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Biomedical subjects

H Feng

Publications and source records attributed to H Feng.

107 records · Page 6Linked to original sources
PubMed1995

Bradykinin acting on B2 receptors contracts colon circular muscle cells by IP3 generation and adenylate cyclase inhibition.

Receptor subtypes and intracellular signaling events involved in bradykinin-evoked contraction of colonic circular muscle are unknown. We studied the roles of inositol trisphosphate (IP3) and cyclic AMP generation and the selectivity for B1 and B2 receptors in guinea pig colon. Bradykinin induced concentration-dependent contraction of circular muscle strips with an EC50 of 2 x 10(-8) M that was inhibited by the B2 antagonist D-Argo-(Hyp3,Thi5,8,D-Phe7)-bradykinin but not the B1 antagonist des-Arg9-[Leu8]bradykinin. The B1 agonist des-Arg9-bradykinin did not evoke contraction or relaxation. Bradykinin induced concentration-dependent shortening of isolated myocytes from circular muscle with an EC50 of 2 x 10(-11) M that was inhibited by the B2 but not the B1 antagonist, confirming the myogenic nature of the bradykinin receptors. Persistence of myocyte contraction in a calcium-free medium with EGTA confirmed the lack of dependence on extracellular calcium. In colon muscle tissue, bradykinin evoked concentration-dependent IP3 generation with an EC50 of 10(-7) M and a maximal level of 58 +/- 17 pmol/mg of protein at 10(-4) M that was inhibited by the B2 but not the B1 antagonist. Bradykinin, acting on B2 receptors, inhibited cyclic AMP formation after forskolin (10(-5) M) with an EC50 of 3 x 10(-8) M and maximal inhibition of 48% at 10(-5) M. In conclusion, bradykinin induces colon muscle contraction via myogenic non-B1 receptors, which are likely of the B2 subtype, with phosphoinositide turnover activation and adenylate cyclase inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclase Inhibitors↗
PubMed1994

P1 and cosmid clones define the organization of 280 kb of the mouse H-2 complex containing the Cps-1 and Hsp70 loci.

A 280 kilobase (kb) contig was isolated from mouse genomic P1 and cosmid libraries, using as probes human cDNA and genomic DNA fragments that map in the interval between the second component of complement and tumor necrosis factor genes of the HLA complex. The clone contig demonstrates synteny of eleven mouse genes that are homologous to genes initially mapped within the human major histocompatibility complex. These include the mouse homologs of BAT2 (HLA-B-associated transcript 2) through BAT9 and also three HSP70-related genes. Five P1 clones form a contig of 240 kb that spans from BAT9 through BAT3. Twelve cosmid clones are arranged in three contigs that confirm most of the structure of the P1 contig and link the mouse BAT3 homolog to the BAT2 homolog approximately 15 kb farther telomeric. Polymorphic DNA markers within the cloned region were used to map the cleft palate susceptibility-1 (Cps-1) locus to the interval between Hsp70.1 and BAT6 (valyl-tRNA synthetase). This refines the location of the Cps-1 locus to a 45 kb region contained in the H2-124 P1 insert.

Adenosine Triphosphatases↗
PubMed1994

Evidence, from family studies, for linkage disequilibrium between TGFA and a gene for nonsyndromic cleft lip with or without cleft palate.

The inheritance of alleles of the transforming growth factor alpha (TGFA) locus has been studied in families affected with cleft lip with or without cleft palate (CL/P), by using the transmission/disequilibrium test described by Spielman and colleagues. Only heterozygous parents with an affected child can be included in this test, but within such families a significantly greater frequency of C2 alleles were transmitted to affected children than would be expected by chance. There was no evidence that the total number of C2 alleles transmitted to affected and unaffected children differed significantly from random segregation. These data provide evidence from within families that a gene for susceptibility to CL/P is in significant linkage disequilibrium with the C2 allele of the TGFA locus.

Alleles↗
PubMed1993

Association between alleles of the transforming growth factor-alpha locus and the occurrence of cleft lip.

DNA samples from 100 patients with cleft lip with or without cleft palate (CL/P) were compared with those of 98 unaffected control individuals with respect to transforming growth factor alpha (TGFA) genotypes. Among the Caucasians in this population (83 CL/P, 84 controls), there was a significant difference in the restriction fragment length polymorphisms (RFLPs) observed after digestion with TaqI (chi 2 = 4.68, P = 0.03). The frequency of the C2 allele in the Caucasian CL/P population was 0.169, whereas that in the control group was 0.089. When the data for Caucasians, African-Americans, and Asians were examined jointly, the chi 2 value for the pooled sample was 5.08 (P = 0.02). This confirms the hypothesis of Ardinger et al. [1989, Am J Hum Genet, 45:348-353] that TFGA itself or a closely linked gene contributes to the development of CL/P in humans.

Alleles↗
PubMed1993

Purified antichick Thy-1 IgG abolishes intermediate and long-term memory.

One- to 2-day-old chicks administered purified antichick Thy-1 IgG showed substantial amnesia for a single-trial passive discriminated avoidance task. Amnesia was clearly evident at 30 min after learning, during the intermediate stage of a three-stage model of memory processing, and persisted for at least 3 h. A similar effect was also observed with Fab and F(ab')2 fragments. Fc fragments, the non-IgG fraction of ascites, and saline yielded normal retention levels at all times. These results contrast with our earlier reports that both polyclonal and monoclonal antibodies to chick Thy-1 inhibited long-term memory formation only. The present findings are interpreted as possibly representing a dual effect of the purified IgG.

Animals↗
PubMed1992

CT-guided stereotactic injection of radionuclide for treatment of brain tumors.

The authors report on 40 brain tumor patients treated with CT-guided stereotactic injection of 198Au and 32P. Among the 40 cases were astrocytoma in 23 cases, craniopharyngioma in 9, meningioma in 4, pituitary adenoma in 2, and pinealoma and metastatic carcinoma each in 1 case. The tumors were all located in deep or important areas of the brain which were difficult to deal with by conventional operation. 62 injections of colloidal isotopes were performed, and all were successful. No major adverse effects or complications occurred on follow-up of 6-12 months, 28 patients were improved in their clinical symptoms, and CT scanning showed that the tumor sizes were diminished. The effective rate is 70%.

Adenoma↗
PubMed1990

Studies on medicamentous inhibitory therapy for esophageal precancerous lesions--3- and 5-year inhibitory effects of antitumor-B, retinamide and riboflavin.

Since 1983, we have been conducting inhibitory therapy for precancerous lesions of the esophagus in two regions of Henan Province considered high-risk areas of esophageal carcinoma. Our goal was to effect a 50% reduction in the canceration rate of marked esophageal dysplasia. By means of a cytological survey, 2531 cases of marked esophageal dysplasia and 3393 cases of mild esophageal dysplasia were selected. The former were randomly divided into 3 groups for antitumor-B (ATB, a mixture of Chinese herbs), retinamide (4-ethoxycarbophenylretinamide) and placebo treatment respectively, and the latter into 2 groups treated with riboflavin and placebo respectively. Treatment was continued for 3 or 5 years (administration rate greater than 90% in all groups) and esophageal cytology reexamined (reexamination rates were 94.1% and 92.5% respectively). Our results were as follows: 1) ATB 3- and 5-year subjects saw the canceration rate of marked esophageal dysplasia drop by 52.2% and 47.3% respectively as compared to control (P less than 0.01). 2) Retinamide lowered the canceration rate by 37.3% after a 3-year treatment period, with this reduction reaching 43.2% after an additional 2 years of treatment with increased dosages (P less than 0.05, P less than 0.01). 3) In the riboflavin group, the canceration rate of mild esophageal dysplasia was reduced by 22.2% and 34.8% after 3 and 5 years of treatment respectively, but these differences were not statistically significant. The above results verify the efficacy of medicamentous inhibitory therapy for esophageal precancerous lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Multiecho magnetic resonance angiography.

Several pulse sequences which generate projected MR angiograms are presented. These pulse sequences exploit multiple-gradient refocused echoes to obtain several independent angiograms, which can be combined or separately analyzed to provide more information than an individual angiogram. For example, a series of angiograms, each with a different projection axis, can be obtained in the time required to obtain a single angiogram using a single-echo method. If the view angle of each echo is the same, then the acquired angiograms can be added to enhance the signal-to-noise ratio. Another pulse sequence simultaneously obtains two or more angiograms, sensitive to orthogonal flow components of the overall blood flow. These angiograms are then added to give an angiogram which is sensitive to flow in all directions.

Angiography↗
PubMed1987

Definition of myasthenogenic sites of the human acetylcholine receptor using synthetic peptides.

Experimental autoimmune myasthenia gravis (EAMG) and antibodies that modulate AChRs from cultured human muscle are induced by a disulfide-looped peptide comprising the human acetylcholine receptor (AChR) alpha-subunit residues 125-147 (H alpha 125-147). To delineate the essential antigenic requirements for induction of EAMG by this peptide, a series of peptides was synthesized: (a) a nonlooped analog (Cys 128 replaced by Ser) stimulated modulating autoantibodies, induced EAMG, and bound antibodies induced by native AChR; (b) H alpha 131-147, a heptadecylpeptide shorter by 6 N-terminal residues, induced modulating antibodies, EAMG, and T cells that responded to H alpha 125-147, but not to H alpha 137-147; (c) H alpha 137-147, an undecapeptide shorter than H alpha 125-147 by 12 N-terminal residues, did not stimulate T cells or induce antibody production, but it bound antibodies generated by the longer peptides. Thus, when coupled to an epitope that could stimulate helper T cells, the region 137-147 was able to stimulate B cells. This study has defined a myasthenogenic region of the human AChR's alpha-subunit, 17 amino acids long, that contains several distinct epitopes, including at least one N-terminal site inducing T-cell responses (region 131-136) and two possibly overlapping sites that induce antibodies (regions 131-136 and 137-147). Further definition of antigenic sites inducing helper and suppressor T-cell responses and stimulating production of autoantibodies to AChR is essential to the goal of antigen-specific immunotherapy for myasthenia gravis.

Action Potentials↗
PubMed1979

Endplates after esterase inactivation in vivo: correlation between esterase concentration, functional response and fine structure.

Mouse sternomastoid muscles were incubated with diisopropylfluorophosphate (DFP) in vivo, and the time course of recovery was studied using histochemistry, EM autoradiography and physiology. We found that: (1) the ability of the muscle to sustain tetanus in response to nerve stimulation is eliminated when the esterases at the neuromuscular junctions are saturated with DFP. This ability is regained partially when less than 10% of the DFP-binding sites have recovered. (2) There is a positive correlation between the frequency of stimulation at which the tetanic response can be maintained and the extent of acetylcholinesterase (AChE) recovery. (3) Tetanic responses at fusion frequency (about 100 Hz) appear indistinguishable from controls with only about 25% of normal AChE. (4) Butyrylcholinesterase (BuChE) possibly of Schwann cell origin recovers more rapidly than does AChE. (5) The muscle shows fine structural changes involving Z band dissolution and the breakdown of sarcoplasmic reticulum within hours after esterase inactivation. (6) This myopathy reaches a peak at three days after esterase inactivation and is almost fully recovered by two weeks. (7) It can be eliminated if, at the time of esterase inactivation, the nerve is cut or the acetylcholine receptors at the endplate are inactivated by alpha-bungarotoxin. We suggest that the myopathy, seen after DFP, is mediated by Ca2+ fluxes due to prolonged action of acetylcholine (ACh) in the absence of esterases.

Acetylcholinesterase↗
PubMedDate not supplied

Deficits in water escape performance and alterations in hippocampal cholinergic mechanisms associated with neonatal monosodium glutamate treatment in mice.

Mice treated neonatally with monosodium glutamate (MSG) were found to have learning and memory deficits in performing a non-spatial water escape task. Scopolamine impaired the water-escape performance of the control mice but not that of the MSG-treated mice. It was suggested that the water-escape performance deficit in the MSG-treated mice was a result of impaired central cholinergic mechanisms. As such, scopolamine was unable to further incapacitate an already impaired cholinergic system. This is strongly supported by the decreased affinity of the sodium-dependent high-affinity choline uptake observed in the hippocampus. D-Cycloserine, a partial agonist at the glycine site of the NMDA receptor, did not affect the water-escape performance of the MSG-treated and control mice; nor did it alter the effects of scopolamine. This lack of effect of D-Cycloserine may imply that the NMDA receptors are not involved in non-spatial learning, in contrast to their reported involvement in spatial learning.

Animals↗