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Biomedical subjects

J Steiner

Publications and source records attributed to J Steiner.

At least 37 records · Page 2Linked to original sources
PubMed1999

Impact and reversibility of chronic ethanol feeding on the reproductive axis in the peripubertal male rat.

Teenage drinking continues to be a major problem in the United States as well as abroad. A significant depression in serum testosterone in adolescents who consume EtOH has been well described. In the male rodent model, a similar fall in testosterone has been reported, and prevention with the opiate blocker naltrexone has been demonstrated. To explore further the impact of chronic EtOH exposure on the reproductive axis in peripubertal rats, we designed this study specifically to define whether or not there was recovery after abstinence by examining reproductive hormones and their genes during and after EtOH exposure. Peripubertal male rats 35 d old were fed an EtOH-containing diet or a calorically matched control diet for 60 d. A third group was fed the control liquid diet ab libitum. EtOH was then withdrawn and all animals were fed standard rat chow and water ad libitum for an additional 3 mo. The EtOH-imbibing animals were found consistently to weigh less than their pair-fed mates and liquid diet ad libitum animals. Serum testosterone levels and testicular weights were significantly decreased by EtOH whereas serum estradiol levels were higher, suggesting enhanced peripheral conversion by EtOH. Spermatogenesis, assessed by histological parameters, was unaltered by EtOH. Serum luteinizing hormone levels were not different among the groups. Hypothalamic luteinizing hormone-releasing hormone mRNA levels were unaffected by EtOH. During the 3-mo recovery period, all the changes reversed, with a significant increase noted in testosterone. All other parameters remained the same among the groups. Thus, although chronic EtOH exposure in the peripubertal age period results in significant reproductive alterations, there is complete recovery on withdrawal.

Animals↗
PubMed1999

Reversal of chronic ethanol-induced testosterone suppression in peripubertal male rats by opiate blockade.

Teenage drinking continues to be a significant problem in the U.S., as well as abroad. We have previously demonstrated that opiate blockade with naltrexone, a drug currently used in patients to diminish alcohol craving, prevented the fall in serum testosterone seen after acute ethanol (EtOH) exposure in young, peripubertal male rats. To follow-up on this reversal, a series of experiments was performed to determine if naltrexone would also prevent the testosterone suppression caused by chronic EtOH exposure. Peripubertal rats either 45 days old (mid-pubertal) or 55 days old (late pubertal) were fed an EtOH-containing liquid diet or pair-fed control diet for 14 days. Each animal was implanted with either a naltrexone containing or placebo pellet before starting the liquid diet. In each age group, EtOH alone significantly suppressed testosterone, whereas naltrexone prevented this fall, although it had no effect alone. Serum luteinizing hormone was also suppressed by EtOH; however, naltrexone did not abrogate this fall. In the 45-day-old animals, beta-luteinizing hormone mRNA levels rose significantly in the EtOH group, but not when naltrexone was coadministered with EtOH. There was no change in hypothalamic luteinizing hormone releasing hormone (LHRH) mRNA, pro-LHRH, or LHRH in any group at either age. Thus, naltrexone is able to partially prevent the EtOH-induced suppression of gonadal testosterone of young, adolescent male rats. This effect appears to be mediated directly at gonadal level, because hypothalamic and pituitary hormone changes were minor and nonsignificant.

Age Factors↗
PubMed1999

Effects of Nitric oxide synthase blockade on the acute response of the reproductive axis to ethanol in pubertal male rats.

The effects of ethanol (EtOH) and nitric oxide (NO) are well known in the adult male rat reproductive axis. In the present study, we investigate the effects of EtOH, NO, and their interaction on key genes and reproductive hormone levels in mid- (45-day) and late pubertal (55-day) male rats. Using three different NO synthase blockers--N'omega-nitro-L-arginine methyl ester (L-NAME), N'omega-nitro-L-arginine (L-NA), and 7-nitroindazole--we show that it is possible to block, in part, some of the disruptive effects of EtOH. L-NAME totally prevented the EtOH-induced fall in serum testosterone in both 45- and 55-day-old rats (p < 0.05 and p < 0.001, respectively). On the other hand, the D-NAME, an inactive isomer of L-NAME, did not protect testosterone from suppression caused by EtOH. Similarly, L-NA and 7-nitroindazole prevented the suppression of testosterone caused by EtOH in 55-day-old animals (p < 0.001 L-NA and p < 0.05 for 7-nitroindazole), but not in the 45-day-old rats. Serum luteinizing hormone (LH) was significantly reduced by EtOH in all the studies in both age groups. L-NAME (but not D-NAME) and L-NA prevented this inhibition in 55-day-old animals (p < 0.001 for L-NAME and p < 0.01 for L-NA). However, only L-NA was able to prevent the effects of EtOH on LH in the 45-day-old rats. 7-Nitroindazole was unable to prevent the decrease in LH in either age group. Despite changes in the other reproductive hormones, there were no consistent changes in hypothalamic concentrations of either LH releasing hormone (LHRH) or its precursor, pro-LHRH. No treatment caused any change in steady-state levels of beta-LH mRNA. There were no consistent changes in pro-LHRH mRNA; but, interestingly, in 45-day-old rats, L-NA given with or without EtOH lead to a significant fall in LHRH gene expression. Our findings indicate that the acute suppressive effects of EtOH on the hypothalamic-pituitary-gonadal axis of the pubertal male rat can be at least partially prevented by NO synthase blockade.

Animals↗
PubMed1999

Chronic alcohol consumption during male rat adolescence impairs skeletal development through effects on osteoblast gene expression, bone mineral density, and bone strength.

BACKGROUND: The effect of chronic alcohol ingestion on bone formation is mediated through its direct actions on osteoblasts. The affected population of mature osteoblasts declines in both number and function resulting in decreased cancellous bone volume and cortical bone strength. Although the mechanism of action on osteoblasts is unknown, alcohol alters osteoblast gene expression and matrix synthesis. METHODS: Male rats consuming alcohol (EtOH) daily for 60 days from 35 days of age until 95 days of age (unrecovered group) were compared to rats switched to a regular diet of rat chow without EtOH for an additional 90 days (recovered group). The effects of chronic dietary EtOH on skeletal development during adolescence were examined in the unrecovered and recovered rats by hormonal analysis, bone mineral density determination, bone histomorphometry, metaphyseal gene expression for osteoblast-specific proteins, and biomechanical analysis. RESULTS: The unrecovered EtOH imbibing rats weighed less than their paired isocaloric-fed and ad libitum mates. Statistically significant reductions occurred in femur lengths in the unrecovered EtOH-fed group compared to controls. Serum testosterone levels were significantly decreased by EtOH consumption but returned to higher normal levels during the recovery period. Serum insulin-like growth factor-1 (IGF-1) levels were unaffected by EtOH. Serum osteocalcin levels in the unrecovered EtOH-fed group were higher than those in the recovered group but EtOH intake did not elevate the unrecovered levels compared to isocaloric or ad libitum control rats. Quantitative computed tomography (QCT) determination of bone mineral density (BMD) revealed a statistically significant reduction only in the distal femur metaphysis in the unrecovered EtOH-fed rats. BMD increased during recovery in the distal femur metaphysis and femur mid-cortex. Image analysis of midsagittal sections of the proximal tibial metaphysis of unrecovered rats revealed reductions in cancellous area, trabecular cellularity and thickness, and increased trabecular separation. Cortical widths were significantly reduced by chronic EtOH consumption. These changes remained statistically significant at the end of the recovery period. Four-point biomechanical testing of femurs from EtOH-fed and control unrecovered groups revealed significant reductions in cortical strength, energy-to-failure, and stiffness. These cortical characteristics returned to normal values with abstinence. Tibial metaphyseal alpha-1 type I collagen and osteocalcin mRNA expression levels were significantly elevated above the paired isocaloric control levels after 60 days of EtOH consumption. Metaphyseal alkaline phosphatase mRNA levels remained unaltered by EtOH consumption in the unrecovered group. After 90 days of abstinence alpha-1 type I collagen and alkaline phosphatase gene expression levels remained significantly elevated over the isocaloric and ad libitum control levels (collagen) and the isocaloric control value (alkaline phosphatase). However, metaphyseal osteocalcin mRNA levels declined to normal levels during abstinence. CONCLUSIONS: Chronic consumption of EtOH during the peripubertal period of skeletal growth leads directly to decreased metaphyseal and cortical bone mediated through effects on osteoblasts. Removal of EtOH from the diet is accompanied by incomplete restoration of normal bone metabolism during skeletal growth.

Age Factors↗
PubMed1998

The role of gonadectomy and testosterone replacement on thymic luteinizing hormone-releasing hormone production.

We and others have identified luteinizing hormone-releasing hormone (LHRH) in cells of the immune system in both animals and humans. LHRH is an immunostimulant, and testosterone is an immunosuppressant. Because testosterone is known to modulate the concentrations of hypothalamic LHRH, we wondered whether testosterone might also alter the concentrations of rat thymic LHRH. Two weeks after castration or sham castration, adult male rats were implanted with either vehicle or testosterone capsules. All animals were killed 4 days after capsule implantation. Thymic LHRH concentration increased significantly in castrated animals. Testosterone replacement prevented this increase. The concentration of the LHRH precursor, proLHRH, decreased significantly, but testosterone replacement prevented this decrease. Steady-state concentrations of LHRH mRNA were not changed by castration or by hormonal replacement. In contrast to the post-castration increase in thymic LHRH, LHRH content of the hypothalamus decreased significantly. Whereas concentrations of LHRH were lower in the thymus than in the hypothalamus, proLHRH concentrations were much greater in the thymus. These data suggest that gonadal manipulation modulates LHRH molecular processing and its tissue concentration in the thymus in addition to those in the hypothalamus, and that the regulation of LHRH molecular processing by testosterone in the hypothalamus is different from that in the thymus.

Analysis of Variance↗
PubMed1998

Leptin alters the response of the growth hormone releasing factor- growth hormone--insulin-like growth factor-I axis to fasting.

Proper nutritional status is critical for maintaining growth and metabolic function, playing an intimate role in neuroendocrine regulation. Leptin, the recently identified product of the obese gene, may very well be an integral signal which regulates neuroendocrine responses in times of food deprivation. The present study examines leptin's ability to regulate hormonal synthesis and secretion within the GRF-GH-IGF axis in the adult male rat during almost 3 days of fasting. Serum levels of GH and IGF-I were drastically suppressed by fasting. Daily leptin administration was able to fully prevent the fasting-induced fall in serum GH. Leptin failed to restore IGF-I to control levels, however, suggesting possible GH resistance. Fasting caused an insignificant increase in GH mRNA, while leptin injections significantly increased steady-state levels of this message. The GRF receptor (GRFr) message was not altered with fasting or leptin treatment. Leptin also exhibited effects at the hypothalamic level. Fasting induced a sharp fall in GRF mRNA expression and leptin injections partially prevented this fall. However, there were no observed changes in the hypothalamic GRF content. These results provide evidence that leptin may function as a neuromodulator of the GRF-GH-IGF axis communicating to this hormonal system the nutritional status of the animal.

Animals↗
PubMed1998

Reversal of ethanol-induced testosterone suppression in peripubertal male rats by opiate blockade.

Teenage drinking is a major problem in the United States, as well as abroad. Besides psychosocial implications, ethanol (EtOH) has detrimental effects on the reproductive system. Clinical problems associated with reduced reproductive hormones include osteoporosis, decreased muscle function, anemia, altered immune function, prostate involution, and decreased reproductive abilities. Education coupled with strategies aimed at preventing these deleterious consequences even in the face of continued EtOH intake is extremely important. We have tested the possibility that naltrexone, a drug currently used in patients to decrease alcohol craving, might also prevent the fall in the male hormone, testosterone, caused by EtOH exposure. Rats aged 35 days old (prepubertal), 45 days old (midpubertal), and 55 days old (late pubertal) were injected (intraperitoneally) with either saline, EtOH, naltrexone, or EtOH plus naltrexone. In the two older age groups, EtOH significantly suppressed testosterone, which was prevented by administration of naltrexone. In the youngest animals, there was no treatment effect presumably due to low basal levels of testosterone. EtOH similarly reduced luteinizing hormone (LH), but this suppression was not prevented by naltrexone. There was no consistent effect of any treatment on hypothalamic concentration of pro-LH releasing hormone (RH) (LHRH), LHRH, or on steady-state levels of LHRH mRNA. We conclude that, as animals progress through puberty, EtOH suppresses LH and testosterone. The testosterone decline can be prevented by opiate blockade with naltrexone, an effect primarily seen at gonadal level. Thus, naltrexone, a drug already used clinically to reduce EtOH intake, also has protective physiological effects on the endocrine system.

Animals↗
PubMed1997

Cloning, sequencing and expression of the cDNA of endoxylanase B from Penicillium purpurogenum.

The cDNA for xylanase B from Penicillium purpurogenum was cloned and sequenced. This DNA encodes a protein of 208 amino acids which is expected to yield a protein of 183 residues upon processing of the N terminus. The sequence of the predicted protein is very similar to that of 40 other xylanase domains which belong to family G of cellulases/xylanases (73-21% identity).

Amino Acid Sequence↗
PubMed1997

Normalizing acute care: a day hospital/crisis residence alternative to inpatient hospitalization.

Normalization is the use of culturally valued means to enable people with disabilities to live culturally valued lives. In this article, the authors describe an effort to bring normalization practices to acute psychiatric care. They describe a day hospital/crisis respite diversion program that serves as an alternative to acute inpatient hospitalization and sketch the research project that fostered it. The authors argue that a day hospital/ crisis respite provides effective clinical care comparable to inpatient hospitalization but achieves greater potential for recovery through a normalizing philosophy and practice. An implication of this finding is that such programs based on the principle of normalization may be both cost effective as well as more empowering for patients.

Acute Disease↗
PubMed1997

Prevalence of dissociative disorders in an acute care day hospital population.

To estimate the prevalence of dissociative disorders in a day hospital and examine their relation to traumatic experiences, trained clinicians evaluated 70 of 229 patients consecutively admitted to an acute care day hospital. They used the Mini-Structured Clinical Interview for DSM-III-R Dissociative Disorders and the Traumatic Experience Questionnaire. Six of the 70 patients (9 percent) received a definite diagnosis of a dissociative disorder. Five of the six patients reported a childhood history of sexual or physical abuse. The results show that dissociative disorders are not rare among general psychiatric patients in a day hospital setting and are associated with histories of childhood trauma.

Adult↗
PubMed1997

Ethanol, growth hormone and testosterone in peripubertal rats.

The deleterious effects of ethanol on the hypothalamic pituitary growth hormone axis in adult male humans and animals have been well documented. It is also well established that ethanol has toxic effects on testicular function in adult humans and animals. Much less is known, however, about the effects of ethanol on the growth hormone (GH) axis and testicular function in adolescence. Recent studies have established that adolescent problem drinking is a widespread and growing threat to the health of young people in the United States. In the present study, therefore, we investigated if acute ethanol exposure in peripubertal male Sprague-Dawley rats altered normal pituitary and testicular function. Serum levels of GH and testosterone were measured at 1.5, 3, 6, and 24 h after a single i.p. injection of either saline or 3 g/kg body weight ethanol. Histologic analysis as well as serum testosterone levels allowed us to assign animals to either early puberty (35-day-old animals), mid-puberty (41-day-old animals), or young adult (51- and 66-day-old animals) status. Ethanol produced significant decrements in serum testosterone in the 51- and 66-day-old animals, with a trend toward suppression in the 41-day-old group. Furthermore acute ethanol administration significantly decreased serum GH (P < 0.0001 by 3 way ANOVA) demonstrating a significant effect of ethanol on serum GH in all age groups and at all time points studied when compared with saline injected controls (P < 0.01 by Turkey's studentized range test). Despite this significant fall in peripheral GH levels, there was no decrease in either GH mRNA or growth hormone-releasing factor (GRF) mRNA levels nor in hypothalamic concentration of GRF peptide. We conclude that, as in adult animals, acute exposure to ethanol causes a prolonged and severe decrement in serum GH which is possibly mediated at the level of secretion. In addition, there is attenuation in testosterone secretion. These data are all the more important since GH and testosterone play critical roles in organ maturation during this stage of development.

Analysis of Variance↗
PubMed1997

Jurkat cell proliferative activity is increased by luteinizing hormone-releasing hormone.

Jurkat cells were used to study the immunomodulatory role of luteinizing hormone-releasing hormone (LHRH) in immune cells. The Jurkat cell, a human mature leukemic cell line, phenotypically resembles resting human T lymphocytes and has been widely used to study T cell physiology. The data from this study demonstrate that the Jurkat cell concentration of immunoreactive LHRH was 210 +/- 36 pg/10(6) cells and that of proLHRH was 188 +/- 27 pg/10(6) cells (means +/- S.E.M.). The authenticity of this LHRH immunoreactivity is documented in two ways. First, both Jurkat LHRH and proLHRH immunoreactivity demonstrate dilutional parallelism with hypothalamic LHRH and proLHRH. Second, Jurkat lysates show LHRH bioactivity by releasing luteinizing hormone from rat anterior pituitary cells in culture. The presence of substantial amounts of LHRH in medium in which Jurkat cells were cultured for 72 h indicated that LHRH can be released from the cells. Using specific primers to exons 2 and 4 of the LHRH gene, we have found that Jurkat cells (like human T cells) express LHRH mRNA. The LHRH agonist, des-Gly10,D-Trp6-LHRH ethylamide, significantly increases the proliferative activity of Jurkat cells, as assessed by tritiated thymidine incorporation, from 15980 +/- 1491 c.p.m. in control to 28934 +/- 3395, 30457 +/- 3861 (P = 0.05 vs control) or 35299 +/- 5586 c.p.m. (P < 0.01 vs control) with 10(-11), 10(-9) or 10(-7) M agonist respectively. LHRH antagonist, [D-pGlu1,D-Phe2,D-Trp3,6]-LHRH, at a concentration of 10(-8) M decreases Jurkat cell proliferative activity form 17145 +/- 526 c.p.m. in control medium to 10653 +/- 1323 c.p.m. (P = 0.05). Co-incubation with the LHRH antagonist completely inhibits the proliferative stimulation induced by the LHRH agonist. Furthermore, applying monoclonal LHRH antibody to Jurkat cells inhibits the cell proliferative activity assessed by tritiated thymidine incorporation from 19900 +/- 2675 c.p.m. in control to 15680 +/- 2254, 15792 +/- 1854 and 9700 +/- 908 c.p.m. in media with 1:40, 1:20 and 1:10 dilution of purified antibody respectively (P < 0.01, 1:10 dilution compared with control). In addition, the cAMP level in LHRH-stimulated Jurkat cells is decreased to 74, 27 and 57% of control levels after 15, 30 and 45 min respectively of exposure to 10(-7) M LHRH agonist. In summary, Jurkat cells produce, process and release immunoreactive and bioactive LHRH, as do normal human T cells. Endogenous and exogenous LHRH increase Jurkat cell proliferative activity, and cAMP may be involved in LHRH-induced Jurkat cell proliferation. The Jurkat cell may be a useful model with which to study the role of LHRH in human T cell function.

Animals↗
PubMed1997

Geographic analysis of pertussis infection in an urban area: a tool for health services planning.

OBJECTIVE: This study examined whether incident cases of pertussis cluster in urban census tracts and identified community characteristics that predict high-incidence areas. METHODS: An ecological study design was used. The study population included all persons diagnosed with pertussis from January 1, 1986, through December 31, 1994. Maps of rates were constructed via a geographic information system and clustering was statistically confirmed. Associations between pertussis rates and community characteristics were tested. RESULTS: Mapping and statistical analysis revealed spatial clustering of pertussis. Higher age-adjusted rates of pertussis infection were associated with higher proportions of residents below poverty level. CONCLUSIONS: In urban areas pertussis infection clusters in areas of poverty.

Age Distribution↗
PubMed1997

The impact of acute ethanol on reproductive hormone synthesis, processing, and secretion in female rats at proestrous.

It is the purpose of this study to investigate the effects of acute ethanol (EtOH) on the female rat hypothalamic-pituitary-gonadal (HPG) axis. The molecular and cellular mechanistic details of such effects have been studied intensively in the male rat. However, there has been relatively little in-depth study of EtOH's effects on the adult, postpubertal female rat. Adult female rats with confirmed 4- or 5-day estrous cycles were given a single injection of EtOH or saline between noon and 1:00 PM on proestrous and were killed at 4:00 PM. EtOH caused a sharp 97% reduction in luteinizing hormone (LH) serum levels (p < 0.001), compared with controls with no concomitant change in LH mRNA. EtOH also significantly reduced hypothalamic LH releasing hormone (LHRH) by 49% (p < 0.01), with no change in content of the precursor pro-LHRH compared with saline-injected controls. The ratio of LHRH to pro-LHRH was also significantly reduced by EtOH (p < 0.05), compared with control. There was no EtOH-induced change in LHRH mRNA. Compared with saline, EtOH reduced both serum estradiol by 37% (p < 0.02) and progesterone by 47% (p < 0.001). These results show that EtOH has profound disruptive effects on the female HPG axis. Our data suggests that EtOH decreases the releasable LHRH pool either by decreasing conversion of pro-LHRH to LHRH and/or by increasing local LHRH degradation. This acutely restricts the release of LH and subsequent estradiol and progesterone secretion.

Animals↗
PubMed1996

In vitro import of pre-ferredoxin-NADP+-oxidoreductase from Cyanophora paradoxa into cyanelles and into pea chloroplasts.

Using a novel cyanelle isolation procedure we showed that pre-ferredoxin-NADP+-oxidoreductase (pre-FNR) from C. paradoxa is translocated in vitro across the peptidoglycan-containing cyanelle envelope. Efficient import was also observed in a heterologous system with pea chloroplasts as the recipient organelles. These results support the conclusion derived from comparative analysis of plastid genome organization, that all plastids originate from a common semi-autonomous endosymbiotic ancestor.

Cell Fractionation↗
PubMed1996

Hypomelanosis of Ito and brain abnormalities: MRI findings and literature review.

We report the results of a 14-year retrospective study of brain MRI abnormalities in 12 pediatric patients presenting with hypomelanosis of Ito (HI). Miscellaneous brain abnormalities were found: one patient had a medulloblastoma, three had cortical malformations, and five demonstrated "minor" abnormalities such as dilated Virchow-Robin spaces or brain atrophy. We emphasize the polymorphism of brain abnormalities associated with HI.

Adolescent↗