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Biomedical subjects

J Cheng

Publications and source records attributed to J Cheng.

At least 415 records · Page 23Linked to original sources
PubMed1994

[Relationship between summating potentials and perilymphatic fistula].

Serial electrocochleogram (ECochG) recordings were obtained within 24 hours from 40 guinea pigs with experimentally induced PLF, and the cochlears of 30 guinea pigs (60 ears) were histopathologically observed under light microscope. -SP occurred in 100% experimented ears within 1-3 hours after PLF, but distention of Ressner's membrane was found only in 30% ones. CAP thresholds and N1 latencies of 10 animals were improved, accompanying disappearance of -SP in 6 of the 10 animals in 24 hours after PLF. It is presumed that -SP is not a specifically electrophysiologic indicator of ELH, and that the generation of -SP may chiefly result from reversible damage of cochlear hair cells. The mechanical factor of basilar membrane displacement can hardly be considered as a main cause of SP abnormality. The mechanism of the ELH following PLF was also discussed.

Animals↗
PubMed1994

Role of ERCP in the management of bile duct lesions post bile duct surgery.

INTRODUCTION: Therapeutic Endoscopic Retrograde Cholangio-Pancreatography (ERCP) is an established mode of treatment for bile duct lesions. AIM: This paper reviews the role of ERCP in the management of bile duct lesions developing after biliary surgery. PATIENTS AND METHODS: Of the 894 ERCPs performed in our department between January 1990 and May 1992, 23 (13 female, 10 male) were for patients with post-operative bile duct lesions. The mean age of these 23 patients was 59 years (range 38-91 years). The previous biliary surgical procedures were conventional cholecystectomy (n = 19), laparoscopic cholecystectomy (n = 3) and a cholecystectomy with choledochojejunostomy. Associated medical conditions of ischaemic heart disease, unstable angina, hypertensive heart disease, chronic obstructive airway disease and hepatitis B cirrhosis were present in 7 of these patients. RESULTS: Ten patients had benign biliary strictures. Endoscopic stenting (with one or 2 stents) was successful in 9. The strictures reopened in 2 patients after a total stenting duration of 12 and 18 months respectively. Four patients had biliary leakages that were successfully treated with stenting. Two patients had spontaneous sealing of biliary leak at 3 and 6 months respectively. Nine patients had retained stones (7 with solitary stone, 2 with multiple stones) that were successfully removed with Dormia basket after sphincterotomy. Complications were few and manageable. CONCLUSIONS: Therapeutic ERCP is safe and effective. It is a useful adjunct in the management of patients with post-operative biliary lesions.

Adult↗
PubMed1994

[Effects of electro-acupuncture on EEG during transient global ischemia and reperfusion in gerbils].

In the model of gerbil of acute global ischemia and reperfusion, we studied the effects of electro-acupuncture (EA) on total power of EEG at different periods of global ischemia and reperfusion. The "Fengfu" (GV 16) and "Jinsuo" (GV 8) points were stimulated by electrical pulse with frequency 7 Hz and intensity of 5-6 mA for 30 min. Recording was made before ischemia and 0 min, 15 min, 30 min, 60 min, 120 min and 240 min after reperfusion respectively. The results were as follows: 1. In the control group, after 10 min of ischemia, the amplitude of EEG was severely inhibited, even became flatten, and the total power of EEG was significantly decreased to 1.41 + 1.29%. After reperfusion, the recovery of total power was very slow. The peak level of recovery occurred at 120 min following reperfusion was 27.39 + 11.31%. 2. In comparison with the control group, the EA remarkably improved the recovery of EEG after ischemia and reperfusion. The recovery of total power was 71.45 + 16.46% (P < 0.01), and 75.27 + 18.43% (P < 0.01) at 120 min and 240 min after reperfusion respectively. These results strongly indicate that EA could reduce the EEG inhibition during global ischemia and improve the recovery after reperfusion.

Animals↗
PubMed1994

Biochemical and pharmacological characterization of mu, delta and kappa 3 opioid receptors expressed in BE(2)-C neuroblastoma cells.

Total opioid binding in the human neuroblastoma cell line BE(2)-C has a density similar to that found in brain, with a Bmax value of 383 +/- 60 fmol/mg protein and a KD of 0.4 +/- 0.07 nM for the nonselective opioid antagonist 3H-diprenorphine. Selective assays reveal a binding distribution of mu (38%), delta (16%) and kappa 3 (43%) opioid receptors. There is no observable kappa 1 or kappa 2 binding. The sum of the Bmax values in the selective binding assays (370 +/- 39 fmol/mg protein) approximates closely that observed with 3H-diprenorphine, suggesting that mu, delta and kappa 3 sites account for most of the binding. The binding selectivities of various opiates and opioid peptides in the BE(2)-C cells are similar to those in rat brain. Delta and mu binding are defined easily by traditional selective ligands. The binding profiles also distinguish clearly mu from kappa 3 binding. The selective mu ligand DAMGO competes with mu binding over 35-fold more potently than kappa 3 binding, whereas morphine shows a 10-fold selectivity. Functionally, selective mu, delta and kappa 3 agonists inhibit forskolin-stimulated cAMP accumulation through distinct receptor mechanisms that are pertussis toxin-sensitive. In addition to demonstrating that BE(2)-C cells provide a useful model system for studying mu, kappa 3 and delta receptors, these studies confirm that kappa 3 receptors represent a pharmacologically distinct receptor class in this cell line.

Animals↗
PubMed1994

Opioid binding in giant toad and goldfish brain.

Opiate receptor expression in phylogenetically different species has played an important role in the study of opioid receptor pharmacology. Total opioid binding measured with the nonselective ligand 3H-diprenorphine reveals a Bmax of 21.7 +/- 1.37 fmol/mg tissue wet wt and a KD of 0.17 +/- 0.03 nM in Bufo marinus (giant toad), as well as a Bmax of 18.17 + 0.41 fmol/mg tissue wet wt and a KD of 0.47 +/- 0.18 nM in Carassius auratus (goldfish). Despite the similar levels of 3H-diprenorphine binding, the composition of binding subtypes in the two species differs. Approximately 30% of total binding corresponds to mu receptors in both species, whereas neither kappa 1 nor delta binding can be detected. However, the remaining 70% of binding differs between the toad and goldfish. In the toad, the non-mu binding corresponds to kappa 2 sites, whereas in the goldfish, the non-mu binding corresponds to kappa 3 sites. The sites can be distinguished biochemically, as well as pharmacologically. After affinity labeling the sites with 3H-NalBzoH, the retention times on an ion-exchange column differ for the peaks of kappa binding in the two species. Although Bufo marinus (giant toad) and Carassius auratus (goldfish) brains express kappa and mu opioid binding, the kappa subtypes in these two species differ.

Animals↗
PubMed1994

Nucleolar organizer regions (NORs) in lymphoproliferative disorders of the human salivary gland.

The relationship between the silver-stained proteins of the nucleolar organizer regions (AgNORs) and proliferative activity was studied in 30 patients with lymphoproliferative disorders of the major salivary gland. The salivary gland lesions were microscopically and immunohistochemically differentiated into myoepithelial sialadenitis (MESA, n = 6), low-grade B-cell lymphoma (n = 16), high-grade B-cell lymphoma (n = 5), and T-cell lymphoma (n = 3). The mean AgNOR count per nucleus for MESA was 2.48; for low-grade B-cell lymphoma, 2.19; for high-grade B-cell lymphoma, 6.37; and for T-cell lymphoma, 5.46. There was no significant difference in AgNOR counts per nucleus between the MESA and low-grade B-cell lymphoma, whereas the high-grade B-cell lymphomas exhibited significantly increased mean AgNOR number. Furthermore, the mean numbers of AgNOR were compared with cellular types of lymphoproliferative disorders. A statistically significant difference did exist among AgNOR counts of centroblasts, centrocytes and mantle zone lymphocytes or interfollicular lymphocytes in MESA. There was no significant difference in AgNOR counts per nucleus among the centroblasts of MESA, neoplastic centroblasts of centroblastic/centrocytic lymphoma, and centroblastic lymphoma. It was shown that AgNOR enumeration of tumor cells in mucosa-associated lymphoid tissue (MALT) lymphoma was similar to those seen in mantle zone and interfollicular lymphocytes of MESA. Therefore, we propose that MALT lymphoma may represent a mucosal counterpart of mantle zone lymphocyte- or interfollicular lymphocyte-related low-grade B-cell lymphomas.

Humans↗
PubMed1994

Modulation of morphine tolerance by the competitive N-methyl-D-aspartate receptor antagonist LY274614: assessment of opioid receptor changes.

Recent reports have demonstrated that the coadministration of morphine with an N-methyl-D-aspartate (NMDA) receptor antagonist can attenuate and/or reverse the development of morphine tolerance. In the present study we used an experimental tolerance paradigm using morphine pellets (75 mg) to produce an 1-fold shift in the morphine dose-response curve in rats. Coadministration of the competitive NMDA receptor antagonist LY274614 [(+-)-6-phosphonomethyl-decahydroisoquinolin-3-carboxylic acid] via continuous s.c. infusion (24 mg/kg/24 hr) significantly attenuated the development of morphine tolerance. In addition, animals made tolerant to morphine and then infused with LY274614 (24 mg/kg/24 hr) regained their analgesic sensitivity to morphine more rapidly than morphine-tolerant animals given a saline infusion. To determine whether LY274614 treatment modifies the subsequent development of tolerance, LY274614 was administered to nontolerant animals for 1 week. One week after LY274614 treatment was discontinued the animals were challenged with morphine and then implanted with morphine pellets. Neither the expression of morphine analgesia nor the development of morphine tolerance differed when LY274614- and saline-treated animals were compared. The infusion of LY274614 for 7 days did not increase the affinity or density of mu, delta, kappa-1 or kappa-3 opioid receptors in rat brain homogenates as measured by ligand binding assays. Additionally, the IC50 values for LY274614 in mu-1, mu-2, delta, kappa-1 or kappa-3 ligand binding assays were greater than 10 microM. Taken together these results demonstrate that the competitive NMDA receptor antagonist LY274614 can both attenuate and reverse the development of morphine tolerance.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1993

cDNA cloning and characterization of the protein encoded by RD, a gene located in the class III region of the human major histocompatibility complex.

The RD gene, initially defined in the mouse, has been mapped between the Bf and C4A genes in the human major histocompatibility complex class III region. Using the mouse cDNA as a probe, we isolated and sequenced human RD cDNA clones. The composite nucleotide sequence consisted of 1301 nucleotides, excluding a poly(A) tail at the 3' end. It contained a single open reading frame encoding a polypeptide of 380 amino acid residues with a calculated molecular mass of 42274 Da. The most striking structural feature of the deduced amino acid sequence is a region consisting entirely of 24 tandem repeats of an Arg-Asp (or Glu) dipeptide. The human RD cDNA was expressed in Escherichia coli as a fusion protein with glutathione S-transferase and used to produce antisera in rabbits. Western blot analysis and immunoprecipitation of lysates of biosynthetically labelled HeLa cells indicated that RD is a 44 kDa nuclear protein.

Amino Acid Sequence↗
PubMed1993

Evidence to implicate translation by ribosomes in the mechanism by which nonsense codons reduce the nuclear level of human triosephosphate isomerase mRNA.

The abundance of the mRNA for human triosephosphate isomerase (TPI) is decreased to 20-30% of normal by frameshift and nonsense mutations that prematurely terminate translation within the first three-quarters of the reading frame. The decrease has been shown to be attributable to a reduced level of TPI mRNA that copurifies with nuclei. Given that the translational reading frame of an mRNA is assessed in the cytoplasm during protein synthesis, cytoplasmic and nuclear RNA processes may be linked. Alternatively, a nuclear mechanism may exist whereby in-frame nonsense codons can be identified. To differentiate between these two possibilities, two distinct modulators of protein synthesis have been tested for the ability to influence the nonsense-codon-mediated reduction in the mRNA level. (i) A suppressor tRNA, which acts in trans to suppress an amber nonsense codon within TPI mRNA, and (ii) a hairpin structure in the 5' untranslated region of TPI mRNA, which acts exclusively in cis to inhibit initiation of TPI mRNA translation, were found, individually, and to a greater extent, together, to abrogate the decrease in mRNA. These results show that tRNA and ribosomes coordinately mediate the effect of a nonsense codon on the level of newly synthesized TPI mRNA. We suggest that the premature termination of TPI mRNA translation in the cytoplasm can reduce the level of TPI mRNA that fractionates with nuclei.

Animals↗
PubMed1993

Nonsense codons can reduce the abundance of nuclear mRNA without affecting the abundance of pre-mRNA or the half-life of cytoplasmic mRNA.

The abundance of the mRNA for human triosephosphate isomerase (TPI) is decreased to approximately 20% of normal by frameshift and nonsense mutations that cause translation to terminate at a nonsense codon within the first three-fourths of the reading frame. Results of previous studies inhibiting RNA synthesis with actinomycin D suggested that the decrease is not attributable to an increased rate of cytoplasmic mRNA decay. However, the step in TPI RNA metabolism that is altered was not defined, and the use of actinomycin D, in affecting all polymerase II-transcribed genes, could result in artifactual conclusions. In data presented here, the nonsense codon-mediated reduction in the level of TPI mRNA is shown to be characteristic of both nuclear and cytoplasmic fractions of the cell, indicating that the altered metabolic step is nucleus associated. Neither aberrancies in gene transcription nor aberrancies in RNA splicing appear to contribute to the reduction since there were no accompanying changes in the amount of nuclear run-on transcription, the level of any of the six introns in TPI pre-mRNA, or the size of processed mRNA in the nucleus. Deletion of all splice sites that reside downstream of a nonsense codon does not abrogate the reduction, indicating that the reduction takes place independently of the splicing of a downstream intron. Experiments that placed TPI gene expression under the control of the human c-fos promoter, which can be transiently activated by the addition of serum to serum-deprived cells, verified that there is no detectable effect of a nonsense codon on the turnover of cytoplasmic mRNA.

Animals↗
PubMed1993

Sequences within the last intron function in RNA 3'-end formation in cultured cells.

In cultured cells, little if any mRNA accumulates from an intronless version of the human gene for triosephosphate isomerase (TPI), a gene that normally contains six introns. By deleting introns either individually or in combinations, it was demonstrated by Northern (RNA) blot hybridization that while the deletion of a greater number of introns generally results in a lower level of product mRNA, not all introns contribute equally to mRNA formation. For example, intron 1 appeared to be dispensable, at least when the remaining introns are present, but deletion of the last intron, intron 6, reduced the level of product mRNA to 51% of normal. To determine how intron 6 contributes to mRNA formation, partial deletions of intron 6 were constructed and analyzed. Deletion of the lariat and acceptor splice sites or the donor, lariat, and acceptor splice sites, each of which precluded removal of the intron 6 sequences that remained, reduced the level of product mRNA to < 1 or 27% of normal, respectively. As measured by RNase mapping and cDNA sequencing, the decrease in mRNA abundance that was attributable to the complete and partial intron 6 deletions was accompanied by an increase in the abundance of pre-mRNA that lacked a mature 3' end, i.e., that was neither cleaved nor polyadenylated. We infer from these and other data that sequences within the final intron facilitate proper 3'-end formation, possibly through an association with the components of a productive spliceosome.

Alleles↗
PubMed1993

P53 mutation in acute T cell lymphoblastic leukemia is of somatic origin and is stable during establishment of T cell acute lymphoblastic leukemia cell lines.

Samples donated by patients with T cell acute lymphoblastic leukemia (T-ALL) were screened for mutations of the p53 tumor suppressor gene. Peripheral blood cells of T-ALL relapse patient H.A. were found to possess a heterozygous point mutation at codon 175 of the p53 gene. To determine whether this was an inherited mutation, a B cell line (HABL) was established. Leukemic T cell lines (HATL) were concurrently established by growing peripheral blood leukemic T cells at low oxygen tension in medium supplemented with IGF-I. Previously we had shown that > 60% of leukemic T cell lines possessed mutations in the p53 gene (Cheng, J., and M. Hass. 1990. Mol. Cell. Biol. 10:5502), mutations that might have originated with the donor's leukemic cells, or might have been induced during establishment of the cell lines. To answer whether establishment of the HATL lines was associated with the induction of p53 mutations, cDNAs of the HATL and HABL lines were sequenced. The HATL lines retained the same heterozygous p53 mutation that was present in the patient's leukemic cells. The HABL line lacked p53 mutations. Immunoprecipitation with specific anti-p53 antibodies showed that HATL cells produced p53 proteins of mutant and wild type immunophenotype, while the HABL line synthesized only wild-type p53 protein. The HATL cells had an abnormal karyotype, while the HABL cells possessed a normal diploid karyotype. These experiments suggest that (a) p53 mutation occurred in the leukemic cells of relapse T-ALL patient HA; (b) the mutation was of somatic rather than hereditary origin; (c) the mutation was leukemia associated; and (d) establishment of human leukemia cell lines needs not be associated with in vitro induction of p53 mutations. It may be significant that patient HA belonged to a category of relapse T-ALL patients in whom a second remission could not be induced.

Adult↗
PubMed1993

Social deprivation indices of patients on renal replacement therapy (RRT) in Grampian.

The social deprivation scores of 169 patients who resided in Grampian region and commenced renal replacement therapy (RRT) in Aberdeen during the period 1 January 1985-30 June 1991 were measured when their serum creatinine concentrations were first > = 300 mumol/l, using the Jarman Underprivileged Area (UPA) and Carstairs indices. The numbers in the population of Grampian for each score were obtained from the Information Services team of Grampian Health Board based on the 1981 census. Comparison of the numbers of patients in each category of both Jarman and Carstairs indices showed no differences between the observed numbers of patients and the numbers in the general population. Thus in this study social deprivation occurred no more frequently in those commencing RRT than in the general population.

Health Care Rationing↗