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Biomedical subjects

J Yin

Publications and source records attributed to J Yin.

At least 127 records · Page 7Linked to original sources
PubMed1997

Some changes of receptor and postreceptor signal transduction regulated by somatostatin in pituitary hGH-secreting adenomas.

OBJECTIVE: To investigate the disturbance in the function of SRIF receptor, Gi protein and Ca2+ channel in hGH adenoma cells and to evaluate their significance in the pathogenesis of pituitary hGH adenomas. METHODS: All 25 patients with pituitary hGH adenoma who were involved in this study had typical acromegalic manifestation and high fasting serum hGH levels of > 5.0 micrograms/L which were not suppressed to < 3.0 micrograms/L by oral glucose tolerance test. The pituitary hGH adenoma tissue obtained from transphenoidal operation was digested by collagenase and the dispersed adenoma cells were cultured in the monolayer. The effects of octreotide (SMS), a long-acting agonist of somatostatin, on hGH secretion and intracellular cAMP level were observed and the influences of pertussis toxin (PT), an inhibitor of Gi protein, and Ca2+ ionophore A23187 or KCl on the inhibitory action of octreotide on hGH secretion were also investigated in the cultured pituitary hGH adenoma cells. RESULTS: A total of 16.0% (4/25) of cultured pituitary hGH adenomas did not respond to octreotide (100 nmol). The inhibitory effect of octreotide on hGH secretion was not blocked by PT (50 ng/ml) and A23187 (10 mumol) or KCl (22.5 nmol) in 31.6% (6/19) and 35% (7/20) of hGH adenomas, respectively. The effects of octreotide on hGH secretion and intracellular cAMP levels were studied in 10 cultured hGH adenomas. Octreotide suppressed both hGH secretion and cAMP levels in 5 cases; inhibited only hGH secretion or the cAMP level in 3 cases and 1 case respectively; and affected neither hGH secretion nor cAMP level in the last case. CONCLUSION: There were abnormalities in the SRIF receptor and/or postreceptor signal transduction in 16.0% of hGH adenomas which did not respond to octreotide. The defects in Gi and/or Ca2+ channels were found in 52.4% (11/21) of hGH adenomas which had responded to octreotide. These defects might induce diminution of the inhibitory action of SRIF on hGH secretion and might be the causes of hypersecretion in some pituitary hGH adenomas.

Adenoma↗
PubMed1997

[An instrument for estimating human body composition using impedance measurement].

According to the impedance feature of biological tissue, the instrument was designed at 1, 5, 10, 50, 100kHz to measure human impedance, and then to calculate human FAT, FFM, FAT%, TBW, ECW, ICW and so on. A 8031 singlechip microprocessor contacuting used as a control center in the instrument. The part of electric circuit contacuting human body in the instrument was unreally earthing. The instrument was safty, effective, repeatable, and easily manpulative. Prelimintary clinical experiment showed the results measured with the instrument could effectively reflect practical, status of human composition.

Adolescent↗
PubMed1996

Infrequent DPC4 gene mutation in esophageal cancer, gastric cancer and ulcerative colitis-associated neoplasms.

Homozygously Deleted in Pancreatic Cancer 4 (DPC4), a recently identified candidate tumor suppressor gene, was previously shown to be altered in human pancreatic cancers. We examined DPC4 mutation in 30 examples of three other types of gastrointestinal malignancy: 10 esophageal cancers, 10 gastric cancers and 10 colorectal cancers occurring in the preneoplastic condition, ulcerative colitis. The entire coding region of DPC4 (including all 11 exons) was analysed by either direct sequencing of PCR product or the in vitro synthesized protein assay. No coding region mutations of DPC4 were found in any of the samples examined. Our results suggest that inactivation of DPC4 may not be important in the majority of these types of gastrointestinal cancer.

Colitis, Ulcerative↗
PubMed1996

Determination of the amino acid residue involved in [3H]beta-funaltrexamine covalent binding in the cloned rat mu-opioid receptor.

We previously demonstrated that [3H]beta-funaltrexamine ([3H]beta-FNA) labeled the rat mu opioid receptor expressed in Chinese hamster ovary cells with high specificity, and [3H]beta-FNA-labeled receptors migrated as one broad band with a mass of 80 kDa. In this study, we determined the region and then the amino acid residue of the mu receptor involved in the covalent binding of [3H]beta-FNA. [3H]beta-FNA-labeled receptors were solubilized and purified to approximately 10% purity by immunoaffinity chromatography with antibodies against a C-terminal domain peptide. The site of covalent bond formation was determined to be within Ala206-Met243 by CNBr cleavage of partially purified labeled mu receptors and determinations of sizes of labeled receptor fragments. The amino acid residue of beta-FNA covalent incorporation was then determined by site-directed mutagenesis studies within this region. Mutation of Lys233 to Ala, Arg, His, and Leu completely eliminated covalent binding of [3H]beta-FNA, although these mutants bound beta-FNA with high affinity. Mutations of other amino acid residues did not affect covalent binding of [3H]beta-FNA. These results indicate that [3H]beta-FNA binds covalently to Lys233. Since [3H]beta-FNA is a rigid molecule, the information will be very useful for molecular modeling of interaction between morphinans and the mu receptor.

Amino Acid Sequence↗
PubMed1996

The region in the mu opioid receptor conferring selectivity for sufentanil over the delta receptor is different from that over the kappa receptor.

We determined the binding domains of sufentanil and lofentanil in the mu opioid receptor by comparing their binding affinities to seven mu/delta and six mu/kappa chimeric receptors with those to mu, delta and kappa opioid receptors. TMHs 6 and 7 and the e3 loop of the mu opioid receptor were important for selective binding of sufentanil and lofentanil to the mu over the kappa receptor. TMHs 1-3 and the e1 loop of the mu opioid receptor conferred binding selectivity for sufentanil over the delta receptor. Thus, the region that conferred binding selectivity for sufentanil differs, depending on chimeras used. In addition, the interaction TMHs 1-3 and TMHs 6-7 was crucial for the high affinity binding of these two ligands. These two regions are likely to contain sites of interaction with the ligands or to confer conformations specific to the mu receptor.

Animals↗
PubMed1996

Irreversible binding of cis-(+)-3-methylfentanyl isothiocyanate to the delta opioid receptor and determination of its binding domain.

Binding of cis-(+)-3-methylfentanyl isothiocyanate (SUPERFIT) to cloned opioid receptors stably expressed in Chinese hamster ovary cells was characterized. SUPERFIT inhibited [3H]diprenorphine binding with much higher affinity for the delta than the mu or kappa receptor. Pretreatment with SUPERFIT followed by extensive washing reduced delta binding with an IC50 value of 7.1 nM, yet it did not affect mu and kappa binding up to 0.1 microns. The reduction in delta binding by SUPERFIT pretreatment was due to a decrease in Bmax with no change in Kd. These results indicate that SUPERFIT is a highly selective delta irreversible ligand. We then determined the region in the delta receptor that confered binding selectivity for SUPERFIT by examining its binding to six mu/delta chimeric receptors. SUPERFIT bound to delta, mu/delta 1 (amino acids mu 1-94/delta 76-372), delta/mu 3 (delta 1-134/mu 154-398), and delta/mu 4 (delta 1-187/mu 207-398) receptors with high affinity but to mu, delta/mu 1 (delta 1-75/mu 95-398), mu/delta 3 (mu 1-153/delta 135-372), and mu/delta 4 (mu 1-206/delta 188-372) receptors with low affinity. Pretreatment with SUPERFIT potently inhibited [3H]diprenorphine binding to delta, mu/delta 1, delta/mu 3, and delta/mu 4 but affected binding to mu, delta/mu 1, mu/delta 3, and mu/delta 4 only at much higher concentrations. Thus, the segment from the beginning of the first intracellular loop to the middle of the third transmembrane helix of the delta receptor is important for selective binding of SUPERFIT.

Amino Acid Sequence↗
PubMed1996

Metal-ion discrimination by phage T7.

The discovery of new metal-selective complexing agents may be facilitated by applying an in vitro selection strategy. Such a strategy was recently devised to identify and enrich populations of bacteriophage that rely on Mg(II)-, Zn(II)-, or Au(III)-selective stabilization for survival in the presence of denaturing urea. The potential for extension of the strategy to other metal ions is investigated here. The kinetics of phage inactivation in 5 M urea was measured for a spectrum of metals. At a concentration of 1 mM, Mg(II), Ca(II), Co(II), and Ni(II) were found to be the most stabilizing, followed by Cd(II), Cu(II), and Zn(II), respectively. K(I) had virtually no effect. In contrast, Al(III) and Au(III) significantly destabilized the phage, even at concentrations of 0.25 mM.

Aluminum↗
PubMed1996

Allelic imbalance on chromosome 5q predicts long-term survival in neuroblastoma.

Neuroblastoma is the most common extracranial solid tumour of childhood. Amplification of the proto-oncogene, N-myc, confers a poor prognosis in neuroblastoma, while hyperdiploidy is associated with a favourable outcome. Little is known about the contribution of tumour-suppressor genes to the development or progression of neuroblastoma. We examined allelic imbalance at the locus of the tumour-suppressor gene, APC (adenomatous polyposis coli), on chromosome 5q using a polymerase chain reaction (PCR)-based assay. Nine of 24 (37.5%) informative neuroblastoma tumours showed allelic imbalance (AI) at this locus. Clinical data concerning N-myc amplification and DNA content were correlated with these results in the same patients. Allelic imbalance was found only in tumours containing a single copy of the N-myc gene and exhibiting hyperdiploidy. All nine patients with AI of chromosome 5q were alive after a median follow-up period of 46 months, while 7 of 15 (47%) of those lacking AI at this locus had died (P = 0.018). Allelic imbalance at three additional loci on chromosome 5 was demonstrated in tumours that exhibited AI at the APC locus, suggesting that endoreduplication of chromosome 5 had occurred. Fluorescent in situ hybridisation (FISH) analysis of tumour tissue from one patient exhibiting AI demonstrated two, three, four or six copies of the APC gene per cell, consistent with this hypothesis. These data suggest that allelic imbalance of chromosome 5 is involved in at least a subset of neuroblastomas and influences survival in patients with neuroblastoma.

Alleles↗
PubMed1996

Detection of evolving viruses.

The spread of viruses on a homogeneous lawn of receptive hosts provides an opportunity to detect the dynamics of their evolution. We have previously found that when repeated virus passages are confined to the expanding perimeter of a growing plaque, the appearance and outgrowth of genetically diverse strains (all descended from the same parent strain) can be traced along different radii of the plaque. As a plaque grows, the random mutation and selection of new fast-growing strains reduce the roundness or circularity of the growing plaque. Here we have quantified such changes in growing plaques of bacteriophage T7 using a digital imaging system. We find that T7 populations not adapted for fast growth exhibit a broader diversity of growth rates than populations adapted for fast growth. These results provide a foundation for understanding how viruses exploit mutation and selection processes to persist in nature.

Bacteriophage T7↗
PubMed1996

Comparison of regional variability in lung-specific gene expression using a novel method for RNA isolation from lung subcompartments of rats and mice.

The lung is composed of a complex assemblage of more than 40 different cell types. Therefore, investigative techniques that rely on samples derived from whole lung homogenates, whether for biochemical measurements of metabolism or the analysis of gene expression, are inherently insensitive to cell type or region-specific differences. Microdissection has previously been successful for defining region-specific metabolic activity in the lung. Tissues obtained by this technique exhibit good viability and permit reproducible enzyme activity measurements. In this paper, a technique for isolating RNA from lung subcompartments obtained by microdissection is described. The method is straight forward and results in high quality RNA that can be used to quantify specific mRNAs in microscopically selected lung subcompartments by complementary DNA or RNA hybridization techniques. This technique provides a significant increase in sensitivity over techniques based on whole lung homogenates because RNA contributed by relevant lung subcompartments is enriched. The high sensitivity of the method makes it feasible to compare differences in mRNA expression 1) within different regions of the lung in the same animal, 2) in the same region in different animals and between different species, and 3) between susceptible and nonsusceptible sites in conditions of focal lung injury.

Animals↗
PubMed1996

[The effect of mitomycin C on filtration surgery of glaucoma with poor prognosis].

OBJECTIVE: To determine the anticicatrization effect of mytomycin C (MMC). METHODS: We randomly divided 30 cases (40 eyes) into two groups: 21 eyes in MMC group and 19 eyes in control group. Intra-operatively, 0.4 mg/ml MMC was used in the trabeculectomy in MMC group, and no MMC was used in the control group. The post-operative follow-up periods ranged from 6 to 25 months (mean, 10.0 months). RESULTS: The successful rate of the operation of MMC group was 90.4% and that of the control group, 26.3% (P < 0.0001). The rate of eyes with functional filtering blebs was 17/21 and that of the control group, 4/19 (P = 0.002). Macular edema occurred in 3 eyes of MMC group and none in the eyes in the control group. There were no corneal complication and leakage of the wound. CONCLUSION: The results show that MMC can promote the formation of functional filtering bleb and elevate the successful rate of filtration surgery.

Adolescent↗
PubMed1996

Esophagin cDNA cloning and characterization: a tissue-specific member of the small proline-rich protein family that is not expressed in esophageal tumors.

Cancer may be understood as the net effect of differences in gene expression between normal and transformed cells. In a novel direct approach applying this principle, complete genes expressed at altered mRNA levels in malignant versus normal esophageal epithelium were identified and isolated from cDNA libraries. One clone was expressed in normal esophageal mucosae but absent in esophageal carcinomas. By in situ hybridization, Northern blotting, and immunohistochemistry, expression of this gene was restricted to normal esophageal mucosa; it is designated esophagin. Esophagin expression was greatest in the superficial, most mature layers of esophageal squamous mucosa and was restricted to this organ, being undetectable in other squamous epithelia. A genomic clone localized esophagin to chromosomal region 1q21-q22. The expressed protein contains multiple direct repeats of an 8-amino acid motif rich in proline, with significant homology to the cornifin, pig 20K, monkey MT5, and human small proline-rich genes spri and spril. Esophagin constitutes the newest and largest member of this small proline-rich gene family and is associated with differentiation and the benign phenotype of the human esophageal epithelial cell.

Amino Acid Sequence↗
PubMed1996

Alterations of transforming growth factor-beta 1 receptor type II occur in ulcerative colitis-associated carcinomas, sporadic colorectal neoplasms, and esophageal carcinomas, but not in gastric neoplasms.

BACKGROUND & AIMS: Gastric cancers, sporadic colorectal cancers, and ulcerative colitis (UC)-associated colorectal carcinomas and dysplasias manifest microsatellite instability (MI); however, esophageal carcinomas rarely exhibit MI. Recently, a transforming growth factor-beta 1 type II receptor (TGF-beta 1RII) mutation in a coding microsatellite was described in primary colorectal carcinomas demonstrating MI. No previous studies of TGF-beta 1RII have addressed mechanisms of inactivation other than MI in human tumors; furthermore, MI-negative tumors have not been examined for TGF-beta 1RII mutation. We evaluated 138 primary human neoplasms for mutation in the poly-A microsatellite tract of TGF-beta 1RII. Additionally, a group of esophageal tumors was evaluated for the expression of TGF-beta 1RII messenger RNA (mRNA). METHODS: First, we determined whether MI was present at other chromosomal loci in these lesions. The poly-deoxyadenine (poly-A) microsatellite tract within the TGF-beta 1RII coding region was then PCR-amplified. In a group of MI-negative esophageal tumors, RT-PCR was performed to determine the expression of TGF-beta 1RII mRNA. RESULTS: Among 17 MI+ UC specimens, 3 (18%) demonstrated TGF-beta 1RII poly-A tract mutation (2 cancers and 1 dysplasia), while 2 (4%) of 44 MI-negative UC specimens (1 dysplasia and 1 tumor), and 13 (81%) of 16 MI+ sporadic colorectal cancers, contained TGF-beta 1RII poly-A mutation. No gastric or esophageal tumors contained TGF-beta 1RII mutation. Among 21 MI-negative esophageal carcinomas. 6 cases (28.5%) had TGF-beta 1RII transcripts that were low or undetectable by RT-PCR. CONCLUSIONS: Mutation within the poly-A microsatellite tract of TGF-beta 1RII occurs early in a subset of UC-neoplasms and commonly in sporadic colorectal cancers, but may be rare in MI+ gastric tumors. Diminished expression of TGF-beta 1RII mRNA in esophageal tumors suggests that mechanisms of inactivation in this gene other than MI play a role in esophageal carcinogenesis.

Colitis, Ulcerative↗
PubMed1996

The role of GRH mediated AC-cAMP system in the pathogenesis of human pituitary GH-secreting adenomas.

OBJECTIVE: To investigate the role of AC-cAMP system in the transmission of the action of the growth hormone releasing hormone (GRH) on growth hormone (GH) release in pituitary GH-secreting adenomas. METHODS: The effects of GRH (10(-7) mol/L) on intracellular cAMP levels and GH release and the effects of AC-cAMP stimulators, cholera toxin (Ct, 50 micrograms/L), forskolin (10(-5) ml/L) and db-cAMP (10(-3) mol/L) on GH secretion were studied in cultured cells of 21 GH-secreting adenomas obtained from operation for acromegalic patients. RESULTS: GRH and Ct failed to stimulate GH secretion in 61.9% (13/21 cases) and 57.1% (12/21 cases) pituitary GH adenoma cell cultures respectively. Forskolin stimulated GH release in 88.9% (8/9 cases), while db-cAMP induced GH secretion in all cases tested (5/5 cases). The intracellular cAMP levels were elevated by GRH in the 4 out of 9 cases of tumor cell cultures, but not in the other 5 cases. According to the GH secretory responses to GRH and Ct, the 21 GH tumors were divided into 4 groups. In group A and B, GRH can stimulate GH release, but Ct has stimulative role only in group A. In group C and D, GRH fails to stimulate GH secretion. However group A can respond to Ct, but group D has no response. CONCLUSIONS: The GH hypersecretion in most acromegalic patients is mainly due to the defects of pituitary adenoma cells, especially the abnormalities of GRH receptor and/or stimulative guanosine protein.

Adenoma, Acidophil↗
PubMed1996

[The role of Ca2+ in the pathogenesis of human pituitary GH-secreting adenomas].

Effects of Ca2+ channel blockers (nicardipin and nifedipin) and Ca2+ ionophore A23187 on the basal secretion and on the secretion stimulated by GRH or inhibited by SMS, a SRIF analogne of GH were investigated in monolayer cell cultures of 23 cases of human pituitary GH-secreting adenomas. The roles of GRH and SMS in 45Ca influx were investigated also. The GH secretion of most GH adenomas was depended on Ca2+, but the abnormality in different link of GH secretion mediated by Ca2+ was observed. The defects of receptor and post-receptor including Ca2+ channel and Ca(2+)-GH secretion couple regulated by GRH and SRIF were found in 66.7% and 55.6% of GH adenomas respectively. These abnormalities may contribute to GH hypersecretion in GH adenomas.

Adenoma↗
PubMed1996

The role of calcium ion in the pathogenesis of human pituitary GH-secreting adenomas.

To study the role of Ca2+ in the pathogenesis of pituitary growth hormone secreting adenomas, the function of Ca2+ in 23 cases of human pituitary GH-secreting adenoma was investigated in monolayer cell culture. It was found that Ca2+ channel blockers nicardipin and nifedipin inhibited basal and growth hormone releasing hormone (GRH)-stimulated GH secretion in 87.5% and 100.0% of the GH adenomas, respectively, demonstrating that in most human pituitary GH adenomas, the basal and GRH regulated GH secretion is Ca2+ dependent. The GRH and sometostatin (SRIF) agonist octreotide regulated the processes of GH secretion via Ca2+ had defects in different steps including receptor, postreceptor Ca2+ channel and Ca(2+)-GH secreting coupling in 6(66.6%) and 5(55.5%) cases of 9 GH adenomas respectively. Among them, the defects in GRH receptor and SRIF regulated Ca2+ channel are the main causes of the dysfunction of GH adenomas. These defects may be related to GH hypersecretion in GH adenomas. Our data provides advance evidences for intrinsic defects of GH adenomas.

Adenoma↗
PubMed1996

[Quality control of semen Cassiae].

A reversed-phase HPLC method was developed for determination of chrysophanol in Semen Cassiae. The extraction conditions were examined for free and combined chrysophanols. 14 samples collected from 6 different areas were determined. The average recoveries for two kinds of compounds were 101.2% and 103.3% respectively, and the RSDs were 3.5% and 1.8%.

Anthraquinones↗