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Biomedical subjects

K Hsiao

Publications and source records attributed to K Hsiao.

45 records · Page 3Linked to original sources
PubMed1988

Identification of more than 500 RFLPs by screening random genomic clones.

As part of our genome-mapping effort, we undertook a large-scale screening study to identify RFLPs useful as genetic markers. Some 1,664 single-copy or repeat-containing phage clones from a Charon 4A genomic library were tested for polymorphism against a panel of DNAs, from five unrelated individuals, digested with eight restriction enzymes. Approximately 30% (515) of the clones revealed polymorphism by Southern hybridization; 67 loci detected had PIC values greater than .5. Restriction enzymes MspI, TaqI, and RsaI were most efficient in detecting polymorphism within the 1-20-kb-fragment size range resolved. With only one exception each of the clones detected polymorphism originating from a single locus.

Cloning, Molecular↗
PubMed1987

Scrapie prion protein contains a phosphatidylinositol glycolipid.

The scrapie (PrPSc) and cellular (PrPC) prion proteins are encoded by the same gene, and their different properties are thought to arise from posttranslational modifications. We have found a phosphatidylinositol glycolipid on both PrPC and PrP 27-30 (derived from PrPSc by limited proteolysis at the amino terminus). Ethanolamine, myo-inositol, phosphate, and stearic acid were identified as glycolipid components of gel-purified PrP 27-30. PrP 27-30 contains 2.8 moles of ethanolamine per mole. Incubation of PrP 27-30 with a bacterial phosphatidylinositol-specific phospholipase C (PIPLC) releases covalently bound stearic acid, and allows PrP 27-30 to react with antiserum specific for the PIPLC-digested glycolipid linked to the carboxyl terminus of the trypanosomal variant surface glycoprotein. PIPLC catalyzes the release of PrPC from cultured mammalian cells into the medium. These observations indicate that PrPC is anchored to the cell surface by the glycolipid.

Animals↗
PubMed1984

Cloning of eukaryotic genes in single-strand phage vectors: the human interferon genes.

Using oligonucleotide probes with defined sequences, we have selected clones from a human lymphocyte cDNA library which represent human leukocyte (HuIFN-alpha) and fibroblast (HuIFN-beta) interferon gene sequences. Double-stranded f1 phage DNA was used as the vector for initial cloning of cDNA. Clones carrying interferon gene sequences were identified by hybridization with the oligonucleotide probes. The same oligonucleotide probes were used as primers for dideoxy chain termination sequencing of the clones. One HuIFN-alpha clone, 201, has a nucleotide sequence different from published HuIFN-alpha sequences. Under control of the lacUV5 promoter, the 201 gene has been used to express biologically active HuIFN-alpha in Escherichia coli.

Base Sequence↗
PubMed1984

A minute fraction of Syrian golden hamster retinal ganglion cells project bilaterally.

Bilaterally projecting retinal ganglion cells (BPRGCs) in the adult Syrian golden hamster were identified through the use of two retrogradely transported neuronal labels, horseradish peroxidase and Nuclear Yellow, placed separately in each optic tract. The distribution and size of doubly labeled retinal ganglion cells were characterized and their numbers were determined. Strict criteria were used to exclude artifactual doubly labeled cells. This work revealed that: (a) BPRGCs comprise less than 0.01% of the entire retinal ganglion cell population, averaging 7.4 (SD = 3) cells per retina; (b) BPRGCs are found primarily in the upper, peripheral retina and not along the vertical meridian or in the temporal crescent; and (c) BPRGCs correspond in size to ordinary retinal ganglion cells in their immediate vicinity, thus providing no evidence that they comprise a separate population of cells. Electrophysiological collision experiments were also performed, with stimulating electrodes in the two brachia of the superior colliculi and a recording electrode in one optic nerve. A collision effect was not detected, thus supporting the anatomical findings of rare bilateral branching of optic nerve axons. The occurrence of BPRGCs may reflect occasional ambiguities in the cues that guide axons through the chiasm.

Animals↗
PubMed1984

Bilateral branching contributes minimally to the enhanced ipsilateral projection in monocular Syrian golden hamsters.

Studies of the plasticity of retinal projections following neonatal eye ablations in rats and hamsters have demonstrated an enhanced ipsilateral projection which affects both the terminal fields and the number of ipsilaterally projecting cells. The enhancement has been attributed to an excess of bilateral branching by single optic nerve axons, but this claim was not supported by the present study. Double retrograde labels were used to quantify the ipsilateral enhancement and measure the extent of bilateral branching in hamsters with neonatal eye removals. In 19 normal Syrian golden hamster retinas the average number of bilaterally projecting retinal ganglion cells (BPRGCs) was 7.4 (SD = 3), and the average number of ipsilaterally projecting retinal ganglion cells (IPRGCs) was 1349 (SD = 478) (Hsiao, K., G. M. Sachs, and G. E. Schneider (1984) J. Neurosci. 4: 359-367). In nine retinas of hamsters with removal of one eye at birth, the average number of BPRGCs was 25.3 (SD = 9.2), and the average number of IPRGCs per retina was 2036 (SD = 414). Although the increase in BPRGCs is statistically significant, it accounted for only 2 to 3% of the 51% increase in the number of IPRGCs. Various possible mechanisms underlying the formation of the enhanced projection are enumerated, and it is concluded that the predominant mechanism is a reduction of cell death in the developing population of IPRGCs. The responses of IPRGCs and BPRGCs to early eye enucleations were also examined with respect to age at enucleation and cell size. No difference in size was found between IPRGCs and BPRGCs in monocular hamsters compared to normal hamsters.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Effect of medroxyprogesterone and an aorta-derived cell growth inhibitor on B16 melanoma in mice.

An aorta-derived inhibitor of endothelial cell and tumor cell growth and medroxyprogesterone, which depresses collagenase expression in vivo, were tested alone and in combination against B16-F10 melanoma in C57BL/6 mice in such doses that either agent alone had little effect. Together, these agents retarded growth of subcutaneously transplanted tumor cells and reduced the number and size of pulmonary tumors after iv tumor cell injection. Of the treatments used, only the aortic factor administered alone prolonged life in mice with pulmonary tumors.

Animals↗
PubMed1981

Calcium uptake mechanisms affected by some convulsant and anticonvulsant drugs.

An anticonvulsant (phenytoin) and a convulsant barbiturate (5-(2-cyclohexylidene ethyl)-5-ethyl-barbituric acid) (CHEB) reduced depolarization-coupled 45Ca uptake by synaptosomes from rat brain. CHEB reduced uptake to the level of undepolarized control samples. Phenobarbital failed to affect synaptosomal 45Ca uptake. Phenobarbital inhibited mitochondrial 45Ca uptake by 38%. CHEB was even more effective, lowering mitochondrial 45Ca uptake nearly to the levels induced by the mitochondrial inhibitors KCN, ruthenium red and dinitrophenol. Phenytoin, phenobarbital and CHEB did not affect ATP-dependent 45Ca uptake by the endoplasmic reticulum in lysed synaptosomes. In view of the effect of CHEB, a known convulsant, in limiting Ca uptake by depolarized synaptosomes, an effect which was greater than either that of phenytoin or phenobarbital, an identification of such a mechanism with anticonvulsant or sedative properties may be oversimplified.

Adenosine Triphosphate↗
PubMedDate not supplied

Transgenic mice expressing Alzheimer amyloid precursor proteins.

Nearly a decade after the identification of the Alzheimer amyloid precursor protein (APP) gene several groups of investigators have created transgenic mice expressing APP that simulate some of the prominent behavioral and pathological features of Alzheimer's disease (Quon et al., 1991; Games et al., 1995; Hsiao et al., 1995, 1996; Moechars et al., 1996; Sturchler-Pierrat et al., 1997). These features, which are present to various degrees in different lines of mice, include age-related impairment in learning and memory, neuronal loss, gliosis, neuritic changes, amyloid deposition, and abnormal tau phosphorylation. No mouse model exhibiting every neuropathological feature of Alzheimer's disease exists. Whether an exact simulation of Alzheimer neuropathology is required to understand neural dysfunction in Alzheimer's disease is unclear. Various mouse models of Alzheimer's disease are summarized in this article.

Amyloid beta-Protein Precursor↗