Biomedical subjects

X Bian

Publications and source records attributed to X Bian.

At least 19 recordsLinked to original sources

PubMed2003

The NCI/CIT microArray database (mAdb) system - bioinformatics for the management and analysis of Affymetrix and spotted gene expression microarrays.

A scalable, modular, enterprise-level system for both microarray databasing and analysis over the Internet has been developed over the past four years by the National Cancer Institute's Center for Cancer Research in collaboration with NIH's Center for Information Technology. This completely Web-based system, called mAdb (for microArray database), is currently supporting over 810 registered users and collaborators at NIH and contains over 22,000 microarray experiments, making it one of the largest collections of microarray data in existence. In addition, the mAdb system has been ported for the Netherlands Cancer Institute, the Genome Institute of Singapore, and the CDC. This system has been used for a wide variety of scientific experiments spanning the range from cancer to studies of early development, and for human, mouse, rat, yeast, and numerous microbial organisms.

Animals↗

PubMed2001

NF-kappa B activation mediates doxorubicin-induced cell death in N-type neuroblastoma cells.

Neuroblastoma is the most common extracranial solid tumor of childhood. N-type neuroblastoma cells (represented by SH-SY5Y and IMR32 cell lines) are characterized by a neuronal phenotype. N-type cell lines are generally N-myc amplified, express the anti-apoptotic protein Bcl-2, and do not express caspase-8. The present study was designed to determine the mechanism by which N-type cells die in response to specific cytotoxic agents (such as cisplatin and doxorubicin) commonly used to treat this disease. We found that N-type cells were equally sensitive to cisplatin and doxorubicin. Yet death induced by cisplatin was inhibited by the nonselective caspase inhibitor z-Val-Ala-Asp-fluoromethylketone or the specific caspase-9 inhibitor N-acetyl-Leu-Glu-His-Asp-aldehyde, whereas in contrast, caspase inhibition did not prevent doxorubicin-induced death. Neither the reactive oxygen species nor the mitochondrial permeability transition appears to play an important role in this process. Doxorubicin induced NF-kappa B transcriptional activation in association with I-kappa B alpha degradation prior to loss of cell viability. Surprisingly, the antioxidant and NF-kappa B inhibitor pyrrolidine dithiocarbamate blocked doxorubicin-induced NF-kappa B transcriptional activation and provided profound protection against doxorubicin killing. Moreover, SH-SY5Y cells expressing a super-repressor form of I-kappa B were completely resistant to doxorubicin killing. Together these findings show that NF-kappa B activation mediates doxorubicin-induced cell death without evidence of caspase function and suggest that cisplatin and doxorubicin engage different death pathways to kill neuroblastoma cells.

Amino Acid Chloromethyl Ketones↗

PubMed2001

[Pregnancy and its outcome in women with malformed uterus].

OBJECTIVE: To analyze the clinical characteristics of fertility and pregnancy in women with congenital uterine malformations and explore optimal treatments to improve the prognosis. METHODS: A retrospective study was conducted on the fertility and obstetric outcome in 153 in patients with uterine malformations treated in our hospital from January 1984 to December 1998. Twenty-seven cases with other kinds of genital and/or urinary anomalies but with normal uterus was used as the control group. RESULTS: The infertility rate was 22.2% (34/153). The miscarriage rate was 44.3% (86/194), preterm labor rate was 9.3% (18/194). Abnormal fetal presentation rate was as high as 28.4% (29/102), the cesarean section rate was 61.8% (63/102), perinatal mortality rate was 11.8% (12/102). CONCLUSION: Women with congenital uterine malformation usually have higher incidence of infertility and complications during pregnancy and delivery. Bicornuate and septate uterus could be associated with poorer obstetric outcome.

Abortion, Spontaneous↗

PubMed2001

Cognitive deficits following blast injury-induced neurotrauma: possible involvement of nitric oxide.

Blast injuries, that is injuries caused by the complex pressure wave generated by some explosions, show increasing frequency throughout the world. However, whether blast injury is capable of inducing memory dysfunction has not been previously investigated. The present study examines the effects of blast injury-induced neurotrauma on memory deficit in rats. Furthermore, it is hypothesized that blast injury, stimulating nitric oxide production in the medial mesodiencephalic reticular formation and the dorsal hippocampus, both structures being involved in memory processing, may induce memory deficits. Prior to blast injury, Wistar rats were trained for an active avoidance task for 6 days. On day 6, rats that had acquired the avoidance response were subjected to whole-body blast injury, using a BT-I shock tube. Neurotrauma was confirmed by electron microscopical examination. At the completion of cognitive testing, rats were sacrificed at 3, 24 hours and 5 days after injury. The nitric oxide production in the brain structures was determined by the total nitrite/nitrate concentration, and by the expression of inducible nitric oxide synthase mRNA. The rats with blast injury revealed significant deficits in performance of the active avoidance task that persisted up to 5 days post-injury. Electron microscopical findings in both brain structures showed swellings of neurons, glial reaction, myelin debris, and increased pinocytotic activity on the fifth day following trauma. In blast injured rats, there was a significant elevation in total nitrite/nitrate levels 3 and 24 hours following injury which was comparable with the changes in the expression of inducible nitric oxide synthase mRNA. The results indicate that blast injury-induced neurotrauma is able to cause cognitive deficits.

Animals↗

PubMed2001

Ultrastructural and functional characteristics of blast injury-induced neurotrauma.

OBJECTIVE: The present study investigates whether whole-body or local (chest) exposure to blast overpressure can induce ultrastructural, biochemical, and cognitive impairments in the brain. METHODS: Male Wistar rats were trained for an active avoidance task for 6 days. On day 6, rats that had acquired the avoidance response were subjected to whole-body blast injury (WBBI), generated by large-scale shock tube (n = 40); or local (chest) blast injury (LBI), induced by blast overpressure focused on the right middle thoracic region and generated by small-scale shock tube (n = 40) while the heads of animals were protected. At the completion of cognitive testing, rats were killed at 3 hours, 24 hours, and 5 days after injury. Ultrastructural changes in the hippocampus were analyzed electron microscopically. Parameters of oxidative stress (malondialdehyde and superoxide anion generation) and antioxidant enzyme defense (superoxide dismutase and glutathione peroxidase activity) were measured in the hippocampus to assess biochemical changes in the brain after blast. RESULTS: Ultrastructural findings in animals subjected to WBBI or LBI demonstrated swellings of neurons, glial reaction, and myelin debris in the hippocampus. All rats revealed significant deficits in performance of the active avoidance task 3 hours after injury, but deficits persisted up to day 5 after injury only in rats subjected to WBBI. Oxidative stress development and altered antioxidant enzyme defense was observed in animals in both groups. Cognitive impairment and biochemical changes in the hippocampus were significantly correlated with blast injury severity in both WBBI and LBI groups. CONCLUSION: These results confirm that exposure to blast overpressure induces ultrastructural and biochemical impairments in the brain hippocampus, with associated development of cognitive deficits.

Animals↗

PubMed2001

Right ventricular oxygen supply/demand balance in exercising dogs.

This is the first investigation of right ventricular (RV) myocardial oxygen supply/demand balance in a conscious animal. A novel technique developed in our laboratory was used to collect right coronary (RC) venous blood samples from seven instrumented, conscious dogs at rest and during graded treadmill exercise. Contributions of the RV oxygen extraction reserve and the RC flow reserve to exercise-induced increases in RV oxygen demand were measured. Strenuous exercise caused a 269% increase in RV oxygen consumption. Expanded arteriovenous oxygen content difference (A-V(Delta)O2) provided 58% of this increase in oxygen demand, and increased RC blood flow (RCBF) provided 42%. At less strenuous exercise, expanded A-V(Delta)O2 provided 60-80% of the required oxygen, and increases in RCBF were small and driven by increased aortic pressure. RC resistance fell only at strenuous exercise after the extraction reserve had been mobilized. Thus RC resistance was unaffected by large decreases in RC venous PO2 until an apparent threshold at 20 mmHg was reached. Comparisons of RV findings with published left ventricular data from exercising dogs demonstrated that increased O2 demand of the left ventricle is met primarily by increasing coronary flow, whereas increased O2 extraction makes a greater contribution to RV O2 supply.

Animals↗

PubMed2001

Endogenous nitric oxide modulates myocardial oxygen consumption in canine right ventricle.

The role of endogenous nitric oxide (NO) in modulating myocardial oxygen consumption (MVO2) is unclear, in part because of systemic and coronary hemodynamic effects of blocking NO release. This study evaluated the effect of NO on right ventricular MVO2 under controlled hemodynamic conditions. In 12 open-chest dogs, N(omega)-nitro-L-arginine methyl ester (L-NAME, 150 microg/min), a NO synthase (NOS) blocker, was infused into the right coronary artery. Heart rate and mean aortic pressure were constant. Right coronary blood flow and right ventricular MVO2 were measured at normal and elevated right coronary perfusion pressures (RCP) before and after L-NAME. To avoid effects of NO synthesis blockade on right coronary blood flow, which might have altered right ventricular MVO2, experiments, were conducted during adenosine-induced maximal coronary vasodilation. L-NAME did not affect right coronary blood flow (P = 0.51). However, L-NAME significantly increased right ventricular MVO2 (6% at RCP 100 mmHg, and 21% at RCP 180 mmHg). Right coronary blood flow varied with perfusion pressure (P < 0.02), and the elevation of MVO2 produced by L-NAME increased at higher flows (P < 0.04), consistent with the greater shear stress-mediated release of NO. These findings indicate that endogenous NO limits right ventricular MVO2.

Animals↗

PubMed2001

Optimal management of postpartum hemorrhage.

OBJECTIVE: To review the management of postpartum hemorrhage (PPH). METHODS: Fifteen cases of severe PPH were retrospectively analyzed for clinical parameters and management. RESULTS: Nine patients had a hysterectomy while selective arterial embolization was carried out in 7 cases. One patient had focus clearance. The main causes of postpartum hemorrhage requiring operative management were disseminated intravascular coagulation (DIC), uterine arteriovenous fistula and malformation, placental abnormality, uterine myoma and laceration. CONCLUSION: Upon recognition of postpartum hemorrhage, the most effective management should be initiated. Every effort should be made to stabilize the patient and maintain her reproductive capability.

Adult↗

PubMed2001

[The effects of the polysaccharides from Dermatocarpon miniatum on oxygen radicals and lipid peroxidation].

OBJECTIVE: To study the effects of Dermatocarpon miniatum (DEM) polysaccharides scavenging oxygen radicals and inhibiting lipid peroxidation. METHODS: .OH was produced by Fenton reaction and O2-. was produced by the oxidation of pyrogallol. The inhibition to LPO was determined by the colorimetry for testing the relative content of MDA. RESULTS: DEM polysaccharides could scavenge oxygen radical. The amounts of scavenging 50% (EC50) .OH was 1.72 mg/ml, the EC50 for O2-. was 2.12 mg/ml. DEM polysaccharides could also decrease the content of MDA. CONCLUSION: DEM polysaccharides has the effects of scavenging oxygen radicals and the inhibition to LPO. Its activities showed positive correlation with the amounts.

Antioxidants↗

PubMed2001

Comparative observation with MRI and pathology of brain edema at the early stage of severe burn.

OBJECTIVE: To investigate the correlation between MRI features and pathology in brain edema at the early stage of severe burn (5 0% TBSA III degree) in dogs. METHODS: Fifty-two dogs were randomized into control, simple b urn (SB), burn plus sodium lactate (BSL), and burn plus glucose solution groups (BGS). The manifestation of the brain of control group was compared with that of burn groups at 6, 12, 18 and 24 hours postburn with MRI and pathological examination (gross appearance, electron microscopy and light microscopy). RESULTS: The earliest findings of brain edema were seen at 12 h ours after burn in BGS group, in which brain swelling was the main feature of MR I. The decrease of SIR on T(1)WI was not observed until it was exceeded 10%. Sig nal of T(2)WI increased by 8.29% at 24 hours after burn. It was difficult to distinguish the gray matter from the white matter at the boundary line, which became blurred later. Histological changes of brain edema were observed as early as 6 hours after burn, being accompanied by swelling of endothelial cells and peri-vescular astrocytes, and vacuolation took place in neurons at 12 hours after burn, with different degrees of necrosis of capillary endothelium, neurons, and axons. These changes became more marked with elapse of time. The BGS group showed the most obvious changes mentioned above at 24 hours after burn. CONCLUSIONS: The model of the brain edema after severe burn has the feature of both vasogenic edema and cytotoxic edema on the MRI and pathology. Positive MRI findings lagged behind that of the pathomorphological changes.

Animals↗

PubMed2001

[A quantitative pathological study on angiogenesis, vascular endothelial growth factor and inducible nitric oxide synthase in astrocytomas].

OBJECTIVE: To investigate whether the expression of vascular endothelial growth factor (VEGF) and inducible nitric oxide synthase (iNOS) are associated with angiogenesis and malignancy of astrocytomas. METHODS: Immunohistochemistry, semiquantitation and image analysis were used to study the expression features of VEGF and iNOS in 61 cases of astrocytomas having follow-up data. Factor VIII related antigen (FVIII RAg) was also analysed in reflecting the epithelial cell amount and the microvessel density. RESULTS: Microvessels in astrocytomas could be divided into seven types. The positive reaction areas and IA values of FVIIIRAg expression in the endothelium were significantly increased with the increase of tumor grade (P < 0.001) and VEGF labeling index (LI) (P < 0.05). The patients with high VEGF LIs (LI >or= 25%) had a poor prognosis. VEGF expression was significantly related to that of iNOS (P < 0.001), i.e., VEGF level was reduced along with the decrease of iNOS reaction. CONCLUSION: Detection of FVIIIRAg could reflect the angiogenesis activities in astrocytomas. VEGF and iNOS could up-regulate each other to promote angiogenesis and are of importance in determining the malignancy degree of astrocytomas.

Astrocytoma↗

PubMed2001

Investigation of thrombomodulin and plasminogen activator inhibitor type-I in pregnancy induced hypertension and its clinical significance.

OBJECTIVE: To measure the circulating levels of thrombomodulin (TM) and plasminogen activator inhibitor type-I (PAI-I) in women with pregnancy induced hypertension (PIH). METHODS: Blood samples were drawn from 97 pregnant women in their third trimester, grouped as 25 mild PIH, 26 moderate PIH, 22 severe PIH and 24 normotensive healthy pregnant women for determining levels of TM by ELISA, PAI-I by colorimetric assay methods, and creatinine (Cr) in serum by biochemical method. RESULTS: Circulating levels of TM, PAI-I and TM/Cr ratio increased with increasing severity of PIH. There were no significant differences between mild and normotensive pregnant women. The parameters were significantly changed in the moderate and severe PIH groups. CONCLUSION: TM and PAI-I may serve as meaningful clinical markers for the assessment of the endothelial damage in PIH, which is very important in evaluating and following the development of PIH.

Adult↗

PubMed2000

Descending inhibitory reflexes involve P2X receptor-mediated transmission from interneurons to motor neurons in guinea-pig ileum.

The role of P2X receptors in descending inhibitory reflexes evoked by distension or mucosal distortion in the guinea-pig ileum was studied using intracellular recording from the circular muscle in a two-chambered organ bath. This allowed separate superfusion of the sites of reflex stimulation and recording, thereby allowing drugs to be selectively applied to different parts of the reflex pathway. Inhibitory junction potentials (IJPs) evoked by electrical field stimulation (EFS) in the recording chamber were compared with those evoked during reflexes to control for effects of P2 receptor antagonists on neuromuscular transmission. The P2 receptor antagonists suramin (100 microM) and pyridoxal phosphate-6-azophenyl-2',4'-disulphonic acid (10 and 60 microM; PPADS), when added to the recording chamber, depressed reflexly evoked IJPs significantly more than those evoked by EFS. In particular, 10 microM PPADS depressed IJPs evoked by distension or mucosal distortion by about 50 %, but had little effect on IJPs evoked by EFS. Blockade of synaptic transmission in the stimulation chamber with a low Ca2+-high Mg2+ solution depressed, but did not abolish, IJPs evoked by distension. The residual reflex IJPs were unaffected by PPADS (10 microM), hyoscine (1 microM), hyoscine plus hexamethonium (200 microM), or hysocine plus hexamethonium plus PPADS in the recording chamber. We conclude that P2X receptors are important for synaptic transmission from descending interneurons to inhibitory motor neurons in descending inhibitory reflex pathways of guinea-pig ileum. Transmission from anally directed axons of distension-sensitive intrinsic sensory neurons to inhibitory motor neurons is unlikely to involve P2X, muscarinic or nicotinic receptors.

Animals↗

PubMed2000

Myocardial oxygen consumption modulates adenosine formation by canine right ventricle in absence of hypoxia.

Myocardial adenosine formation varies with myocardial oxygen consumption (MVO(2)), but whether concurrent hypoxia is required for adenosine formation is uncertain. Changes in right coronary (RC) perfusion pressure (RCP) produce directionally similar alterations in right ventricular (RV) MVO(2)and in RC venous P O(2)(P(v)O(2)), an index of myocardial P O(2). RCP was varied in 10 anesthetized, open chest dogs to determine if, under these conditions, RV formation of adenosine would increase with MVO(2)in absence of myocardial hypoxia. Dialysis probes were implanted in the mid myocardium of RV free wall for collecting dialysate samples for HPLC analyses to estimate interstitial adenosine and other purines. Coronary venous blood was sampled from a superficial vein draining the RC artery (RCA) perfusion territory. At 115+/-3 mmHg baseline RCP, RC blood flow (RCBF)=0.51+/-0.04 ml/min/g, MVO(2)=4.6+/-0.5 ml/min/100 g, P(v)O(2)=34+/-1.5 mmHg, and dialysate adenosine=0. 27+/-0.03microM. When RCP was lowered to 61+/-1 mmHg by adjusting an occluder on the proximal RCA, RCBF decreased to 0.36+/-0.03 ml/min/g, MVO(2)fell to 3.7+/-0.4 ml/min/100 g, lactate uptake remained positive, P(v)O(2)fell to 30+/-1.7 mmHg, and dialysate adenosine decreased to 0.20+/-0.03microM. Reactive hyperemia of 1.25+/-0.13 ml/min/g was observed when the RCA constriction was released, although dialysate adenosine had fallen. When RCP was elevated to 164+/-2 mmHg by inflating a balloon catheter in the descending aorta, RCBF increased to 0.70+/-0.06 ml/min/g, MVO(2)increased to 5.8+/-1. 0 ml/min/100 g, P(v)O(2)rose to 39+/-2.3 mmHg, and dialysate adenosine increased to 0.33+/-0.04microM. These data indicate that (1) RV oxygen demand varies with RCP; (2) if RV ischemia is absent, myocardial adenosine formation is modulated by MVO(2), with no requirement for hypoxia; (3) pressure-flow autoregulation is relatively ineffective in the RC circulation, where adenosine does not mediate and may even blunt autoregulation.

Adenosine↗

PubMed2000

Hyperlipidemia with hypoglycemia reduces myocardial oxygen utilization efficiency but not contractile function during coronary hypoperfusion.

This study was designed to determine changes in myocardial contractile function and fuel selection during moderate coronary hypoperfusion in the presence of elevated plasma free fatty acid (FFA) at normal and reduced blood glucose concentrations. Coronary perfusion pressure (CPP) was sequentially lowered from 100 to 60, 50, and 40 mmHg in the left anterior descending coronary artery (LAD) of anesthetized, open-chest dogs. Regional glucose uptake (GU), fatty acid uptake (FAU), percentage segment shortening (%SS), and oxygen consumption (MV O(2)) were determined with normal arterial plasma FFA concentrations (Group 1) or with elevated FFA concentrations (Groups 2 and 3). In Group 3, glucose in the coronary perfusate blood was reduced from 3.53+/-0.36 to 0.15+/-0.03 m M by hemodialysis. In Group 1, FAU fell by 85% as CPP was lowered to 60 mmHg and remained depressed as CPP was reduced further; GU did not fall significantly. Hyperlipidemia in Group 2 did not alter GU at any CPP, but maintained FAU at baseline levels until CPP was lowered to 40 mmHg. At 40 mmHg CPP, myocardial function and metabolic variables were similar in Groups 1 and 2. In Group 3 at 40 mmHg, FAU increased four-fold and MV O(2)doubled v Groups 1 and 2, and GU fell to zero. Despite these metabolic changes, %SS in Group 3 was unchanged relative to Group 2. Addition of glucose to the dialysate prevented the effects of dialysis on FAU, GU, and MV O(2). Thus, preferential glucose oxidation sustains myocardial oxygen utilization efficiency [(heart rate x %SS x maximum left ventricular pressure)/MV O(2)] during hypoperfusion. Blocking preferential glucose oxidation by combined hyperlipidemia and hypoglycemia lowers oxygen utilization efficiency, but does not compromise myocardial contractile function.

Animals↗

PubMed2000

Vascular endothelial growth factor is increased following coronary artery occlusion in the dog heart.

Vascular endothelial growth factor (VEGF) is a hypoxia-inducible factor expressed into several molecular forms in mammalian tissues of which VEGF 120, VEGF 164, and VEGF 188 are the major isoforms. While VEGF 164 is the predominant isoform in most tissues, VEGF 188 has been reported to be dominant in cardiac tissues such as that in guinea pig, rat, and mouse. In the dog heart, an important model for studies of myocardial ischemia and angiogenesis, the expression of VEGF remains to be established. We investigated the expression of the various isoforms of VEGF in normal and ischemic dog heart tissues using Reverse transcription-Polymerase chain reaction, Ribonuclease Protection Assay and Western blotting. The nucleotide sequences of the major isoforms of VEGF were also determined using homology cloning techniques. Our study showed that the nucleotide sequences of dog VEGF were highly homologous to human VEGF especially in the c-terminal region spanning exons 58. A single amino acid-deletion (Glu5 in human VEGF), similar to that reported in other animal species, was observed in the major isoforms resulting in monomers of 120, 164, and 188 amino acids. A novel splice site similar to that in human VEGF183 was also identified in the dog heart, resulting in the 182 amino acid-containing isoform (VEGF 182). Moreover, VEGF 164 was expressed at a higher level as compared with VEGF 182 or VEGF 188 in both normal and ischemic tissues. The identification of the nucleotide sequences of VEGF isoforms in the dog heart should prove useful in investigating the molecular expression of VEGF in canine tissues.

Amino Acid Sequence↗

PubMed2000

Dobutamine enhances both contractile function and energy reserves in hypoperfused canine right ventricle.

Although the beta(1)-adrenergic agent dobutamine is used clinically to provide inotropic support to the failing myocardium, it could jeopardize the myocardium by depleting energy reserves. This investigation delineated the contractile and energetic effects of low versus high dobutamine doses in the hypoperfused right ventricular (RV) myocardium. The right coronary artery (RCA) of anesthetized dogs was cannulated for controlled perfusion with arterial blood, and regional RV contractile function was measured. RCA perfusion pressure was lowered from 100 mmHg baseline to 40 mmHg, and flow fell by 54%. At 15-min hypoperfusion, dobutamine was infused into the RCA at either 0.01 (low-dose dobutamine) or 0.06 microgram. kg(-1). min(-1) (high-dose dobutamine) for 15 min. Regional power (systolic segment shortening x isometric developed force x heart rate) stabilized at 63% of baseline during hypoperfusion. Low-dose dobutamine restored power to baseline but did not increase RV myocardial O(2) consumption (MVO(2)) and thus increased myocardial O(2) utilization efficiency (O(2)UE:power/MVO(2)). At 5 min, high-dose dobutamine enhancement of power was similar to that of low-dose dobutamine, but by 15 min, power and O(2)UE fell to untreated levels. Remarkably, low-dose dobutamine tripled cytosolic phosphorylation potential; in contrast, high-dose dobutamine lowered phosphorylation potential to 45% of the untreated value. Analyses of glucose uptake and glycolytic intermediates revealed sustained enhancement of glycolysis by low-dose dobutamine, but glycolysis became limited at glyceraldehyde 3-phosphate dehydrogenase during high-dose dobutamine treatment. In summary, low-dose dobutamine improved mechanical performance and efficiency of the hypoperfused RV myocardium while increasing myocardial energy reserves, but high-dose dobutamine failed to sustain improved function and depleted energy reserves. Dobutamine is capable of improving both contractile function and cellular energetics in the hypoperfused RV myocardium, but dosage should be carefully selected.

Animals↗

PubMed2000

Risk factors for development of diabetes mellitus in women with a history of gestational diabetes mellitus.

OBJECTIVE: To determine whether diabetes recurs in their later life when women have a history of gestational diabetes mellitus (GDM) or abnormal glucose tolerance test (impaired glucose tolerance, IGT). METHODS: Three groups of women were investigated at 5-10 years postpartum. GDM group (n = 45) had been diagnosed as having GDM in their previous pregnancy. IGT group (n = 31) had a history of abnormal glucose tolerance test during previous pregnancy. Normal control group (n = 39) was normal previous pregnant population. Their previous obstetric and medical histories were thoroughly reviewed. Fasting plasma glucose (FPG) and oral glucose (75 g) tolerance test (OGTT) were repeated in all women. RESULTS: Diabetes mellitus (DM) was diagnosed in 33.3% of patients in the GDM group, while in 9.7% in the IGT group and in 2.6% in the normal control group. Incidence of recurring DM in later life was significant higher in the GDM group (P = 0.017). When one or more blood glucose values exceeding WHO criteria for diagnosis of diabetes in their previous pregnancy, the incidence of DM in later life was 60% (3/5, including GDM in women having four abnormal OGTT values), 41.7% (5/12) in women having three, 25% (7/28) in women having two and 9.7% (3/31) in women having one. The women with DM, also with a history of GDM and abnormal OGTT in previous pregnancy, tends to have a high pregnant body mass index (BMI > 25 kg/m2). CONCLUSION: The women suffering from GDM during previous pregnancy have a high risk of recurrence DM. Two or more abnormal OGTT values during pregnancy, blood glucose level exceeding the maximal values at 1 and 2 hours after oral glucose loading and high pregnant BMI are concluded to be useful factors in predicting the recurring DM in their later life.

Adult↗