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Biomedical subjects

A M Wang

Publications and source records attributed to A M Wang.

At least 19 recordsLinked to original sources
PubMed1995

[Clinical observation of the effect of blood gas with two different methods of sputum suction].

The authors observed the preventive effect of the oxygen supplied double channel sucker on low blood oxygen. Thirty patients with channel sputum sucker under the mechanical respiratory support were taken as the contrast group, in comparison with the experimental group A and B respectively. Patients (n = 30) with one channel sputum sucking for 15 sec. were designated as experimental group A, while the other patients (n = 30) with the oxygen supplied double channel sucking for 15 sec were the group B, Blood gas analysis was done in every patient of each group. Significant difference of PO2 was found between group A and the contrast group (P < 0.01). No significant difference was found between group B and the contrast group (P > 0.05). It shows that oxygen supplied double channel sucker has preventive effect on low blood oxygen, and is suitable for sputum sucking in severe patients.

Blood Gas Analysis↗
PubMed1995

Inhibition of kainic acid binding to glutamate receptors by extracts of Gastrodia.

S-(4-hydroxybenzyl)glutathione was isolated as the major principle responsible for the inhibition of the in vitro binding of kainic acid to brain glutamate receptors by water extracts of the plant Gastrodia elata. The affinity (IC50 value) of the compound is slightly lower compared to glutamate and glutathione.

Drugs, Chinese Herbal↗
PubMed1995

Langerhans cell histiocytosis involving the sphenoid sinus and superior orbital fissure.

We report Langerhans cell histiocytosis involving the sphenoid sinus and extending to the orbital apex. MR and CT imaging, particularly with contrast, both were helpful in defining the extent of the lesion before treatment. MR was a useful examination for follow-up after treatment. Langerhans cell histiocytosis should be considered in the differential diagnosis of lesions of this region in the pediatric age group.

Adolescent↗
PubMed1995

MR staging of acute dural sinus thrombosis: correlation with venous pressure measurements and implications for treatment and prognosis.

PURPOSE: To correlate parenchymal brain changes, venous sinus pressure measurements, and outcome in 29 patients with acute dural sinus thrombosis. METHODS: A retrospective review of 29 patients with angiographically proved acute dural sinus thrombosis was made from January 1989 to December 1993. MR examinations were performed on either a 0.5- or 1.5-T superconductive scanner in multiple planes. Direct dural sinus venography, cerebral angiography, and MR venography were performed. Venous sinus pressure measurements were obtained in 11 of 29 patients. RESULTS: We identified five distinct stages of brain parenchymal changes; each stage correlated with increasing intradural sinus pressure. The pressures measured in this study ranged from 20 to 50 mm Hg. Brain parenchymal changes were reversible up to stage III if thrombolytic treatment was performed. Beyond stage III, there were some residual changes, even after thrombolysis. All stage V patients died. CONCLUSION: Acute dural sinus thrombosis leads to distinct stages of parenchymal changes, the severity of which depends on the degree of venous congestion, which, in turn, is closely related to intradural sinus pressure. As intradural sinus pressure increases, progression from mild parenchymal change to severe cerebral edema and/or hematoma may occur if thrombolysis is delayed.

Acute Disease↗
PubMed1994

The molecular lesion in the alpha-N-acetylgalactosaminidase gene that causes angiokeratoma corporis diffusum with glycopeptiduria.

Angiokeratoma corporis diffusum with glycopeptiduria is a recently recognized inborn error of glycoprotein catabolism resulting from the deficient activity of human alpha-N-acetylgalactosaminidase (E.C. 3.2.1.49; alpha-GalNAc). The first patient with this autosomal recessive disorder, a 46-yr-old consanguineous Japanese woman, presented with diffuse angiokeratoma, mild intellectual impairment, and peripheral neuroaxonal degeneration. Deficient alpha-GalNAc activity also has been reported in consanguineous brothers with an infantile-onset form of neuroaxonal dystrophy resulting from a missense mutation (designated E325K) in the alpha-GalNAc gene. To identify the mutation causing the phenotypically distinct adult-onset disorder, Southern and Northern hybridization analyses of DNA and RNA from the affected homozygote were performed which revealed a grossly normal alpha-GalNAc gene structure and normal transcript size and abundancy. Reverse transcription, amplification, and sequencing of the alpha-GalNAc transcript identified a single C to T transition at nucleotide (nt) 985 that predicted an arginine to tryptophan substitution in residue 329 (designated R329W) of the alpha-GalNAc polypeptide. This base substitution was confirmed by hybridization of PCR-amplified genomic DNA from family members with allele-specific oligonucleotides. Transient expression of an alpha-GalNAc construct containing the R329W mutation resulted in the expression of an immunoreactive polypeptide which had no detectable alpha-GalNAc activity. Comparison of the biosynthesis and stabilities of the transiently expressed and radiolabeled normal, E325K (infantile-onset) and R329W (adult-onset) alpha-GalNAc polypeptides in COS-1 cells indicated that both the mutant precursors were processed to the mature form; however, the E325K mutant polypeptide was more rapidly degraded than the R329W subunit, thereby providing a basis for the distinctly different infantile- and adult-onset phenotypes.

Base Sequence↗
PubMed1994

BAER, EOG, MRI and 3-D MR angiography correlates in a case of Locked-In syndrome.

A case of Locked-in syndrome is reported with correlation of BAER and EOG with MRI for localization and identification of brain lesions, and 3-D MRA and 2-D gradient echo MR imaging, a non-invasive new diagnostic modality for confirmation and visualization of vascular pathology. There was thrombosis of the basilar artery with extensive infarct of ventral pons and lower mid-brain. The patient had ocular bobbing. This eye movement in its classical form consists of irregular vertical oscillations, the fast component being downward with complete absence of horizontal eye movements. To our knowledge, the change from ocular bobbing to upbeat nystagmus has not been previously reported in the Locked-in syndrome. Bilateral involvement of the lateral lemniscus might have contributed to its appearance in our patient.

Basilar Artery↗
PubMed1994

Venous sinus occlusive disease: MR findings.

PURPOSE: To study MR patterns of venous sinus occlusive disease and to relate them to the underlying pathophysiology by comparing the appearance and pathophysiologic features of venous sinus occlusive disease with those of arterial ischemic disease. METHODS: The clinical data and MR examinations of 26 patients with venous sinus occlusive disease were retrospectively reviewed with special attention to mass effect, hemorrhage, and T2-weighted image abnormalities as well as to abnormal parenchymal, venous, or arterial enhancement after intravenous gadopentetate dimeglumine administration. Follow-up studies when available were evaluated for atrophy, infarction, chronic mass effect, and hemorrhage. RESULTS: Mass effect was present in 25 of 26 patients. Eleven of the 26 had mass effect without abnormal signal on T2-weighted images. Fifteen patients had abnormal signal on T2-weighted images, but this was much less extensive than the degree of brain swelling in all cases. No patient showed abnormal parenchymal or arterial enhancement. Abnormal venous enhancement was seen in 10 of 13 patients who had contrast-enhanced studies. Intraparenchymal hemorrhage was seen in nine patients with high signal on T2-weighted images predominantly peripheral to the hematoma in eight. Three overall MR patterns were observed in acute sinus thrombosis: 1) mass effect without associated abnormal signal on T2-weighted images, 2) mass effect with associated abnormal signal on T2-weighted images and/or ventricular dilatation that may be reversible, and 3) intraparenchymal hematoma with surrounding edema. CONCLUSION: MR findings of venous sinus occlusive disease are different from those of arterial ischemia and may reflect different underlying pathophysiology. In venous sinus occlusive disease, the breakdown of the blood-brain barrier (vasogenic edema and abnormal parenchymal enhancement) does not always occur, and brain swelling can persist up to 2 years with or without abnormal signal on T2-weighted images. Abnormal signal on T2-weighted images may be reversible and does not always indicate infarction.

Adolescent↗
PubMed1993

A prospective study to identify high-yield criteria associated with acute intracranial computed tomography findings in head-injured patients.

We conducted a multicenter, prospective study of head-injured patients to identify high-yield clinical criteria for acute intracranial injuries. Emergency patients with a history of blunt head trauma occurring within 2 weeks and who underwent nonenhanced cranial computed tomography (CT) were entered onto the study during a 12-month period. Of the 264 patients, 32 (12%) had abnormal CT findings. Nine high-yield variables were associated with abnormal CT findings: alcohol use before injury, antegrade amnesia, prolonged loss of consciousness, anisocoria and/or fixed and dilated pupils, abnormal Babinski reflex, focal motor paralysis, cranial nerve deficit, Glasgow coma scale score of less than 15, and clinical signs of basilar skull fracture. Patients 2 years old or younger or older than 60 years of age showed a significantly greater prevalence of abnormal CT findings than patients of other ages.

Acute Disease↗
PubMed1993

Angiokeratoma corporis diffusum with glycopeptiduria due to deficient lysosomal alpha-N-acetylgalactosaminidase activity. Clinical, morphologic, and biochemical studies.

BACKGROUND: Angiokeratoma corporis diffusum is a prominent cutaneous feature of certain lysosomal storage diseases. In this article, the clinical, morphologic, and biochemical features of a new, adult-onset lysosomal disease with angiokeratoma are described. OBSERVATIONS: A 46-year-old Japanese woman had diffuse angiokeratoma, mild intellectual impairment, and peripheral neuroaxonal degeneration. The angiokeratoma first appeared on her lower torso when she was 28 years old, and then it became diffusely distributed. Histopathologically, the telangiectasia had localized hyperkeratosis; ultrastructural examination revealed clear cytoplasmic vacuoles in all dermal cells, particularly in vascular and lymphatic endothelial cells and in eccrine sweat gland cells. The lysosomal pathologic features and increased urinary excretion of O-linked glycopeptides suggested the deficiency of a specific glycosidase. Enzyme analyses revealed less than 2% of normal alpha-N-acetylgalactosaminidase activity and the absence of immunodetectable enzyme protein. Her two unaffected children had half-normal alpha-N-acetylgalactosaminidase levels, consistent with the autosomal recessive inheritance of the enzymatic defect. CONCLUSIONS: Since this enzyme deficiency was previously identified in patients with an infantile form of inherited neuroaxonal dystrophy, the occurrence of the enzymopathy in the 46-year-old proband described herein represents an adult-onset form of alpha-N-acetylgalactosaminidase deficiency. This newly recognized entity should be considered in the differential diagnosis of angiokeratoma corporis diffusum.

Fabry Disease↗
PubMed1992

Modulation of macrophage colony stimulating factor in cultured human retinal pigment epithelial cells.

Steady-state mRNA expression and protein production of macrophage colony stimulating factor were measured in visually confluent monolayers of unstimulated cultured human retinal pigment epithelial cells and after cells were stimulated with recombinant cytokines. Using reverse transcription polymerase chain reaction, macrophage colony stimulating factor mRNA expression was detected in unstimulated cells obtained from each of four separate donors. In these cells, mRNA expression was accompanied by secretion of macrophage colony stimulating factor protein into cell-conditioned medium; 48 hr after cells were switched to fresh medium, the mean (+/- S.D.) quantity of macrophage colony stimulating factor, measured by enzyme-linked immunoassay, was 5.1 +/- 2.3 ng 10(-6) cells. There was a dose- and time-dependent induction of macrophage colony stimulating factor mRNA after cells were exposed to recombinant human interleukin-1 and tumor necrosis factor alpha. Maximal mRNA induction was observed in cells exposed for 4 hr to interleukin-1 beta (5 U ml-1) or for 4-8 hr to tumor necrosis factor alpha; under these conditions, macrophage colony stimulating factor mRNA was induced up to 23- and 46-fold after exposure to interleukin-1 beta and tumor necrosis factor alpha, respectively. Similarly, macrophage colony stimulating factor protein production was enhanced after cells were exposed to recombinant cytokines. Protein secretion increased 1.3-2.5-fold (P less than 0.001) after exposure to interleukin-1 beta (5 U ml-1), and 1.2-1.6-fold after exposure to tumor necrosis factor alpha (P less than 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Cells, Cultured↗
PubMed1992

Electromyographic detection of paraspinal muscle metastasis. Correlation with magnetic resonance imaging.

Electromyographic (EMG) examination demonstrating marked segmental compromise of the posterior primary ramus distal to the spinal root with relative sparing of the anterior ramus may be the earliest objective evidence of paraspinal muscle metastasis. Antecedent studies are often initially normal, failing to disclose the underlying cause of back pain. Although paraspinal muscle metastasis has been histopathologically demonstrated at postmortem, attempts to image the suspected malignancy with computed tomography have been unsuccessful because the tumor in muscle remains isodense. This study reports the use of magnetic resonance imaging (MRI) to substantiate the existence of EMG-suspected paraspinal muscle metastasis. An EMG pattern of segmental posterior primary ramus denervation is not pathognomonic of metastasis. A confirmatory MRI, however, does permit earlier treatment with palliative radiation therapy.

Adenocarcinoma↗
PubMed1991

Purification and substrate specificity of a T4 phage intron-encoded endonuclease.

The T4 phage td intron-encoded endonuclease (I-Tev I) cleaves the intron-deleted td gene (td delta I) 23 nucleotides upstream of the intron insertion site on the noncoding strand and 25 nucleotides upstream of this site on the coding strand, to generate a 2-base hydroxyl overhang in the 3' end of each DNA strand. I-Tev I-157, a truncated form in which slightly more than one third (88 residues) of the endonuclease is deleted, was purified to homogeneity and shown to possess endonuclease activity similar to that of I-TEV I, the full-length enzyme (245 residues). The minimal length of the td delta I gene that was cleaved by I-Tev I and I-Tev I-157 has been determined to be exactly 39 basepairs, from -27 (upstream in exon1) to +12 (downstream in exon2) relative to the intron insertion site. Similar to the full-length endonuclease, I-Tev I-157 cuts the intronless thymidylate synthase genes from such diverse organisms as Escherichia coli, Lactobacillus casei and the human. The position and nature of the in vitro endonucleolytic cut in these genes are homologous to those in td delta I. Point mutational analysis of the td delta I substrate based on the deduced consensus nucleotide sequence has revealed a very low degree of specificity on either side of the cleavage site, for both the full-length and truncated I-TEV I.

Base Sequence↗
PubMed1991

Bladder cancer. Human leukocyte antigen II, interleukin-6, and interleukin-6 receptor expression determined by the polymerase chain reaction.

The prediction of tumour biology rarely rests upon a single characteristic of the malignancy. The analysis of a single gene can complement standard histologic evaluation. The investigation of new parameters as well as the routine clinical analysis of gene expression is often limited because of the small amount of tissue available. This is particularly true of de novo human bladder cancers because they are generally small or handled in such a way as to hinder the analysis of multiple different parameters. Analysis of expressed mRNA by the polymerase chain reaction (RNA/PCR) is a method that allows the development of a profile of bladder cancer gene expression. The authors report the use of the RNA/PCR method to examine in bladder cancer the expression of the human leukocyte antigen (HLA) class II gene family (HLA-DR, DQ, and DP) as well as interleukin-6 (IL-6) and the interleukin-6 receptor (IL-6R). All de novo transitional cell carcinomas, one squamous carcinoma, and two transitional cell carcinoma cell lines expressed the majority of HLA class II genes. All samples expressed IL-6R RNA whereas production of IL-6 message was limited to one of the cell lines and to the high-grade bladder cancers. These results were combined with stage, grade, and DNA content to develop a profile of the cancers examined. Although an improved predictive index based on gene expression analysis by RNA/PCR has not been realized, a broader survey of human tumors for expression of these genes and others is likely to refine the classification of bladder cancer.

Base Sequence↗
PubMed1991

Positive therapeutic interaction between thiopurines and alkylating drugs in human glioma xenografts.

We used human anaplastic glioma xenografts to evaluate the therapeutic efficacy of combinations of alkylating drugs, either 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), 1-(2-chloroethyl)-3-(2,5-dioxo-3-piperidyl)-1-nitrosourea (PCNU), or procarbazine, and thiopurines, either 6-mercaptopurine (6MP) or 6-thioguanine (6TG). Using growth delay as the endpoint in subcutaneous (s.c.) tumors and increased life span as the endpoint in intracranial (i.c.) tumors, we found that combinations of chloroethylnitrosoureas (CENUs) and thiopurines were significantly more active than either type of agent alone. In contrast, combinations of procarbazine and thiopurines were not significantly more active than procarbazine alone. The therapeutic potentiation of the CENU was greater when the latter was given on the 4th day of the thiopurine treatment cycle than when it was given on the 1st day. Characterization of the interaction between CENUs and thiopurines also revealed a supraadditive therapeutic response at higher BCNU doses in combination with 6TG. Interaction between the nitrosoureas and the thiopurines probably occurs in the guanine base of tumor DNA and has important therapeutic implications.

Alkylating Agents↗
PubMed1991

Structural organization and complete sequence of the human alpha-N-acetylgalactosaminidase gene: homology with the alpha-galactosidase A gene provides evidence for evolution from a common ancestral gene.

Human alpha-N-acetylgalactosaminidase (alpha-GalNAc; EC 3.2.1.49), the lysosomal glycohydrolase that cleaves alpha-N-acetylgalactosaminyl moieties in glycoconjugates, is encoded by a gene localized to chromosome 22q13----qter. The deficient activity of this enzyme results in Schindler disease, an autosomal recessive disorder characterized by the increased urinary excretion of glycopeptides and oligosaccharides containing alpha-N-acetylgalactosaminyl moieties. Recently, the 3.6-kb full-length alpha-GalNAc cDNA sequence was isolated and found to have remarkable nucleotide and predicted amino acid homology (55.8 and 46.9%, respectively) with the human alpha-galactosidase A (alpha-Gal A) cDNA. To investigate the possible evolutionary relatedness of the two glycosidases, the alpha-GalNAc chromosomal gene was isolated and characterized. Screening of a human genomic DNA cosmid library resulted in the identification of a clone, gAGB-1, with an approximately 35-kb insert that contained the entire alpha-GalNAc gene. A single approximately 15-kb EcoRI fragment of gAGB-1, which contained the complete 3.6-kb cDNA sequence, was digested and the subcloned fragments were sequenced in both orientations. The 13,709-bp alpha-GalNAc gene had nine exons ranging from 95 to 2028 bp and intronic sequences of 304 to 2684 bp. All exon/intron junctions conformed to the GT/AG consensus rule. Analysis of 1.4 kb of 5' flanking sequence revealed three Sp1 and two CAAT-like promoter elements. This region was GC-rich (56%), but no HTF island was identified. The gene contained six Alu-repetitive elements, all in the reverse orientation. Comparison of the structural organization of the alpha-GalNAc and the alpha-Gal A genes revealed that all six alpha-Gal A introns were identically positioned in the homologous alpha-GalNAc exonic sequence. Two additional introns, 1 and 8, were identfied in the alpha-GalNAc gene. The predicted amino acid sequences of alpha-GalNAc exons 2 through 7 and those of corresponding alpha-Gal A exons 1 through 6 were 46.2 to 62.7% identical. In contrast, there was little, if any, similarity between the deduced amino acid sequences of alpha-Gal A exon 7 and alpha-GalNAc exons 8 and 9. The remarkable amino acid identity and the identical exonic interruption by six introns of the alpha-GalNAc and alpha-Gal A genes suggest that this region in both genes is evolutionarily related and arose through duplication and divergence from a common ancestral gene.

Base Sequence↗