rate was 77.34%. No correlation was observed between anti-F-ab and nAchRab and CAEab. The antibody-absorbtion test were positive. The result demonstrated that anti-F-ab may play some role in the pathology of MG. The clinical use of ELISA for detection of anti-F-ab may help to diagnose MG.

Adolescent↗
PubMed1992

Na-dependent pHi regulatory mechanisms in native human retinal pigment epithelium.

This study provides the first information about pHi regulatory mechanisms in human retinal pigment epithelium (RPE). The experiments were carried out on fresh explant tissues from adult donor and fetal eyes, and pHi was measured using fluorescence microscopy techniques and the pH-sensitive dye 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. In adult donor RPE, the resting pHi is 7.30 +/- 0.14 (mean +/- standard deviation; n = 6) in HCO3 Ringer's solution. In HCO3 Ringer's solution, apical Na removal caused rapid cell acidification with an initial rate of 0.40 +/- 0.10 pH U/min (n = 4). This Na-dependent acidification was partially inhibited by apical amiloride (n = 1) and DIDS (n = 1). In HCO3 Ringer's solution, pHi recovery from an acid load (NH4 prepulse) also was blocked by apical Na removal. In nominally HCO3-free Ringer's solution, apical amiloride (1 mmol/l) acidified the cells. These results suggest that the apical membrane of adult human RPE contains an Na/H exchanger and possibly a Na-dependent, DIDS-inhibitable pH regulatory mechanism, perhaps a NaHCO3 cotransporter. For the fetal RPE, the resting pHi was 7.16 +/- 0.10 (n = 9) and 7.19 +/- 0.10 (n = 20) in HCO3 and HCO3-free Ringer's solution, respectively. In HCO3 and HCO3-free Ringer's solution, apical amiloride (1 mmol/l) acidified the cells and the removal of apical Na caused cell acidification with an initial rate of 0.30 +/- 0.08 (n = 32) and 0.58 +/- 0.29 (n = 6) pH U/min, respectively. The pHi recovery from an acid load also was blocked by apical amiloride and apical Na removal. These results suggest that the apical membrane Na/H exchanger is the dominant acid extrusion mechanism in human fetal RPE.(ABSTRACT TRUNCATED AT 250 WORDS)

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1991

Dystrophin is a component of the subsynaptic membrane.

A subsynaptic protein of Mr approximately 300 kD is a major component of Torpedo electric organ postsynaptic membranes and copurifies with the AChR and the 43-kD subsynaptic protein. mAbs against this protein react with neuromuscular synapses in higher vertebrates, but not at synapses in dystrophic muscle. The Torpedo 300-kD protein comigrates in SDS-PAGE with murine dystrophin and reacts with antibodies against murine dystrophin. The sequence of a partial cDNA isolated by screening an expression library with mAbs against the Torpedo 300-kD protein shows striking homology to mammalian dystrophin, and in particular to the b isoform of dystrophin. These results indicate that dystrophin is a component of the postsynaptic membrane at neuromuscular synapses and raise the possibility that loss of dystrophin from synapses in dystrophic muscle may have consequences that contribute to muscular dystrophy.

Amino Acid Sequence↗