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Biomedical subjects

R H Wu

Publications and source records attributed to R H Wu.

At least 37 records · Page 2Linked to original sources
PubMed1988

Effect of growth hormone treatment on sleep EEGs in growth hormone-deficient children.

Total sleep time, sleep stages 1-4, REM, REM latency, and sleep efficiency were analyzed in seven children with growth hormone deficiency (GHD) before and after growth hormone (GH) therapy. Before GH therapy, GHD children spent 19.5% of their total sleep time in REM sleep, 9.7% in stage 1, 41.0% in stage 2, 10.0% in stage 3, and 19.7% in stage 4. GHD children had more stage 1 and 3 sleep and less REM as compared with age-matched normal children reported by Williams et al. After GH therapy was initiated, six of the seven patients had decreases in the duration of stage 3 sleep, with an average decrease of 21.8 min. The difference between stage 3 sleep before and during GH treatment was significant, with a p value of less than 0.025. When the results were expressed as the percentage of the total sleep period, the difference was also significant, (10.0 +/- 2.0 to 7.5 +/- 3.1%, mean +/- SD; p less than 0.05). No other sleep parameters were significantly affected by GH therapy. The changes observed in stage 3 sleep, non-REM sleep, and the lack of any other changes in sleep before and after GH therapy have not been described before in GH-deficient children. They differ from studies in normal humans and animals which showed that REM sleep increased with administration of growth hormone. These differences suggest that GH deficiency is associated with a specific sleep EEG anomaly that is corrected in part by GH therapy.

Child↗
PubMed1987

Reversibility of deficient sleep entrained growth hormone secretion in a boy with achondroplasia and obstructive sleep apnea.

Obstructive sleep apnea may lead to disordered sleep architecture and impair the physiologic slow wave sleep related growth hormone release. Obstructive sleep apnea occurs with craniofacial syndromes and in children with airway narrowing, pharyngeal hypoplasia, tonsillar adenoidal hypertrophy, micrognathia and achondroplasia. To examine the relationship between disordered sleep and growth hormone release we studied a 9 year old male with achondroplasia, growth failure (3 cm/year) and obstructive sleep apnea. Polysomnography data and a 20 min sampling for sleep entrained growth hormone showed before therapeutic tracheostomy numerous apneic episodes, absent slow wave sleep and abnormal low growth hormone secretion during sleep. Normalized slow wave sleep entrained growth hormone secretion after tracheostomy led to a sustained increase in growth rate. Normal growth rate (greater than 5 cm/year) continues 2 years after tracheostomy. We conclude that obstructive sleep apnea may impair sleep related growth hormone release. Obstructive sleep apnea may be a useful model for other diseases in which growth failure and sleep disturbances are linked.

Achondroplasia↗
PubMed1987

[Reactivity of monoclonal antibodies ALT-01 and ALT-04 and identification of lung cancer-associated antigens].

Two IgG1 type monoclonal antibodies ALT-01 and ALT-04 were prepared by two different immunization schedules. ALT-01 was generated by fusing murine myeloma NS-1 cells with splenocytes from a BALB/c mouse immunized by human lung squamous carcinoma cells, which were coated by antisera to mixed human lymphocytes. For preparation of ALT-04, human lung squamous carcinoma xenograft-bearing nude mice were injected I. P. with the spleen cells of normal BALB/c mice in order to acquire immunofunction. The spleen cells from these tumor-bearing nude mice were fused with NS-1 cells. Then, these hybridomas were screened and cloned for 3 times. Two antibodies were shown to recognize the surface antigen on human lung carcinoma cells and several kinds of tumor cell lines but not those on normal cell lines. ALT-01 reacted to neither human lung carcinoma tissue nor its xenograft. ALT-04 reacted to human lung carcinoma tissue, of which, reaction to adenocarcinoma was the strongest but not to various normal tissues. Immunoprecipitation followed by SDS-polyacrylamide gel electrophoresis and autoradiography was used to detect the associated antigen in 35S-labeled human lung carcinoma cells. Antigens, reacting to ALT-01, show one band of Mr 38,000 but those to ALT-04 reveal two bands of Mr 48,000 and 36,000.

Animals↗
PubMed1987

[Radioimmunodetection of human lung cancer xenografts by isotope labeling monoclonal antibody ALT-04 in nude mice].

Three nude mouse models bearing the human lung cancer were established from two fresh surgical specimens and one cell line. Tumor histological structure and cell morphology were similar before and after transplantation. The monoclonal antibody ALT-04 (McAb ALT-04) against human lung cancer was labeled by 125I, 131I and 201Tl. Radioimmunodetection study showed that all the three kinds of xenografts in nude mice were specifically located by McAb ALT-04. Imaging examination confirmed the ability of isotope labeling McAb ALT-04 to detect the presence of transplanted human lung cancer tissues without the aid of background subtraction manipulations. It is suggested that McAb ALT-04 have the possibility of locating in the tumor diagnosis and guiding in the treatment.

Animals↗
PubMed1987

[Kinetic observation and analysis of the radioactivity distribution of 125I-labelled F(ab')2 fragments of monoclonal antibody against human lung cancer cells in normal mice].

Radioactivity distribution of 125I-labelled F(ab')2 fragments in 14 organs and tissues of normal mice for 11 time-phases from 0.5 hour to 7 days after injection was observed. The radioactivity-time curves of these organs and tissues were divided into three types according to their characteristics: excreting type (blood and liver), absorbing type (thyroid), absorbing-excreting type (the other organs and tissues). The organs fully perfused with blood had shorter peak-time and higher peak-value, such as heart, lung, kidney and liver. All of the peak-times were equal to or less than 2 days after injection, therefore the image taking should be kept away from this period. The excreting rate constants of slow metabolic component were similar for various organs and tissues except thyroid and brain. The brain had a low peak in the curve and small excreting rate constant. It was demonstrated that F(ab')2 fragments were able to penetrate the blood-brain barrier but absorption and excretion were slower compared with the other organs and tissues. The radioiodine was obviously concentrated in the subcutaneous tissue, which may have been the main cause of the subcutaneous tissue tumor induced by radioiodine. The radioactivity-time curve in which the peak value and inflect point existed simultaneously shows that radioactivity metabolism after injection of 125I-F(ab')2 follows three compartment models. The biological meanings corresponding to three sections of the blood radioactivity-time curve are pure distribution, distribution-recycle and catabolic-excretory phases, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Testicular failure in an adolescent with mesoappendicular testis.

A fifteen-year-old male presented with delayed puberty and cryptorchidism. Previous exploratory surgery for bilateral cryptorchidism resulted in left orchiectomy. The right testis was very high and intimately adherent to the mesentery of the appendix, and was left in situ. Subsequently progressive testicular failure was demonstrated by falling plasma testosterone and rising plasma gonadotropin levels. On elective surgical exploration, an atrophic testis with an independent blood supply was found adherent to the mesentery of the appendix. No spermatic duct was present, and orchiectomy was performed. The reasons for orchiectomy and the role of serial hormonal evaluations in the management of this unusual mesoappendicular testis case are reviewed.

Adolescent↗
PubMed1985

Achondroplasia and obstructive sleep apnea: correction of apnea and abnormal sleep-entrained growth hormone release by tracheostomy.

Severe obstructive sleep apnea in a patient with achondroplasia syndrome was found to result in a definitive deficiency of overnight growth hormone secretion related to absence of slow-wave sleep. Resolution of the apnea by tracheostomy resulted in normalization of growth hormone release and normal growth rates postoperatively. Sleep-related growth hormone deficiency may contribute to the short stature so often seen in a variety of craniofacial syndromes. Furthermore, this short stature may be reversible.

Achondroplasia↗
PubMed1981

Primary hypogonadism and 13/15 chromosome translocation in Prader-Labhart-Willi syndrome.

A 14-year-old male with Prader-Labhart-Willi syndrome (PLW) had hypogonadism, normal serum gonadotropin levels and 13/15 chromosome translocation. The 24-hour pattern of LH and FSH secretion was normal and comparable to that observed in males at the middle to late stage of puberty. LH rose during sleep and LRH infusion. Basal serum testosterone was low, in the 60-136 ng/dl range, and rose modestly during sleep, LRH and HCG. The 24-hour mean concentrations of androsterone, androsterone sulfate, dehydroepiandrosterone, dehydroepiandrosterone sulfate and prolactin were comparable with normal adolescent males. Biopsy of an undescended testis revealed poor morphology with disorganized spermatogenesis and normal Leydig and Sertoli cells. The 13/15 chromosome aberration was a balanced Robertsonian translocation occurring in his mother and in 5 of 6 siblings, although only the patient had PLW. These data indicate that hypogonadism in PLW is not necessarily hypothalamic-pituitary in origin and that D-chromosome translocations, or deletions per se are not sufficient to explain the etiology of PLW.

Adolescent↗
PubMed1977

Endocrine and cytogenetic studies in a patient with Turner's phenotype and a ring chromosome.

A 27-year-old woman with secondary amenorrhea and some of the somatic stigmata of Turner's syndrome was found to have a ring chromosome. Laparoscopy and ovarian biopsy showed hypoplastic ovaries and an absence of primordial follicles. Endocrine evaluation showed a normal 24-h mean LH level (12.5 mIU/ml), an elevated FSH level (28 mIU/ml) and a normal plasma estradiol level (64 pg/ml). The augmented FSH and normal LH response to LH-RH is similar to what is found in men with germinal cell aplasia (Sertoli-cell only). The synchronous initiations of normal LH and abnormally augmented FSH secretory episodes in this patient suggests the absence or decrease of some factor normally produced by the ovarian follicle which modulates the release of FSH in response to LH-RH.

Adult↗
PubMed1976

Endocrine studies in a phenotypic girl with XY gonadal agenesis.

An 18-year-old phenotypic girl with XY gonadal agenesis had endocrine studies. The patient had a small amount of sexual hair, a slightly enlarged clitoris, normal labia and no posterior fusion. Her vagina was of normal length, but no cervix was palpable. At laparoscopy, no gonads, uterus or fallopian tubes were identified. The buccal smear was chromatin negative and the karyotype was 46XY. The 24 h LH plasma pattern was qualitatively similar to that found in normal late pubertal subjects, but the values were in the castrate range. The 24h mean plasma concentrations of testosterone and dihydrotestosterone were 16.4 ng/dl and 14.2 ng/dl, respectively. Urinary estrogen excretion was 15 and 19 mug/day. These clinical and endocrine findings suggest that the patient was a genetic male in whom Mullerian regression occurred normally; however, the testes probably ceased functioning early in gestation preventing normal development of the Wolffian system. This set of events resulted in agenesis of the gonaductal system and female external genitalia. The patient represents the second example of this variation of male pseudohermaphroditism associated with XY gonadal agenesis.

Adolescent↗
PubMed1976

Clinical and laboratory heterogeneity in idiopathic hypogonadotropic hypogonadism.

Six young men with idiopathic hypogonadotropic hypogonadism had 24-h frequent blood sampling studies for measurement of LH, FSH and testosterone. Five of the patients had LH and FSH measured after administration of 100 mug LH-RH during waking and then during sleep. Four of the patients had testicular biopsies performed. The results of the present studies showed that 4 of the patients had no evidence of episodic LH, FSH, or testosterone secretion. The two patients who showed significant sleep related pulses of LH had the highest 24 h mean testosterone concentrations, the best responses to exogenous LH-RH and the most differentiated testicular biopsies. Sleep had no effect on the release of LH or FSH in response to LH-RH. These sutdies suggest that the clinical and laboratory heterogeneity of idiopathic hypogonadotropic hypogonadism may be the result of differences in the degree of endogenous LH-RH deficiency.

Adult↗