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Biomedical subjects

J Gong

Publications and source records attributed to J Gong.

At least 73 records · Page 4Linked to original sources
PubMed1999

Lemierre's syndrome.

Postanginal sepsis, or Lemierre's syndrome, is rare but with life-threatening potential involving mainly infants and adolescents. The morbidity or mortality is caused mainly by lack of knowledge of the syndrome. The 18-year-old boy described here developed a jugular thrombosis 7 days after an angina. Fusobacterium necrophorum was isolated from the culture of the excised jugular vein. Secondary embolism involved the lungs, associated with an iliac osteomyelitis and sacroiliitis. Computed tomography was used for diagnosis and follow-up.

Adolescent↗
PubMed1999

Effect of dietary fish oil, vitamin E, and probucol on renal injury in the rat.

Dietary fish oil, vitamin E, and probucol have been considered in a variety of human and experimental models of kidney disease. Using subtotal nephrectomized cholesterol-fed rats as a model for progressive kidney disease, we examined the effect of 5% dietary fish oil, or a combination of 5% dietary fish oil with 500 IU vitamin E/kg diet or 1% probucol on renal injury. Three-month-old Sprague Dawley rats were fed a control diet (C group) or a cholesterol supplemented (2%) diet (Ch group) containing either fish oil (FO group) or fish oil plus vitamin E (FO+E group) or fish oil plus probucol (FO+P group). After 4 weeks of dietary treatment, the right kidney was electrocoagulated and the left kidney nephrectomized. After 8 weeks, 24-hour urine was collected before sacrifice. No effect of the dietary treatments was noted on serum creatinine, blood urea nitrogen, or proteinuria, except that proteinuria was highest in FO+P group. Rats receiving the cholesterol diets had higher serum low density lipoprotein (LDL) + very low density lipoprotein (VLDL) cholesterol (P < 0.05). In contrast, rats in the FO+P group had the lowest serum total cholesterol and LDL+VLDL cholesterol among all groups. The FO group had 26% lower kidney alpha-tocopherol concentrations than the C group. However, inclusion of vitamin E in the diet (FO+E group) increased the kidney alpha-tocopherol status to a level comparable to that in the C group, whereas inclusion of probucol in fish oil diet (FO+P group) did not improve the kidney alpha-tocopherol status. Rats fed the cholesterol diet had a 2.5-fold higher glomerular segmental sclerosis (GSS) score and 1.5-fold higher glomerular macrophage (GM) subpopulation than the C group. These effects of the cholesterol diet were ameliorated by a fish oil diet (FO group: GSS by 30%, GM by 24%). The inclusion of vitamin E in the fish oil diet (FO+E group) did not further improve the GSS score or GM subpopulation. However, inclusion of probucol in fish oil diet (FO+P group) lowered the GSS score by 73% and reduced GM subpopulation by 83% compared with the Ch group. These remarkable changes can be attributed to the powerful hypocholesterolemic activity of probucol. Our findings indicate that progression of glomerular sclerosis in the rat remnant kidney model of progressive kidney disease can be significantly modulated with fish oil treatment.

Journal Article↗
PubMed1999

Structure, function and regulation of p63 and p73.

The p53 tumor suppressor gene is one of the most frequently mutated genes in human cancers.1 p53 is a sequence-specific transcription factor and plays a critical role in activating the expression of genes involved in cell cycle arrest or apoptosis under conditions of genotoxic stress.2,3 For over two decades, p53 was thought to be the only gene of its kind in the vertebrate genomes. This strong conviction, which was widely accepted in the p53 field, has now been proven to be incorrect. Two genes, referred to as p63 and p73, have been found to encode proteins that share a significant amino-acid identity in the transactivation domain, the DNA binding domain, and the oligomerization domain with p53. In the short period since their cloning, a number of investigators have reported on the structure, the function and the regulation of p63 and p73. This review summarizes the current information on the p63 and the p73 genes, with a focus on the differences between the three members in this newly defined p53-gene family.

Alternative Splicing↗
PubMed1999

Cyclin D2 promoter disrupted by t(12;22)(p13;q11.2) during transformation of chronic lymphocytic leukaemia to non-Hodgkin's lymphoma.

In a unique case of chronic lymphocytic leukaemia (CLL) we performed a longitudinal cytogenetic and molecular genetic study of tumour cells from diagnosis through progression and transformation to non-Hodgkin's lymphoma (NHL) and lymphomatous meningitis. CLL cells at diagnosis had trisomy 12 and a t(14;19)(q32;q13.3). At relapse, the leukaemic cells had a subclone carrying a t(12;22)(p13;q11.2) in addition to the initial changes. We cloned reciprocal translocation junctions at the 22q11.2- chromosome and the 12p13+ chromosome and the corresponding germline DNA fragments. Restriction map analysis and nucleotide sequence analysis of the cloned DNA fragment from the 22q11.2- chromosome mapped the translocation break within the immunoglobulin (Ig)-lambda-C complex at the nt3889; nts 3890, 3891 were lost from the translocation site. A probe from the 3'-end of the clone derived from the 22q11.2- chromosome showed single copy hybridization which was different from the Ig-lambda probe. Nucleotide sequence analysis of the exact junction region and the corresponding germline DNA showed that the translocation at 12p13 occurred in the negative regulatory region of the cyclin D2 gene at the nt -1602, and a pentamer consisting of nts -1603 to -1599 was lost at the break site. We sequenced another 227 bp upstream of the known 5'-end of the promoter and did not find any open reading frame. From these results we hypothesize that, in this patient, the t(12;22) disrupted the negative regulator in the promoter of cyclin D2 which in turn might have deregulated cyclin D2.

Base Sequence↗
PubMed1999

Enhanced capacity of a widespread strain of Mycobacterium tuberculosis to grow in human macrophages.

To determine whether the extent of spread of Mycobacterium tuberculosis strains in the community correlated with their capacity to replicate in human macrophages, intracellular growth rates of M. tuberculosis patient isolates were measured. Strain 210 caused disease in 43 patients in central Los Angeles, 3 "small-cluster" strains caused disease in 8-23 patients, and 5 "unique" strains each caused disease in only 1 patient who was positive by sputum acid-fast smear and spent substantial amounts of time at homeless shelters that were tuberculosis transmission sites. Strain 210 isolates grew significantly more rapidly than small-cluster and unique strains in macrophages. All strains elicited production of similar amounts of tumor necrosis factor-alpha, interleukin (IL)-6, IL-10, and IL-12 and were equally susceptible to reactive nitrogen intermediates. It was concluded that the extensive spread of an M. tuberculosis strain correlated with its capacity to replicate rapidly in human macrophages, which may be a marker of virulence.

Cells, Cultured↗
PubMed1999

Cytokine production in children with tuberculous infection and disease.

To determine if the manifestations of initial infection with Mycobacterium tuberculosis reflect changes in the balance of T cell cytokines, we evaluated cytokine production by M. tuberculosis-stimulated peripheral blood mononuclear cells (PBMCs) from 24 children with tuberculosis and 22 children who were healthy tuberculin reactors. PBMCs from patients with tuberculosis had lower production and mRNA expression of interferon gamma (IFN-gamma) than did PBMCs from healthy tuberculin reactors. IFN-gamma production was most severely depressed in patients with moderately advanced and far-advanced pulmonary disease and in malnourished patients. Production of IL-12, IL-4, and IL-10 was similar in tuberculosis patients and healthy tuberculin reactors. These results indicate that, during the initial immune response to M. tuberculosis, development of tuberculosis is associated with diminished IFN-gamma production, which is not due to reduced production of IL-12 or enhanced production of IL-4 or IL-10.

Child↗
PubMed1999

Decoherence and correspondence in conservative chaotic dynamics.

The quantum and classical dynamics of a conservative nonlinear Hamiltonian system in the chaotic regime are compared in the absence and presence of decoherence effects. Results show marked improvement in classical-quantum correspondence with the introduction of decoherence, even though the initial quantum dynamics is far from the semiclassical limit.

Journal Article↗
PubMed1999

[Genetic polymorphisms of serum orosomucoid in Han population in Nanjing of China].

OBJECTIVE: To determine the genetic polymorphisms of serum orosomucoid (ORM) in Han population in Nanjing of China and provide genetic data for studying the individual variance in the plasma protein binding of weak alkaline drugs. METHODS: The desialylated sera from 220 unrelated subjects were analyzed by isoelectric focusing on polyacrylamide gels followed by immunoblotting. RESULTS: The band patterns of ORM showed that the polymorphism of the structural locus ORM1 was controlled by three codominant autosomal alleles, ORM1*F1, ORM1*F2 and ORM1*S, which presented five phenotypes, ORM1 F1(47.27%), ORM1 S(5.46%), ORM1 F1F2 (3.18%), ORM1 F1S(43.64%), and ORM1 F2S(0.45%). The allele frequencies were: ORM1*F1=0.7068, ORM1*F2=0.0182, ORM1*S=0.2750. CONCLUSION: The ORM1 locus is polymorphic and the ORM2 locus is monomorphic in sera from the Han people in Nanjing of China.

Alleles↗
PubMed1999

Selective in vivo mobilization with granulocyte macrophage colony-stimulating factor (GM-CSF)/granulocyte-CSF as compared to G-CSF alone of dendritic cell progenitors from peripheral blood progenitor cells in patients with advanced breast cancer undergoing autologous transplantation.

Dendritic cells (DCs) are potent antigen-presenting cells that are essential for the initiation of T cell-mediated immunity. DCs develop from myeloid progenitor populations under the influence of granulocyte macrophage colony-stimulating factor (GM-CSF) and pass through an intermediate stage of maturation that is characterized by CD14 expression. Interest has focused on generating human-derived DCs for antigen-specific tumor vaccines to be used as adjuvant immunotherapy in minimal disease settings, such as after autologous transplantation. In the present study, mobilized peripheral blood progenitor cells (PBPCs) were obtained from 18 patients with locally advanced or metastatic breast cancer preparing to undergo autologous stem cell transplantation. PBPCs mobilized in 10 patients with GM-CSF for 1 week, followed by the combination of GM-CSF and G-CSF, were compared with those obtained from patients receiving G-CSF alone with respect to the presence of DC progenitors and the capacity to generate functionally active mature DCs. PBPCs mobilized with GM-CSF/G-CSF were markedly enriched for CD14+ DC progenitor cells as compared with those mobilized with G-CSF alone. Consistent with an immature progenitor population, the CD14+ cells express Ki-67 antigen but not nonspecific esterase. CD14+ cells purified by fluorescence-activated cell sorting from PBPCs mobilized with either regimen and cultured for 1 week in GM-CSF and interleukin-4 generated nearly pure populations of cells with characteristic DC phenotype and function. The addition of GM-CSF to the mobilization regimen resulted in greater yields of functionally active DCs for potential use in posttransplant immunotherapy.

Breast Neoplasms↗
PubMed1999

[Morphological cure of cerebral arteriovenous malformations by endovascular therapeutics].

OBJECTIVE: To sum up the clinical characteristics and typical manifestation by analysing clinical materials from total embolized cerebral arteriovenous malformations (AVM) via endovascular embolization. METHODS: We reviewed clinical and image materials of 50 patients whose cerebral AVM were embolized entirely and found the cerebral AVM morphological cure by endovascular embolization after studying the size, position, artery supply, therapeutics and follow-up. RESULTS: 50 patients with cerebral AVM were embolized by endovascular therapy, accounting for 17% of all patients. Malformation lesions were medium or small type, with a diameter less than 3 cm, 95% of them were located in the tentorium superior. Terminal end blood supply was common to AVM and especially medium cerebral artery (MCA) or its branches. 97% of the patients were graded III or below by spectzler grading system. 70% of them had a history of intracranial hemorrhage and were cured by one therapy. CONCLUSIONS: It is a reliable and feasible method for morphological cure in cerebral AVM via endovascular therapeutics only, but case selection is important, that is, medium or small AVM with single branch terminal end blood supply in the tentorium superior.

Adolescent↗
PubMed1999

[Studies on immunization strategies for hepatitis B in different endemic areas of China].

OBJECTIVE: To compare the cost-benefit of immunization with hepatitis B (HB) vaccine in different endemic areas of HB and to explore the optimal strategy for it. METHODS: Cost-benefit analysis and comprehensive weighted score analysis (CWSA) were used to screen the optimal immunization strategy for low, medium and heavy endemic areas of HB. RESULTS: Significant economic benefit was obtained in Long-An County, Guangxi Zhuang Autonomous Region, Shanghai and Jinan, Shandong Province from HB immunization programs for infants. The greatest benefit cost ratio (BCR) was provided by the low-dose immunization strategy, which was 49.91, 54.53 and 37.68, respectively for heavy, medium and low endemic areas of HB. The maximal net benefit could be obtained by the high-dose immunization strategy with better immune protective efficacy. CWSA showed that the low-dose immunization strategy was the optimal one for HB immunization. CONCLUSION: It is suggested that the low-dose immunization strategy be implemented in undeveloped areas to obtain a greater BCR, and the high-dose one be implemented in more developed areas to obtain more net benefit and lower prevalence of hepatitis B surface antigen carriage.

China↗
PubMed1999

[Use of diagnostic ultrasound of sinus in the paranasal sinus disease].

OBJECTIVE: To utilize the diagnostic A ultrasound of sinuses in the diagnosis of paranasal sinus disease. METHOD: Through history enquirement, careful clinical otorhinolaryngological examination, X-ray examination of paranasal sinus, CT, maxillary sinus puncture and examination of the diagnostic ultrasound of sinus, we observed 115 patients with paranasal sinus disease and compared them with 22 normal people who were in control group. RESULTS: In normal people, the according rate between ultrasound examination and clinicaly diagnostic methods, include history enquirement, otorhinolaryngological examination, X-ray examination, CT and maxillary puncture, is 100%. And in the group of patients with paranasal disease, the according rate is 62.5%-92%. CONCLUSION: The diagnostic A ultrasound of sinus has high accuracy, the control is easy, the cost is relatively lower, it can be used repeatedly and do no harm to the patient's health. It is a good method and assistant technigue in the diagnosis of frontal and maxillary sinus disease.

Adolescent↗
PubMed1998

Endomorphins fully activate a cloned human mu opioid receptor.

Endomorphins were recently identified as endogenous ligands with high selectivity for mu opioid receptors. We have characterized the ability of endomorphins to bind to and functionally activate the cloned human mu opioid receptor. Both endomorphin-1 and endomorphin-2 exhibited binding selectivity for the mu opioid receptor over the delta and kappa opioid receptors. Both agonists inhibited forskolin-stimulated increase of cAMP in a dose-dependent fashion. When the mu opioid receptor was coexpressed in Xenopus oocytes with G protein-activated K+ channels, application of either endomorphin activated an inward K+ current. This activation was dose-dependent and blocked by naloxone. Both endomorphins acted as full agonists with efficacy similar to that of [D-Ala2,N-Me-Phe4,Gly-ol5]enkephalin (DAMGO). These data indicate that endomorphins act as full agonists at the human mu opioid receptor, capable of stimulating the receptor to inhibit the cAMP/adenylyl cyclase pathway and activate G-protein-activated inwardly rectifying potassium (GIRK) channels.

Analgesics, Opioid↗
PubMed1998

Single-nucleotide polymorphism in the human mu opioid receptor gene alters beta-endorphin binding and activity: possible implications for opiate addiction.

Opioid drugs play important roles in the clinical management of pain, as well as in the development and treatment of drug abuse. The mu opioid receptor is the primary site of action for the most commonly used opioids, including morphine, heroin, fentanyl, and methadone. By sequencing DNA from 113 former heroin addicts in methadone maintenance and 39 individuals with no history of drug or alcohol abuse or dependence, we have identified five different single-nucleotide polymorphisms (SNPs) in the coding region of the mu opioid receptor gene. The most prevalent SNP is a nucleotide substitution at position 118 (A118G), predicting an amino acid change at a putative N-glycosylation site. This SNP displays an allelic frequency of approximately 10% in our study population. Significant differences in allele distribution were observed among ethnic groups studied. The variant receptor resulting from the A118G SNP did not show altered binding affinities for most opioid peptides and alkaloids tested. However, the A118G variant receptor binds beta-endorphin, an endogenous opioid that activates the mu opioid receptor, approximately three times more tightly than the most common allelic form of the receptor. Furthermore, beta-endorphin is approximately three times more potent at the A118G variant receptor than at the most common allelic form in agonist-induced activation of G protein-coupled potassium channels. These results show that SNPs in the mu opioid receptor gene can alter binding and signal transduction in the resulting receptor and may have implications for normal physiology, therapeutics, and vulnerability to develop or protection from diverse diseases including the addictive diseases.

Base Sequence↗
PubMed1998

Reversal of tolerance to human MUC1 antigen in MUC1 transgenic mice immunized with fusions of dendritic and carcinoma cells.

Immunological unresponsiveness established by the elimination or anergy of self-reactive lymphocyte clones is of importance to immunization against tumor-associated antigens. In this study, we have investigated induction of immunity against the human MUC1 carcinoma-associated antigen in MUC1 transgenic mice unresponsive to MUC1 antigen. Immunization of adult MUC1 transgenic mice with irradiated MUC1-positive tumor cells was unsuccessful in reversing unresponsiveness to MUC1. By contrast, fusions of dendritic cells with MUC1-positive tumor cells induced cellular and humoral immunity against MUC1. Immunization with the dendritic cell fusions that express MUC1 resulted in the rejection of established metastases and no apparent autoimmunity against normal tissues. These findings demonstrate that unresponsiveness to the MUC1 tumor-associated antigen is reversible by immunization with heterokaryons of dendritic cells and MUC1-positive carcinoma cells.

Adult↗
PubMed1998

Aspartate-279 in aminolevulinate synthase affects enzyme catalysis through enhancing the function of the pyridoxal 5'-phosphate cofactor.

5-Aminolevulinate synthase (ALAS) catalyzes the first step in the heme biosynthetic pathway in nonplant eukaryotes and some prokaryotes, which is the condensation of glycine with succinyl-coenzyme A to yield coenzyme A, carbon dioxide, and 5-aminolevulinate. ALAS requires pyridoxal 5'-phosphate as an essential cofactor and functions as a homodimer. D279 in murine erythroid enzyme was found to be conserved in all aminolevulinate synthases and appeared to be homologous to D222 in aspartate aminotransferase, where the side chain of the residue stabilizes the protonated form of the cofactor ring nitrogen, thus enhancing the electron sink function of the cofactor during enzyme catalysis. D279A mutation in ALAS resulted in no detectable enzymatic activity under standard assay conditions, and the conservative D279E mutation reduced the catalytic efficiency for succinyl-CoA 30-fold. The D279A mutation resulted in a 19-fold increase in the dissociation constant for binding of the pyridoxal 5'-phosphate cofactor. UV-visible and CD spectroscopic analyses indicated that the D279A mutant binds the cofactor in a different mode at the active site. In contrast to the wild-type and D279E mutant, the D279A mutant failed to catalyze the formation of a quinonoid intermediate upon binding of 5-aminolevulinate. Importantly, this partial reaction could be rescued in D279A by reconstitution of the mutant with the cofactor analogue N-methyl-PLP. The steady-state kinetic isotope effect when deuteroglycine was substituted for glycine was small for the wild-type enzyme (kH/kD = 1.2 +/- 0.1), but a strong isotope effect was observed with the D279E mutant (kH/kD = 7.7 +/- 0.3). pH titration of the external aldimine formed with ALA indicated the D279E mutation increased the apparent pKa for quinonoid formation from 8.10 to 8.25. The results are consistent with the proposal that D279 plays a crucial role in aminolevulinate synthase catalysis by enhancing the electron sink function of the cofactor.

5-Aminolevulinate Synthetase↗