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H S Wang

Publications and source records attributed to H S Wang.

At least 19 recordsLinked to original sources
PubMed2001

Regulation of glutamine transport by the type I insulin-like growth factor receptor in a human neuroblastoma cell line.

We examined the effects of the monoclonal antibody against the type I insulin-like growth factor receptor (IGF-IR), alphaIR3, on cell growth and membrane glutamine (Gln) transport in a human neuroblastoma cell line, SK-N-SH. In the presence of alphaIR3 (2 microg/ml), the cell proliferation rate was significantly attenuated. Gln transport was decreased in the alphaIR3-treated group with the mechanism of decreasing maximum transport velocity without affecting transport affinity. The addition of alphaIR3 significantly decreased DNA and protein biosynthesis. Our results support the concept that the activation of IGF-IR partially mediates neuroblastoma cell proliferation by regulating membrane Gln transport.

Apoptosis↗
PubMed2001

Regulation of KChIP2 potassium channel beta subunit gene expression underlies the gradient of transient outward current in canine and human ventricle.

Expression of four members of the KChIP family of potassium channel beta subunits was examined in canine heart. Only one member of the gene family, KChIP2, was expressed in heart. There was a steep gradient of KChIP2 mRNA expression across the canine ventricular free wall. KChIP2 mRNA was 25-fold more abundant in the epicardium than in the endocardium, and this gradient paralleled the gradient in transient outward current (Ito) expression. In contrast, Kv4.3 potassium channel alpha subunit mRNA was expressed at equal levels across the ventricular wall. There was no difference in the pharmacological sensitivity of epicardial and endocardial Ito channels to flecainide, suggesting that the current is produced by the same channel in the two tissues. A similar gradient of KChIP2 expression was found across the ventricular wall of human heart, but not rat heart. It is concluded that transcriptional regulation of the KChIP2 beta subunit gene, rather than the Kv4.3 [alpha] subunit gene, is the primary determinant regulating the transmural gradient of Ito expression in the ventricular free wall of canine and human heart.

Animals↗
PubMed2001

Insulin-like growth factor-I stimulates amino acid transport in a glutamine-deprived human neuroblastoma cell line.

It is still unknown how insulin-like growth factor-I (IGF-I) regulates cancer cell growth in the condition of the limited availability of key nutrients, such as glutamine. We investigated the effects of IGF-I on cell growth and amino acid transport in a glutamine-deprived human neuroblastoma cell line, SK-N-SH. Cell growth was measured, and 3H-labeled amino acid transport was assayed after treatment with or without IGF-I (50 ng/ml) in 2 mM (control) and 100 microM glutamine concentrations. Cell growth rates were dependent on glutamine concentrations. IGF-I stimulated cell growth in both 2 mM and 100 microM glutamine. IGF-I stimulated glutamine transport in 100 microM glutamine with the mechanism of increasing carrier Vmax, but had no effect in 2 mM glutamine. IGF-I also stimulated leucine, glutamate and 2-(methylamino)isobutyric acid transport in 100 microM glutamine. There were significant increases in [3H]thymidine and [3H]leucine incorporation in IGF-I-treated cells in both 2 mM and 100 microM glutamine. These data suggest that IGF-I stimulates cell growth by increasing amino acid transport in the condition of low glutamine levels in a human neuroblastoma cell line. This mechanism may allow to maintain cell growth even in nutrient-deprived tumor tissues.

Amino Acids↗
PubMed2001

Carcinoembryonic antigen in monitoring of response to systemic chemotherapy in patients with metastatic colorectal cancer.

The response to chemotherapy of solid tumors is generally assessed by measuring tumors visualized by imaging. However, the response assessment based on imaging is not always feasible because patients often have disease not measurable by imaging, such as diffuse peritoneal dissemination. We evaluated the correlation between the change on imaging and change in CEA levels for assessing chemotherapeutic response of patients with metastatic colorectal cancer. Between July 1993 and August 1999 we retrospectively examined 136 patients with metastatic colorectal carcinoma, all of whom had measurable lesions. Forty patients received oral tegafur-uracil (300 mg/m2/day) plus folinic acid (60 mg/day) for 4 weeks, repeated every 5 weeks, as the firstline treatment. Another 96 patients received either a weekly intravenous bolus injection of 5-fluorouracil (400 mg/m2) plus folinic acid (20 mg/m2), or an intravenous bolus injection of 5-fluorouracil (425 mg/m2) plus folinic acid (20 mg/m2) for 5 consecutive days every month. Responders, based on CEA assessment, were defined as those with a greater than 50% drop in CEA level for more than 4 weeks. The pretreatment CEA levels were elevated beyond the normal cutoff value in 110 (81%) patients. A response rate of 18.4% (95% CI, 11.9-24.9%), including 8 complete remissions and 17 partial remissions, was achieved according to imaging studies. The response rate assessed by CEA was 25% (34/136). Sixteen responders (47%) based on CEA had no remission on imaging. The sensitivity of change in CEA levels in the prediction of true responders and progressive diseases on imaging were 72% and 81%, respectively. In terms of the positive predictive value, change in CEA levels in the prediction of true responders and progressive disease on imaging were 53% and 85%, respectively. Patients with remarkable falls on CEA levels survived significantly longer than nonresponders (P < 0.001, log-rank test). At follow-up of 48 months the median survival for responders and nonresponders assessed by CEA was 28 months and 13 months, respectively. These data suggest that measurement of CEA levels might be helpful in monitoring chemotherapeutic response when imaging study is unsuitable for assessing the response in clinical practice. Furthermore, measurement of CEA levels may be helpful in determining the prognosis of patients with metastatic colorectal cancer receiving chemotherapy.

Adult↗
PubMed2001

Cdk5 mediates changes in morphology and promotes apoptosis of astrocytoma cells in response to heat shock.

The cyclin-dependent kinase member, Cdk5, is expressed in a variety of cell types, but neuron-specific expression of its activator, p35, is thought to limit its activity to neurons. Here we demonstrate that both Cdk5 and p35 are expressed in the human astrocytoma cell line, U373. Cdk5 and p35 are present in the detergent-insoluble cytoskeletal fraction of this cell line and Cdk5 localizes to filopodia and vinculin-rich regions of cell-matrix contact in lamellopodia. When exposed to a 46(o)C heat shock, U373 cells change shape, lose cell-matrix contacts and show increased levels of apoptosis. To test whether Cdk5 activation might play a role in these events, U373 cells were stably transfected with histidine-tagged or green fluorescent protein-tagged constructs of Cdk5 or a dominant negative mutation, Cdk5T33. Under normal growth conditions, growth characteristics of the stably transfected lines were indistinguishable from untransfected U373 cells and Cdk5 localization was not changed. However, when subjected to heat shock, cells stably transfected with Cdk5-T33 remained flattened, showed little loss of cell-matrix adhesion, and exhibited significantly lower levels of apoptosis. In contrast, cells that overexpressed wild-type Cdk5 showed morphological changes similar to those seen in untransfected U373 cells in response to heat shock and had significantly higher levels of apoptosis. Heat-shocked cells showed changes in p35 mobility and stability of the Cdk5/p35 complex consistent with endogenous Cdk5 activity. Together these findings suggest that endogenous Cdk5 activity may play a key role in regulating morphology, attachment, and apoptosis in U373 cells, and raise the possibility that Cdk5 may be a general regulator of cytoskeletal organization and cell adhesion in both neuronal and non-neuronal cells.

Apoptosis↗
PubMed2001

Acute necrotizing encephalopathy of childhood.

Symmetric change of the entire area of the bilateral thalami, as with panthalamic lesions, plus involvement of other regions in the brain rarely occurs to previously healthy children. The term, acute necrotizing encephalopathy of childhood, has recently been proposed. Its clinical, radiological, and pathological features are described. This disease predominantly affects infants and young children living in Taiwan and Japan, and manifests itself as acute encephalopathy following 2 to 4 days of fever and minor symptoms of the respiratory and/or gastrointestinal systems. The hallmark of this encephalopathy consists of multifocal, symmetric brain lesions affecting the bilateral thalami, and/or cerebral periventricular white matter, brainstem tegmentum, or cerebellar medulla, which can be documented by ultrasonography, computed tomography, and magnetic resonance imaging of the brain. The prognosis is usually poor. Less than 10% of patients recover completely. Cases with good outcome were reported to have reversible imaging changes. Focal neurologic deficits are common sequelae. The pathogenesis of acute necrotizing encephalopathy of childhood is still not known. Some diseases, such as Reye's syndrome, vascular occlusion, tumor, hemorrhage of the thalamus, Sandhoff disease, or Leigh and Wernicke encephalopathies must be differentiated clinically, radiologically, or pathologically. By excluding other disease entities, acute necrotizing encephalopathy of childhood can be diagnosed.

Acute Disease↗
PubMed2000

Immunohistochemistry of advanced glycation end products in neurofilamentous axonal spheroids induced by beta-beta'-iminodipropionitrile in lower motor neurons of rat.

Chronic parenteral administration of beta-beta'-iminodipropionitrile (IDPN) in adult female rats induces large neurofilament-rich axonal spheroids (AXS) in spinal motor neurons closely resembling those AXS in early phases of amyotrophic lateral sclerosis. Immunohistochemistry of advanced glycosylation end-products (AGEs) in axonal spheroids was performed in the present study. Anti-AGE and anti-neurofilament antibodies strongly co-labeled IDPN-induced axonal spheroids, whereas motor neuron soma showed little AGE immunoreactivity. In an attempt to modify and intensify glycosylation, another group of IDPN rats was made hyperglycemic with streptozotocin after IDPN intoxication. These hyperglycemic rats showed AXS with striking AGE immunoreactivity. An additional group of rats made hyperglycemic before IDPN intoxication showed markedly diminished AXS formation, with a few small AGE-positive AXS in anterior horns. Findings suggest that AGEs are involved in neurofilament crosslinking as well as disassembly of neurofilament induced by IDPN with or without hyperglycemia. Hyperglycemia did not intensify neurofilament aggregation. Additional immunohistochemistry revealed not only aberrant phosphorylation, but also intense local production of Cu/Zn superoxide dismutase and nitrotyrosine in axonal spheroids, probably secondary to superoxide generation as a consequence of AGE production at neurofilament protein, impeding its assembly as hypothesized in motoneuron diseases.

Animals↗
PubMed2000

Paclitaxel-induced cell death: where the cell cycle and apoptosis come together.

BACKGROUND: Compelling evidence indicates that paclitaxel kills cancer cells through the induction of apoptosis. Paclitaxel binds microtubules and causes kinetic suppression (stabilization) of microtubule dynamics. The consequent arrest of the cell cycle at mitotic phase has been considered to be the cause of paclitaxel-induced cytotoxicity. However, the biochemical events, downstream from paclitaxel's binding to microtubules, that lead to apoptosis are not well understood. METHODS: The authors examined recent scientific literature about the mechanisms by which paclitaxel exerts cytotoxicity. RESULTS: In addition to an arrest of the cell cycle at the mitotic phase in paclitaxel-treated cells, recent discoveries of activation of signaling molecules by paclitaxel and paclitaxel-induced transcriptional activation of various genes indicate that paclitaxel initiates apoptosis through multiple mechanisms. The checkpoint of mitotic spindle assembly, aberrant activation of cyclin-dependent kinases, and the c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) are shown to be involved in paclitaxel-induced apoptosis. Consistent with observations that microtubules of different status (e.g., cytoskeletal microtubules vs. mitotic spindles) have different sensitivity to paclitaxel, the concentration of paclitaxel appears to be the major determinant of its apoptogenic mechanisms. CONCLUSIONS: Advances in research of the cell cycle and apoptosis have extended our understanding of the mechanisms of paclitaxel-induced cell death. Further elucidation of resistance and enhancement of paclitaxel-induced apoptosis should expedite the development of better paclitaxel-based regimens for cancer therapy.

Animals↗
PubMed2000

Elevation of insulin-like growth factor-binding protein-1 mRNA expression following hormone replacement therapy.

The purpose of this study was to investigate the possible regulatory roles of insulin-like growth factors (IGF) and IGF binding protein-1 (IGFBP-1) on postmenopausal endometrium in women undergoing hormone replacement therapy (HRT). Endometrial tissues and blood samples were collected from 25 postmenopausal women with abnormal uterine bleeding before and after HRT. As a control, blood and endometrial samples were also obtained at mid-luteal phase (days 18-23 of the menstrual cycle) from 10 women with benign uterine leiomyoma during surgical intervention. Expression of mRNA for IGF-I, IGF-II, type 1-IGF receptor, IGFBP-1, oestrogen receptor (ER) and progesterone receptor (PR) in the endometrium was explored by a semiquantitative reverse transcription-polymerase chain reaction (RT-PCR). Serum concentrations of IGFBP-1, oestradiol, progesterone, follicle stimulating hormone (FSH) and sex hormone-binding globulin (SHBG) were also determined. In the endometrium obtained from postmenopausal women with abnormal uterine bleeding (before HRT), expression of IGFBP-1 was undetectable, whereas PR expression was abundant. HRT significantly up-regulated expression of IGFBP-1 but down-regulated PR. Moderate expression of IGF-I, IGF-II, type 1-IGF receptor and ER was identified in the postmenopausal endometrium before HRT. HRT significantly down-regulated IGF-I, up-regulated IGF-II, but had no effects on expression of type 1-IGF receptor and ER. In conclusion, up-regulation of IGFBP-1 collaboratively with down-regulation of IGF-I may account for the protective effect of progesterone in HRT on the endometrium.

Endometrium↗
PubMed2000

Preoperative carcinoembryonic antigen level as an independent prognostic factor in colorectal cancer: Taiwan experience.

BACKGROUND: Preoperative carcinoembryonic antigen (CEA) level is considered as a factor predictive of survival in colorectal cancer patients. Patients with normal (<5 ng/ml) or lower preoperative CEA levels were reported to have significantly longer survival. This study was carried out in an effort to evaluate the prognostic significance of preoperative CEA levels of patients with colorectal cancer in Taiwan. METHODS: Between 1990 and 1994, 218 patients with histologically confirmed colorectal cancers were evaluated retrospectively at the Veterans General Hospital-Taipei. All the patients had undergone potentially curative surgery. Patients with metastatic diseases were not included. 5-Fluorouracil-based adjuvant chemotherapy was administered if the patients had Dukes' C disease. Reference to the Dukes' classification was according to the classical criteria described in 1932 for carcinoma of the rectum and adapted for use in colonic tumors. Data on gender, age, degree of tumor differentiation, location of the tumor, tumor size, lymph node metastasis, penetration of the bowel wall and preoperative CEA levels were analyzed to determine their association with survival. Blood samples for CEA measurement were taken a few days before operation and were analyzed using the radioimmunoassay method. Multivariate analysis by Cox's proportional hazards regression model was performed to determine the most important predictors of survival among all of the possible variables. RESULTS: By univariate analysis, the size of the tumor (p = 0.012), lymph node metastases (p = 0.007), penetration of the bowel wall (p < 0.001) and preoperative CEA levels (p < 0.001) were found to be significant prognostic factors, while gender, age, degree of tumor differentiation and location of the tumor were not significant. By multivariate Cox analysis, lymph node metastases (p = 0.003), penetration of the bowel wall (p = 0.0001) and preoperative CEA levels (p = 0.0001) were found to be independent prognostic factors in colorectal cancer patients. CONCLUSIONS: The data from our study indicate that in addition to lymph node metastases and penetration of the bowel wall, the preoperative CEA levels are also an independent prognostic factor in non-metastatic colorectal cancer patients after curative surgery. This could serve as an appropriate modification to the initial Dukes' scheme in colorectal cancer.

Adenocarcinoma↗
PubMed2000

Phase II study of oral tegafur-uracil and folinic acid as first-line therapy for metastatic colorectal cancer: Taiwan experience.

BACKGROUND: Tegafur-uracil has become an important regimen in the treatment of metastatic colorectal cancer. Tegafur is a prodrug that is converted to 5-fluorouracil (5-FU) and has been reported to be less toxic and to have a higher therapeutic index. The additional advantage of tegafur is oral administration, an important consideration to improve the quality of life in these patients. Tegafur in combination with uracil is thought to have greater anti-tumor activity due to the inhibitory effect of uracil on the degradation of 5-FU by hepatic dihydropyrimidine dehydrogenase. Tegafur with folinic acid has been reported with modest efficacy and acceptable toxicity. The purpose of this study was to evaluate the effectiveness and toxicity profile of oral tegafur-uracil plus folinic acid in Chinese patients with metastatic colorectal cancer. METHODS: Between May 1998 and August 1999, 40 patients with metastatic colorectal carcinoma were enrolled in this study. All the patients had to have measurable lesions. The initial dose of tegafur-uracil was 300 mg/m2/day for 28 days, followed by a 7-day rest period. Folinic acid was administered orally at a dose of 60 mg/day concurrently with tegafur-uracil. For patients with neutrophil count <1500/microl or a platelet count <100,000/microl after treatment, the treatment was postponed for a maximum of 2 weeks. After that time, if the neutrophil count was 1000-1500/microl and the platelet count was 70,000-100,000 microl, the dose of tegafur-uracil was reduced by 50%, and if lower values resulted, the treatment was discontinued. RESULTS: Forty patients received a total of 318 courses of treatment and a response rate of 32.5% (95% CI, 18-47%), including five complete remissions and eight partial remissions, was achieved. Toxicity was mild and generally tolerable. Gastrointestinal toxicities, including diarrhea, nausea and vomiting, were the major side effects. Seven incidences (17.5%) of grade 3-4 gastrointestinal toxicity were observed. Hematological toxicities were minimal with no evidence of severe (grade 3 or 4) leukopenia and thrombocytopenia. No episode of hepatic, renal, cardiac or neurological toxicity occurred. Two patients (5%) developed transient painful fissuring erythroderma over their palms and soles (the hand-foot syndrome). CONCLUSIONS: The data from our study indicate that oral tegafur-uracil plus folinic acid is an active and tolerable first-line treatment for Chinese patients with metastatic colorectal cancer, with the additional advantage of being easily administered at home.

Adenocarcinoma↗
PubMed2000

Cyclic changes in serum levels of insulin-like growth factor binding protein-1 in women treated with clomiphene citrate and tamoxifen.

In order to investigate the cyclic changes of serum insulin-like growth factor-I (IGF-I), IGF binding protein-1 (IGFBP-1) and IGFBP-3 levels in menstrual cycles treated with or without antiestrogens (clomiphene citrate and tamoxifen), we treated 24 young women having irregular menstrual cycles with either clomiphene citrate (100 mg/day) (n = 12) or tamoxifen (60 mg/day) (n = 12) from the 5th to the 9th day of the menstrual cycle. Without antiestrogens, 12 women with regular menstrual cycles were recruited as controls. There was a preovulatory (day 13) peak of circulating IGFBP-1 in women treated with or without antiestrogens. A significant concomitant increase in serum estradiol was also observed on day 13 of the menstrual cycle in subjects treated with clomiphene citrate and in controls. However, no significant elevation in preovulatory estradiol was detected in women treated with tamoxifen. In clomiphene citrate and control groups, a significant positive correlation was found between circulating IGFBP-1 and estradiol, and between serum levels of IGFBP-1 and inhibin A at the preovulatory stage (on day 13). In contrast, no such association was observed in the tamoxifen group. Unlike cyclic changes in circulating IGFBP-1, serum concentrations of IGF-I and IGFBP-3 remained unchanged throughout the menstrual cycle in all groups. In conclusion, the preovulatory peak of circulating IGFBP-1 can be induced in cycles treated with both clomiphene citrate and tamoxifen. In addition, a significant positive correlation between estradiol, inhibin A and IGFBP-1 at the preovulatory stage indicates that IGFBP-1 may also reflect follicular development and may further be used as an additional indicator to monitor folliculogenesis under clomiphene citrate treatment.

Adult↗
PubMed2000

Molecular basis for differential sensitivity of KCNQ and I(Ks) channels to the cognitive enhancer XE991.

Channels formed by coassembly of the KCNQ1 (KvLQT1) subunit and the minK subunit underlie slowly activating cardiac delayed rectifier (I(Ks)) in the heart, whereas two other members of the KCNQ channel family, KCNQ2 and KCNQ3, coassemble to underlie the M current in the nervous system. Because of their important physiological function, KCNQ channels have potential as drug targets, and an understanding of possible mechanisms that would enable tissue-specific targeting of these channels will be of significant value to drug development. In this study, we examined the role of the minK subunit in determining the response of KCNQ1 channels to blockade by the cognitive enhancer XE991. Coexpression with minK markedly decreased the sensitivity of KCNQ1 to blockade by XE991. When measured at the end of a 500-ms step, XE991 blockade of the KCNQ1+minK current had a K(D) value of 11.1 +/- 1.8 microM, approximately 14-fold less sensitive than the block of the KCNQ1 current (K(D) = 0.78 +/- 0.05 microM). In addition, XE991 reduced activation and deactivation time constants and caused a rightward shift in the activation curve of KCNQ1+minK, but affected none of these parameters for KCNQ1 alone. Also, XE991 block of KCNQ1+minK, but not of KCNQ1, was time- and voltage-dependent. We conclude that the presence of minK in the I(Ks) channel complex gives rise to differential sensitivity of KCNQ and I(Ks) channels to blockade by XE991. Our results have implications for drug development by demonstrating the important potential role of accessory subunits in determining the pharmacological properties of KCNQ channels.

Animals↗
PubMed2000

Regulation and functions of c-Jun N-terminal kinase/stress-activated protein kinase.

The cell uses a complex signal transduction network both to respond to changes in its microenvironment and to integrate all of its intracellular signals. Actions of various signals in the cellular signal transduction network converge at the mitogen-activated protein kinase (MAPK) cascades, which lead to and activate transcription factors in the nucleus and other effectors throughout the cell. Extracellular signal-regulated kinases (ERKs), c-Jun N-terminal kinases/stress-activated protein kinases (JNK/SAPK), and p38 are some of the better characterized members of the MAPK family. Unlike ERK mainly responding to mitogens, JNK/SAPK was originally identified as a stress-related kinase and it has been extensively demonstrated to be associated with apoptosis. However, recent studies have further indicated that JNK/SAPK also has many functions other than the promotion of apoptosis. The repertoire of the JNK/SAPK pathway is wide-ranging, and its functions can vary, and even oppose each other, depending on the cell types and stimuli. It remains a challenge for biomedical scientists to elucidate the distinct role of JNK/SAPK in each model system.

Animals↗
PubMed2000

gamma-sarcoglycan deficiency muscular dystrophy in two adults.

All dystrophin-associated proteins contain sarcoglycan complex. Different forms of muscular dystrophy are caused by defective expression of different proteins of this structure. gamma-Sarcoglycan deficiency muscular dystrophy, so-called severe childhood autosomal recessive muscular dystrophy (SCARMD), is a rare disease that has not been previously reported in Taiwan. This paper describes two Taiwanese adults with this disease: a 26-year-old man with calf pseudohypertrophy who had weakness in both legs for 1 year; and a 43-year-old woman who had progressive weakness in all four limbs, with the initial symptom of gait disturbance at the age of 32 years. Analysis of muscle biopsy specimens, which showed total deficiency of gamma-sarcoglycan protein on immunostaining, confirmed the diagnosis of SCARMD in both cases. However, the clinical manifestations in these two patients, including lower proximal limb weakness initially developing in adulthood with a slow progressive course, are different from previously reported cases of SCARMD. The literature on this disease is reviewed and possible mechanisms of these distinct clinical presentations are discussed.

Adult↗
PubMed2000

Changes in mRNA expression of insulin-like growth factors and insulin-like growth factor-binding proteins in ovarian granulosa cells after cotreatment with growth hormone in low responders.

BACKGROUND: Insulin-like growth factors (IGFs) in the intraovarian autocrine control mechanism may serve as a central signal, and the granulosa cell is their site of production, reception, and action. In addition, various IGF-binding proteins (IGFBPs) are thought to modulate and regulate the actions of IGFs and in turn influence the growth and maturation of ovarian follicles. METHODS: To further investigate the follicular growth and maturation regulated by IGFs and IGFBPs in the ovary of low responders, 14 cases of low responders cotreated with growth hormone (GH) were studied. Another 14 normal responders without GH treatment were also recruited as controls. RESULTS: Serum levels of estradiol on day 6 and day 9 of the cycle and on the day of HCG administration, and the numbers of oocytes retrieved and follicles on the day of oocyte retrieval were significantly lower in low responders before growth hormone (GH) treatment than those in low responders after GH treatment as well as those in normal responders. Expression of both IGF-II and IGFBP-1 mRNA was elevated (by 23% and 35%, respectively) in granulosa cells from low responders after GH treatment as compared to that in low responders before GH treatment. In contrast, there was a substantial decrease (16%) in expression of IGFBP-3 mRNA in granulosa cells from low responders after GH treatment. Clinically, the pregnancy rate was lower in low responders after GH treatment as compared to controls (7% vs. 29%). CONCLUSION: Cotreatment with growth hormone in low responders might not increase the pregnancy rate.

Anovulation↗