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Biomedical subjects

G Gong

Publications and source records attributed to G Gong.

At least 19 recordsLinked to original sources

A study of the viral etiology of histiocytic necrotizing lymphadenitis (Kikuchi-Fujimoto disease).

Histiocytic necrotizing lymphadenitis (HNL) or Kikuchi's disease is a distinctive, self-limited disorder characterized by necrotizing cervical lymphadenopathy in young individuals. HNL is more prevalent among Asians and is a relatively common disorder among Koreans. A preceding fever, lymphopenia, and occasional skin rashes suggest a viral etiology and there have been sporadic reports of viral association. However, so far, no infectious agent has been proven to be etiologically related. In the present study, the authors examined HNL tissue samples for the presence of the genome of herpesviridae. A polymerase chain reaction was performed on 12 freshly frozen lymph nodes with HNL with a single pair of consensus primers selected within a highly conserved region of the DNA polymerase gene of the Epstein-Barr virus (EBV), designed to detect herpes simplex type 1 (HSV1), herpes simplex virus type 2 (HSV2), and cytomegalovirus (CMV) in addition to EBV. The amplified products of known sizes were then analyzed by a single restriction enzyme treatment for confirmation. No viral DNA was amplified in any of the 12 cases of histiocytic necrotizing lymphadenitis. The authors conclude that there is no evidence that HSV1, HSV2, CMV, or EBV plays any role in the pathogenesis of histiocytic necrotizing lymphadenitis.

Adolescent

Usual interstitial pneumonia: relationship between disease activity and the progression of honeycombing at thin-section computed tomography.

The authors estimate the relationship between the progression of honeycombing and disease activity of usual interstitial pneumonia (UIP) by open lung biopsy specimen and ground-glass opacity on thin-section computed tomography (CT). Open lung biopsy specimens and the initial and follow-up thin-section CT of 29 patients with proven UIP are reviewed. Follow-up thin-section CTs were performed from 2 to 61 months (mean, 15.3 months) after biopsy. The interval between the initial CT and open lung biopsy was from 2 to 30 days (mean, 10.0 days). Areas of ground-glass opacity and honeycombing were quantified respectively on each CT slice by using a 0%-100% scale with 10% increments. Each open lung biopsy specimen was scored semiquantitatively for alveolar desquamation, alveolar septal inflammation, inflammatory airway narrowing, obstructive pneumonitis, and lymphoid nodules. Patients were classified into either a mild or severe activity group according to the median value of the pathologic score and the median value of the area of ground-glass opacity. The authors compared the progression of honeycombing on follow-up thin-section CT between the groups. The progression of honeycombing in UIP was significantly faster in the severe activity group than in the mild group according to the pathologic score (p = 0.003) and the area of ground-glass opacity (p = 0.0024). In patients with UIP, more active inflammation of the pulmonary interstitium results in faster progression of honeycombing in long-term follow-up.

Adult

Bone dimensional change with age: interactions of genetic, hormonal, and body size variables.

Changes in bony dimensions with age were assessed longitudinally from standardized X-ray films in 170 middle-aged Caucasian women, starting at age 40 years and with a median duration of observation of 21.125 years. Consistent with earlier work, cortical area of the metacarpals and radial shaft declined with age at rates ranging from 0.57 to 0.86%/year. As predicted, estrogen replacement therapy decreased this loss in a dose-dependent manner. Not previously reported is the fact that weight gain over the period of observation reduced upper extremity bone loss. Moreover, this protection was independent of the estrogen effect. In contrast with bone loss in the upper extremity, both femur shaft diameter and femur shaft cortical area increased significantly with age (0.23 and 0.26%/year, respectively). Estrogen replacement therapy inhibited femur shaft expansion but had no effect on femur cortical area. Weight change, however, strongly influenced gain (or loss) of femur cortical area: those in the highest weight change tertile gained 4 times as much cortical area as those in the lowest weight change tertile. VDR genotype also significantly influenced femoral shaft changes: women with the bb genotype had both greater shaft expansion and a greater increase in cortical area. The VDR effects were independent of the effects of weight change and estrogen. Femoral shaft expansion was of sufficient magnitude to suggest that the mechanical properties of the entire femur may change appreciably with age. Finally, contrary to widespread belief, there was significant, if modest, expansion at the femoral neck with age.

Adult

The value of pancreatoscopy in patients with mucinous ductal ectasia.

We report here on three cases of mucinous ductal ectasia in which the diagnosis was suggested by abdominal computed tomography and finally established by duodenoscopy with pancreatoscopy. Duodenoscopic examination of the ampulla of Vater demonstrated a patulous papillary orifice and extrusion of viscid mucus. Pancreatoscopic examination was carried out in all three patients, and characteristic findings such as papillary or villous mucosal projections coated with whitish gelatinous mucus were noted. In patients with mucinous ductal ectasia in whom the radiographic findings are equivocal, pancreatoscopic examination may provide valuable information for the differential diagnosis of amorphous filling defects in the main pancreatic duct, and may provide information that helps to determine the extent of the pathology and the resection margin.

Adenocarcinoma, Mucinous

Linkage of a gene causing high bone mass to human chromosome 11 (11q12-13)

The purpose of this paper is to report the linkage of a genetic locus (designated "HBM") in the human genome to a phenotype of very high spinal bone density, using a single extended pedigree. We measured spinal bone-mineral density, spinal Z(BMD), and collected blood from 22 members of this kindred. DNA was genotyped on an Applied Biosystems model 377 (ABI PRISM Linkage Mapping Sets; Perkin Elmer Applied Biosystems), by use of fluorescence-based marker sets that included 345 markers. Both two-point and multipoint linkage analyses were performed, by use of affected/unaffected and quantitative-trait models. Spinal Z(BMD) for affected individuals (N = 12) of the kindred was 5.54 +/- 1.40; and for unaffected individuals (N = 16) it was 0.41 +/- 0.81. The trait was present in affected individuals 18-86 years of age, suggesting that HBM influences peak bone mass. The only region of linkage was to a series of markers on chromosome 11 (11q12-13). The highest LOD score (5.21) obtained in two-point analysis, when a quantitative-trait model was used, was at D11S987. Multipoint analysis using a quantitative-trait model confirmed the linkage, with a LOD score of 5.74 near marker D11S987. HBM demonstrates the utility of spinal Z(BMD) as a quantitative bone phenotype that can be used for linkage analysis. Osteoporosis pseudoglioma syndrome also has been mapped to this region of chromosome 11. Identification of the causal gene for both traits will be required for determination of whether a single gene with different alleles that determine a wide range of peak bone densities exists in this region.

Absorptiometry, Photon

cGMP level that reduces cardiac myocyte O2 consumption is altered in renal hypertension.

We tested the hypothesis that cardiac myocytes from hypertensive (one kidney, one clip; 1K,1C) cardiac-hypertrophied rabbits require higher guanosine 3',5'-cyclic monophosphate (cGMP) to similarly lower O2 consumption than control myocytes and that this effect is caused by differences in guanylate cyclase activity. Using isolated myocytes from control and 1K,1C New Zealand White rabbits, we obtained O2 consumption (nl O2 x min(-1) x 10(5) cells) and cGMP (fmol/10(5) cells) levels after stimulation of guanylate cyclase with nitroprusside, CO, or guanylin (10(-8)-10(-5) M). Soluble guanylate cyclase activity was also determined. Basal cGMP was elevated in 1K,1C vs. control (176 +/- 28 vs. 85 +/- 13) myocytes. cGMP increased in 1K,1C and control myocytes after stimulation with nitroprusside, CO, and guanylin. Guanylate cyclase activity in 1K,1C vs. control myocytes was not statistically different. Basal O2 consumption in 1K,1C vs. control myocytes was comparable (307 +/- 1 vs. 299 +/- 22). O2 consumption was similarly decreased when guanylate cyclase was stimulated. Control regression equations correlating cGMP and O2 consumption were O2 consumption = -1.46 x [cGMP] + 444.65 (r = 0.96) for CO, O2 consumption = -0.58 x [cGMP] + 328.48 (r = 0.82) for nitroprusside, and O2 consumption = -1.25 x [cGMP] + 389.15 (r = 0.88) for guanylin. The 1K,1C regression equations were O2 consumption = -1.36 x [cGMP] + 537.81 (r = 0.97) for CO, O2 consumption = -0.23 x [cGMP] + 307.30 (r = 0.88) for nitroprusside, and O2 consumption = -1.27 x [cGMP] + 502.91 (r = 0.89) for guanylin. These data indicate that 1K,1C hypertrophic myocytes had higher cGMP than controls at every level of O2 consumption. This effect was not caused by differences in basal or maximal guanylate cyclase activity.

Animals

Gastrointestinal involvement in Henoch-Schönlein syndrome: CT findings.

OBJECTIVE: The purpose of this study was to describe the CT features of gastrointestinal involvement in seven patients with Henoch-Schönlein syndrome. CONCLUSION: Although the incidence of Henoch-Schönlein syndrome is low, it should be considered when CT scans show multifocal areas of bowel-wall thickening, mesenteric edema, vascular engorgement, and nonspecific lymphadenopathy. It should be considered especially in young patients with acute gastrointestinal symptoms.

Adolescent

Prevalence and contribution of BRCA1 mutations in breast cancer and ovarian cancer: results from three U.S. population-based case-control studies of ovarian cancer.

We investigate the familial risks of cancers of the breast and ovary, using data pooled from three population-based case-control studies of ovarian cancer that were conducted in the United States. We base estimates of the frequency of mutations of BRCA1 (and possibly other genes) on the reported occurrence of breast cancer and ovarian cancer in the mothers and sisters of 922 women with incident ovarian cancer (cases) and in 922 women with no history of ovarian cancer (controls). Segregation analysis and goodness-of-fit testing of genetic models suggest that rare mutations (frequency .0014; 95% confidence interval .0002-.011) account for all the observed aggregation of breast cancer and ovarian cancer in these families. The estimated risk of breast cancer by age 80 years is 73.5% in mutation carriers and 6.8% in noncarriers. The corresponding estimates for ovarian cancer are 27.8% in carriers and 1.8% in noncarriers. For cancer risk in carriers, these estimates are lower than those obtained from families selected for high cancer prevalence. The estimated proportion of all U.S. cancer diagnoses, by age 80 years, that are due to germ-line BRCA1 mutations is 3.0% for breast cancer and 4.4% for ovarian cancer. Aggregation of breast cancer and ovarian cancer was less evident in the families of 169 cases with borderline ovarian cancers than in the families of cases with invasive cancers. Familial aggregation did not differ by the ethnicity of the probands, although the number of non-White and Hispanic cases (N = 99) was sparse.

Adult

Familial juvenile polyposis coli with APC gene mutation.

Familial juvenile polyposis has been known to have malignant potential, but their genetic relation to familial adenomatous polyposis has not been proven yet. Two young brothers with intermittent rectal bleeding revealed multiple juvenile polyposis. Their father had a history of rectal cancer with multiple colonic polyps. Four frequent exons of APC gene mutation were tested from these patients' white blood cells by polyacrylamide gel electrophoresis and sequencing. The 21-yr-old brother had a missense mutation (GAA-->GGA) at codon 1309, whereas the 18-yr-old brother showed a missense mutation (ATA-->GTA) at codon 1304 in exon 15 of APC gene. Three of four first-degree relatives were affected with familial juvenile polyposis, familial juvenile polyposis with adenomatous change, and rectal cancer with multiple polyps. The APC gene mutation of familial juvenile polyposis in this case suggests a genetic relationship with familial adenomatous polyposis.

Adenomatous Polyposis Coli

[Determination of lead in blood by polarography].

A method for determination of trace lead in blood with complex catlysis polarography was develop. The peak potential of lead is -0.54 V in the system of hydrochloric acidpotassium iodide-vanadium (IV)-ethanol-ascorbic acid. There is good linelar relationship between peak current and lead concentration in the range of 0-1.0 microgram/3 ml. The recoveries of spiked samples ranged from 76.0% to 105.0% and the average recovery was 91.0% with RSD of 3.6% to 7.0%. The detection limit was 45 micrograms/L. The blood samples of 24 normal people and 6 workers with occupational exposure to lead were measured and the results were concordant with the clinical diagnoses. The proposed method is simple, rapid, sensitive and reliable. It is suitable for determination of trace lead in blood.

Humans

Vitamin D receptor gene polymorphism, bone mass, body size, and vitamin D receptor density.

We determined vitamin D receptor (VDR) gene alleles (based on the BsmI restriction site polymorphism), duodenal mucosal receptor density, bone mass at spine and total body, and body size in 32 healthy premenopausal females. While we found no relationship between allele and receptor density in duodenal mucosa, bone mineral content (BMC) at both spine and total body was significantly associated with VDR gene alleles. BMC was highest for the bb allele, lowest for BB, and intermediate for Bb. A similar association was noted between allele and body size variables, particularly weight. When BMC was adjusted for body weight, the association with VDR polymorphism disappeared. The VDR gene polymorphism may be affecting bone mass not through classical nutritional mechanisms (e.g., intestinal calcium absorption), but through an influence on body size.

Adult

Significance of magnetic resonance signal enhancement in evaluation of myocardial infarction in cats.

RATIONALE AND OBJECTIVES: To correlate magnetic resonance (MR) signal enhancement with pathophysiologic changes occurring during ischemia and reperfusion in evaluation of myocardial infarction in cats. METHODS: Seven cats were subjected to 150 minutes of occlusion of the left anterior descending coronary artery followed by 90 minutes of reperfusion. Gadolinium (Gd) diethylenetriaminepentaacetic acid-polylysine (molecular weight [mw] = 40 to 50 kd, DP230) contrast-enhanced MR images were acquired with coinjection of poly-L-lysine-fluorescein isothiocyanate (mW = 40 to 50 kd, DP219) as a fluorescent tracer molecule of the contrast agent. Signal intensities on the MR images and fluorescence activities on the resected cardiac specimens were measured. Pathologic examinations by electron and light microscopes and 2,3,5-triphenyltetrazolium chloride histochemical staining were performed on the specimens. RESULTS: Magnetic resonance signal intensity was lower in the center (3.49 +/- 0.36) than in the periphery (4.71 +/- 0.89) of the enhanced area. Fluorescence activities were absent in the normal myocardium; they were scant as nonspecific discrete dots in the center and numerous as specific interstitial distribution in the periphery of the ischemic myocardium. Electron and light microscopic examinations showed severely damaged ultrastructures of the center and moderately distorted ultrastructures of the periphery. CONCLUSIONS: The center of the MR signal-enhanced area is the infarct center with severe ultrastructural damages, which also might be an area of little or absent of blood reflow. Conversely, the peripheral-enhanced area is the infarct periphery with moderate myocardial damages.

Animals

Testosterone regulation of renal alpha 2B-adrenergic receptor mRNA levels.

Androgens regulate blood pressure and renal alpha 2-adrenergic receptors in a parallel fashion in the spontaneously hypertensive rat (SHR). The present studies investigated whether this regulation of renal alpha 2B-adrenergic receptors occurs at the mRNA level. Male and female SHR were gonadectomized at 4 weeks of age. The gonadectomized rats were implanted with or without testosterone propionate. Sham-gonadectomized rats served as controls. Total kidney RNA was purified, and alpha 2B-adrenergic receptor mRNA was quantified with a reverse transcriptase-polymerase chain reaction (RT-PCR) assay. The assay uses a mimic RNA added at known concentrations to the sample RNA. The mimic was constructed from the target sequence in the alpha 2B-adrenergic receptor mRNA plus a 20-bp insertion of a random nucleotide sequence. The amount of alpha 2B-adrenergic receptor mRNA present in each sample was obtained by determining the equivalence point between the amount of RT-PCR product formed in the target band versus the mimic band, which were resolved by gel electrophoresis. Intact males had more than two times as much alpha 2B-adrenergic receptor mRNA as intact females. Castration of males reduced the male-female difference by more than 60%. Ovariectomy slightly increased the alpha 2B-adrenergic receptor mRNA level compared with that of intact females. Treatment with testosterone elevated alpha 2B-adrenergic receptor mRNA levels of gonadectomized males and females to the level of intact males. The alpha 2B-adrenergic receptor mRNA levels correlated remarkably well with renal alpha 2-adrenergic receptor density. We conclude that testosterone regulates renal alpha 2B-adrenergic receptor gene expression at the mRNA level in the SHR.

Animals

Sex influence on renal alpha 2-adrenergic receptor density in the spontaneously hypertensive rat.

Male spontaneously hypertensive rats (SHR) have higher blood pressure than females. We compared renal alpha 2-adrenergic receptor density among intact SHR and Wistar-Kyoto (WKY) rats of both sexes, male and female SHR gonadectomized at 4 weeks of age, and gonadectomized SHR supplemented with testosterone. Additional groups of SHR were treated with enalapril (30 mg/kg per day), an angiotensin-converting enzyme inhibitor, from 5 to 14 weeks of age. Renal alpha 2-adrenergic receptor density was higher in males than females in both SHR and WKY rats. Female SHR and WKY rats had identical low renal alpha 2-adrenergic receptor density. Castration of male SHR reduced the male-female differences in blood pressure and renal alpha 2-adrenergic receptor density by 60%. Treatment with testosterone raised blood pressure and renal alpha 2-adrenergic receptor density to the intact male levels in both gonadectomized males and females. Treatment with enalapril decreased blood pressure but not renal alpha 2-adrenergic receptor density in both male and female SHR. We conclude that (1) both renal alpha 2-adrenergic receptor density and blood pressure are influenced by sex in SHR and WKY, (2) renal alpha 2-adrenergic receptor density like blood pressure is regulated by androgens, and (3) increased renal alpha 2-adrenergic receptor density is not a consequence of high blood pressure in male SHR.

Animals

Extrafollicular reticulum cells in pathologic lymph nodes.

Extrafollicular reticulum cells in lymph nodes are heterogeneous. They express cytokeratins, desmin, and/or vimentin as their intermediate filament profile. Using those markers, we undertook an immunohistochemical study of human lymph nodes under various pathologic conditions. Samples included 15 simple reactive lymph nodes, 7 follicular hyperplasia, 1 necrotizing lymphadenitis, 4 tuberculous lymphadenitis, 13 malignant lymphoma (9 non-Hodgkin's and 4 Hodgkin's lymphomas), and 11 metastatic adenocarcinoma. In lymph nodes with follicular hyperplasia, cytokeratin and/or desmin expressing reticulum cells displayed a characteristic dendritic meshwork in the subcapsular, perisinusoidal, and paracortical regions. In other forms reactive lymph nodes, they were similarly distributed but were less prominent. By SDS-PAGE and immunoblotting, cytokeratin polypeptides were identified. In necrotizing lymphadenitis, they were increased and the pattern of distribution was disturbed. In tuberculous lymphadenitis, they were also increased and located at nongranulomatous as well as in perigranulomatous areas. In lymphomas the reticular meshwork was entirely obliterated. Cytokeratin or desmin expressing reticulum cells were rarely seen within tumors. The reticular meshwork was also obliterated in metastatic carcinoma. However, the meshwork was maintained in uninvolved areas. In conclusion, extrafollicular reticulum cells displayed characteristic patterns of distribution under various pathologic conditions, and may be implicated in the pathogenesis of those pathologic conditions in human lymph nodes.

Antibodies, Monoclonal

Endodermal sinus tumor: immunophenotypic expression of a carcinoma.

A series of five endodermal sinus tumors was studied for their cytoskeletal and other phenotypic markers. They included 2 ovarian, 2 testicular, and 1 inguinal tumors. The cytoskeletal expression was also studied by gel electrophoresis and immunoblotting. Every tumor was diffusely and strongly immunostained for cytokeratin. By SDS-PAGE and immunoblotting, cytokeratins 8 & 18 were detected. Vimentin was focally coexpressed in 4 cases. The stroma was diffusely immunostained for vimentin. None of them expressed desmin, neurofilament, or glial filament protein. Desmoplakin was expressed only in one ovarian tumor. Alpha-fetoprotein and S-100 protein were also diffusely positive among the neoplastic cells; intracytoplasmic globules were especially strongly immunostained. These findings suggest that endodermal sinus tumors represent a group of pure malignant epithelial neoplasms, and may be regarded as primitive carcinomas.

Adult