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Biomedical subjects

H Yan

Publications and source records attributed to H Yan.

At least 199 records · Page 11Linked to original sources
PubMed1996

Frequencies of cystic fibrosis mutations in the Maine population: high proportion of unknown alleles in individuals of French-Canadian ancestry.

Cystic fibrosis (CF) is one of the most common severe autosomal recessive disorders in Caucasian populations. A mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene causes this disorder. Reported here is the first analysis of CF mutations in the Maine population. We have screened 263 CF chromosomes for 16 previously reported mutations. Analysis of DNA from 124 apparently unrelated CF patients and 15 obligate carrier parents (whose partner and affected child were unavailable for study) resulted in the identification of 91% of the CF alleles and complete genotyping of 85% of the patients. The frequencies (%) of these mutations in the Maine population are delta F508 (75% of the chromosomes), G85E (0.76), R117H (0.76), I148T (1.1), 621 + 1G --> T (1.1), 711 + 1G --> T (3.0), A455E (1.1), 1717-1G --> A (1.1), G542X (1.9), G551D (1.9), R560T (0.76), Y1092X (0.38), W1282X (0.38), and N1303K (1.5). The exon 10 mutation, delta I507, and the exon 11 mutation, R553X, were not observed. Surprisingly, whereas only 5% of the alleles remain unidentified in the non-French population, the unidentified proportion in the French population is 19%. CF testing for the Maine population will be further improved as the as yet unidentified CF mutations in this population are characterized.

Alleles↗
PubMed1996

Arcuate keratotomy to correct naturally occurring astigmatism.

PURPOSE: To evaluate retrospectively the safety, efficacy, and complications of arcuate keratotomy (AK) in correcting naturally occurring astigmatism. SETTING: Laser Ultravision Institute, Montreal, Canada. METHODS: Surgically induced refractive change was evaluated in 25 eyes of 15 patients with naturally occurring astigmatism. All patients had mixed or compound myopic astigmatism and were treated with AK alone or both AK and radial keratotomy (RK). Minimum follow-up of 24 months was necessary for inclusion in this study. We used vector analysis to evaluate the refractive and keratometric astigmatic change at 1 month and 1 and 2 years. RESULTS: Ten eyes (40%) had AK only and 15 eyes (60%), both AK and RK. It was necessary to redeepen the original incisions in 21 eyes (84%). All patients had improved uncorrected visual acuity postoperatively. The reduction in refractive cylinder, quantified by vector analysis, was significant. Two years postoperatively, mean reduction was 3.30 diopters (D) +/- 1.32 (SD) in eyes that had AK alone and 2.71 +/- 1.53 D in eyes that had both AK and RK. CONCLUSION: Arcuate keratotomy is an effective and safe method for correcting naturally occurring astigmatism. Further analysis of this series of patients is planned.

Adult↗
PubMed1996

Organization of DNA into foci during replication.

In metazoan cells, DNA replication during the S phase of the cell cycle takes place at discrete locations within the nucleus. These sites, or foci, appear to participate in clustering many replicons together and synchronously regulating the activation of these replicon units. Consistent with this role. many replication proteins have been observed to attach to foci during the S phase of the cell cycle. Recently, cell-free replication extracts have been used both to characterize the events that are involved in either the formation of these sites or in the regulation of foci assembly, and to purify candidate proteins which may be integral core structural proteins responsible for forming foci. These advances provide a foundation for investigating foci structure and function at a biochemical level.

Animals↗
PubMed1996

Pulmonary parenchymal manifestations surrounding small peripheral masses: pathologic correlation with chest radiographs and diagnostic value.

RATIONALE AND OBJECTIVES: We evaluated pathologic correlations of pulmonary parenchymal manifestations surrounding small peripheral masses and their usefulness in differentiating small peripheral bronchogenic carcinomas from tuberculomas. METHODS: We evaluated 29 resected lobe specimens with 1.5- to 3.5-cm solitary pulmonary masses, including 24 carcinomas and five tuberculomas. These specimens were prospectively studied with preoperative chest radiographs, postoperative specimen radiographs, 10- to 15-microns-thick wholemount sections, and 5-microns-thick slices. A total of 100 chest X-rays and conventional tomography scans of 1- to 3-cm peripheral pulmonary masses, including 60 carcinomas and 40 tuberculomas, were retrospectively reviewed and analyzed. RESULTS: The pulmonary parenchymal manifestations surrounding the masses presented as small infiltrates and nodular protrusions, thickened strands, and "double track" shadows, which extended from the proximal margin of five tuberculomas (100%, 5 of 5) and from the distal margin of 17 carcinomas (71%, 17 of 24). These pulmonary changes represented caseous material spreading from tuberculomas into the proximal bronchus and alveolar inflammatory exudation distal to the carcinomas. The proximal pulmonary manifestations were significantly more frequent in tuberculomas than in carcinomas (p < .01), whereas the distal pulmonary manifestations were more often found in carcinomas than in tuberculomas (p < .01). CONCLUSION: The radiologic findings of the pulmonary parenchymal manifestations proximal or distal to the masses may be valuable radiologic signs for distinguishing between tuberculomas and small peripheral bronchogenic carcinomas, even though there is still considerable crossover between the two disease populations in the findings.

Carcinoma, Bronchogenic↗
PubMed1996

Malignant conversion of human cells by antisense cDNA to a putative tumor suppressor gene.

A cell line, SCC83-01-82, derived from a human oral squamous carcinoma, was non-tumorigenic in nude mice, a characteristic of premalignant cells. Conversion of these cells to a tumorigenic phenotype with chemical mutagens did not increase mutations in hot spots or other conserved regions of p53 or H-ras genes. Investigation of the tumorigenic conversion using an expression library resulted in isolation of a previously unidentified gene, CATR1, located on the long arm of chromosome 7 at band approximately q31-32. Evidence for the involvement of this gene in conversion to tumorigenicity was demonstrated by introduction of a eukaryotic expression CATR1 construct into SCC83-01-82 cells. Transfection with the antisense construct reduced the expression of CATR1 in tumors formed by the transfected cells, suggesting that the antisense suppression of endogenous CATR1 expression appeared to be sufficient for tumorigenic conversion. These results are consistent with previous reports of cytogenetic analyses of tumors, that 7q31-32 contains a gene(s) with tumor suppressor activity; CATR1 is a candidate for this putative suppressor gene.

Animals↗
PubMed1996

Vascular manifestations of small solitary pulmonary masses. Angiographic-pathologic correlations and clinical significance.

RATIONALE AND OBJECTIVES: By performing pulmonary specimen angiographies, the authors attempted to determine the pathologic correlations of the vascular-related radiologic manifestations within, at the edge of, and adjacent to the small solitary pulmonary masses, and to evaluate their usefulness in differentiating small bronchogenic carcinomas from tuberculomas. METHODS: A total of 29 resected lobe specimens with 1.5- to 3.5-cm solitary pulmonary masses, including 24 carcinomas and 5 tuberculomas, were studied prospectively with preoperative radiographs, postoperative specimen arteriographies (in 19 carcinomas and 5 tuberculomas), and venographies (in 5 carcinomas), 10- to 15 micrograms-thick whole-mount sections, and 5-micrograms-thick slices for the examination of angiographic-pathologic correlation. Another series of chest radiographs and conventional tomographs of 100 patients with 1- to 3-cm peripheral pulmonary masses, including 60 carcinomas and 40 tuberculomas, were reviewed retrospectively and analyzed with the chi-square test. RESULTS: Specimen angiographies showed the intralesion avascularity, small arterial speculation, and lobulation or notch at the mass margin with arterial compression, as well as vascular convergence to the mass, in both carcinoma and tuberculoma groups. The irregular arterial wall (79.2%) and venous dilation distal to the mass (100%) were found in the carcinoma group only. Microscopically, arterial or venous fibrous hyperplasia was observed in both carcinomas and tuberculomas, whereas the arterial erosion by tumor tissue and tumor emboli within the vessels were found in carcinomas only. The retrospective review of the 100 patients showed that two radiologic signs of the vascular convergence to the mass and the vascular dilation distal to the mass occurred at similar frequencies (12%-13%) between the carcinoma and tuberculoma groups. CONCLUSIONS: In addition to compression of vessels by tumor and vessel occlusion by tumor embolus, pulmonary vascular fibrotic hyperplasia can cause intramass avascularity. Small vessels running vertically into or from the mass margin can construct the spiculation sign of the tuberculomas. Any evidence of pulmonary vascular irregularity will indicate a bronchogenic carcinoma. The vascular convergence to the mass and the vascular dilation distal to the mass are not specific radiologic signs for small solitary bronchogenic carcinomas.

Adenocarcinoma↗
PubMed1996

Enteropathogenic Escherichia coli markedly decreases the resting membrane potential of Caco-2 and HeLa human epithelial cells.

It is presumed, but not proven, that enteropathogenic Escherichia coli (EPEC) causes secretory diarrhea by altering ion transport in enterocytes. In this study we used the whole-cell, current clamp variant of the patch clamp technique to demonstrate that EPEC infection of HeLa and Caco-2 human epithelial cells reduces cell resting membrane potential. The observed reduction of resting membrane potential in HeLa cells results from EPEC-mediated signal transduction to the host cell but is not dependent upon EPEC-mediated elevation of levels of intracellular free calcium. These findings indicate that EPEC can directly alter the relative distribution of ions across epithelial host cell membranes. This may be relevant to the etiology of diarrhea caused by EPEC infection.

Caco-2 Cells↗
PubMed1996

Molecular characterization of an alpha interferon receptor 1 subunit (IFNaR1) domain required for TYK2 binding and signal transduction.

Binding of alpha interferon (IFNalpha) to its receptors induces rapid tyrosine phosphorylation of the receptor subunits IFNaR1 and IFNaR2, the TYK2 and JAK1 tyrosine kinases, and the Stat1 and Stat2 transcription factors. Previous studies have demonstrated that TYK2 directly and specifically binds to and tyrosine phosphorylates IFNaR1 in vitro. We now report a detailed analysis of the TYK2 binding domain on the IFNaR1 subunit. First, we used an in vitro binding assay to identify the TYK2 binding motif in IFNaR1 as well as the critical residues within this region. The most striking feature is the importance of a number of hydrophobic and acidic residues. A minor role is also ascribed to a region resembling the proline-rich "box 1" sequence. In addition, mutations which disrupt in vitro binding also disrupt the coimmunoprecipitation of the receptor and TYK2. We also provide direct evidence that the binding region is both necessary and sufficient to activate TYK2 in vivo. Specifically, mutations in the binding domain act in a dominant-negative fashion to inhibit the IFNalpha-induced tyrosine phosphorylation of TYK2 and Stat2. Further, introduction of dimerized glutathione S-transferase-IFNaR1 fusion proteins into permeabilized cells is sufficient to induce phosphorylation of TYK2 and the receptor, confirming the role of the binding domain in IFNalpha signal transduction. These studies provide clues to the sequences determining the specificity of the association between JAK family tyrosine kinases and cytokine receptors as well as the functional role of these kinases in cytokine signal transduction.

Amino Acid Sequence↗
PubMed1996

Insulin-like growth factor II induces DNA synthesis in fetal ventricular myocytes in vitro.

Insulin-like growth factor II (IGF2) belongs to a family of growth factors that includes insulin and insulin-like growth factor I (IGF1). Although the accumulating evidence indicates that IGF1 is involved in regulating proliferation of ventricular myocytes, the role of IGF2 is less clear. To gain more insight into the functions of IGF2, rat ventricular expression of IGF2 mRNA at four developmental stages was examined by Northern analysis. An abundant IGF2 mRNA of approximately 3.8 kb was detected in fetal ventricles. It was dramatically decreased in neonatal ventricles and became undetectable in juvenile and adult ventricles. Similar expression patterns of the mRNA encoding IGF1 receptor and IGF2 receptor were observed. Since the results of Northern analysis strongly suggest the importance of IGF2 in regulating proliferation of fetal rat ventricular myocytes, the effects of an exogenous IGF2 on DNA synthesis in cultured rat ventricular myocytes were determined. DNA synthesis, which was monitored by measuring 5-bromo-2'-deoxyuridine (BrdU) and [3H]thymidine incorporation, was increased by twofold to threefold in IGF2-stimulated fetal ventricular myocytes, whereas no change in BrdU or [3H]thymidine incorporation was observed in neonatal ventricular myocytes. Instead, IGF2 seemed to induce hypertrophy in neonatal ventricular myocytes. An antisense oligonucleotide against rat IGF2 mRNA was able to significantly reduce BrdU incorporation, and this effect was quantitatively reversed by the addition of exogenous IGF2. Reversion by exogenous IGF2 was abolished by a monoclonal antibody against IGF1 receptor. In conclusion, our results suggest that IGF2 directly regulates proliferation of fetal rat ventricular myocytes in a paracrine/autocrine fashion.

Animals↗
PubMed1996

Assessment of early radiation effects on the liver. Comparison of SPECT and MR.

PURPOSE: To evaluate the early effects of radiation on the liver using single photon emission CT (SPECT) with 99mTc-phytate combined with a pinhole collimator and MR imaging with superparamagnetic iron oxide (SPIO) and to compare 2 modalities regarding the assessment of the reticuloendothelial cell function. MATERIAL AND METHODS: The right sides of the livers of 12 anesthetized rats were irradiated with X-rays (4000 cGy). On the 3rd and 4th days postirradiation, SPECT and MR imaging pre- and postcontrast were performed. RESULTS: On SPECT, the irradiated areas appeared as areas with reduced 99mTc-phytate uptake in 9 rats. In the remaining 3 rats, irradiated lesions were not evident on SPECT. On the early postcontrast MR images, differential negative enhancement of the irradiated and nonirradiated areas in the same 9 rats as on SPECT was apparent. However, on the later postcontrast images of 3 of these rats, the irradiated areas, which were brighter than the nonirradiated areas, were visually less clear than those on the earlier postcontrast images. In the remaining 3 rats, no radiation damage was evident on MR images. CONCLUSION: SPECT with 99mTc-phytate and early postcontrast MR imaging with SPIO can show early radiation damage of the liver. The serial assessment of the postcontrast MR images provides functional information on the Kupffer cells.

Animals↗
PubMed1996

A mutant form of p135tyk2, an interferon-alpha inducible tyrosine kinase, suppresses the transformed phenotype of Daudi cells.

The type I interferons induce an anti-viral state and suppress cell growth. The p135tyk2 non-receptor tyrosine kinase appears to initiate, at least in part, the type I interferon signal transduction pathway, and thereby activates type I interferon-dependent gene expression. To determine if p135tyk2 can suppress growth and/or tumorigenesis, derivatives of the tyk2 gene were introduced into the tumorigenic cell line Daudi. Transfectants expressing a tyk2 construct missing the carboxy-terminal 22 amino acids cloned with a greatly reduced efficiency in soft agar and displayed a partial decrease in the ability to form tumors in athymic mice. In addition, transfectants producing a kinase deficient version of tyk2 show an increase in both growth rate and agar cloning efficiency, suggesting that the inactive kinase can act in a dominant-negative manner. Surprisingly, the carboxyl-terminal deleted protein lacks both auto-kinase activity, and activity towards a putative substrate, even though it induces a phenotype which is precisely the opposite of that produced by another kinase-deficient tyk2 mutant containing an altered ATP binding site. Thus, while these results add tyk2 to a growing list of interferon-alpha regulated proteins that might be able to suppress tumor formation, the biochemical basis of this activity remains unknown.

Animals↗
PubMed1996

[A 63-year-old woman with muscle weakness, myotonia, and parkinsonism].

We report a 63-year-old woman who presented myotonia and parkinsonism. The patient was well until 15 years of the age when she noted that the ring finger of her left hand at times flexed when she did not intend to do so. She noted weakness in her left upper extremity at the age of 40, and difficulty in relaxing her hand grip at 45. She had an onset of tremor in her right foot at age 50, which was followed by difficulty in gait and hand writing. She was admitted to Juntendo University Urayasu Hospital when she was 63-year-old. Her mother, two sisters, and a son were affected with similar muscle weakness and myotonia. Although some of them developed stooped posture in the late stage of the disease, none of them had overt parkinsonism. General physical examination was unremarkable. Neurologic examination revealed an alert and oriented woman with some recent memory loss. She had bilateral ptosis, facial weakness, and a masked face. Myerson's sign was present. Her speech was small and monotonous. The sternocleidomastoid muscles were markedly atrophic and weak. The remaining of the cranial nerves were intact. She walked in small steps with freezing with support. She showed bradykinesia, retropulsion, and resting tremor in her right leg. Slight distal dominant weakness was noted in both upper and lower extremities more on the left. No cerebellar signs were noted. Muscle stretch reflexes were within normal limits in the upper extremities and diminished in the lower limbs. Sensation was intact. Routine laboratory findings were unremarkable. Cranial CT scan and MRI revealed slight cortical atrophy and leukoaraiosis. She responded to levodopa and she became able to walk by herself. She was transferred to another hospital one month after her admission. She had several bouts of airway obstruction with one episode of respiratory arrest. She expired six month after the transfer. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that this patient suffered from myotonic dystrophy and Parkinson's disease which set in later years. Postmortem examination on the iliopsoas muscle revealed uneven muscle fiber diameters, central nuclei, and type 1 fiber predominance; the pathologic finding was consistent with myotonic dystrophy. The substantia nigra showed marked cell loss and Lewy bodies in the remaining neurons. The finding was consistent with Parkinson's disease. In myelin stain, diffuse myelin pallor was noted in the cerebral white matter which was the pathologic substrate of leukoaraiosis in this patient. Combination of these two disorders have never been reported in the literature to our knowledge. It appears to be that the coincidence is just a by-chance phenomenon, but it seems interesting to note that accelerated aging process appears to be present in both myotonic dystrophy and Parkinson's disease.

Diagnosis, Differential↗
PubMed1996

[The PCR amplification, cloning, sequencing, expression in E. coli of gene encoding endoflagella subunit protein (fla B) from Leptospira interrogans serovar lai].

A pair of oligonucleotide primers were designed by ourselves to amplify the endoflagella gene of L. interrogans serovar lai. A fragment about 840 bp was generated with PCR and inserted into plasmid pUC8 after the fragment and pUC8 were digested respectively with Bam HI and Pst I. A recombinant plasmid (designated as pLF1) was obtained. SDS-PAGE analysis indicated that a 33 kd was expressed in E. coli JM103 harboring pLF1 and the expression level of the protein was 11% of total bacterial soluble proteins. Western blot analysis showed that the protein band could be recognized by the antiserum against the endoflagella (Axiall filament) of Leptospira interrogans serovar lai. Nucleotide seguence data showed an open reading frame encoding 282 aminoacids residues, corresponding to a protein of molecular weight 33.6 kd. The G + C content of endoflagella subunit protein gene was 48 mol%. Therefore, the G + C content of the leptospiral fla B Gene is significantly higher than the reported 39 mol% G + C content of leptospiral genome of L.interrogans serovar lai but similar to the G + C of the Treponema pallidum genome. Comparison of the deduced endoflagellar subunit protein (fla B) amino acid sequence with flagellins from other bacteria revealed a high level of identity with the Treponema pallidum fla B proteins. Immunization/protection experiment was performed on the model of BALB/c mice and showed that the survival rate in the group JM103-pLF1 was higher than that in the group JM103-pUC8, but statistically the difference between them was significant (P < 0.05) and pLF1 did not induce significant levels of agglutinating antibodies against L.interrogans serovar lai.

Amino Acid Sequence↗
PubMed1996

[Selenium levels in human bodies and environment in Qinghai province].

To study selenium level, its distribution in human bodies and environment and its effects on health, 3,035 specimens of human hair, blood, urine, and environmetal water, soil, food were collected from 91 sampling spots in 23 cities and counties of Qinghai Province and determined for selenium levels with fluorescence analysis. Results showed overall biological selenium level of human bodies in Qinghai Province was low and blood selenium level was lower than the normal reference value in 84.73% of the population, same as that in selenium-poor nations. Environmental selenium was poor or in a deficient status in Qinghai Province, 69.57% of the areas in the Province was in low, poor, or severely deficient selenium. Selenium level in vegetable food correlated closely with that in human blood, which indicated low selenium level in environment caused human selenium deficient in their internal environment via food chain. There were difference in biological selenium levels of human bodies in seven districts and six ethnic nationalities, which suggests selenium levels in human bodies correlate closely with economic development, selenium intake, geographical environment, living habits and customs, etc., and are nothing to do with the altitude above sea level.

Adolescent↗
PubMed1996

A dynamic and quantitative study of pattern visual evoked potentials and gamma-aminobutyric acid neurones in the lateral geniculate nucleus and the visual cortex of monocular deprivation cats.

PURPOSE: To assess the effects of monocular lid closure during critical period on cortical activity. METHOD: Pattern visual evoked potentials (PVEP) of the normal and the monocular deprivation (MD) cats were dynamically measured and the number of gammaaminobutyric acid immunopositive (GABA-IP) neurones of the area 17 of the visual cortex and the lateral geniculate nucleus (LGN) was quantitatively compared by using immunohistochemical method (ABC). RESULTS: The amplitude of the N1-P1 attenuated in deprived eyes (DE), NE/DE at postnatal week (PNW) 7-8 (P < 0.05), NE/DE at PNW 15-16 (P < 0.01); while P1 latency delayed, NE/DE at PNW 7-8 (P > 0.05), NE/DE at PNW 15-16 (P< 0.05). The numbers of GABA-IP neurones in layer A1 of the ipsilateral LGN and in layer A of the contralateral LGN, compared to those in the corresponding normal laminae, were not significant at PNW 7-8 and PNW 11-12 (P > 0.05), while in the same cats a reduction in the number of GABA-IP neurones was found in layer IV of area 17 at PNW 11-12 (P < 0.05). However, with longer survival of 3-4 weeks in duration, the numbers of GABA-IP neurones in the deprived laminae of LGN were remarkably reduced (P < 0.05). CONCLUSIONS: The amplitude of N1-P1 components is sensitive to the effects of monocular deprivation. Monocular deprivation in cats during critical period leads to dramatic changes of the number of GABA-IP neurones in the LGN and cortical layer IV receiving inputs from the deprived eye in cats. The deprivation-induced reduction in GABA-IP neurones is delayed in the LGN compared with the visual cortex. PVEP of the MD cats is consistent with the damage of its GABA system in visual cortex.

Animals↗
PubMed1996

[Surgical treatment for congenital motive defect nystagmus by the parks (5, 6, 7, 8mm) procedure or the augmented Parks procedure].

PURPOSE: The purpose of the surgical treatment for patients with congenital motive detect nystagmus was to correct deviation of the eye and the head tilt, to improve vision and eliminate nystagmus. METHODS: 19 patients underwent the Parks (5, 6, 7, 8mm) or the augmented Parks procedure from 1987 to 1994. For patients with abnormal head turn > or = 30 degrees, We used a 40-60% augmented Parks procedure. RESULTS: A follow up of 19 patients ofr an average of 22 months revealed a marked improvemtnts. After operation, the head turn was decreased form 30.5 degrees to 4.9 degrees, the intensity of nystagmus was decreased from 36.0 to 9.7, 21 eyes (55.3%) of 19 patients improved by two or more lines of Snellen visual acuity. CONCLUSIONS: The Parks (5, 6, 7, 8mm) and the augmented Parks (5, 6, 7, 8mm) procedure produce a marked correction for congenital motive defect nystagmus.

Adolescent↗