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Biomedical subjects

J Fang

Publications and source records attributed to J Fang.

At least 343 records · Page 19Linked to original sources
PubMed1990

Cervical magnetic stimulation.

We stimulated the cervical region with a 9-cm-diameter magnetic coil on centered on the spinous processes in 21 normal subjects. We obtained maximal amplitudes with clockwise coil current in right-sided upper extremity muscles and counterclockwise coil current in left-sided upper extremity muscles. Optimal stimulation sites for biceps, triceps, and abductor digiti minimi were C-3 or C-4, C-4 or C-5, and C-4, C-5, or C-6, respectively. The latencies of the muscle responses varied little in the same subject in spite of marked amplitude changes due to suboptimal position of the coil or submaximal stimulator output. In abductor digiti minimi, the amplitude of the muscle response on cervical magnetic stimulation was 9 to 100% of the supramaximal amplitude on wrist electrical stimulation. We established normal values for latency, amplitude, and interside differences for the above 3 upper extremity muscles. The findings were reproducible, and the latencies obtained with large coils from different manufacturers in the same subjects were comparable. We found no advantage in bipolar recording over tendon-belly montage. Comparison of magnetic and electrical needle root stimulation in the same subjects showed that the magnetic stimulus was more proximal in biceps and triceps, and that the site of excitation was approximately the same in abductor digiti minimi. Indirect assessment of the longitudinal site of excitation based on F-wave minimal latency indicated that excitation occurred within millimeters of the emergence of axon of the peripheral motor neuron.

Adult↗
PubMed1988

Glial fibrillary acidic protein immunohistochemical study of Alzheimer I & II astrogliosis in Wilson's disease.

This study compared the relationships of the development of both Alzheimer I & II cells to reactive astrogliosis and also their distributional patterns in the demyelinated and non-demyelinated lesions in 6 cases of Wilson's disease by the use of PAP immunohistochemical technique for glial fibrillary acidic protein (GFAP). The development of GFAP positive Alzheimer I (A-I) cells was found to be directly proportional to the capability of reactive astrogliosis, and inversely proportional to the severity of Alzheimer II (A-II) change. The GFAP negative A-II cells could be identified morphologically into 2 subtypes: one with well-developed nuclei, the other with "shrunken" nuclei. They were believed to stand for the "compensatory" and "decompensatory" stages of this dynamic astrogliotic process respectively. The distribution patterns of these 2 types of astrogliosis were different: A-I cells were found only in the regions of demyelination with intensive reactive astrogliosis, while A-II cells were found diffusely in both the grey and white matter, affecting both the protoplasmic and fibrous astrocytes without special predilection.

Adult↗
PubMed1981

Avian leukosis virus-induced tumors have common proviral integration sites and synthesize discrete new RNAs: oncogenesis by promoter insertion.

Unlike other RNA tumor viruses, avian leukosis viruses (which cause lymphomas and occasionally other neoplasms) lack discrete "transforming genes". We have analyzed the virus-related DNA and RNA of avian leukosis virus (ALV)-induced tumors in an attempt to gain insight into the mechanism of ALV oncogenesis. Our results show that viral gene products are not required for maintenance of neoplastic transformation. Primary and metastatic tumors are clonal and thus presumably derived from a single infected cell. Most importantly, tumors from different birds have integration sites in common. Tumor cells synthesize discrete new poly(A) RNAs consisting of viral sequences covalently linked to cellular sequences. These RNA species are expressed at high levels in tumor cells. Our results suggest that in lymphoid tumors, an ALV provirus is integrated adjacent to a specific cellular gene, and the insertion of the viral promoter adjacent to this gene results in its enhanced expression, leading to neoplasia. These results have potentially important implications for the mechanism of non-viral carcinogenesis.

Animals↗
PubMedDate not supplied

Metabolism of clozapine by rat brain: the role of flavin-containing monooxygenase (FMO) and cytochrome P450 enzymes.

The atypical antipsychotic clozapine has been reported to be metabolised mainly to its N-oxide and N-demethylated products. Brain, the target organ of clozapine, is known to contain numerous drug-metabolising enzymes which could alter the local concentrations of the drug. The metabolism of clozapine was, therefore, studied in rat brain preparations. Clozapine N-oxide was the major metabolic pathway in rat brain. We characterised the N-oxygenation of clozapine by rat brain preparations. The Km and Vmax values were found to be 319.6 microM and 28.1 pmol/min/mg protein, respectively. The formation of clozapine N-oxide was shown to be inhibited by thiourea (a flavin-containing monooxygenase inhibitor) but not by ketoconazole, quinidine or furafylline. This finding suggests prominent involvement of FMO in the N-oxygenation of clozapine in rat brain. This conclusion was further confirmed by the observation that the formation of clozapine N-oxide is sensitive to heat treatment of the brain preparation and can be partially protected from thermal degeneration by the presence of an NADPH generating system. It was further observed that the rate of clozapine N-oxygenation was much higher at pH 8.5 than at pH 7.4. Taken together, the data suggest that N-oxygenation is the major metabolic pathway catalysed by rat brain and this reaction is catalysed mainly by FMO. As significant interindividual differences have been observed in brain FMO activities, these differences may contribute to the interindividual differences in patient response to clozapine.

Animals↗
PubMedDate not supplied

Brain organization and sleep function.

A view of brain organization and sleep function is presented. Sleep is hypothesized to begin at the neuronal group level. Sleep results in the use and thus maintenance, of synapses that are insufficiently stimulated during wakefulness thereby serving to preserve a constancy of a synaptic superstructure. It is further hypothesized that sleep at the neuronal group level is regulated by the production of substances whose rate of production or catabolism is synaptic use-dependent. If sufficient number of neuronal groups are in a sleep state (also called disjunctive state) then the perception of sleepiness occurs. Coordination of neuronal group sleep results from humoral and neuronal projection systems previously linked to sleep regulation. The theory presented is unique in that it: (a) hypothesizes an organizational level at which sleep occurs; (b) hypothesizes that sleep is neuronal--use-dependent, not wakefulness-dependent; (c) hypothesizes that sleep first occurs in evolution when complex ganglia evolved; and (d) hypothesizes the both non-rapid eye movement sleep (NREMS) and REMS serve the same function of synaptic reorganization. The theory is consistent with past theories of sleep function, yet provides a fundamentally new paradigm for sleep research.

Animals↗
PubMedDate not supplied

Type I insulin-like growth factor receptors in the BeWo choriocarcinoma cell (b30 clone) during cell differentiation.

The expression of insulin-like growth factor (IGF) receptors in the differentiating human trophoblast was studied using the b30 clone of the BeWo choriocarcinoma cell line (BeWob30) as a model system. This clonally derived cell line differentiates over 48-72 h, in culture, to form syncytiotrophoblasts when intracellular cAMP levels are elevated by exposure to 100 microM forskolin (FSK). IGF receptors were studied at various times during the differentiation process by measuring the specific binding of [125I]-IGF-I and [125I]-IGF-II to attached cells. First, [125I]-IGF-I bound to a single class of binding sites in the untreated cells (KD approximately 1-2 x 10-10 M) that exhibited binding specificity characteristic of the type I IGF receptor (IGF-I > or = IGF-II > > Insulin). FSK treatment resulted in a two- to threefold increase in the number of these binding sites. Increased receptor expression was observed as early as 24 h after FSK treatment and remained elevated for at least 72 h. Next, [125I]-IGF-II bound to two classes of binding sites in the untreated cells, a high-affinity (KD approximately 2.5 x 10(-10) M), low-capacity site and a low-affinity (KD approximately 6 x 10(-9) M), high-capacity site. The Bmax and KD of the high-affinity site suggested that it represented the type I IGF receptor. Competition studies revealed that 15-20 per cent of total [125I]-IGF-II binding only was sensitive to IGF-I competition in the untreated cells. After FSK treatment, however, unlabelled IGF-I inhibited 60-70 per cent of specific [125I]-IGF-II binding. Scatchard analysis revealed a two- to fourfold increase in the number of both binding sites with no change in their respective binding affinities. Cross-linking analysis demonstrated that [125I]-IGF-II bound to two structurally distinct binding sites in the untreated BeWob30 cell consistent with both the type I and II IGF receptors. After FSK treatment, however, there was an increase in the relative amount of [125I]-IGF-II associated with the higher affinity type I IGF receptor. The BeWob30 cells expressed no insulin receptors at any stage of differentiation. These data demonstrate that the BeWob30 choriocarcinoma cell line expresses both type I and II IGF receptors. Induction of cell differentiation is associated with an increase in type I IGF receptors expressed at the cell surface. These receptors bind IGF-II with high-affinity, providing additional binding capacity for locally available IGF-II. These data are consistent with specific roles for the type I IGF receptor in regulating differentiated trophoblast cell function. Furthermore, the early rise in type I IGF receptor number suggests they may play a regulatory role in the differentiation process itself.

Binding Sites↗
PubMedDate not supplied

Pegylated zinc protoporphyrin: a water-soluble heme oxygenase inhibitor with tumor-targeting capacity.

Heme oxygenase (HO) is a key enzyme in heme metabolism; it oxidatively degrades heme to biliverdin, accompanied by formation of free iron and carbon monoxide. Biliverdin is subsequently reduced by cytosolic biliverdin reductase to form bilirubin, a potent antioxidant. We recently found that tumor cells utilize HO to protect themselves from oxidative stress by producing the antioxidant bilirubin. This result suggested an important potential therapeutic strategy: suppression of bilirubin production with the use of HO inhibitors; hence, cancer cells become vulnerable to oxidative stress induced by anticancer drugs or leukocytes of the host. This concept was validated by using the intraarterial administration of an HO inhibitor, zinc protoporphyrin, in nonphysiological solution. In the present study, zinc protoporphyrin (ZnPP) was conjugated with poly(ethylene glycol) (PEG) with molecular weight of 5000, to make ZnPP, a water-soluble compound (PEG-ZnPP), and to improve its tumor-targeting efficiency. PEG was conjugated to ZnPP through newly introduced amino groups, where ethylenediamine residues were added at C6 and C7 of protoporphyrin. The divalent zinc cation was chelated into the protoporphyrin ring to obtain PEG-ZnPP. PEG-ZnPP did become highly water-soluble, and it formed multimolecular associations with molecules larger than 70 kDa in aqueous media. PEG-ZnPP inhibited splenic microsomal HO activity in vitro in a competitive manner in the presence of hemin, with an apparent inhibitory constant of 0.12 microM. Most important, PEG-ZnPP injected intravenously significantly suppressed intratumor HO activity in a murine solid tumor model, which suggests that tumor-targeted inhibition of HO is possible with the use of PEG-ZnPP.

Animals↗
PubMedDate not supplied

Production of alpha-galactosyl epitopes via combined use of two recombinant whole cells harboring UDP-galactose 4-epimerase and alpha-1,3-galactosyltransferase.

alpha-Galactosyl epitopes (or alpha-Gal, oligosaccharides with a terminal Galalpha1,3Gal sequence) are a class of biologically important oligosaccharides in great demand in bulk quantities for basic and clinical studies on preventing hyperacute rejection in pig-to-primate organ xenotransplantation. A truncated bovine alpha-1, 3-galactosyltransferase, the key enzyme responsible for the biosynthesis of the terminal structure of alpha-Gal, was cloned and overexpressed previously. The acceptor specificity was further studied in the present paper, and lactose and galactose derivatives were found to be good acceptors. To develop a more proficient reaction process, we report herein an example of an efficient enzymatic synthesis of alpha-Gal oligosaccharides catalyzed by the combination of two recombinant Escherichia coli whole cells harboring the genes of a UDP-galactose 4-epimerase and the alpha-1, 3-galactosyltransferase, respectively. Using lactosyl azide (LacN(3)) as the acceptor for the glycosyltransferase, the combined use of the two recombinant cells efficiently produced alpha-Gal epitope Gal alpha1,3LacN(3) in 60-68% yield.

Carbohydrate Sequence↗
PubMedDate not supplied

Two acidic polysaccharides from the flowers of Chrysanthemum morifolium.

Two new acidic polysaccharides, F4 and F5, were isolated from the flowers of Chrysanthemum morifolium. Monosaccharide analysis indicated that F4 contained arabinose, galactose and galacturonic acid units in a molar ratio of 1.0:2.3:6.8 and F5 contained arabinose, rhamnose galactose and galacturonic acid units in a molar ratio of 1.0:3.2:1.0:4.3. The results of methylation analysis, partial acid hydrolysis and NMR spectral analysis indicated that F4 had a homogalacturonan main chain with arabinogalactan side chain linked to 3 position of (1 --> 3,4)-linked galacturonan and F5 had a rhamnogalacturonan main chain with arabinogalactan side chain linked to 3 position of (1 --> 3,4)-linked galacturonan or 4 position of (1 --> 2,4)-linked rhamnose. Biological tests revealed that F4 and F5 could simulate the mitogen induced T and B lymphocyte proliferation in vitro.

Animals↗