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T H Chiu

Publications and source records attributed to T H Chiu.

At least 19 recordsLinked to original sources

Hypoxic preconditioning attenuated in kainic acid-induced neurotoxicity in rat hippocampus.

The neuroprotective effect of hypoxic preconditioning on kainate (KA)-induced neurotoxicity, including apoptosis and necrosis, was investigated in rat hippocampus. Female Wistar-Kyoto rats were subjected to 380 mm Hg in an altitude chamber for 15 h/day for 28 days. Intrahippocampal infusion of KA was performed in chloral hydrate anesthetized rats, which acutely elevated 2,3-dihydroxybenzoic acid levels in normoxic rats. Seven days after the infusion, KA increased lipid peroxidation in the infused hippocampus and resulted in hippocampal CA3 neuronal loss. A 4-week hypoxic preconditioning attenuated KA-induced elevation in hydroxyl radical formation and lipid peroxidation as well as KA-induced neuronal loss. The effects of hypoxic preconditioning on KA-induced apoptosis and necrosis were investigated further. Two hours after KA infusion, cytosolic cytochrome c content was increased in the infused hippocampus. Twenty-four hours after KA infusion, pyknotic nuclei, cellular shrinkage, and cytoplasmic disintegration, but not TUNEL-positive staining, were observed in the CA3 region of hippocampus. Forty-eight hours after KA infusion, both DNA smear and DNA fragmentation were demonstrated in the infused hippocampus. Furthermore, TUNEL-positive cells, indicative of apoptosis, in the infused hippocampus were detected 72 h after KA infusion. Hypoxic pretreatment significantly reduced necrotic-like events in the KA-infused hippocampus. Moreover, hypoxic preconditioning attenuated apoptosis induced by KA infusion, including elevation in cytosolic cytochrome c content, TUNEL-positive cells, and DNA fragmentation. Our data suggest that hypoxic preconditioning may exert its neuroprotection of KA-induced oxidative injuries via attenuating both apoptosis and necrosis in rat hippocampus.

Animals↗

Hydrogen peroxide increases the activity of rat sympathetic preganglionic neurons in vivo and in vitro.

Reactive oxygen species (ROS) have been shown to modulate neuronal synaptic transmission and have also been implicated in cardiovascular diseases such as hypertension. The hypothesis that H(2)O(2) acting on sympathetic preganglionic neurons (SPNs) affects spinal sympathetic outflow was tested in the present study. H(2)O(2) was applied intrathecally via an implanted cannula to the T7-T9 segments of urethane-anesthetized rats. Blood pressure and heart rate were used as indices to evaluate the spinal sympathetic effects of H(2)O(2) in vivo. Intrathecal H(2)O(2) (100-1000 nmol) dose-dependently increased both the mean arterial pressure and heart rate. Reproducible pressor effects of H(2)O(2) (1000 nmol) applied consecutively at intervals of 30 min were observed. The pressor effects of intrathecal H(2)O(2) (1000 nmol) were attenuated by pretreatment with intrathecal administration of catalase (500 units), or N-acetyl-cysteine (1000 nmol). The pressor effects of intrathecal H(2)O(2) (1000 nmol) were also antagonized dose-dependently by prior intrathecal injection of AP-5 (DL-2-amino-5- phosphonovaleric acid, 10 and 30 nmol), or 6-cyano-7- nitroquinoxaline-2,3-dione, 10 and 30 nmol. In vitro electrophysiological study in spinal cord slices showed that superfusion of 1 mM H(2)O(2) for 3 min, which had no effect on membrane potential, caused an increase in amplitude of excitatory postsynaptic potentials in SPNs, but had little effect on that of inhibitory postsynaptic potentials. Taken together, these results demonstrated that oxidative stress in spinal cord may cause an increase in spinal sympathetic tone by acting on SPNs, which may contribute to ROS-induced cardiovascular dysfunction.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

Acute exposure to trichloroethylene differentially alters the susceptibility to chemoconvulsants in mice.

The effects of a common industrial solvent, trichloroethylene (TCE), which was once used as an anesthetic agent but its in vivo mechanism is still unknown, on convulsant-induced seizures in mice were examined. Pretreatment with TCE (250-2000 mg/kg, i.p.) significantly increased pentylenetetrazol (PTZ)-, picrotoxin (PIC)-, bicuculline (BIC)-, strychnine (STY)-, 4-aminopyridine (4-AP)- and N-methyl-D-aspartate (NMDA)-induced convulsion thresholds and lethal doses. However, the increase in convulsion thresholds and lethal doses was much greater for GABAergic antagonists (PIC, BIC, and PTZ) than non-GABAergic convulsants (STY, 4AP, and NMDA) following 2000 mg/kg TCE administration. Pre-treatment of mice with disulfiram (an inhibitor of CYP 4502E1) but not 4-methyl pyrazole (an inhibitor of alcohol dehydrogenase) significantly prolonged the time required for TCE (5000 mg/kg, i.p.) to induce the loss of righting reflex. These results suggest that acute exposure to TCE differentially alters the susceptibility to chemically induced convulsions in mice. The anticonvulsive effect of TCE may be predominantly mediated by GABA(A) receptors. In addition, TCE appears to exert a direct anesthetic effect.

Animals↗

Ethanol effects on nitric oxide production in cerebral pial cultures.

BACKGROUND: Although alcohol abusers are known to have higher incidences of hemorrhagic cerebrovascular diseases, it is not known whether these changes are associated with ethanol (EtOH) action on nitric oxide (NO) production in the cerebrovascular cells. The purpose of this study was to examine the effects of EtOH treatment on basal and cytokine-induced NO production in cortical pial cultures. METHODS: Cell cultures for this study included murine primary pial vascular cells, primary glial cells and cortical neurons. These cells were exposed to cytokines or EtOH for 24 to 48 hr. The culture media were used for measurement of nitrite, as an indication for NO release, and lactate dehydrogenase (LDH), as an index of cell membrane integrity. In addition, immunocytochemical determinations were carried out to identify cell types and to assess inducible nitric oxide synthase (iNOS). RESULTS: Exposure of primary pial vascular cultures to cytokines that consisted of interleukin-1 beta (IL-1 beta; 250 pg/mL) and interferon-gamma (IFNgamma; 2 ng/mL) or to EtOH (50 to 100 mM) for 24 to 48 hr significantly elevated NO production. NO production could be attenuated by N-nitro-L-arginine (N-arg), a nonspecific NOS inhibitor, or aminoguanidine (AG), an iNOS inhibitor. Increased iNOS immunoreactivity was observed in cytokines- or EtOH-treated pial cells. When pial cells were cocultured with cortical neurons, prolonged EtOH exposure led to a large increase in NO production as well as LDH release. However, this increase was not observed in pial culture alone or in mixed cortical culture. Nevertheless, inhibition of NO production with N-arg or AG did not alter the EtOH-induced LDH release in the pial cells cocultured with cortical neurons. CONCLUSION: These results show that EtOH exposure led to increased production of NO in primary pial cell culture. In mixed culture that contained cortical neurons and pial cells, EtOH induced increase in NO as well as LDH release, which is an indication of loss of cell membrane integrity. However, EtOH-mediated LDH release in mixed cortical pial cultures was not a consequence of the increase in NO production by these cells. Studies that use mixed cortical-pial cultures may provide a unique in vitro system for examining the interactions among glial cells, neurons, and cerebrovascular cells.

Animals↗

Arecoline excites rat locus coeruleus neurons by activating the M2-muscarinic receptor.

The action of arecoline on rat locus coeruleus neurons was studied by intracellular recording from the in vitro brain slice preparation. Superfusion of arecoline (0.1-100 microM) caused two dose-related effects, an increased firing rate and, in neurons previously hyperpolarized to a constant potential by passing a steady hyperpolarizing current across the membrane, depolarization. Both effects were associated with a reduction in membrane input resistance. Moreover, the arecoline-induced excitatory effects were antagonized by the muscarinic receptor antagonist, atropine, but not by the nicotinic receptor antagonist, hexamethonium. Methoctramine, a selective M2-muscarinic receptor antagonist, was also effective in reversing the arecoline-induced effects, with a dissociation equilibrium constant of 14.2+/-1.2 nM (n=6). These results therefore suggest that arecoline exerts its excitatory actions by binding to M2-muscarinic receptors on the cell membrane of neurons of the locus coeruleus.

Alzheimer Disease↗

Risk factors for pre-eclampsia in an Asian population.

OBJECTIVE: To identify the risk factors for pre-eclampsia in an Asian population. METHOD: We conducted a retrospective cohort study involving 29375 Taiwanese women who delivered between July 1990 and September 1998, excluding pregnancies complicated by chronic hypertension or fetal malformations. RESULT: Four hundred and fifteen women had pre-eclampsia (1.4%). Women who had a history of pre-eclampsia (OR 6.3, 95% CI 4.4, 9.2), multiple gestation (OR 3.6, 95% CI 2.4, 5.5), a prepregnancy BMI > 24.2 kg/m(2) (OR 2.4, 95% CI 1. 8, 3.1), were > 34 years of age (OR 1.8, 95% CI 1.4, 2.4), nulliparous (OR 1.3, 95% CI 1.2, 1.5), had urinary tract infection (OR 4.8, 95% CI 1.5, 15.8), or worked during pregnancy (OR 1.9, 95% CI 1.4, 2.4) were at increased risk of pre-eclampsia. CONCLUSION: Some of the risk factors for pre-eclampsia among Asian women are the same as those of other ethnic groups, whereas some of the risk factors are different.

Adult↗

Activation of rat locus coeruleus neuron GABA(A) receptors by propofol and its potentiation by pentobarbital or alphaxalone.

The action of propofol on the rat locus coeruleus was examined using intracellular recording from in vitro brain slice preparations. Concentrations of propofol between 3 and 300 microM were tested. At 100 microM, propofol completely inhibited the firing of all neurons tested (n=34); this was associated with a 5.7-mV hyperpolarization (range 0-16 mV, n=33) and a 35.6% reduction in input resistance (range 7.3-66.1%, n=33). The propofol-induced responses were not affected by 2-hydroxysaclofen (50 microM) or BaCl(2) (300 microM), but were completely blocked by bicuculline methiodide (100 microM) or picrotoxin (100 microM), indicating that propofol acts on GABA(A) receptors. As assessed by inhibition of the spontaneous firing rate, propofol was 5.6-fold more potent than GABA (gamma-aminobutyric acid). Potentiation of the propofol effect by other general anesthetics or other drugs was also investigated. When pentobarbital (100 microM) was tested alone on locus coeruleus cells, no change in membrane potential or input resistance was seen and there was only a 20.3+/-7.2% (n=8) inhibition of firing rate; however, in combination with 30 microM propofol, it caused a 6.1-fold greater increase in membrane hyperpolarization and a 9.7-fold greater reduction in input resistance than 30 microM propofol alone. A relatively low concentration of alphaxalone (10 microM), when tested alone, had little effect on the membrane potential or input resistance and only produced a 46.0+/-8.9% (n=8) inhibition of firing rate; however, in combination with 30 microM propofol, it caused a 9.3-fold greater hyperpolarization and an 8.6-fold greater reduction in input resistance compared with 30 microM propofol alone. In contrast, diazepam caused no potentiation of either propofol- or GABA-induced responses. Our data also indicate that locus coeruleus neuron GABA(A) receptors possess distinctive pharmacologic characteristics, such as blocking of the propofol effects by zinc and insensitivity to diazepam and the direct action of pentobarbital. On the basis of these pharmacologic properties, we suggest that locus coeruleus neuron GABA(A) receptors do not contain the gamma subunit.

Anesthetics↗

Structure-activity relationships of naturally occurring and synthetic opioid tetrapeptides acting on locus coeruleus neurons.

Intracellular recording was used to study the effects of eight opioid tetrapeptides with similar amino acid sequences, namely endomorphin-1 (Tyr-Pro-Trp-Phe-NH2), endomorphin-2 (Tyr-Pro-Phe-Phe-NH2), morphiceptin (Tyr-Pro-Phe-Pro-NH2), hemorphin-4 (Tyr-Pro-Trp-Thr), Tyr-MIF-1 (Tyr-Pro-Leu-Gly-NH2), Tyr-W-MIF-1 (Tyr-Pro-Trp-Gly-NH2), TAPS (Tyr-D-Arg-Phe-Sar) and DALDA (Tyr-D-Arg-Phe-Lys-NH2), on neurons of the rat locus coeruleus, using a submerged brain slice preparation. All the tetrapeptides inhibited the spontaneous firing of all neurons of the locus coeruleus tested. Higher concentrations also caused hyperpolarization of the neurons and a reduction in input resistance. These inhibitory effects were rapidly and completely reversed by CTAP (D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2, a selective micro-opioid receptor antagonist). The IC50 of the opioid tetrapeptides, in terms of inhibition of spontaneous firing of locus coeruleus neurons, as compared to the concentrations which produced a 5-mV hyperpolarization (HC5 mV) were calculated, giving the same rank order of potency: TAPS (IC50 = 1.9 nM, HC5 mV = 3.4 nM) > endomorphin-1 (IC50 = 8.8 nM, HC5 mV = 22.1 nM) and endomorphin-2 (IC50 = 5.3 nM, HC5 mV = 16.1 nM)> DALDA (IC50 = 20 nM, HC5 mV = 143 nM) > morphiceptin (IC50 = 65 nM, HC5 mV = 335 nM) > Tyr-W-MIF-I (IC50 = 3.8 microM, HC5 mV = 6.7 microM) > hemorphin-4 (IC50 = 6.7 microM, HC5 mV = 36.9 microM) > Tyr-MIF-1 (IC50 = 37.5 microM, HC5 mV = 76.2 microM). Comparison of the ability of endomorphin-1 and endomorphin-2 to inhibit spontaneous firing based on single-cell recordings (n = 5) showed these two peptides to be equipotent. Based on these results, the structure-activity relationships of these opioid tetrapeptides are discussed herein.

Animals↗

Risk factors for placenta accreta.

OBJECTIVE: To identify risk factors associated with placenta accreta in a large cohort study. METHODS: Data for this study came from the Taiwan Down Syndrome Screening Group, an ongoing project on feasibility of serum screening in an Asian population. Women who had serum screening for Down syndrome at 14-22 weeks' gestation using alpha-fetoprotein (AFP) and free beta-hCG between January 1994 and June 1997, and delivered in the same institution, were included (n = 10,672). Those who had multiple gestations (n = 200), overt diabetes (n = 11), or fetal malformations (n = 101) were excluded. If a woman was involved more than once, one randomly selected pregnancy was included in the analysis (n = 9349). Twenty-eight pregnancies were complicated by placenta accreta, diagnosed by clinical presentation (n = 26) or histologic confirmation (n = 2). Multiple logistic regression with adjustment for potentially confounding variables was used to identify independent risk factors for placenta accreta. RESULTS: Women who had placenta previa (odds ratio [OR] 54.2; 95% confidence interval [CI] 17.8, 165.5) and second-trimester serum levels of AFP and free beta-hCG greater than 2.5 multiples of the median (OR 8.3; 95% CI 1.8, 39.3 and OR 3.9; 95% CI 1.5, 9.9, respectively), and were 35 years and older (OR 3.2; 95% CI 1.1, 9.4) were at increased risk of having placenta accreta. CONCLUSION: Risk factors for placenta accreta include placenta previa, abnormally elevated second-trimester AFP and free beta-hCG levels, and advanced maternal age.

Adult↗

Tumor vascular pattern and blood flow impedance in the differential diagnosis of leiomyoma and adenomyosis by color Doppler sonography.

PURPOSE: Our objective was to evaluate the differences between leiomyoma and adenomyosis by color Doppler sonography with new criteria. METHODS: A total of 78 patients with symptomatic uterine nodularities who were sonographically suspected to have leiomyoma or adenomyosis without other coexisting pathologic conditions was enrolled in the study. All patients underwent transvaginal color Doppler sonography (7.0-MHz vaginal probe) or transabdominal color Doppler sonography (5.0 MHz) during the early follicular phase. The morphology, tumor vascular pattern, and blood flow impedance of the uterine tumors were measured. All of the patients underwent surgery and the pathologic reports were used as references. RESULTS: The mean age was not statistically significant in patients with adenomyosis versus leiomyoma (P > 0.05). The morphologic criteria for adenomyosis and leiomyoma by sonography detected 79% of adenomyosis and 84% of leiomyoma. Adenomyosis had 87% randomly scattered vessels or intratumoral signals and 88% of leiomyomas showed peripheral scattered vessels or outer feeding vessels. Eighty-two percent of adenomyosis had a pulsitility index (PI) of arteries within or around uterine tumors > 1.17 and 84% of leiomyomas had a PI < or = 1.17. The reliability test of tumor vascular pattern and blood flow impedance were better than that of using morphological criteria alone. CONCLUSIONS: With the aid of color Doppler sonography, tumor vascular pattern and blood flow impedance of the arteries within or around uterine tumors could more accurately diagnose adenomyosis and leiomyoma in addition to the morphologic criteria on transvaginal sonography.

Adult↗

Effect of panax notoginseng extracts on inferior sperm motility in vitro.

The purpose of this study was to investigate the effects of Panax notoginseng extracts on inferior sperm motility in vitro. Semen samples were collected from 23 patients with sperm motility between 20% and 40%. The sperm count was over 20 x 10(6)/ml in accordance with the World Health Organization standard. 1.0 mg/ml and 2.0 mg/ml of Panax notoginseng extracts including aqueous extract, n-butanol extract, and polysaccharide fraction on sperm motility and progression were evaluated by computer assisted semen analysis. The results demonstrated that sperm motility as well as progression on inferior sperm motility were enhanced at 1 hour and 2 hours after incubation with all three types of extracts.

Adult↗

Acute pentylenetetrazol injection reduces rat GABAA receptor mRNA levels and GABA stimulation of benzodiazepine binding with No effect on benzodiazepine binding site density.

The effects of a single convulsive dose of pentylenetetrazol (PTZ, 45 mg/kg i.p.) on rat brain gamma-aminobutyric acid type A (GABAA) receptors were studied. Selected GABAA receptor subunit mRNAs were measured by Northern blot analysis (with beta-actin mRNA as a standard). Four hours after PTZ, the GABAA receptor gamma2-mRNA was decreased in hippocampus, cerebral cortex, and cerebellum; alpha1-mRNA was decreased in cerebellum; and beta2 subunit mRNA was decreased in cortex and cerebellum. The alpha5 subunit mRNA level was not altered. Those mRNAs that had been reduced were increased in some brain regions at the 24-h time point, and these changes reverted to control levels by 48 h. PTZ effect on GABAA receptors was also studied by autoradiographic binding assay with the benzodiazepine agonist [3H]flunitrazepam (FNP), the GABAA agonist [3H]muscimol, and the benzodiazepine antagonist [3H]flumazenil. There was an overall decrease in [3H]FNP binding 12 but not 24 h after PTZ treatment. In contrast, [3H]muscimol binding was minimally affected, and [3H]flumazenil binding was unchanged after PTZ treatment. Additional binding studies were performed with well-washed cerebral cortical homogenates to minimize the amount of endogenous GABA. There was no PTZ effect on specific [3H]FNP binding. However, there was a significant reduction in the stimulation of [3H]FNP binding by GABA. The results showed that an acute injection of PTZ caused transient changes in GABAA receptor mRNA levels without altering receptor number but affected the coupling mechanism between the GABA and benzodiazepine sites of the GABAA receptor.

Animals↗

Electrophysiological and behavioral effects of Tyr-D-Arg-Phe-Sar on locus coeruleus neurons of the rat.

The effect of Tyr-D-Arg-Phe-Sar (TAPS), a mu-selective tetrapeptide analog of dermorphin, was studied in the rat both in vitro, using slices of the locus coeruleus, and in vivo, after microinjection into the locus coeruleus. In electrophysiological studies, TAPS (1-100 nM) was able to inhibit spontaneous firing, cause hyperpolarization of the membrane potential and reduce the input resistance of neurons of the locus coeruleus, suggesting that there was an effect on the potassium channels. Based on the inhibition of the spontaneous firing rate, the average IC50 for TAPS was calculated to be 1.9 nM, a value lower than that reported for dermorphin or morphine. The TAPS-induced effects were antagonized by naloxone, with a dissociation equilibrium constant of 1.96 +/- 0.14 nM. The results indicate that TAPS binds to mu-opioid receptors on the cell membrane of neurons of the locus coeruleus to cause its inhibitory actions. In behavioral study, TAPS was microinjected bilaterally via chronically implanted cannulae into the locus coeruleus of non-anesthetized rats and its effects on locomotor activity determined. TAPS, at concentrations of 1 microM and 10 microM, but not of 0.1 microM, induced hypolocomotion/sedation and the effect was significantly reversed by naloxone (5 mg/kg i.p.). Taken together, these data suggest that TAPS has an inhibitory effect on neurons of the locus coeruleus and produces hypolocomotive/sedative effects in vivo.

Analgesics↗

Striatal glutamate release is important for development of ischemic damage to striatal neurons during rat heatstroke.

This study attempted to ascertain whether heatstroke-induced ischemia is associated with augmented striatal glutamate release and can be attenuated by NMDA receptor antagonists. Mean arterial pressure (MAP), striatal cerebral blood flow (CBF), striatal glutamate release and striatal neuronal damage score were assessed in saline-treated rats and in rats treated with NMDA receptor antagonists. Heatstroke was induced by exposing the animals to a high ambient temperature; the moment at which MAP and CBF began to decrease from their peak levels was taken as the onset of heatstroke. During onset of heatstroke, rats displayed higher values of colonic temperature, striatal glutamate release and striatal neuronal damage score, and lower values of MAP and striatal blood flow compared with normothermic control rats. The decreased MAP, the diminished striatal blood flow, the augmented striatal glutamate release and the increased striatal neuronal damage score during onset of heatstroke were significantly attenuated by pretreatment with an NMDA receptor antagonist such as MK-801 or ketamine. In addition, the survival time (interval between onset of heatstroke and death) of the rats was extended by pretreatment with one of these two NMDA receptor antagonists. These results suggest that marked accumulation of glutamate in the striatum is important for the development of ischemic damage to striatal neurons during the onset of heatstroke.

Animals↗

Electrochemical studies of the effects of substance P on dopamine terminals in the rat striatum.

The purpose of this study was to investigate the regulation of dopamine (DA) release and clearance by Substance P (SP) in striatum. In vivo high speed chronoamperometric recording techniques, with Nafion-coated carbon-fiber electrodes, were used to evaluate extracellular DA concentrations in urethane-anesthetized Sprague-Dawley rats. SP was locally applied to striatum. Our data indicate that SP can induce DA release in striatum. However, only about half of the striatal sites respond to SP. Readministration of SP to the same site elicited a smaller DA release. These data suggest that SP-evoked release shows tachyphyllaxis and is heterogeneous in the striatum. Lesioning of DA neurons with 6-OHDA into the medial forebrain bundle abolished DA release induced by SP. It has been shown that SP interacts with three different tachykinin receptors. We found that application of the Neurokinin-1 (NK1) agonist [Sar9, Met (O2)11]SP, but not the NK3 agonist senktide, induced DA release, suggesting that SP-induced DA release may be mediated through NK1 receptors. We further examined SP effects on DA clearance in striatum. We found that pretreatment with SP significantly attenuated extracellular levels of DA after exogeneous application of DA, suggesting that DA clearance is augmented by SP. Taken together, our data demonstrate that substance P facilitates dopamine release and clearance in the striatum.

Animals↗

Primary hyperparathyroidism in pregnancy--report of 3 cases.

Three cases of primary hyperparathyroidism in pregnancy are described. Patient 1 developed left thigh pain and lower abdominal pain at 34 weeks' gestation. Patient 2 had right flank pain and lower abdominal pain at 32 weeks' gestation. Both patients accepted medical therapy initially, which resulted in poor control of hypercalcemia. Patient 1 delayed her parathyroidectomy until the postpartum period; she had maternal hypercalcemia and neonatal hypocalcemia. Patient 2 accepted parathyroidectomy at 32 weeks' gestation with an uneventful outcome for both mother and baby. Patient 3 was asymptomatic; her hyperparathyroidism was diagnosed postpartum after neonatal hypocalcemia and agreed to parathyroidectomy. All 3 patients had a parathyroid adenoma.

Adenoma↗

The antral follicle count predicts the outcome of pregnancy in a controlled ovarian hyperstimulation/intrauterine insemination program.

PURPOSE: Our purpose was to test whether age-related changes in antral follicle counts can predict the pregnancy outcome in the early follicular phase of a controlled ovarian hyperstimulation/intrauterine insemination (COH/IUI) program. METHODS: A selected group of 107 women (36 healthy women requesting child sex preselection, 52 women with unexplained infertility, and 19 with minimal endometriosis) who underwent controlled ovarian hyperstimulation with clomiphene citrate (CC) plus human menopausal gonadotrophin (hMG) and subsequent intrauterine insemination were enrolled in the study. Transvaginal ultrasonography (7.0 MHz) was used to determine the total number of antral follicles (2-8 mm) in the right and left ovaries. The association among the antral follicle count, age, dominant follicle, and estradiol (E2) level on the day of human chorionic gonadotropin (hCG) was analyzed. The association of the pregnancy rate and OHSS with the antral follicle count, dominant follicle count, and age was also examined. RESULTS: The total antral follicle number decreased with age (P < 0.0001). Dominant follicle number increased with total antral follicle number in women who received CC plus hMG/ IUI(P < 0.0001). The pregnant group had a higher number of antral follicle and dominant follicles in comparison with the nonpregnant group (P < 0.01 and P < 0.02, respectively). The E2 level on the day of hCG injection increased positively with the total number of antral follicles (P < 0.0001) and the total number of dominant follicles (P < 0.0001). In women aged younger than 35 years, the pregnancy rate and dominant follicle number rose as the number of antral follicles increased (P < 0.03 and P < 0.0001, respectively). The pregnancy rate was low (2/39) in women aged older than 35 years regardless of the number of antral follicles (P < 0.05) and the extent of hMG administration (P < 0.02). Women aged older than 35 also produced fewer dominant follicles (P < 0.001). No pregnancy was achieved in a patient with an antral follicle number of less than five (17 cases). CONCLUSIONS: Age-related changes in antral follicle count significantly predicted the dominant follicle count and the pregnancy outcome. In women with antral follicle counts of less than five or who are older than 35 years, the application of COH/IUI may not be indicated.

Age Factors↗

Perinatal outcome of oligohydramnios without associated premature rupture of membranes and fetal anomalies.

To investigate the perinatal outcome of patients with oligohydramnios (amniotic fluid index < or = 5 cm), but without premature rupture of membranes and fetal congenital anomalies, data from 245 singleton pregnancies were analyzed and compared to those with normal amniotic fluid volumes (5 < amniotic fluid index < 24 cm, n=27,261). Significantly higher incidences of primiparity, pregnancy-induced hypertension, premature separation of placenta, past history of intrauterine fetal death, past history of preterm delivery, postterm pregnancy, and advanced maternal age were noted to be associated with the occurrence of oligohydramnios. Pregnancies complicated by a markedly diminished amniotic fluid volume assessed antenatally by ultrasound were significantly more frequently associated with adverse perinatal outcomes such as preterm delivery, low or very low birth weight, low Apgar scores, intrauterine fetal death, small-for-gestational-age newborns, meconium staining, cesarean delivery, neonatal intensive care, and neonatal death.

Cohort Studies↗