Biomedical subjects

L A Lane

Publications and source records attributed to L A Lane.

6 recordsLinked to original sources

PubMed2000

Procedure for assessing myeloperoxidase and inflammatory mediator responses in hairless mouse skin.

A preparation procedure for making multiple inflammatory biomarker measurements from the same skin tissue was assessed. The backs of euthymic hairless mice were exposed to sulfur mustard (HD) vapor for 6 min. Animals were euthanized 24 h following exposure, dorsal skin tissue was excised and 12-mm, full-thickness biopsy punches of the exposed skin sites were taken. Specimens were snap-frozen, crushed to a powder using a biopulverizer unit, solubilized in buffer and centrifuged. Supernatant was assayed for pro-inflammatory cytokines and the acute-phase reactive protein, serum amyloid P (SAP). Myeloperoxidase (MPX), which is indicative of neutrophil infiltration into the skin, was associated with the pellet fraction. Results indicate an elevation of interleukin-6, SAP and MPX in mouse skin tissue specimens 24h following HD vapor exposure. The tissue preparation procedure allows the use of a single skin specimen to make multiple inflammatory endpoint measurements requiring different preparation processes, and it will be used in subsequent studies to characterize further the inflammatory nature of HD-exposed skin tissue.

Administration, Cutaneous↗

PubMed1987

Neuroendocrine aspects of primary endogenous depression. II. Serum dexamethasone concentrations and hypothalamic-pituitary-adrenal cortical activity as determinants of the dexamethasone suppression test response.

To determine the contribution of serum dexamethasone concentrations and hypothalamic-pituitary-adrenal cortical activity before dexamethasone administration to the dexamethasone suppression test (DST) response, a series of stepwise discriminant function analyses were performed for 40 patients with definite endogenous depression and 40 matched normal control subjects. The 24-hour serum cortisol concentration before dexamethasone administration and the serum dexamethasone concentrations at 8, 16, and 24 hours after administration served as the independent variables, and the DST "escaper"/"suppressor" dichotomy served as the dependent variable. While both types of independent variables significantly influenced the DST response, the major factor that contributed to the discrimination of escapers from suppressors was the 24-hour cortisol concentration before dexamethasone administration. Sixteen hours after dexamethasone administration, when the DST had the highest positive predictive value, serum dexamethasone concentrations significantly influenced DST outcome only when they were below a certain threshold level. At this time, hypothalamic-pituitary-adrenal cortical hyperactivity before dexamethasone administration accounted for approximately two thirds of the incidence of DST nonsuppression.

Circadian Rhythm↗

PubMed1986

Influence of prenatal ethanol exposure on hormonal responses to clonidine and naloxone in prepubescent male and female rats.

The expression of sexually dimorphic behavior has been found to be altered in adult animals following prenatal alcohol exposure. The present study examined whether such exposure would alter the sexually dimorphic response of luteinizing hormone (LH) to clonidine and naloxone observed in normal prepubescent animals. Both LH and corticosterone (CS) were measured in 16 day old male and female rats 30 min after injection of naloxone (2 mg/kg) or clonidine (0.1 mg/kg). Prenatal alcohol exposure did not influence the LH response to either drug in females. An LH response to clonidine in normal males did not occur, but it was present in the males exposed to alcohol in utero and in the pair-fed controls. Prenatal alcohol exposure influenced the CS response to both drugs. CS levels were depressed in the naloxone-treated males prenatally exposed to alcohol compared to their saline-injected counterparts. The CS levels of other groups following naloxone administration were unchanged compared to saline injection. Normal animals of both sexes exhibited an elevation in CS levels following clonidine. However, this stimulatory effect of clonidine on CS release was absent in both female and male animals prenatally exposed to alcohol. The results of this study indicate that prenatal alcohol exposure may alter noradrenergic and opioid modulation of corticosterone and possibly of LH in young animals.

Animals↗

PubMed1985

A modified dexamethasone suppression test for endogenous depression.

In order to simplify the dexamethasone suppression test (DST), we have administered a lower dosage of dexamethasone (DEX) and shortened the sampling time to a single morning blood sample. DEX (in dosage increments from 0.125 to 1.0 mg, p.o.) was administered at 2300 h to normal volunteers in a double-blind randomized fashion, and blood samples were taken at 0700 h the following morning. While significant cortisol suppression occurred after the 0.375 mg, 0.5 mg, and 1.0 mg doses of DEX, the 0.5 mg dose was the smallest that clearly suppressed cortisol in all eight subjects. This dose then was used to test the feedback sensitivity of the central nervous system (CNS)-pituitary-adrenal axis in endogenously depressed patients. Twenty endogenously depressed patients and 20 normal volunteers were given both the standard 1.0 mg DST, with post-DEX serum cortisol determined at 1500 h, and the simplified 0.5 mg DST, with post-DEX serum cortisol determined at 0700 h. Four patients (20%) and one control (5%) were nonsuppressors after the 1.0 mg DST, and nine patients (45%) and one control (5%) were nonsuppressors after the 0.5 mg DST. In addition, nine patients with major depression (nonendogenous subtype) and 15 patients with panic attacks also were studied using the 0.5 mg DST. Only 2 of these 24 patients (8%) were nonsuppressors. The results suggest that the single-sample 0.5 mg DST is more sensitive than the standard 1.0 mg DST, and the specificity of the modified test appears comparable to the standard form of the test.

Adult↗

PubMed1985

Pre- and post-dexamethasone salivary cortisol concentrations in major depression.

Seventy patients fulfilling DSM-III criteria for major depression were given the 1.0 mg overnight dexamethasone suppression test, with salivary cortisol concentrations being measured as the dependent variable. Using both the DSM-III and the Research Diagnostic Criteria, we categorized the patients into four groups based on increasing frequency of endogenous symptomatology. Among these four groups there were no significant differences in salivary cortisol concentrations either before dexamethasone or eight, 16, and 24 h after dexamethasone. Similarly, there were no significant differences among the groups in either the ratios of post- to pre-dexamethasone salivary cortisol or the frequencies of positive tests based on several criterion levels of cortisol for the three post-dexamethasone samples. Multiple regression analyses indicated that the Hamilton depression rating scale item "somatic anxiety" was significantly negatively related to post-dexamethasone cortisol concentrations. We conclude that, for our sample of major depressives, the salivary cortisol dexamethasone suppression test showed no utility as a laboratory correlate of depressive episodes with endogenous features.

Adult↗

PubMedDate not supplied

Prenatal ethanol and ontogeny of pituitary-adrenal responses to ethanol and morphine.

The development of pituitary-adrenal activity was examined in the offspring of rat dams fed a 5.0% w/v ethanol-containing liquid diet or pair-fed an isocaloric diet, as a nutritional control, from day 8 of gestation to parturition. Serum corticosterone responses of the pups to challenges with ethanol (1.5 g/kg) or morphine (3.0 mg/kg) were determined at 5, 7, 10, 12 and 18 days of age. The pituitary-adrenal axis of normal neonates was activated by the drugs at each age, with a characteristic biphasic developmental pattern in which a trough occurred at day 7. The overall pattern was unaffected by prenatal ethanol exposure or pair-feeding. However, both prenatal treatments intensified the trough. Already on day 5 and also on day 7, corticosterone responses of both the ethanol-exposed and pair-fed offspring to ethanol were significantly lower than responses of normal pups. Additionally, on day 7, ethanol-exposed offspring had significantly lower responses to ethanol than pair-fed offspring and significantly lower responses to morphine than normal pups. Thus, both the prenatal ethanol and pair-feeding treatments suppressed pituitary-adrenal responsiveness of 5 and 7 day-old neonates to the drug challenges. This is in marked contrast to our previous findings for adult prenatally ethanol-exposed offspring whose pituitary-adrenal responses to the same drugs, as well as to other stressors, are consistently enhanced in comparison to pair-fed derived rats, whose responses in adulthood no longer differ from normals.

Animals↗