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Biomedical subjects

V K Ganjam

Publications and source records attributed to V K Ganjam.

At least 19 recordsLinked to original sources
PubMed2000

Serum markers of lamellar basement membrane degradation and lamellar histopathological changes in horses affected with laminitis.

In order better to evaluate the extent to which degradation of the lamellar basement membrane (LBM) by matrix metalloproteinases (MMP) occurs in equine laminitis, we determined the concentration of type IV collagen and laminin in normal and laminitic horses, using specific immunoassays. Blood samples were obtained from both the jugular and the cephalic veins of horses (n = 10) before and after the induction of acute alimentary laminitis by carbohydrate overload. Jugular and cephalic venous blood samples were also obtained from horses affected with naturally occurring laminitis (n = 16) and nonlaminitic controls (n = 8). The serum collagen IV concentration was not changed following the induction of laminitis in the experimental group. Serum collagen IV concentration was increased in jugular venous blood obtained from cases of naturally occurring laminitis (mean +/- s.e. 218.04 +/- 18.59 ng/ml) compared with nonlaminitic controls (157.50 +/- 10.93 ng/ml) (P<0.05). Serum collagen IV concentration was also increased in jugular venous blood obtained from severely laminitic horses (219.50 +/- 18.18 ng/ml) compared with nonlaminitic controls (157.50 +/- 10.93 ng/ml) (P<0.05). A difference in serum concentration of collagen IV was not identified based on chronicity of naturally occurring laminitis. Serum laminin concentration did not differ between laminitic and nonlaminitic horses. Differences in serum laminin concentration were not identified based on sampling location (jugular or cephalic vein), severity of laminitic pain, or chronicity of spontaneous laminitis. In conclusion, the circulating concentration of collagen IV was increased in horses affected with naturally occurring laminitis. The potential role for serum collagen IV assay for characterisation of equine laminitis warrants further investigation.

Animals↗
PubMed1999

Extra-adrenal mineralocorticoids and cardiovascular tissue.

In experimental models where chronic inappropriate (relative to sodium intake and intravascular volume) elevations in circulating mineralocorticoids (aldosterone or deoxycorticosterone) are created, a reactive fibrosis with vascular remodeling is observed in systemic organs and the heart. Until recently, it was assumed that aldosterone was derived solely from adrenal glands via the circulation; however, there is now convincing evidence that cells of the heart and vasculature express genes responsible for the formation of both aldosterone and corticosterone and are capable of producing these steroids. Vascular endothelial and smooth muscle cells express CYP11B1 and CYP11B2, genes responsible for 11 beta -hydroxylase and aldosterone synthase, respectively. Furthermore, smooth muscle cells elaborate aldosterone. There is evidence that similar regulatory mechanisms operate in vascular cells as in adrenal cortex, since aldosterone synthase and 11 beta -hydroxylase expression are differentially modulated by low sodium/high potassium, angiotensin II and ACTH. It is likely that such localized corticosteroid production also occurs at sites of tissue repair, where populations of collagen-producing myofibroblasts, nourished by a neovasculature, predominate. Using a subcutaneous pouch model of granulation tissue we have obtained compelling data which would support such a notion. The mineralocorticoid receptor antagonist, spironolactone, severely attenuates pouch formation over a 2-week period and significantly reduces pouch wall hydroxyproline concentration. This effect is apparent even following adrenalectomy, when circulating corticosteroids are undetectable; however, with adrenalectomy alone, pouch formation is barely affected. This we took to be a possible indication of an effect of local, non-adrenal steroids in maintaining pouch tissue. Spironolactone inhibits angiogenesis. A recent clinical study demonstrates the efficacy of low-dose spironolactone in enhancing survival in patients with advanced chronic cardiac failure. Although it is not known how spironolactone brings about such an improvement in survival, we would propose that inhibition of fibrous tissue formation and/or angiogenesis might be important contributory factors. Further studies are required to address the relative contributions of circulating vs local aldosterone in promoting normal vs pathologic connective tissue formation.

Adrenal Glands↗
PubMed1999

Expression of endothelin in equine laminitis.

Biosynthesis of endothelin-1 (ET-1), the most potent endogenous vasoconstrictor yet identified, is increased following myocardial infarction (MI) in man. Pathological events which occur in the connective tissues of the equine hoof during laminitis are similar in some respects, to changes occurring in the myocardial connective tissues following MI in man. The objective of this study was to determine whether ET-1 expression in connective tissues obtained from the hoof of laminitic horses is increased compared with tissues obtained from healthy horses. Expression of ET-1 in connective tissues of the equine hoof was measured following tissue extraction from 3 groups of horses: horses in which acute laminitis had been induced by the administration of starch; chronically foundered horses; nonlaminitic horses. The concentration of ET-1 in laminar connective tissues obtained from all laminitic horses (1573.0 +/- 392.8 pg/g of tissue; n = 10) was increased when compared with tissues obtained from nonlaminitic horses (392.5 +/- 117.4 pg/g of tissue; n = 5) (P<0.05). The concentration of ET-1 in laminar connective tissues obtained from the experimentally induced, acute laminitic horses (1043.6 +/- 254.4 pg/g of tissue; n = 7) and from the spontaneously affected, chronic laminitic horses (2808.3 +/- 878.6 pg/g of tissue; n = 3) was increased compared with the control group (P<0.05, P<0.01, respectively). The concentration of ET-1 in laminar connective tissues obtained from the chronic laminitic horses was greater than that of the experimentally induced, acute laminitic group (P<0.05). It is suggested that the data provide a strong argument that increased ET-1 expression in the connective tissues of the equine hoof represent a potentially important and hitherto unrecognised component of the pathophysiology of equine laminitis. Further studies are needed to determine whether inhibitors of ET-1 converting enzyme or antagonists of ET-1 receptors might be useful in the treatment and prevention of laminitis in horses.

Acute Disease↗
PubMed1998

Activation of extracellular matrix metalloproteinases in equine laminitis.

Samples of connective tissue obtained from the hoof of six laminitic and eight non-laminitic adult horses were analysed zymographically to investigate whether connective tissue matrix metalloproteinases are activated or induced during laminitis. The activity or matrix metalloproteinases was substantially greater in the tissues from the laminitic horses than in the tissues from the non-laminitic horses. A comparison of the collagenolytic activity in the laminitic and control tissues showed that collagenolytic activities corresponding to the 92 kDa (P < 0.001), 72 kDa (P < 0.01) and 66 kDa (P < 0.01) bands were induced in the laminitic tissues.

Animals↗
PubMed1998

Inhibition of tissue repair by spironolactone: role of mineralocorticoids in fibrous tissue formation.

Mineralocorticoids have been implicated in promoting fibrous tissue formation in various organs. In the present study, we sought to address the potential contribution of mineralocorticoids to fibrous tissue formation using a skin pouch model which has proved valuable for the analysis of inflammatory and wound healing responses. Skin pouches were induced in rats by administration of a phorbol ester, croton oil (0.5 ml of a 1% solution). After 2 weeks, rats were killed and intact pouch tissue collected. Pouch weights of control and aldosterone-treated (0.75 microg/h via osmotic minipump) rats were similar (3.33 +/- 0.44 g vs. 3.70 +/- 0.28 g respectively). However, pouch weights were reduced by more than 50% in spironolactone-treated (25 mg/day powdered in food) animals (1.62 +/- 0.22 g and 1.27 +/- 0.23 g respectively in aldosterone and spironolactone alone groups). To ascertain the effects of different treatments on collagen accumulation, hydroxyproline concentration was measured. Compared with controls, hydroxyproline concentration was significantly reduced following spironolactone treatment (17.1 +/- 0.08 vs. 7.5 +/- 2.0 microg/mg dry wt, respectively, p < 0.01). This response to spironolactone was negated by coadministration of aldosterone (hydroxyproline concentration was 18.6 +/- 2.1 microg/mg dry wt). Following bilateral adrenalectomy, spironolactone reduced pouch weight and hydroxyproline concentration, which was not the case for adrenalectomy alone. Two week aldosterone administration in uninephrectomized rats on high salt diet was deemed ineffective in modulating pouch development (pouch wet wts were 3.48 +/- 0.4 g vs. 3.00 +/- 0.19 g in controls and aldosterone-treated rats, respectively). Mineralocorticoid receptor expression in pouch tissue was demonstrated by RT/PCR. Furthermore, NADP+-dependent 11beta-hydroxysteroid dehydrogenase 1 (11beta-HSD1) activity was detected in pouch tissue, together with lower levels of NAD+-dependent 11beta-HSD2. Spironolactone (p < 0.05) significantly reduced 11beta-HSD1 activity compared with controls. Thus, fibrous tissue possesses requisite components of MC action, and antagonism of mineralocorticoid receptors by spironolactone attenuates its formation. Pouch formation is under the influence of circulating MC and, we would like to propose, is also mediated through corticosteroids generated de novo at the site of tissue repair.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1998

Transcription and translation of estrogen receptor-beta in the male reproductive tract of estrogen receptor-alpha knock-out and wild-type mice.

Estrogen receptor-alpha (ERalpha) has been identified in the male reproductive tract, but the role of estrogen in the male has not been well characterized. In vivo mutations in ERalpha genes have demonstrated the necessity for ERalpha-mediated action in male fertility. We asked whether both ERbeta messenger RNA and protein were present in the male reproductive tract of wild-type and ERalpha knock-out (ERalpha KO) mice, and whether ERbeta could compensate for the lack of ERalpha in infertile male ERalpha KO mice. Immunohistochemical localization with both N- and C-terminal anti-ERbeta antibodies demonstrated that ERbeta is present in the Leydig cells of the testes and in the epithelium of both the efferent ductules and the initial segment of the epididymis. RT-PCR amplification was used to confirm ERbeta transcription in these tissues. In conclusion, we observed that ERbeta messenger RNA and protein continue to be expressed in the Leydig cells, elongated spermatids, efferent ductules, and the initial segment of the epididymides of ERalpha KO mice, but the presence of ERbeta is not able to compensate for the absence of ERalpha in male reproductive function.

Animals↗
PubMed1998

Morphometric analysis of endometrial periglandular fibrosis in mares.

OBJECTIVES: To develop an objective, quantifiable assay for endometrial periglandular fibrosis (EPF) and correlate assay results with histologic and ultrastructural changes in equine endometrial biopsy specimens. SAMPLE POPULATION: Endometrial biopsy specimens from 70 mares from 3 to 27 years old in estrus. PROCEDURE: In a double-blinded study design, endometrial biopsy specimens were graded histologically (modified Kenney classification) for EPF and inflammation. Endometrial periglandular collagen volume fraction (%EPCVF) was determined by light microscopic image analysis of picrosirius red-stained sections. Specimens from selected mares were examined by transmission electron microscopy. RESULTS: %EPCVF values varied significantly among the 4 modified Kenney EPF categories (I, IIA, IIB, and III) and increased with increasing age of mares. Morphologically, EPF consisted of concentric layers of transformed fibroblasts with myofibroblastic features and deposition of fibrillar collagen around unaltered glandular basal laminae. CONCLUSIONS AND CLINICAL RELEVANCE: %EPCVF correlates well with morphologic changes in endometrial biopsy specimens. Determination of %EPCVF could be useful in evaluation and clinical management of subfertile mares and in investigations of the pathogenesis of EPF.

Animals↗
PubMed1997

Prostate enlargement in mice due to fetal exposure to low doses of estradiol or diethylstilbestrol and opposite effects at high doses.

On the basis of results of studies using high doses of estrogens, exposure to estrogen during fetal life is known to inhibit prostate development. However, it is recognized in endocrinology that low concentrations of a hormone can stimulate a tissue, while high concentrations can have the opposite effect. We report here that a 50% increase in free-serum estradiol in male mouse fetuses (released by a maternal Silastic estradiol implant) induced a 40% increase in the number of developing prostatic glands during fetal life; subsequently, in adulthood, the number of prostatic androgen receptors per cell was permanently increased by 2-fold, and the prostate was enlarged by 30% (due to hyperplasia) relative to untreated males. However, as the free serum estradiol concentration in male fetuses was increased from 2- to 8-fold, adult prostate weight decreased relative to males exposed to the 50% increase in estradiol. As a model for fetal exposure to man-made estrogens, pregnant mice were fed diethylstilbestrol (DES) from gestation days 11 to 17. Relative to controls, DES doses of 0.02, 0.2, and 2.0 ng per g of body weight per day increased adult prostate weight, whereas a 200-ng-per-g dose decreased adult prostate weight in male offspring. Our findings suggest that a small increase in estrogen may modulate the action of androgen in regulating prostate differentiation, resulting in a permanent increase in prostatic androgen receptors and prostate size. For both estradiol and DES, prostate weight first increased then decreased with dose, resulting in an inverted-U dose-response relationship.

Animals↗
PubMed1997

Fibrous tissue and angiotensin II.

Myofibroblasts (myoFb) are cells responsible for fibrous tissue formation in injured systemic organs such as the heart. Cultured myoFb, obtained from rat cardiac scar tissue, express genes that encode components requisite for angiotensin (Ang) II generation, which in turn regulates myoFb collagen turnover in an autocrine/paracrine manner. In this study, we tested the hypothesis that these wound-healing fibroblast-like cells and locally generated Ang II are involved in other repairing tissue. To test this hypothesis, we used a granuloma pouch model, where a subcutaneous air sac is created followed by injection of croton oil. Pouch tissue was collected at days 4, 7, 14 and 21. The presence of myoFb was determined by immunohistochemical alpha-smooth muscle actin (alpha-SMA) labeling and collagen accumulation by picrosirius red staining. Angiotensin converting enzyme (ACE) and Ang II receptor binding were detected by in vitro quantitative autoradiography using 125I-351A and 125I[Sar1, Ile8]Ang II, respectively, while Ang II receptor subtype was defined by displacement studies using either an AT1 (losartan) or AT2 (PD123177) receptor antagonist. Cells expressing ACE were determined by immunohistochemistry. Ang II content in pouch tissue was measured by radioimmunoassay following HPLC separation while its capacity to generate Ang II was assessed in tissue bath, with and without exogenous Ang I or lisinopril, an ACE inhibitor. Collagen accumulation in pouch tissue was examined by determining hydroxyproline content in response to lisinopril, AT1 or AT2 receptor antagonists (losartan or PD123177). In pouch tissue, we found: (1) myoFb at day 4 which became more extensive at days 7, 14 and 21; (2) morphologic evidence of collagen deposition evident at day 4, which gradually became more extensive thereafter; (3) ACE and Ang II receptor binding was evident at day 4 and remained invariant on days 7, 14 and 21; (4) the predominant Ang II receptor subtype expressed was AT1; (5) myoFb express ACE and AT1 receptors; (6) picogram quantities of Ang II (per g tissue) was evident on days 7, 14 and 21; and (7) Ang II was generated from Ang I substrate. Lisinopril and losartan, but not PD123177, significantly attenuated pouch weight and accumulation of collagen. Thus, in this model of cutaneous repair, the appearance of myoFb is associated with Ang II generation that regulates fibrogenesis by AT1 receptor binding. Signals involved in the appearance of myoFb remain uncertain. Further studies are required to address the regulation of Ang II generation in pouch tissue of the rat.

Actins↗
PubMed1996

High affinity NAD(+)-dependent 11 beta-hydroxysteroid dehydrogenase in the human heart.

Receptor-ligand binding is an essential component of mineralocorticoid (MC) activity in target tissues. Detection of type 1 mineralocorticoid receptors (MR) in cardiac tissue is therefore suggestive that, like kidney, the heart is MC responsive. The presence of 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) within MC responsive tissue is essential to prevent saturation of MR by glucocorticoids. Using both high-performance liquid chromatography (HPLC) and thin layer chromatography (TLC), we have found that a high-affinity species of 11 beta-HSD predominates within human heart. Although two 11 beta-HSD isoforms were detected in human cardiac tissues, the activity of high-affinity (type 2) 11 beta-HSD was found to be at least twice that of low affinity (type 1) 11 beta-HSD. Human cardiac type 2 11 beta-HSD possesses characteristics identical to the high-affinity enzyme of distal renal tubules; 11 beta-dehydrogenation of corticosterone or cortisol to their 11-keto metabolites is NAD(+)-dependent and, with corticosterone as substrate, the enzyme has a nanomolar Km (15.1 nM as determined by Lineweaver-Burke analysis). Furthermore, its activity is unidirectional; corticosterone and cortisol are 11 beta-dehydrogenated to inactive 11-keto metabolites, whereas 11-oxoreductase activity (conversion of 11-dehydrocorticosterone and cortisone to corticosterone and cortisol, respectively) is absent. RT/PCR analysis, using primers complementary to the human renal type 2 11 beta-HSD sequence, demonstrated that the high-affinity species of 11 beta-HSD expressed in human heart is indeed the same enzyme as that produced in the kidney. These findings strongly suggest that, as is the case in the distal portion of the nephron, type 2 11 beta-HSD plays an important role in the human heart to promote glucocorticoid metabolism and to confer MC specificity upon MR.

Base Sequence↗
PubMed1996

In situ production of angiotensin II by fibrosed rat pericardium.

Following pericardiotomy in rats, subsequent fibrosis of the visceral pericardium becomes a site of high-density angiotensin-converting enzyme (ACE) binding. This study was undertaken to determine whether this exteriorized site of ACE activity is associated with angiotensin II (AngII) production. Four weeks after pericardiotomy, hearts were isolated and maintained by Krebs-Henseleit perfusion: coronary venous and Thebesian drainage were removed by cannulae. Following a 30-min period of stabilization, a balloon containing superfusate was placed around the heart. Superfusate composition was controlled and included either lisinopril (10(-7) mol/l), angiotensin I (AngI, 10(-7) mol/l), or angiotensinogen (10(-6) mol/l). Sixty min later, superfusate AngII concentration was determined (high-performance liquid chromatography followed by radioimmunoassay). Pericardial fibrosis was confirmed by picrosirius red staining and its high-density ACE binding by quantitative in vitro autoradiography (125I-351A). ACE activity was measured by hippuryl-histidyl-leucine degradation. In coronary effluent, AngII concentration and ACE activity were not different between controls and hearts with pericardial fibrosis. Compared to unoperated, age/sex-matched control hearts, however, we found those with pericardial fibrosis to have: (a) significantly (P < 0.05) greater tissue ACE activity (118.42 +/- 6.66 v 89.45 +/- 7.70 nmol/min/g): (b) significantly (P < 0.01) greater superfusate AngII concentration (4.98 +/- 0.94 v 1.43 +/- 0.28 pg/ml); (c) lisinopril markedly attenuated superfusate AngII concentration to that seen in controls; (d) exogenous AngI markedly increased AngII production (13.76 +/- 1.65 v 4.98 +/- 0.94 pg/ml); and (e) exogenous angiotensinogen did not alter superfusate AngII. Thus, high-density ACE binding and ACE activity of fibrosed pericardium is responsible for AngII production in this in vitro model. Cells involved in generating AngI at this site are uncertain and may involve fibroblast-like cells that express ACE and have ACE activity. The role of local AngII production is unknown, but its autocrine/paracrine properties may regulate collagen turnover of these cells.

Angiotensin I↗
PubMed1995

Effect of dexamethasone administration on serum thyroid hormone concentrations in clinically normal horses.

The effect that 5 consecutive days of treatment with dexamethasone (0.04 mg/kg of body weight, IM, q 24 h) would have on baseline concentrations of triiodothyronine (T3), thyroxine (T4), reverse T3 (rT3), free T3 (FT3), and free T4 (FT4), and on response to thyroid-stimulating hormone (TSH) administration was determined in 12 clinically normal horses. Results of TSH response tests indicated that the horses could be placed into 2 groups: in 6 horses (group A), T4 concentration after administration of TSH was more than twice the baseline concentration; in the other 6 horses (group B), T4 concentration 6 hours after administration of TSH was less than twice the baseline concentration. Baseline serum concentrations of T3, T4, rT3, FT3, and FT4 were not significantly different between group-A and group-B horses. In both groups of horses, serum T3, T4, rT3, and FT4 concentrations were significantly increased 6 hours following TSH administration, compared with baseline concentrations. Treatment with dexamethasone resulted in significant (P < 0.05) increases in baseline concentrations of rT3 and FT3 in group-A horses and baseline concentrations of rT3 in group-B horses. The response to TSH administration following dexamethasone treatment appeared to be blunted with significant (P < 0.05) increases only in T3, T4, and FT4 concentrations in group-A horses and FT4 concentration in group-B horses. The magnitude of change in serum FT3 concentration in response to TSH administration was significantly less (P = 0.05) following dexamethasone treatment, compared with magnitude of change prior to dexamethasone treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Chronic mineralocorticoid excess and cardiovascular remodeling.

Chronic mineralocorticoid (MC) excess, whether due to elevated plasma aldosterone (ALDO) or deoxycorticosterone (DOC), is associated with a perivascular fibrosis of systemic and coronary arterioles. This remodeling of resistance vessels contributes to the appearance of hypertension. Chronic MC excess is also accompanied by cardiac myocyte necrosis, secondary to myocardial potassium depletion, and a subsequent reparative fibrosis that appears in the normotensive, nonhypertrophied right and hypertensive, hypertrophied left ventricles. Fibrosis contributes to the appearance of ventricular arrhythmias and dysfunction. Herein, clinical and experimental evidence linking chronic, inappropriate (relative to dietary sodium) elevations in circulating ALDO and DOC with these reactive and reparative forms of fibrous tissue formation in the heart and other tissues is presented.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1995

Angiotensin-II-induced increase in transcoronary protein clearance: role of hypertension vs. nitric oxide or cyclo-oxygenase products.

Elevations in plasma angiotensin II (AngII) are associated with an efflux of plasma macromolecules into the perivascular and contiguous interstitial space. Whether this exudative response is related to associated hypertension or another effect of AngII is uncertain. We therefore monitored plasma and cardiac lymph total protein, albumin and fibronectin and calculated transvascular clearances for total protein (TVPC) and albumin (TVAC) and lymph fibronectin transport (LFT) every 30 min in open-chested, instrumented dogs. After baseline observations were obtained over 30 min, pressor (250 ng.kg.min-1) or nonpressor (11 ng.kg.min-1) doses of AngII were given intravenously for 90 min. Saline-treated, instrumented dogs served as controls. To address a potential secondary effect of AngII on vascular protein clearance, we monitored lymph prostaglandin E2 and cGMP (a marker of released nitric oxide, NO). At > or = 30 min, each dose of AngII was associated with a significant (P < or = 0.05) and comparable increase in TVPC, TVAC and LFT over baseline, indicating that increase in protein clearance was not related to elevated arterial pressure. Lymph cGMP rose significantly (P < or = 0.05) at 30 min for each dose of AngII and remained elevated thereafter. Lymph PGE2 was increased at > or = 60 min (P < or = 0.05) but only with the pressor dose. To determine the contribution of NO and PGE2 on AngII-induced transcoronary protein clearance, each dose of AngII was accompanied by co-administration of either the NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), or the cyclo-oxygenase inhibitor, indomethacin. L-NAME completely inhibited the release of cGMP and the increase in protein clearance was not seen. Indomethacin suppressed the release of PGE2, but did not prevent the increase in protein clearance. Thus, AngII-induced increase in transcoronary protein clearance is not related to arterial hypertension or the release of PGE2, but instead appears to be mediated by NO release.

Angiotensin II↗
PubMed1995

Effect of food deprivation on baseline iodothyronine and cortisol concentrations in healthy, adult horses.

Six healthy, adult horses, with normal (mean +/- SEM) baseline serum concentrations of total triiodothyronine (T3, 1.02 +/- 0.16 nmol/L), free T3 (FT3, 2.05 +/- 0.33 pmol/L), total thyroxine (T4, 19.87 +/- 1.74 nmol/L), free T4 (FT4, 11.55 +/- 0.70 pmol/L), total reverse T3 (rT3, 0.68 +/- 0.06 nmol/L), and cortisol (152.75 +/- 17.50 nmol/L), were judged to be euthyroid on the basis of response to a standardized thyroid-stimulating hormone response test. Serum concentrations of T3, FT3, T4, FT4, rT3, and cortisol were determined immediately before and every 24 hours during a 4-day period of food deprivation, when water was available ad libitum. Similar variables were measured 72 hours after refeeding. Decreases (to percentage of baseline, prefood deprivation value) in circulating T3 (42%), T4 (38%), FT3 (30%), and FT4 (24%) concentrations were maximal after 2, 4, 2, and 4 days of food deprivation, respectively (P < 0.05). Increases (compared with baseline, prefood deprivation value) in rT3 (31%) and cortisol (41%) concentrations were maximal after 1 and 2 days of food deprivation, respectively (P < 0.05). Refeeding resulted in increase in serum T4 and FT4, and decrease in rT3 and cortisol concentrations toward baseline values, after 72 hours (P < 0.05). Refeeding did not effect a return of T3 or FT3 concentration to baseline values after 72 hours (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1995

Androgen receptors in the pelvic diaphragm muscles of dogs with and without perineal hernia.

Levator ani and coccygeus muscle estrogen and androgen receptors were measured in 6, healthy, > or = 5-year-old, noncastrated, male Beagles (controls) and in 24 dogs with perineal hernia. Estrogen and androgen receptor analyses were performed on levator ani and coccygeus muscle specimens obtained from control dogs at the time of castration; contralateral levator ani and coccygeus muscle specimens were assayed 2 months after castration. During herniorrhaphy of dogs with perineal hernia, levator ani (non-castrated, n = 12; castrated, n = 7) and/or coccygeus (noncastrated, n = 5; castrated, n = 4) muscle biopsy specimens were obtained for estrogen and androgen receptor analyses. For estrogen and androgen receptor assays, each muscle biopsy specimen was homogenized in Tris-EDTA-glycerol buffer, and centrifuged at 30,000 x g; extracts were used for binding with ligands: [3H]methyltrienolone (3HR1881) for androgen receptors, and [3H]estradiol-17 beta for estrogen receptors. Extracts were incubated overnight at 0 to 4 C. Nonspecific binding was estimated, using 100-fold concentration of cold ligands. Bound and free hormones were separated, using hydroxylapatite batch assay. Receptor numbers for each tissue were calculated as femtomoles (fmol) per milligram of protein. Quantified data were compared between precastration and postcastration controls, using a paired t-test. One-way ANOVA and Bonferroni post-hoc test were used to compare values for precastration controls, postcastration controls, castrated dogs with perineal hernia, and noncastrated dogs with perineal hernia. Significance was set at P < 0.05.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗