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S B Kim

Publications and source records attributed to S B Kim.

At least 91 records · Page 5Linked to original sources

Chemokines, osteopontin, ICAM-1 gene expression in cultured rat mesangial cells.

To investigate whether MCP-1, CINC, RANTES, osteopontin and ICAM-1 mRNA could be induced in cultured rat mesangial cells by interleukin-1beta(IL-1beta), tumor necrosis factor-alpha (TNF-alpha) and lipopolysaccharide (LPS), and whether MCP-1 and CINC gene expression could be modulated by dexamethasone, Northern blot assays were performed. IL-1beta induced MCP-1, CINC, RANTES and ICAM-1 gene expression in a time dependent manner. IL-1beta-induced MCP-1, CINC and ICAM-1 mRNA amount were maximal at 3 hours exposure around 14.5, 15.7, 2.2 folds increase and IL-1beta-induced RANTES mRNA at 24 hours around 2.0 folds. TNF-alpha and LPS also induced MCP-1 and ICAM-1 gene expression. TNF-alpha also induced RANTES gene expression but LPS did not. On the other hand, IL-1beta, TNF-alpha and LPS had little effect on osteopontin gene expression but fetal calf serum could increase osteopontin mRNA. Dexamethasone suppressed the IL-1beta-induced MCP-1 and CINC mRNA. These results suggest that, through these gene expressions, mesangial cells are able to communicate directly or indirectly with macrophages or neutrophils, which may lead to glomerulosclerosis.

Animals↗

Severe aplastic anemia induced by ticlopidine: report of two cases.

Aplastic anemia is a rare side-effect associated with ticlopidine therapy. We report two cases of severe aplastic anemia developed after the use of ticlopidine. A 51-year-old woman took ticlopidine at 500 mg/day for 49 days to prevent a secondary stroke. She developed fever and dizziness within 49 days of initiating ticlopidine therapy. A 70-year-old woman was started on ticlopidine after coronary stent insertion. Fifty days after starting ticlopidine, she developed fever and dizziness. Both patients showed pancytopenia and were diagnosed as aplastic anemia which were confirmed by bone marrow examination. Both patients were hospitalized and received antibiotics, blood products and hematopoietic growth factors. Four and seven weeks after the withdrawal of ticlopidine, the hematologic parameters of each patient improved. A complete blood count should be monitored during ticlopidine therapy to check for cytopenia.

Aged↗

Low prevalence of activated protein C resistance and coagulation factor V Arg506 to Gln mutation among Korean patients with deep vein thrombosis.

Activated protein C (APC) is a naturally occurring anticoagulant that interacts with factor V and VIII to inhibit the clotting cascade. The prevalence of APC resistance among Korean patients with deep vein thrombosis is ill defined. The aim of the present study was to investigate the prevalence of APC resistance and factor V Leiden mutation in Korean patients with deep vein thrombosis. The presence of factor V Leiden mutation was determined in 49 patients who visited Asan Medical Center. APC ratio was performed in 33 individuals from the above 49 patients. Three patients were excluded from the analysis because their baseline aPTT was prolonged. Resistance to APC was diagnosed when the APC ratio was below 2.55. APC resistance was documented in 8 individuals, representing 27% (8/30) of the patients on whom APC resistance test was performed. The 2 patients, who showed APC resistance, were positive for lupus anticoagulant. None of the 49 patients demonstrated factor V Leiden mutation. These findings indicate that factor V Leiden mutation is rare and APC resistance is less prevalent in Korean patients with deep vein thrombosis than in Caucasians. APC resistance not caused by factor V Leiden mutation may be a risk factor for deep vein thrombosis in this population.

Activated Protein C Resistance↗

Effect of increasing serum albumin on serum lipoprotein(a) concentration in patients receiving CAPD.

Lipoprotein(a) [Lp(a)], an independent risk factor for atherosclerotic cardiovascular disease in the general population, is known to be elevated in patients with renal disease accompanied by hypoalbuminemia such as nephrotic syndrome and end-stage renal disease. In this study, the role of hypoalbuminemia in the elevation of serum Lp(a) was investigated in 20 continuous ambulatory peritoneal dialysis (CAPD) patients with serum albumin below 3.5 g/dL. The patients were divided into two groups. In group 1 (n = 10), fasting serum Lp(a) and albumin were measured before, after repeated infusion of 20% albumin 100 mL three times per week for 2 weeks, and 4 weeks after withdrawal of albumin infusion. In group 2 (n = 10), serum albumin and Lp(a) were measured similarly without albumin infusion. C-reactive protein was monitored in both group as an indicator of acute-phase reactant. Serum Lp(a) was also measured in 20 age- and sex-matched normal controls. Apolipoprotein(a) [apo(a)] phenotype was determined in all the subjects. CAPD patients as a whole (n = 20; median, 70.2 mg/dL; interquartile range, 45.0 to 86.2 mg/dL) had higher serum Lp(a) than normal controls (n = 20; median, 9.9 mg/dL; interquartile range, 2.4 to 24.3 mg/dL) (P < 0.0001), although the distribution of apo(a) phenotype was similar. Serum albumin in group 1 increased from 2.6+/-0.5 g/dL to 3.5+/-0.6 g/dL (P < 0.0005) at the end of repeated infusion of albumin, whereas serum Lp(a) decreased from 73.7 mg/dL (range, 43.2 to 89.0 mg/dL) to 25.6 mg/dL (range, 10.7 to 71.7 mg/dL) (P < 0.01). Four weeks after withdrawal of albumin infusion, serum albumin decreased again to 2.9+/-0.5 g/dL (P < 0.001), whereas serum Lp(a) increased to 65.2 mg/dL (range, 43.3 to 106.0 mg/dL) (P < 0.05). Serum albumin in group 2 was 2.8+/-0.6 g/dL, 3.0+/-0.4 g/dL, and 2.9+/-0.7 g/dL, respectively. The change of serum Lp(a) was not significant (67.0 mg/dL [range, 46.8 to 84.8 mg/dL], 62.8 mg/dL [range, 45.1 to 81.0 mg/dL], and 63.0 mg/dL [range, 44.7 to 74.0 mg/dL]). C-reactive protein was stable during the study period in both groups. These findings support the hypothesis that hypoalbuminemia is one of the important trigger factors in the elevation of serum Lp(a) in CAPD patients.

Albumins↗

Inter- and intraspecific genetic analysis of the genus Saccharomonospora with 16S to 23S ribosomal DNA (rDNA) and 23S to 5S rDNA internally transcribed spacer sequences.

In order to clarify interspecific relationships and to investigate the intraspecific phylogenetic structure of the genus Saccharomonospora, 16S to 23S ribosomal DNA (16S-23S) and 23S to 5S ribosomal DNA (23S-5S) internally transcribed spacers (ITSs) were used for sequence analyses. The 16S-23S and 23S-5S ITSs from 22 Saccharomonospora strains were amplified by PCR and directly sequenced. The average levels of nucleotide similarity of the 16S-23S and 23S-5S ITSs for the four valid species were 87.6% +/- 3.9% and 83% +/- 2.2%, respectively. For the most part, intraspecific sequence differences were not found in the two ITSs; the only exception was Saccharomonospora glauca K194, which differed from other S. glauca strains by 1 bp in the 23S-5S ITS. The Saccharomonospora viridis strains had a smaller 16S-23S ITS region than the other strains, which may be useful for differentiating these organisms from other Saccharomonospora species. The characteristics of the two ITS regions make them more useful than 16S rRNA sequences as a tool for defining and identifying Saccharomonospora strains. However, Saccharomonospora azurea K161T had two types of 23S-5S ITSs; rrnB, separated by XhoI digestion, had two additional nucleotides inserted between positions 52 and 55. Most of the 16S-23S and 23S-5S ITS sequences of S. azurea K161T and strains of "Saccharomonospora caesia" were identical; the only exception was rrnB in S. azurea K161T. The lengths and levels of sequence divergence of the two ITSs of Saccharomonospora sp. strain K180 were different from the lengths and levels of sequence divergence of the ITSs of other species. These findings suggest that a taxonomic revision of the genus Saccharomonospora is necessary. Two trees based on 16S-23S and 23S-5S ITS sequences revealed distinct interspecific relationships in the genus Saccharomonospora.

Actinomycetales↗

Benign and malignant esophageal strictures: treatment with a polyurethane-covered retrievable expandable metallic stent.

PURPOSE: To evaluate the clinical effectiveness of a polyurethane-covered, retrievable, self-expandable metallic stent and hook catheter in the treatment of esophageal strictures. MATERIALS AND METHODS: Stents were constructed of 0.4-mm stainless steel wire in a cylindric zig-zag configuration of six to nine bends. Four to eight stents were connected in tandem by dipping in a polyurethane solution. A nylon loop was hooked inside to each bend of the proximal portion of the stent and strung with a thread. Under fluoroscopic guidance, 22 stents were placed in 16 patients with a malignant stricture and five patients with a benign stricture. The stent was removed with a hook catheter 2 months after placement in patients with a benign stricture and when complications occurred in patients with a malignant stricture. All patients had dysphagia with ingestion of soft foods or liquids. RESULTS: Stent placement was technically successful and well tolerated in 20 patients. In one patient, the stent was misplaced but relocated successfully. After stent placement, all patients were able to ingest solid and/or soft foods without dysphagia. After stent removal, strictures showed improvement but recurred in two patients. CONCLUSION: Use of polyurethane-covered, retrievable expandable stents seems to be a feasible and effective method of treatment of benign and malignant esophageal strictures.

Adolescent↗

Treatment of hepatitis B virus associated glomerulonephritis with recombinant human alpha interferon.

To evaluate the therapeutic effect of recombinant human alpha-interferon (alpha-IFN) on hepatitis B virus associated glomerulonephritis (HBV-GN) and the relationship between the seroconversion of viral antigens and the change of proteinuria, the hepatitis B viral markers and urinary protein were monitored during alpha-IFN treatment in 8 male adult patients who (1) were positive in serum HBsAg and HBeAg, (2) had chronic hepatitis, (3) had persistent proteinuria > 1 g/day, and (4) showed glomerulonephritis on kidney biopsy. alpha-IFN was given at a dose of 3 million units, subcutaneously, three times a week for 6 months. Kidney biopsy specimens showed membranoproliferative glomerulonephritis (MPGN) in 4 patients, mesangial proliferative glomerulonephritis (MesPGN) in 2, and membranous glomerulonephritis (MGN) in 2 patients. Seven of the 8 patients received a 6-month course of alpha-IFN therapy; 1 patient with MGN quitted therapy 2 months after the initial dose because of side effects. In 5 of the 7 patients who received a 6-month therapy, serum HBeAg disappeared, and anti-HBe appeared during the therapy. In 2 of these 5 patients, HBeAg reappeared, in 1 during alpha-IFN therapy and in 1 9 months after the last dose of alpha-IFN. The hepatitis B viral markers of the patient who received a 2-month therapy did not change. HBs antigenemia persisted in all patients. In all 4 patients with MPGN, serum HBeAg was transiently or persistently converted to negative, but the proteinuria persisted. Both patients with MesPGN showed remission of proteinuria; however, only 1 patient had seroconversion of HBeAg. In 2 patients with MGN, proteinuria persisted. In conclusion, alpha-IFN at the doses given was not effective in MPGN type of HBV-GN. Improvement of proteinuria was achieved in MesPGN patients without disappearance of HBs antigenemia which is the finding against the possible role of HBsAg in the pathogenesis of this type of HBV-GN.

Adult↗

Detection of canine parvovirus in naturally infected dogs with enteritis and myocarditis by in situ hybridization.

An improved method for the diagnosis of canine parvovirus using in situ hybridization in standard formalin-fixed, paraffin-embedded tissue sections was developed. A digoxigenin-labeled probe complementary to DNA sequences that code for the entire sequence of the capsid protein VP-1 and the middle part of the sequence of the capsid protein VP-2 was designed. Specific histologic localization of canine parvovirus-infected cells was demonstrated in small intestine, tonsil, lymph node, thymus, spleen, heart, liver, and kidney from dogs diagnosed at necropsy with canine parvovirus infection. The in situ hybridization accurately pinpointed the specific sites of viral infection. The detection of canine parvovirus in liver, kidney, and heart tissues together in the same pups could represent an enhanced virulence of this strain of canine parvovirus and suggests a broadened tissue tropism not seen before in Korean strains of canine parvovirus.

Animals↗

Skin ulcer and immunoblot patterns by inoculation sites in BALB/c mice infected with Leishmania major.

The skin ulcer in Leishmania major infection is known to be variable according to the inoculation sites even in a susceptible host. The present study traced the immunoblot patterns by the site of inoculation and duration of infection in BALB/c mice. L. major were subcutaneously inoculated on the nose, footpad, and back of the mice, in a dose of 3 x 10(6) promastigotes. Sera of the mice were collected every 10 days after inoculation. SDS-PAGE separated soluble protein bands of the promastigotes and immunoblot was carried out with the infection sera. The skin ulcer first appeared on the nose at 15 days, and on the footpad at 17 days after inoculation. The ulcer on the back appeared after 90 days. In the mice with ulcer on the nose or footpad, serum IgG antibody reacted to 202, 139, 98, 83, 81, 67 65, 62, 59, 54, 52, 42, 26 and 23 kDa bands at 20 days after inoculation. In mice inoculated on the back, however, the immunoblot showed visible reactions with 202, 83, 81, 74, 67, 65, 62, 59, 54, 52, 20 and 17 kDa bands at 90 days after inoculation. The present result showed that the antigenic protein bands of L. major promastigotes were differed by the inoculation site and duration of infection. Since the skin ulcer and the serum antibodies to antigenic bands between 67-52 kDa appeared simultaneously, it is suggested that the serum IgG antibodies may play a role in formation of the skin ulcer in BALB/c mice.

Animals↗

Protein intake and the nutritional status in patients with pre-dialysis chronic renal failure on unrestricted diet.

OBJECTIVES: Malnutrition is known to be highly associated with morbidity and mortality in dialysis patients. Malnutrition may begin to develop in patients with chronic renal failure(CRF) before they need dialysis. In this study, the nutritional status of patients with moderate to severe CRF on unrestricted diet was evaluated. METHODS: We measured dietary protein intake (DPI, g/kg/day) in 64 patients with CRF and 42 normal controls(N). Nutritional indices such as serum albumin(SA, g/dl), transferrin(TF, mg/dl), prealbumin(PA, mg/dl) and insulin-like growth factor-1(IGF-1, ng/ml) were measured to evaluate the visceral proteins, and creatinine-height index(C-H, g/d/m) to evaluate the somatic proteins. RESULTS: Mean DPI was 0.80 +/- 0.27(S.D) in CRF and 1.07 +/- 0.30 in N(p < 0.0001). DPI was lower than 0.6 in 15 CRF patients(23%). Serum albumin, transferrin and C-H were significantly lower in CRF patients than in N(p < 0.01). In patients with CRF, nutritional indices were significantly worse with lower DPI(< 0.6 g/kg/d, n = 15) than higher DPI(> 0.6 g/kg/d, n = 49)(SA 2.9 +/- 0.7 vs. 3.6 +/- 0.8, p < 0.005; TF 147 (134-179) vs. 220(182-264), p < 0.0005; PA 24 +/- 8 vs. 32 +/- 9, p < 0.001; IGF-1 123 (66-261) vs. 226(140-344), p < 0.05; C-H 0.52 +/- 0.15 vs. 0.87 +/- 0.23, p < 0.0001). CRF patients with nephrotic range proteinuria (> 3.5 g/d, n = 19) had lower SA (2.8 +/- 0.6 vs. 3.8 +/- 0.8, p < 0.0001) and PA(27 +/- 9 vs. 32 +/- 9, p < 0.05). CRF patients with diabetes mellitus (n = 20) showed worse nutrition than non-diabetic patients(SA 2.8 +/- 0.6 g/dl vs. 3.8 +/- 0.8 g/dl, p < 0.0001; TF 176 mg/dl(148-214) vs. 220 mg/dl(175-266), p < 0.05; PA 24 +/- 10 mg/dl vs. 33 +/- 8 mg/dl, p < 0.0005; IGF-1 138 ng/ml(69-269) vs 231 ng/ml(140-364), p < 0.05; C-H 0.66 +/- 0.23 vs. 0.85 +/- 0.5, p < 0.005). CONCLUSION: A significant protein malnutrition prevails in patients with pre-dialysis CRF on unrestricted diet, especially with low protein intake. The effort to detect and correct malnutrition should be made in patients with CRF even before initiation of maintenance dialysis.

Adult↗

Effects of hypoxia on the extracellular matrix production of cultured rat mesangial cells.

Glomerular changes in patients with cyanotic congenital heart and chronic lung diseases and in persons living at a high altitude might be related to hypoxemia. This study was carried out to examine the effects of hypoxia on the extracellular matrix production by cultured rat mesangial cells (CRMC). Subconfluent CRMC monolayers were grown with 10% oxygen (hypoxia) and 20% oxygen (control) for 1, 3, and 5 days. The production of type IV collagen (CIV), fibronectin (FN), and laminin (LN) by CRMC was evaluated by flow cytometry and immunofluorescent microscopy. Total RNA was extracted and Northern blotting and hybridization were performed with cDNAs for CIV, FN, and LN. The surface expression of CIV on FC was higher in hypoxia than under control conditions at day 5 (158% of control). The surface expression of FN was also higher in hypoxia at day 3 (303%) and at day 5 (332%). The surface expression of LN was lower at day 1 (71%). Immunofluorescent microscopy showed similar changes with flow cytometry. The mRNA level for CIV and FN was maximal at day 5 with 206 and 305% of control, respectively. Hypoxia had little effect on LN mRNA expression. These results show that hypoxia stimulates the synthesis of extracellular matrix of cultured rat mesangial cells. Hypoxia may contribute to the development of glomerular changes in cyanotic congenital heart diseases, chronic lung diseases, and in persons living at a high altitude.

Animals↗

Lipocortin-1 inhibits proliferation of cultured human mesangial cells.

Lipocortin-1, a 37-kDa member of the annexin family of proteins, originally evoked interest as one of the second messengers for the anti-inflammatory actions of glucocorticoids. Studies showed that glucocorticoids inhibited the proliferation of various cell types and lipocortin-1 mediated growth inhibition of glucocorticoids in a human lung adenocarcinoma cell line. The presence of specific lipocortin-1-binding sites (receptor-like molecules) on monocytic cells has been demonstrated. This study was performed to evaluate the effects of hydrocortisone and recombinant human lipocortin-1 on cultured human mesangial cells (CHMC), and the effects of anti-lipocortin-1 antibody on the hydrocortisone-induced inhibition of CHMC proliferation. The existence of specific binding sites for lipocortin-1 was also investigated. Lipocortin-1 inhibited CHMC proliferation in a dose-dependent manner as determined by [3H]thymidine uptake and cell count. Growth of CHMC was inhibited to 18% of the control in the presence of 5 micrograms/ml of lipocortin-1. Similar growth-inhibitory activity by lipocortin-1 was observed in CHMC activated by platelet-derived growth factor. Hydrocortisone also inhibited cell proliferation in a dose-dependent manner. One to 5,000 dilution of anti-lipocortin-1 antibody reversed hydrocortisone-induced inhibition of CHMC proliferation partially, whereas concentrations over 1:1,000 reversed the inhibition completely. Flow cytometry analysis as well as indirect immunofluorescent microscopy revealed specific binding sites on the surface of CHMC. These results support the hypothesis that corticosteroids act by inducing CHMC to synthesize or secrete lipocortin-1, and that lipocortin-1 generates proliferation-suppressive signal(s) through specific binding sites on CHMC.

Annexin A1↗

Veno-occlusive disease (VOD) of the liver in Korean patients following allogeneic bone marrow transplantation (BMT): efficacy of recombinant human tissue plasminogen activator (rt-PA) treatment.

Veno-occlusive disease (VOD) of the liver is a clinical syndrome characterized by hyperbilirubinemia, painful hepatomegaly, and fluid retention. In the bone marrow transplantation (BMT) setting, VOD is caused by dose-intensive chemotherapy and/or radiotherapy used to prepare patients for transplant. VOD occurs in up to 50% of the patients who undergo BMT and is usually associated with a high mortality rate. Until recently, there was no proven effective medical therapy for this condition once it was clinically apparent. We report here on the frequency and treatment result of VOD with rt-PA in our allogeneic BMT patients. Eight patients (median age 28.5 years) underwent allogeneic BMT from December, 1993 to June, 1995 in Asan Medical Center. Six leukemia patients were prepared for BMT with busulfan and cyclophosphmide, while two aplastic anemia patients received cyclophosphamide and antithymocyte globulin. VOD was defined as having two of the following features before day 20 posttransplant: jaundice (bilirubin > or = 2 mg/dL), tender hepatomegaly and/or right upper quadrant pain, ascites and/or unexplained weight gain (> 2% from baseline). All patients who were diagnosed with VOD received rt-PA (10-20 mg/day) and heparin (10,000 U/day). Three (37.5%) of the eight patients developed VOD that occurred between 6 and 10 days posttransplant. All three patients developed jaundice, weight gain, and tender hepatomegaly. Ascites and renal insufficiency occurred in two patients and pleural effusion in one patient. rt-PA and heparin were begun 6 to 26 days posttransplant and rt-PA was administered for 7 to 14 days. All three patients responded to the therapy; bilirubin levels began to decrease at 4 to 13 days from the start of therapy. They are all alive at day 111, 316, and 548 days posttransplant. None of the patients had significant hemorrhagic complications after rt-PA treatment. Prolonged administration of rt-PA was feasible without bleeding episode and it seems that rt-PA may alter the natural course of VOD.

Adolescent↗

Prognostic factors of acute myelocytic leukemia: an analysis of 132 patients in a single institution.

Patients with acute myelocytic leukemia (AML) have varied outlooks for survival after the diagnosis. To identify pretreatment prognostic indicators in AML, we analyzed 132 cases of AML seen at our hospital between June, 1989 and December, 1994. The median age of the patients was 40 years (range, 15-81). There were 63 male and 69 female patients. One hundred eight patients (82%) received induction chemotherapy which was based on cytarabine plus anthracyclines. Sixty six patients achieved complete remission (CR) and the CR rate among the patients given induction chemotherapy was 61%. The median duration of CR was 11.2 months. After median follow up of 6.6 months (range 0.5-51.4), 26 patients (39%) remain in continuous CR. The median duration of overall survival of the patients was 6.7 months. After median follow up of 10.6 months (range, 0.1-52.7), 41 patients (31%) are alive. Variables affecting duration of CR included the age of the patients, performance status of the patients, percentage of blast in the peripheral blood, hemoglobin level, percentage of blast in the bone marrow, FAB subtype, and CD7 marker positivity. Variables affecting survival duration included age of the patients, performance status of the patients, absolute blast count (ABC) in the peripheral blood, bone marrow cellularity, the percentage of blast in the bone marrow, and CD5 marker positivity. Multivariate analysis showed that the age of the patients and percentage of blast in the bone marrow were significant independent indicators for overall survival of the patients. Further studies utilizing cytogenetics and molecular characteristics of leukemic cell are warranted to better define the prognostic factors of patients with AML.

Adolescent↗

Clinicopathologic significance of the K-ras gene codon 12 point mutation in stomach cancer. An analysis of 140 cases.

BACKGROUND: The frequency and clinicopathologic significance of the K-ras gene point mutation in stomach cancer remain to be defined. METHODS: The authors investigated the frequency of K-ras codon 12 point mutations in stomach cancer using a sensitive polymerase chain reaction (PCR)-based method in 140 samples and correlated the findings with various clinicopathologic characteristics of the patients. RESULTS: The overall frequency of K-ras codon 12 point mutations in stomach cancer was 7.9% (11/140). DNA sequencing of nine cases with K-ras codon 12 point mutations identified seven cases with a single-base substitution of GGT to AGT (glycine to serine) and two with single-base substitution of GGT to AGT (aspartic acid). Tumors located in the upper third of the stomach had a significantly higher frequency of K-ras codon 12 mutations (3/8, 37.5%) compared with tumors located in the middle (4/29, 13.8%) or lower (3/99, 3.0%) thirds of the stomach (P = 0.001). No significant difference was observed in the frequency of K-ras codon 12 mutations in terms of other various clinicopathologic characteristics including tumor DNA ploidy and S-phase fraction. After a median follow-up of 26 months, disease free and overall survival were not significantly different between patients with stomach cancer with or without K-ras codon 12 mutation. Among eight patients with stomach cancer located in the upper part of the stomach, none of the three patients with K-ras gene-mutated tumors died versus four of five with tumors without K-ras gene mutations (P = 0.064). CONCLUSIONS: K-ras codon 12 point mutations are uncommon in stomach cancer (7.9%). There was significant correlation between K-ras mutations and vertical tumor location in the stomach, suggesting that different mechanisms may play a role in the pathogenesis of stomach cancer according to the location of tumors in the stomach.

Adult↗

Chronic maternal hypoxia retards fetal growth and increases glucose utilization of select fetal tissues in the rat.

The development of intrauterine growth retardation (IUGR) is frequently associated with fetal hypoxia, hypoglycemia, and abnormal fetal glucose metabolism. To determine the effects of hypoxia (without concomitant hypoglycemia) on fetal glucose metabolism, we continuously exposed pregnant rats to 10% (10.1 kPa) ambient oxygen from day 15 through day 20 of gestation (term, 21.5 days) and used radiolabeled 2-deoxyglucose (2DG) to measure in vivo relative glucose utilization (rGU) of several fetal tissues on day 20 of gestation. Pair-fed rats in room-air oxygen were used as controls. Maternal hypoxia resulted in significant IUGR, fetal hypoxia and acidosis, and fetal lactate accumulation on day 20 of gestation. Following 5 days of hypoxia, rGU values for fetal lung, heart, and kidney were increased by 61%, 54%, and 47%, respectively (P < .05). rGU values for fetal brain, liver, muscle, and placenta were not significantly affected. Fetal plasma glucose concentrations were similar in hypoxic and control fetuses. We speculate that the increased rGU of hypoxic fetal tissues is due in part to anaerobic metabolism and increased glycolysis.

Animals↗

Glomerular hyperfiltration in Koreans with non-insulin-dependent diabetes mellitus.

Glomerular hyperfiltration (GHF) may play an important role in the pathogenesis of diabetic nephropathy. The prevalence of GHF in non-insulin-dependent diabetes mellitus (NIDDM) is reported to vary in different populations, ranging from 35% in black Americans with new-onset diabetes to less than 5% in whites. We measured glomerular filtration rate (GFR) by 51Cr-EDTA clearance methods in 284 Korean NIDDM patients without overt nephropathy. Glomerular hyperfiltration (defined as GFR > 140 mL/min/1.73 m2) was found in 25% (71 of 284) of the patients. Thirty percent and 15% of the patients with known duration of diabetes less than 5 years and more than 10 years, respectively, showed GHF. Microalbuminuria (defined as urinary albumin excretion rate 20 to 200 micrograms/min) was found in 23% (64 of 284) of the patients. The mean GFR of the microalbuminuric patients was not significantly different from that of the normoalbuminuric patients (121.5 +/- 30.1 mL/min/1.73 m2 v 124.9 +/- 26.4 mL/min/1.73 m2; P = NS). However, when the patients with microalbuminuria were divided according to the presence or absence of retinopathy, the microalbuminuric patients with retinopathy had a lower GFR compared with the microalbuminuric patients without retinopathy (109.6 +/- 35.5 mL/min/1.73 m2 v 130.0 +/- 26.3 mL/min/1.73 m2; P < 0.01). These results show that the prevalence of GHF in Korean NIDDM patients without overt nephropathy is higher than that reported in whites and that it is similar to that in black Americans. The high prevalence of GHF in Korean NIDDM patients may contribute to the relatively higher prevalence of clinical diabetic nephropathy in this population.

Adult↗