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D Mayfield

Publications and source records attributed to D Mayfield.

At least 19 recordsLinked to original sources
PubMed2001

Antimicrobial resistance among uropathogens that cause community-acquired urinary tract infections in women: a nationwide analysis.

Current recommendations for empirical therapy for community-acquired urinary tract infection (UTI) in women hinge on knowledge of antimicrobial susceptibility patterns in the geographic region of the practitioner. We conducted a survey of antimicrobial susceptibilities of 103,223 isolates recovered from urine samples that were obtained in 1998 from female outpatients nationally and within 9 geographic regions in the United States. Resistance of Escherichia coli isolates to trimethoprim-sulfamethoxazole varied significantly according to geographic region, ranging from a high of 22% in the western United States to a low of 10% in the Northeast (P<.001). There were no clinically significant age-related differences in the susceptibility of E. coli to any of the study drugs, but the susceptibility to fluoroquinolones of non-E. coli isolates that were recovered from women who were aged >50 years was significantly lower than that of isolates recovered from younger women (P<.001). The in vitro susceptibility of uropathogens in female outpatients varies according to age and geographic region.

Adult↗
PubMed2001

Regulation of B(2)-kinin receptors by glucose in vascular smooth muscle cells.

The development of vascular disease is accelerated in hyperglycemic states. Vascular injury plays a pivotal role in the progression of atherosclerotic vascular disease in diabetes, which is characterized by increased vascular smooth muscle cell (VSMC) proliferation and extracellular matrix accumulation. We previously reported that diabetes alters the activity of the kallikrein-kinin system and results in the upregulation of kinin receptors in the vessel wall. To determine whether glucose can directly influence the regulation of kinin receptors, the independent effect of high glucose (25 mM) on B(2)-kinin receptors (B2KR) in VSMC was examined. A threefold increase in B2KR protein levels and a 40% increase in B2KR surface receptors were observed after treatment with high glucose after 24 h. The mRNA levels of B2KR were also significantly increased by high glucose as early as 4 h later. To elucidate the cellular mechanisms by which glucose regulates B2KR, we examined the role of protein kinase C (PKC). High glucose increased total PKC activity and resulted in the translocation of conventional PKC isoforms (beta(1) and beta(2)), novel (epsilon), and atypical (zeta) PKC isoforms into the membrane. Inhibition of PKC activity prevented the increase in B2KR levels induced by ambient high glucose. These findings provide the first evidence that glucose regulates the expression of B(2) receptors in VSMC and provide a rationale to further study the interaction between glucose and kinins on the pathogenesis of atherosclerotic vascular disease in diabetes.

Animals↗
PubMed1989

Effects of route of administration of ethanol on high-speed reaction time in young and old rats.

The blood ethanol concentrations (BECs) and reactive capacity of young (8 months) and old (24 months) male Fischer 344 rats were compared at 5, 10, 20, 45, 65, and 90 min following the administration of ethanol (EtOH). The time-dependent effects of intragastric intubation (IG; 3 g/kg) and intraperitoneal injection (IP; 1.5 g/kg) of EtOH (20% w/v) were determined. Subsequent to IG delivery, BECs rose most rapidly within the first 20 min, but did not reach peak levels until 90 min for both young (240 mg/dl) and old rats (250 mg/dl). Following IP injections, BECs escalated within 5 min to 250 mg/dl in the young, to 175 mg/dl in the old, and declined gradually to a stabilized value of 150 mg/dl (young) and 130 mg/dl (old). The old rats never achieved the high BECs seen in the young. Reactive capacity, a measure of auditory/visual reaction time, was inversely related to BECs. As BECs (IP) declined, performance improved at a similar rate in both age groups, although the old rats' performance was more impaired than that of the young. However, BEC per se was not an adequate predictor of reactive capacity. When EtOH was delivered by IG so that BECs remained high for long periods of time, reactive capacity was far less impaired compared with IP delivery in which comparable BECs were present for only a few minutes. The possibility was noted that behavioral tolerance may have developed during the 90-min post-EtOH period, and that the IP delivery method may disrupt behavior in ways independent of brain ethanol levels.

Aging↗
PubMed1988

Movement initiation characteristics in young adult rats in relation to the high- and low-affinity agonist states of the striatal D2 dopamine receptor.

Changes in the speed of movement initiation as a function of age, brain damage, or rat strain are associated with altered characteristics of nigrostriatal dopamine (DA) neurons and of striatal D2 DA receptors. In the present study we investigated the relationship between movement initiation (response parameters: percent of successful responses and response latency) and the agonist binding states of the D2 DA receptor in corpus striatum in 3-month-old Sprague-Dawley rats (n = 51). In contrast to the typical experimental procedure, the variances of the behavioral and receptor binding data were intentionally made as small as possible to provide the most stringent test of putative relationships among variables. Rats were trained to release a lever as rapidly as possible in response to a light/buzzer (CS) combination in order to avoid a mild footshock (UCS). Percent avoidance scores, latencies of the fastest successful trials (successful latencies) and mean latencies for all responses (mean latencies) were collected for 1000-, 500-, 300- and 200-ms CS-UCS intervals. Twenty-four hours following the last behavioral test, animals were euthanized for measurements of the high- and low-affinity binding of DA to D2 receptors in corpus striatum. The standard errors of the mean for both behavioral and receptor binding parameters were, generally, less than 10%. The tightness of the receptor binding data appeared to be related to a lack of biological variance in the animals rather than to an artifact associated with the behavioral testing procedure, since a parallel experiment indicated that different numbers of behavioral shaping sessions had no effects on striatal D2 binding characteristics.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Ethanol and aging effects on movement initiation can be dissociated from general behavioral impairment using a high-speed lever-release task in rats.

An animal model of human reaction time was used to assess the effects of ethanol on reactive capacity (RC) as a function of age. Three doses of ethanol (0.5, 1.0 & 1.5 g/kg of 20% v/v, i.p.) were confirmed by gas chromatographic analysis of blood samples taken immediately following every behavioral test. Fisher 344 rats were trained to use their forepaws to hold down a lever until the onset of a buzzer and light that signalled impending foot shock, which occurred within 200-1000 msec of the stimulus. All rats were shaped to release the lever faster than 200 msec, which permitted them to avoid all shock under saline treatment. In the first experiment, only young adult rats (3-4 mos) were tested. Ethanol caused a dose-dependent impairment of RC. In a second experiment, rats aged 4, 12 and 24 mos were tested. As in previous work, RC was reduced by age. Ethanol caused a dose-dependent impairment of response speed (as indicated by the average of the fastest five RTs) that was exaggerated in the 24 mo-old rats. Ethanol also appeared to amplify the trial-by-trial variability in RC that was typical of the old rats under saline conditions. Nevertheless, if given enough time (1000 msec) most rats (except for a few in the oldest group) were able to avoid shock under ethanol as reliably as under saline conditions, even at the highest dose. Thus, ethanol specifically slowed reaction time while sparing memory and motivational and motor capacities required for success in this task. Both extensive practice and pre-test warm up sessions modified the effects of ethanol; however they did not do so differentially across ages.

Aging↗
PubMed1986

Perinatal cannabinoid exposure: effects on hepatic cytochrome P-450 and plasma protein levels in male mice.

Maternal exposure to the major psychoactive delta 9-tetrahydrocannabinol (THC), or to the nonpsychoactive cannabinol (CBN) or cannabidiol (CBD) on day 12 of gestation, or on day 1 postpartum, affected the concentrations of hepatic cytochromes P-450 in adult male offspring. Levels of P-450 were significantly increased in adult males prenatally exposed to cannabinoids, but were reduced after postnatal exposure. The response to exogenous testosterone was also differentially affected by perinatal cannabinoid exposure, with reduced plasma androgen in males prenatally exposed to THC, but increased levels of hormone in mice exposed postnatally to THC or CBN. There was a concomitant decrease in plasma albumin and increased gamma-globulin in adult males postnatally exposed to CBN. Beta-globulin levels were also significantly increased in adult males exposed to cannabichromene (CBC) on day 1 postpartum. Cannabinoid exposure during perinatal periods of development exert effects on hepatic function, plasma androgen levels, and on the immune system. These effects may reflect the ability of perinatal cannabinoid exposure to interfere with androgen-mediated processes of differentiation.

Androgens↗
PubMed1986

Differential effects of follicle-stimulating and luteinizing hormones on testosterone production by mouse testes.

In adult mice, direct intratesticular injection of ovine follicle-stimulating hormone (o-FSH-13; AFP 2846-C, from NIAMDD, less than 1% LH contamination) at 10, 100 or 1000 ng significantly elevated concentrations of testosterone (T) within the testis. These effects were rapid, with peak values attained by 15 min, and transient, with return to values comparable to that in the contralateral, saline-injected testis within 90 min. Intratesticular injection of FSH (1 microgram) significantly increased testicular T levels in 15- and 60-day old mice. This contrasted with the effects of intratesticular administration of human chorionic gonadotropin (hCG), which stimulated T production significantly at 30 days of age through adulthood. In adult mice, the equivalent LH to the possible contamination in the FSH preparation (1 ng) had no effect. Intratesticular injection of 10 ng LH produced comparable stimulation to that by 100 ng FSH (approximately 7-fold). Systemic pre-treatment with a charcoal-treated porcine follicular fluid (PFF) extract for 2 days reduced plasma FSH levels [86 +/- 17 (5) vs 700 +/- 8 (6); P less than 0.05], but had no effect on plasma LH. Twenty-four hours after the last treatment, the response to intratesticular injection of hCG (2.5 mIU), FSH (100 ng) or LH (10 ng) was also significantly attenuated in these mice. Intratesticular injection of PFF had no direct effect on testicular T levels. In vitro T production in the presence of hCG, LH or FSH were differentially affected by the concentrations of calcium (Ca2+) or magnesium (Mg2+) in the incubation media. The stimulatory effects of FSH were apparent at significantly lower levels of Ca2+ or Mg2+, than were those of LH or hCG. The results of these studies indicate that FSH is capable of stimulating testicular T production. Furthermore, the responsiveness to FSH is qualitatively different than that to LH/hCG in terms of the age pattern, as well as the dependence on Ca2+ or Mg2+. In addition, plasma FSH levels appear to influence testicular responsiveness to direct exogenous administration of gonadotropins. These studies indicate that FSH stimulation of T production can be differentiated from those of LH, and that these effects of FSH can be observed under physiological conditions.

Age Factors↗
PubMed1985

Effects of delta 9-tetrahydrocannabinol on testosterone production in vitro: influence of Ca++, Mg++ or glucose.

The major psychoactive component of marihuana, delta 9-tetrahydrocannabinol (THC), influences testicular function. In the present experiments, the addition of THC to incubations of whole decapsulated mouse testes altered testosterone (T) production differentially, depending on the specific gonadotropin used, the dose of THC and/or the amount of divalent cation present in the media. In the presence of luteinizing hormone (LH; 10 ng/ml), and a dose of 25 micrograms THC/ml, T production was significantly decreased, compared to that by testes incubated with LH and vehicle at all Ca++ levels, except at 0.127 or 1.0 mM Ca++. The production of T by these paired testes exposed to either THC or vehicle (ethanol; ETOH), increased as Ca++ concentration approached physiological levels. In contrast, in the presence of follicle-stimulating hormone (FSH; 1 microgram/ml), THC-induced suppression of T production was significant in the absence of Ca++ from the media, and at 12.7 mM Ca++. However, it appeared that the levels of Ca++ did not differentially affect T production in the presence of FSH, whether or not THC was also added. In the presence of human chorionic gonadotropin (hCG; 12.5 mIU/ml), a lower dose of THC (25 ng/ml), stimulated T production at 0.25 to 1 mM Ca++, but had no effect as Ca++ reached 2.5 mM. Without additional Ca++ in the media, this dose of THC significantly reduced T secretion. In contrast, in the presence of hCG, a higher THC dose (25 micrograms/ml), suppressed T accumulation at 0.127, and from 1.0 to 12.7, but had no effect at 0.25 mM, or in the absence of Ca++. In the presence of hCG, the high 25 micrograms/ml dose of THC stimulated T production, in the absence of additional Mg++, and at 0.01 mM Mg++, but THC had no effect at 0.1 mM Mg++, but inhibited T production at 1.1 mM Mg++. In the presence of hCG, 25 micrograms THC/ml produced a consistent suppression of T production across glucose concentrations examined. These findings suggest that the mechanisms by which THC effects testicular steroidogenesis may involve Ca++- and/or Mg++-dependent processes. Differential requirements for these divalent cations by the gonadotropins may explain the interactive effects of THC with LH, hCG or FSH.

Animals↗
PubMed1985

Effects of psychoactive and non-psychoactive cannabinoids on neuroendocrine and testicular responsiveness in mice.

Repeated oral administration of the non-psychoactive cannabinol (CBN; 5 or 50 mg/kg) significantly reduced the concentration of norepinephrine (NE) in median eminence and greatly reduced NE levels 1 and 2 hrs after administration of alpha-methylparatyrosine (alpha-MPT). The levels of dopamine (DA) in median eminence were significantly different, as indicated by the differences in slopes obtained in CBN- treated and control mice before and after alpha-MPT. Plasma levels of luteinizing hormone (LH) were significantly reduced in CBN-exposed mice before alpha-MPT, elevated at 1 hr post-injection, but were also reduced 2 hrs post-injection at 50 mg/kg CBN. Follicle-stimulating hormone (FSH) levels were increased at 1 hr post-alpha-MPT in mice receiving 50 mg/kg CBN. Oral administration of CBN at 50 mg/kg for 4 days enhanced testicular testosterone (T) production in response to intratesticular in vivo injection of 2.5 or 25 mIU human chorionic gonadotropin (hCG). A single oral dose of the psychoactive delta 9-tetrahydrocannabinol (THC) enhanced the production of T 15 min after intratesticular LH (10 ng) injection. However, at 45 or 60 min post-THC treatment, the response to LH was significantly attenuated. These studies demonstrate that both psychoactive and non-psychoactive components of marihuana alter testicular responsiveness to gonadotropins in vivo. These effects may be biphasic, involving stimulation and inhibition of responsiveness, and appear to be correlated with alterations in plasma LH levels. Alterations in plasma gonadotropins may be mediated by cannabinoid effects on catecholamine concentrations in median eminence and THC-induced alterations in testicular responsiveness to gonadotropin probably also involve direct effects of THC at the gonadal level.

Animals↗
PubMed1985

Neonatal exposure to DES in BALB/c male mice: effects on pituitary-gonadal function.

Neonatal male BALB/c mice were injected with diethylstilbestrol (DES), estradiol benzoate (E2B), testosterone propionate (TP), progesterone or DES, in combination with E2B, TP or progesterone and examined in adulthood. Body weight was reduced in males exposed to DES, TP or DES + TP, while testicular weight was reduced in animals injected with DES, E2B, TP, DES + TP or DES + progesterone. Exposure to DES and/or E2B also produced reproductive tract abnormalities and concomitant progesterone exposure did not further affect this parameter. Concomitant DES did not further alter the reduced plasma luteinizing hormone (LH) levels attributable to neonatal TP or E2B treatment. Plasma follicle-stimulating hormone (FSH) levels in intact males were increased by DES, DES + progesterone or progesterone alone. Assessment of the feedback effects of exogenous gonadal steroids on pituitary gonadotropin release in castrated adults indicated that injection of 125 micrograms TP further increased the already elevated post-castration levels of LH and FSH in mice neonatally exposed to progesterone. The increase in testosterone (T) concentration after intratesticular human chorionic gonadotropin (hCG) administration was significantly attenuated in mice neonatally exposed to DES plus E2B or to progesterone. Basal testicular T levels were significantly elevated in males exposed to DES, alone, or in combination with progesterone. Exposure to DES and TP increased hypothalamic serotonin (5-HT) levels in intact mice, while levels of 5-HT were lower after castration compared to controls. DES + E2B-treated mice had higher norepinephrine (NE) levels, and E2B-treated mice also had higher 5-HT levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Early cannabinoid exposure influences neuroendocrine and reproductive functions in male mice: I. Prenatal exposure.

Maternal exposure to delta 9-tetrahydrocannabinol (THC), the major psychoactive constituent in marihuana, or to the non-psychoactive cannabinol (CBN) or cannabidiol (CBD) alters endocrine functions and concentrations of brain biogenic amines in their male offspring. Prenatal CBN exposure on day 18 of gestation resulted in decreased plasma FSH levels, testicular testosterone (T) concentrations, and seminal vesicles weights, but increased plasma levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) post-castration in adulthood. Prenatal exposure to THC significantly enhanced the responsiveness of the testes to intratesticular LH injection in vivo and tended to increase human chorionic gonadotropin (hCG)-stimulated T production by decapsulated testes in vitro. In the CBN-exposed mice, hCG-stimulated T production was enhanced, while CBD exposure had no effect. Prenatal THC exposure altered the negative feedback effects of exogenous gonadal steroids in castrated adults, with lower plasma T and FSH levels after 20 micrograms T than in castrated controls. In contrast, CBD-exposed mice had higher levels of LH in plasma post-castration. In CBN-exposed adults, two weeks post-castration the concentration of norepinephrine (NE) and dopamine (DA) in hypothalamus and remaining brain were reduced, while levels of serotonin (5-HT) and its metabolite, 5-HIAA, were elevated compared to that in castrated OIL-controls. Prenatal CBD-exposure also reduced NE and elevated 5-HT and 5-HIAA, but did not affect DA levels post-castration. Concentrations of brain biogenic amines were not influenced by prenatal THC exposure in the present study. A single prenatal exposure to psychoactive or non-psychoactive components of marihuana results in long term alterations in the function of the hypothalamo-pituitary-gonadal axis. Changes in the concentrations of brain biogenic amines may be related to these effects of prenatal cannabinoids on endocrine function in adult male mice.

Animals↗
PubMed1984

Early cannabinoid exposure influences neuroendocrine and reproductive functions in mice: II. Postnatal effects.

Maternal exposure to delta 9-tetrahydrocannabinol (THC), the major psychoactive component in marihuana, or to the non-psychoactive cannabinol (CBN) or cannabidiol (CBD) alters male reproductive functions and brain biogenic amines in male and female offspring. Postnatal exposure to THC or CBN reduced body weights, while testicular weights were lower in CBD-exposed mice. Testicular testosterone (T) levels were also lower in CBN- and CBD-exposed animals. Postnatal cannabinoid exposure reduced plasma luteinizing hormone (LH) levels in intact and castrated adults. Although basal T production in vitro was not affected by postnatal cannabinoid exposure, testes from CBD-exposed males were more responsive to gonadotropin stimulation. In contrast, in vivo responsiveness to intratesticular human chorionic gonadotropin (hCG) administration was significantly reduced in THC- and CBD-exposed males. Pituitary weights and their basal LH production in vitro was higher in THC- or CBN-exposed mice. Pituitaries from cannabinoid-exposed males were less responsive to LH releasing hormone (RH) stimulation, however, hypothalamic LHRH content was significantly higher in the THC-exposed males. Hypothalamic dopamine (DA) levels were significantly lower in CBN-exposed castrated mice, compared to castrated controls. The reduction in hypothalmic norepinephrine (NE) in THC- and CBN-exposed castrates after alpha-methylparatyrosine (alpha-MPT) was significantly less than that observed in control castrates. Hypothalamic DA levels were depleted to a greater extent in CBD-exposed males. Brain levels of serotonin (5-HT) and 5-HIAA were significantly higher in castrated, than in intact THC-exposed males. In ovariectomized CBN-exposed females, hypothalamic NE levels were lower, while the alpha-MPT-induced depletion of NE was less in CBD-exposed, compared to control females. Levels of 5-HT were lower only in THC-exposed females. Plasma levels of LH were significantly higher in CBN-exposed, while plasma levels of FSH were reduced in THC- and CBD females. Maternal exposure to psychoactive or non-psychoactive cannabinoids on the day of parturition results in long term alterations in neuroendocrine function in male and female offspring. It is possible that the observed alterations in biogenic amines may mediate the effects of cannabinoids on pituitary and gonadal function.

Animals↗
PubMed1984

Dyskinesia and psychosis in a patient following baclofen withdrawal.

A paraplegic man with no history of psychiatric illness developed psychosis and dyskinesia following abrupt withdrawal of baclofen; the symptoms resolved 72 hours after resumption of the drug. The psychosis and dyskinesia may have been a manifestation of baclofen's alteration of cerebral dopaminergic mechanisms.

Adult↗
PubMed1983

Effects of testosterone, estradiol, aromatase inhibitor, gonadotropin and prolactin on the response of mouse testes to acute gonadotropin stimulation.

These studies determined the local acute responsiveness of the testis to intratesticular administration of human chorionic gonadotropin (hCG) under basal, stimulated (systemic hCG pre-treated), hypogonadotropic (steroid pre-treatment) and hyperprolactinemic conditions in male mice. In addition, testicular testosterone (T) levels were determined after intratesticular administration of the aromatase inhibitor, 4-hydroxyandrostenedione (4-OHA) or progesterone under basal or hCG-stimulated conditions. Intratesticular administration of 0.025, 0.25, 2.5 or 25 mIU hCG resulted in a dose-dependent (3- to 14-fold) increase in testicular T concentrations in hCG compared to vehicle-injected testes. Systemic (i.p.) pre-treatment with 5 IU hCG 24 h before prevented any further increases in the already elevated (10-fold basal) T levels after direct intratesticular hCG injection. Pretreatment with 250 micrograms testosterone propionate (TP) reduced basal testicular T concentrations, but resulted in increased responsiveness to intratesticular hCG administration. In contrast, estradiol benzoate (EB) pretreatment, which also reduced basal testicular T concentrations, did not affect the testicular responsiveness to hCG. Hyperprolactinemia reduced testicular responsiveness to intratesticular administration of 0.025, 0.25 or 2.5 mIU hCG, but basal levels of testicular T were elevated. One hour after intratesticular injections of an aromatase inhibitor, 4-OHA; (0.25 micrograms) testis, T levels were increased in males pre-treated with 5 IU hCG (i.p.) 24 h earlier. Higher doses of 4-OHA (2.5, 25 or 250 micrograms) resulted in significant, dose-related increases in basal testicular T levels which were attenuated by hCG-pre-treatment. Intratesticular administration of 20 micrograms progesterone increased testicular T concentrations 2.7-fold, but this effect was attenuated (1.5-fold) in hCG-pre-treated mice, suggesting that enzymatic lesions beyond progesterone may be involved in hCG-induced testicular desensitization. These results indicate that testicular responsiveness to hCG depends on the existing levels of gonadotropic stimulation. However, it is evident that estrogens and prolactin also influence the sensitivity of the testis to gonadotropin.

Androstenedione↗
PubMed1983

Case report of acute disulfiram overdose.

The authors describe the clinical symptoms of a disulfiram overdose in a male patient and present the plasma concentrations of disulfiram and its metabolites 4 and 7 days after the overdose.

Acute Disease↗