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Biomedical subjects

J Schenker

Publications and source records attributed to J Schenker.

At least 19 recordsLinked to original sources

The evolving story of female puberty.

The successful completion of puberty is a pre-requisite for reproduction. Therefore, the gynecologist, who deals daily with reproductive issues, should have a basic knowledge of puberty and the pathology associated with it. The understanding of the basic biological processes involved in pubertal development has advanced considerably in recent years. Also, changes in the timing of normal puberty and modern treatment for pubertal disorders have altered the clinical approach to these problems. In this review we discuss some of the basic science and clinical advances in this field and present the state of the art approach as we see it today.

Adolescent↗

Alcohol and mortality in middle-aged men from eastern France.

To evaluate prospectively the effect on mortality of wine drinking in Eastern France, we conducted an analysis on 34,014 consecutive middle-aged men coming for a comprehensive health appraisal between 1978 and 1983. We evaluated education, physical activity, smoking, and drinking habits by a questionnaire. Electrocardiogram, blood pressure, serum total cholesterol, and gamma-glutamyltransferase level were routinely measured. Seventy-seven per cent of the subjects drank wine; there was little difference between social classes in this proportion. We evaluated mortality over 10-15 years of follow-up. We estimated the relative risk (RR) of death by Cox proportional hazard models using nondrinkers as the reference and adjusting for six covariables. For an intake of 22-32 and 33-54 gm of alcohol per day, the RR of all-cause death was 0.70 [95% confidence interval (CI) = 0.59-0.82] and 0.76 (95% CI = 0.66-0.87), respectively. The lower mortality resulted from fewer deaths from cardiovascular disease and cancer. Above 128 gm per day of alcohol consumption, the RR was 1.37 (95% CI = 1.16-1.61). A moderate intake of wine (2-5 glasses per day) was associated with a 24-31% reduction in all-cause mortality, a proportion that was similar for smokers, ex-smokers, and nonsmokers.

Adult↗

Elevation of serum creatine phosphokinase and its MB isoenzyme during normal labor and early puerperium.

BACKGROUND: Chest pain or discomfort are infrequent complaints among women during labor and early puerperium, but when present they raise the suspicion of myocardial ischemia. The diagnosis of the latter is based upon serum elevatIon of certain enzymes, such as aspartate amino transferase, lactate dehydrogenase and creatine phosphokinase. Nevertheless, the normal patterns of these enzymes in the serum during labor and early puerperium have not been characterized well. OBJECTIVE: To determine serum creatine phosphokinase, lactate dehydrogenase and aspartate amino transferase levels in late pregnancy, and throughout labor and early puerperium. METHODS: Fifty women having normal pregnancies followed by uneventful vaginal deliveries were prospectively studied for serum lactate dehydrogenase, aspartate amino transferase and creatine phosphokinase including its MB isoenzyme before, during and after labor. Cardiac status was evaluated in all women using serial electrocardiographic and physical examinations. RESULTS: All women were found to have low to normal antepartum serum enzymes levels. However, during labor total creatine phosphokinase increased markedly, reaching a peak of 2-4 fold baseline levels 24 hours postpartum. It then declined gradually back to baseline. Nulliparous women reached substantially higher levels than multiparous women. The MB or so-called cardio-specific isoenzyme was found to be an important contributor to creatine phosphokinase surge in most women. Correlation was demonstrated between length of the active phase of labor and both total and MB creatine phosphokinase activity. There was no clinical or electrocardiographic evidence for cardiac muscle damage in any of the study patients. Serum lactate dehydrogenase and aspartate amino transferase were not altered during or after labor. CONCLUSIONS: Serum total creatine phosphokinase and its MB isoenzyme increase substantially during normal vaginal labor without evidence of myocardial ischemia. The uterus and placenta, two organs which were reported to embody substantial amounts of these enzymes, and which participate actively in the process of labor, are thought to release these enzymes to the circulation during labor. Knowing the normal patterns of these enzymes in the serum during labor and puerperium may prevent erroneous diagnoses of myocardial ischemia or infarction. Lack of electrocardiographic abnormalities and low lactate dehydrogenase and aspartate amino transferase levels may assist in excluding such diagnoses.

Aspartate Aminotransferases↗

Patterns of use of obstetrical interventions in 12 countries.

Recent obstetrical practice trends in 12 countries were surveyed. There was a 3-fold difference in caesarean section rates and a 10-fold difference in instrumental vaginal delivery rates among countries. There was a net increase in the caesarean section rate of all countries over the study period and a net decrease in the instrumental vaginal delivery rate of some countries. There was a decrease in the caesarean section rate during the last year of observation in Australia, Denmark and Finland. In general, countries with high caesarean rates also had high instrumental vaginal delivery rates. There was no consistent relationship between use of caesarean section and use of instrumental vaginal delivery, although in several countries increasing use of caesarean section was accompanied by decreasing use of instrumental vaginal delivery. Oxytocin use rates were associated positively with instrumental delivery but not with caesarean section rates. While it was not possible to determine the proportions of women who received appropriate obstetrical care, we can infer that a significant proportion of interventions were unnecessary or only marginally beneficial. Continued increases in rates of obstetrical intervention are unlikely to result in improvements in birth outcome overall and may pose a risk to mothers and their newborns.

Australia↗

Histoincompatibility in couples with unexplained infertility.

Class I human leukocyte antigens (HLA-A, -B) and class II (HLA-DR) antigens were determined in 18 carefully selected couples suffering from unexplained infertility and subsequently compared with 30 normal fertile couples with no history of secondary sterility and with a control group consisting of randomly matched women and men from our laboratory cell panel. No significant differences in the frequencies of HLA antigens were detected between infertile and control groups. The frequency of shared HLA-A, -B, and -DR antigens among members of the couples was similar in all the groups. Finally, the one-way mixed lymphocyte culture showed normal reactivity of both infertile parental pairs in all combinations tested.

Female↗

Mixed lymphocyte reactivity nonresponsiveness in couples with multiple spontaneous abortions.

We have endeavored to ascertain the possible existence of deviant recognition of antigens controlled by the major histocompatibility complex by lymphocytes originating in couples with a history of multiple spontaneous abortions of unknown cause. Human leukocyte antigen (HLA) typing, as well as one-way mixed lymphocyte culture (MLC) tests, were performed on 33 couples with multiple spontaneous abortions and subsequently compared to 30 fertile couples with no abortion history. No significant differences in the frequency of HLA were detected between the fertile and infertile groups. The frequencies of shared HLA-A and -B antigens among members of the couples were similar in both groups. In 70% of the cases studied, the husbands revealed a depressed cellular response to their respective wives; whereas reactivity to cells from other women proved normal. However, the response of allogeneic controls to these infertile women was normal. This implies that women with multiple abortions are not poor stimulators. The specific one-way decrease in the MLC reactivity appeared to be mediated by female-derived suppressor mechanisms and may be considered as one of the causes of the interrupted development of pregnancy in vivo.

Abortion, Habitual↗

Dissociation between sleep-related and TRH-induced prolactin secretion in seminiferous tubule failure.

Prolactin (PRL) secretion has been measured during sleep and following TRH administration in 8 patients aged 24-39 yr with seminiferous tubule failure and 36 controls. Basal LH levels were 25.7 +/- 14.7 mIU/ml in the patients compared to 11.5 +/- 4.2 mIU/ml in the controls (p less than 0.01) Corresponding FSH levels were 26.2 +/- 10.7 mIU/ml and 5.9 +/- 2.1 mIU/ml (p less than 0.001) Mean estradiol 17B and testosterone levels were similar in the 2 groups. The mean PRL secretion during sleep was 16.5 +/- 11.7 ng/ml in the patients and not different in 11 of the controls (12.4 +/- 3.2 ng/ml). One patient had a mean nocturnal PRL concentration of 44.1 ng/ml. In both groups, the mean sleep related PRL concentration was greater than that during waking hours. The average number of peaks in the 2 groups was similar. In the same patients, the peak PRL response to TRH (200 ug IV) was 81.9 +/- 18.8 ng/ml as compared to 32.1 +/- 10.7 ng/ml in the controls (p less than 0.001). It is concluded that PRL concentrations following pharmacological stimulation are increased in seminiferous tubule failure, whereas levels are normal in relation to the physiological stimulus of sleep.

Adult↗

Prolactin response to metoclopramide and chlorpromazine in primary testicular failure and isolated gonadotrophin deficiency.

The aim of the present study was to measure the PRL response to metoclopramide (MET) and chlorpromazine (CPZ) in seventeen patients with primary testicular failure and eight patients with isolated gonadotrophin deficiency (IGD). The responses were compared with those to TRH. Basal gonadotrophins and peak responses to LHRH were increased in testicular failure and reduced in IGD. Basal PRL levels were normal in both groups of patients. However, when compared with controls, the PRL response to both MET and CPZ as well as to TRH was exaggerated in primary testicular failure, whereas the responses wee decreased in IGD. In both patient groups, as well as in the controls, the PRL response to MET exceeded that to TRH and CPZ. It is suggested that alterations in the steroid milieu are responsible for the exaggerated PRL response to MET, CPZ and TRH in primary testicular failure and the reduced response observed in IGD.

Adolescent↗

The TSH response to TRH is exaggerated in primary testicular failure and normal in the male castrate.

Basal TSH levels and the TSH response to TRH have been evaluated in 26 males aged 20-48 years with primary testicular failure, and 6 males aged 58-69 years who had been orchidectomised for prostatic carcinoma. The patients with testicular failure were sequentially challenged at 30 min intervals with iv LRH (100 microgram), TRH (200 microgram) and the dopaminergic antagonist, metoclopramide (10 mg). The castrates received a bolus of LRH and TRH given together. The responses in the 2 patient groups were compared to a group of 28 healthy male controls aged 20-40 years, who received the sequential protocol and 8 elderly controls aged 65-79 years, who were given the LRH, TRH bolus. Mean +/- SD basal TSH levels were 3.0 +/- 1.2 muU/ml in primary testicular failure and significantly greater than both control and castrate groups. The peak TSH response to TRH was 18.4 +/- 7.4 muU/ml in testicular failure and significantly greater than in the young controls, where it was 11.5 +/- 5.0 muU/ml. The peak levels in the castrates and in the elderly controls were similar to the young male controls. Total T4 and T3, as well as FTI, primary testicular failure had a reduction in their T3 resin uptake. The normal TSH profile in the castrates indicates that a testicular factor produces the exaggerated responses in primary testicular failure.

Adult↗

Acute and delayed effects of DSIP (delta sleep-inducing peptide) on human sleep behavior.

A first study of DSIP (= synthetic delta sleep-inducing peptide) application to humans was carried out in six normal volunteers (four males and two females) under extensive psychophysiologic observations and measurements in a double-blind cross-over design. DSIP was applied as slow intravenous infusions at a dosage of 25 nmol/kg in the morning. The subjects immediately reported a feeling of sleep pressure, and sleep increased by 59% (median of total sleep time) within a 130-min interval after the treatment as compared with placebo. Delayed effects on subsequent night sleep were shorter sleep onset, reduced percentage of stage 1, and better sleep efficiency. Nevertheless, sophisticated behavioral and EEG analyses revealed no sedation in the classic pharmacologic way. The results suggest that DSIP in humans is also efficacious by sustaining natural sleep functions. The compound was well-tolerated and no psychologic, physiologic, or biochemical side effects were observed.

Delta Sleep-Inducing Peptide↗

Deficient blood pressure regulation in a case of hypersomnia with sleep drunkenness.

In a 43-year-old man suffering from hypersomnia with sleep drunkenness, a polygraphic sleep study with direct measurement of blood pressure was carried out. The main findings were lack of blood pressure activation with arousals during the sleep period and persistence of sleep levels after morning awakening. This indicates that cardio-vascular responses to the needs of active behaviour are insufficient. Taking into account feedback mechanisms of blood pressure on alertness, this could be a cause for sleep drunkenness and daytime sleepiness. The blood pressure sustaining drug etilefrine seems to alleviate these symptoms.

Adult↗

Exaggerated prolactin response to thyrotropin-releasing hormone and metoclopramide in primary testicular failure.

Twenty-eight severely oligospermic and azoospermic men aged 20 to 42 years were challenged with luteinizing hormone (LH)-releasing hormone (LHRH), thyrotrophin-releasing hormone (TRH), and the dopaminergic antagonist, metoclopramide, given at 30-minute intervals. According to basal gonadotropin levels, the patients were subdivided into three groups: those with severe testicular failure (basal LH > 20 mIU/ml and FSH > 14 mIU/ml); those with moderate testicular failure with predominant seminiferous tubule involvement (LH < 20 mIU/ml and FSH > 14 mIU/ml) and those with mild testicular failure (LH < 20 mIU/ml and FSH < 14 mIU/ml. With one exception, mean basal prolactin (PRL) levels were normal in all patients. In all three groups, however, there was an exaggerated PRL response to TRH, the response in severe and moderate testicular failure being greater than that in mild testicular failure. The response to metoclopramide was increased only in the first two groups, not in the group with mild testicular failure. When individual patients and control subjects were considered together, the peak PRL response to TRH correlated with both basal and peak gonadotropin responses to LHRH. However, the PRL responses did not correlate with 17 beta-estradiol, estrone, testosterone, or the estradiol-testosterone ratio. It is concluded that oligospermic and azoospermic subjects with the most severe testicular failure and the highest gonadotropin levels have the greatest PRL increases after TRH and metoclopramide, indicating that the PRL response is related to the degree of testicular failure.

Adult↗

Prolonged hyperprolactinemia in preterm infants.

Serum PRL levels were followed serially in full term (FT; 39-41 weeks) and preterm (PT; 30-32 weeks) infants, from birth to 12 and 20 postnatal weeks, respectively. Values were higher in FT infants than in PT infants on day 1 after birth (267 +/- 20 vs. 156 +/- 8 ng/ml) but were similar in both by the age of 2-4 weeks (69 +/- 8 vs. 69 +/- 6 ng/ml). Between the ages of 4-12 weeks, the serum PRL in FT infants fell to near adult levels (24 +/- 2 ng/ml), but this fall was seen much later in PT infants, between 12-20 weeks postnatally (23 +/- 2 ng/ml). When values in FT and PT infants were compared at parallel postmenstrual ages in contradistinction to postnatal ages, a similar course of PRL was discernable in both groups. These data may provide indirect evidence for the establishment and maturation of inhibition of PRL secretion (i.e. PRL-inhibitory factor production) postnatally, between 44-52 weeks postmenstrually.

Aging↗