Proceedings: Luteinizing hormone and follicle-stimulating hormone secretion in response to luteinizing hormone releasing hormone in the adult guinea-pig.
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Animals↗
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Plasma growth hormone and prolactin response to thyrotropin releasing hormone, L-dopa and luteinizing hormone-releasing hormone in alcoholic patients with liver cirrhosis.
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Adult↗
[Pituitary hormone secretion studied by simultaneous use of thyrotropin releasing hormone and Hungarian-made luteinizing hormone releasing hormone].
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Adult↗
Oral administration of arginine enhances the growth hormone response to growth hormone releasing hormone in short children.
We have evaluated the effect of oral administration of arginine chlorhydrate on the growth hormone response to growth hormone releasing hormone in a group of nine short prepubertal children (six boys and four girls). Arginine chlorhydrate 10 g, administered orally 60 min before an i.v. bolus injection of growth hormone releasing hormone 1-29, 1 microgram/kg, significantly enhanced the growth hormone response to the neuropeptide, confirming the results of previous studies which used the i.v. route. Furthermore, our data strengthen the view that the effects of arginine chlorhydrate on growth hormone secretion are mediated by inhibition of endogenous somatostatin release.
Administration, Oral↗
Galanin: analysis of its coexpression in gonadotropin-releasing hormone and growth hormone-releasing hormone neurons.
Galanin is coexpressed in a subset of gonadotropin-releasing hormone (GnRH) and growth hormone-releasing hormone (GHRH) neurons in the brain and has an important role in the neuroendocrine regulation of gonadotropin and growth hormone secretion. Our overall goal has been to understand the functional significance of galanin as a cotransmitter with GnRH and GHRH in the regulation of these important physiologic processes. To this end, we studied the regulation of galanin's expression in GnRH and GHRH neurons under a variety of physiologic and experimental conditions. Using double-label in situ hybridization and computerized image analysis, we observed that in GnRH neurons, galanin's expression is increased over the course of development in both sexes. Galanin achieves a higher basal expression in GnRH neurons in females, and it is sexually differentiated in the adult as a result of the differential exposure to testosterone during the neonatal critical period. Galanin is induced in GnRH neurons coincident with and subsequent to the proestrous luteinizing hormone surge (reflecting the combined action of estradiol and progesterone) acting indirectly on GnRH neurons through a synaptic relay. Galanin's expression in GnRH neurons is inhibited during lactation, when the neuroendocrine reproductive axis is relatively quiescent. In GHRH neurons, the expression of galanin is also induced over the course of development in both sexes. Galanin's expression in GHRH neurons in the adult is sexually differentiated, but in this case, its expression is higher in males than females, reflecting the stimulatory effect of testosterone on galanin in the male. Galanin's expression in GHRH neurons is induced by growth hormone (GH), whereas the absence of GH leads to a reduction of galanin mRNA in these same cells. On the basis of these observations, we conclude that galanin is an important target for regulation by many hormones, and we postulate that as a cotransmitter, galanin acts presynaptically to modulate the secretion of GnRH and GHRH, possibly by altering their pulsatile release patterns, which in turn influences the release of the gonadotropins and GH from the pituitary.
Animals↗
Hormonal regulation of rat hypothalamic neuropeptide mRNAs: effect of hypophysectomy and hormone replacement on growth-hormone-releasing factor, somatostatin and the insulin-like growth factors.
Hormonal feedback regulation of hypothalamic peptides putatively involved in growth hormone (GH) regulation has been studied by measurement of steady-state mRNA levels in male hypophysectomized rats with or without thyroid hormone, corticosterone, testosterone or GH replacement. Hypothalamic GH-releasing factor (GRF) mRNA levels increased progressively following hypophysectomy to 420% of sham levels after 15 days while hypothalamic insulin-like growth factor I (IGF-I) and insulin-like growth factor II (IGF-II) mRNA levels decreased to less than 40% of sham levels. Whole hypothalamic somatostatin mRNA levels were not significantly different from sham. One week of continuous GH infusion restored hypothalamic IGF-I mRNA to levels (95%) indistinguishable from those in sham-operated controls but had no effect on either IGF-II or GRF mRNA. Thyroid hormone, corticosterone and testosterone treatment without GH had no effect on the hypophysectomy-induced reduction of either IGF-I or IGF-II mRNA levels but reversed the elevation of GRF mRNA. We conclude that hypothalamic IGF-I may be involved in GH feedback regulation and thus may function as a hypothalamic modulator of GH. In contrast, IGF-II may be regulated by one of the pituitary trophic hormones but not by GH or the target hormones tested. Finally, hypothalamic GRF mRNA regulation appears to be complex and may include target hormone feedback.
Animals↗
Steroids, sex hormone-binding globulin, homocysteine, selected hormones and markers of lipid and carbohydrate metabolism in patients with severe hypothyroidism and their changes following thyroid hormone supplementation.
Laboratory markers of thyroid function, selected steroid hormones, sex hormone-binding globulin (SHBG), homocysteine, prolactin, major markers of lipid- and glucose metabolism and of insular-growth hormone axes were investigated in fasting sera from 16 female patients with severe hypothyroidism after thyroidectomy because of thyroid cancer. The results obtained in severe hypothyroidism within 5-6 weeks after withdrawal of thyroid substitution therapy before control scintigraphy were compared with those obtained after correction of thyroid function. Elevated levels of homocysteine and prolactin in hypothyroidism significantly decreased after correction, while SHBG concentration increased. Correction of thyroid function led to significant changes of growth hormone and immunoglobulin F1 (decrease and increase, respectively), while insulin and proinsulin increased only insignificantly. Elevated levels of total cholesterol and triglycerides in hypothyroidism were normalized, along with a significant increase in high density lipoprotein (HDL)-cholesterol. As revealed by correlation and factor analyses, different relationships characterizing both states were found in hypothyroidism and after correction of thyroid function. A strong inverse relationship between homocysteine and free thyroid hormones confirms the effect of thyroid hormones on homocysteine metabolism. No such inverse relation was found in euthyroid state, however. Similarly, in hypothyroidism only, dehydroepiandrosterone sulfate correlated positively with immunoglobulin F1 and homocysteine and negatively with thyroid hormones and SHBG.
Adult↗
Role of prostaglandin E2 (PGE2) in the growth hormone releasing hormone action on growth hormone, insulin and C-peptide in normal men.
Fourteen healthy men were placed in two treatment groups. 1. Seven men received growth releasing hormone (1 microgram/kg BW) intravenously during either saline or prostaglandin E2 (10 micrograms/min) infusion which were started 60 minutes before testing. Growth hormone response to growth releasing hormone was greater during prostaglandin E2 infusion compared to the control study. These data suggest that exogenous prostaglandin E2 positively modulates growth hormone response to growth releasing hormone. In the second group consisting also of 7 men a GRH test was performed before and after 3 days administration of meclofenamate. Meclofenamate significantly reduced plasma levels of stable metabolites of prostaglandin E2 as well as the growth hormone to growth releasing hormone, suggesting that the GRH effect on GH was at least partly under prostaglandin E2 control. GRH significantly reduced serum insulin in the two treatment groups. PGE2 infusion or meclofenamate did not change insulin response to GRH. Serum C-peptide and blood glucose did not change after GRH injection during saline or PGE2 infusions.
Adult↗
A comparison of the effects of the calcitonins, steroid hormones and thyroid hormones on the response of bone to parathyroid hormone in tissue culture.
A bone culture system was used to compare the effects of several hormones on the response of 5-day-old mouse calvaria to parathyroid hormone (PTH). The results showed that salmon calcitonin was almost 10-5 times more active than any other hormone in preventing the PTH-induced release of calcium and caused a dose-related inhibition of calcium release over a range of 0-2-200 milli MRC units/culture. A high dose of calcitonin (200 milli MRC units) caused a net accretion of calcium in the absence of PTH. Progesterone and testosterone were more active than the naturally occurring oestrogens although a synthetic oestrogen (stillboestrol diphosphate) had approximately the same potency. High concentrations of these hormones caused a net accretion of calcium whether or not PTH was present. Cortisol was only effective at high doses, as was the steroid precursor cholesterol. In the present culture system the thyroid hormones (triiodothyronine and thyroxine) inhibited the action of PTH. It was concluded that these agents acted in a similar fashion to the oestrogens. That is, they prevented the accumulation of citric acid induced by PTH by reducing the rate of glycolysis. None of the hormones affected the inhibition of citrate oxidation caused by PTH. The results also showed that, whilst these hormones inhibited PTH-mediated bone resorption, they had an action on bone independent of PTH. Experiments with clomiphene citrate failed to demonstrate an oestrogen receptor in bone.
Animals↗
[Different effects of tricyclic (clomipramine and amitriptyline) and tetracyclic (maprotiline) antidepressors on the release of thyroid stimulating hormone, prolactin and growth hormone to thyrostimulating releasing hormone in patients with psychoaffective disorders (author's transl)].
The hormonal alterations induced by tricyclic and tetracyclic antidepressors (AD) were studied in patients with psychoaffective disorders (PAD) to ascertain the role of certain biogenic amines in the regulation of thyroid stimulating hormone (TSH), prolactin (PRL) and growth hormone (GH). The responsiveness of plasma TSH, PRL and GH to synthetic thyrostimulating release hormone (TRH; 250 microgram i.v.) was determined in 57 patients distributed in 5 groups according to the treatment: 10 non treated patients, 16 tricyclic (clomipramine and amitriptyline) treated patients, 6 patients treated by clomipramine in association with lithium, 6 tetracyclic (maprotiline) treated patients and 19 patients treated by major neuroleptics. Results of untreated patients were compared to those observed in 10 age and sex matched normal subjects. Basal plasma levels of TSH were normal in all the patients. The TSH response to TRH (delta TSH) was blunted in non treated patients. delta TSH was normal in the patients treated by maprotiline or neuroleptics and increased in the group treated by tricyclic AD in association with lithium. Basal plasma levels of PRL and PRL response to TRH (delta PRL) were decreased in the women treated by tricyclic AD, but remained normal under maprotiline. They were markedly increased in the neuroleptic group. No inadequate response of GH to TRH was noted in our series of patients. The different hormonal effects induced by AD--dissociation between delta TSH and delta PRL under tricyclics and normal or increased delta TSH under maprotiline--may be logically explained by the various ways of action of these AD on the brain monoamines. delta TSH decrease and tendency to an increased delta PRL observed with clomipramine argue for a serotoninergic regulation of these two hormones, whereas the normalisation of delta TSH under maprotiline argues for a noradrenergic regulation of this hormone. Effectively, tricyclic AD inhibits mainly the serotonin recaptation and tetracyclic inhibits rather norepinephrine recaptation. The persistent delta TSH increase observed in the group treated by the association clomipramine-lithium demonstrates that the tricyclics do not interact with the hypophyso-thyroid positive feedback.
Adult↗
Hormonal regulation of hormone-sensitive lipase in intact adipocytes: identification of phosphorylated sites and effects on the phosphorylation by lipolytic hormones and insulin.
In isolated adipocytes, fast-acting lipolytic hormones and insulin have been shown previously to control lipolysis by regulating the activity of hormone-sensitive lipase, the rate-limiting enzyme, through an increase or decrease, respectively, of the extent of phosphorylation of the enzyme. Here, we demonstrate that exposure to lipolytic hormones (corticotropin, noradrenaline) led to phosphorylation at two sites on the Mr 84,000 lipase subunit. One, designated "basal site," was phosphorylated also in the absence of any hormonal stimulation, its phosphorylation apparently not being influenced by hormones. The second, designated "regulatory site," was identical to that phosphorylated by cyclic AMP-dependent protein kinase on the isolated lipase. The regulatory site was not appreciably phosphorylated in the absence of hormones, but exposure of the cells to noradrenaline increased its phosphorylation extent to that of the basal site. Insulin or the beta-adrenergic antagonist propranolol decreased the extent of phosphorylation of the regulatory site to the low level before stimulation, apparently without effect on the basal site. Phosphoserine was the only phosphorylated amino acid residue at both sites. Limited proteolytic digestion indicated that the two sites were separated by less than about 170 amino acid residues. Thus, control of adipose tissue lipolysis by fast-acting lipolytic hormones and by insulin is exerted through the regulation of the phosphorylation state of a single phosphoserine residue in the hormone-sensitive lipase.
Adipose Tissue↗
Effect of endothelin-1 in man--impact on basal and stimulated concentrations of luteinizing hormone, follicle-stimulating hormone, thyrotropin, growth hormone, corticotropin, and prolactin.
The effect of endothelin-1 on basal and stimulated serum (plasma) concentrations of luteinizing hormone (LH), follicle-stimulating hormone (FSH), thyrotropin (TSH), prolactin (PRL), growth hormone (GH), and corticotropin was investigated in healthy male volunteers (n = 5). Intravenous (IV) administration of endothelin-1 (5 ng/kg/min for 15 minutes, followed by 2.5 ng/kg/min for 105 minutes) induced an increase in basal plasma concentrations of corticotropin. Serum concentrations of PRL, TSH, LH, FSH, and GH remained unchanged. The increase in serum concentrations of these pituitary hormones induced by IV administration of LH-releasing hormone ([LH-RH] 100 micrograms), thyrotropin RH ([TRH] 400 micrograms), GH-RH (100 micrograms), and corticotropin-releasing factor ([CRF] 100 micrograms) was suppressed in regard to PRL (P < .01) and GH (P < .01) and enhanced in regard to corticotropin (P < .01). Stimulated serum concentrations of LH and FSH also tended to be higher following administration of endothelin-1 (P < .05), whereas the increase in serum concentrations of TSH remained unchanged. Thus, when administered in pharmacological doses, endothelin-1 influences pituitary hormone secretion in man.
Adrenocorticotropic Hormone↗
Intracerebral expression of gonadotropin-releasing hormone and growth hormone-releasing hormone is delayed until smoltification in the salmon.
A developmental strategy was employed to investigate the functional assembly of neuropeptidergic systems in the migratory species of chum salmon Oncorhynchus keta. Using immunocytochemistry we have demonstrated that different groups of gonadotropin-releasing hormone- (GnRH)- and growth hormone-releasing hormone- (GHRH)-synthesizing neurons emerged according to very different developmental timetables. From the eye pigmentation stage (23 +/- 2 days after fertilisation (DAF)) through to the pre-smoltification stage (136 DAF), salmon-GnRH neurons originating from the olfactory placodes remained restricted to the extracerebral course of the terminal nerve. At the climax of smoltification (downstream migration 167 DAF), basal forebrain and midbrain GnRH neurons with elaborate neurite outgrowths in the brain and the pituitary became detectable. The GnRH neuroanatomical organization in the post-smoltification stage (197 DAF) was similar to that in the smoltification stage (167 DAF). In contrast to the case for other teleosts, chicken-GnRHII neurons were not found in the midbrain but were localized along the medial regions of the olfactory nerve. Growth hormone-releasing hormone immunoreactivity in the olfactory apparatus (21 DAF), and fibers along the basal telencephalon and hypothalamus and in the pituitary were observed during early embryogenesis (51 DAF) and in cells in the preoptic area on 167 DAF. The intracerebral expression of GnRH and GHRH was not detected until the peak of smoltification, which coincided with a peak in thyroid hormones, and precisely with downstream migratory behavior.
Age Factors↗
Preparation of a photoreactive analog of parathyroid hormone [Nle8, Lys(N-epsilon-4-azido-2-nitrophenyl)13,Nle18,Tyr34]bovine parathyroid hormone-(1-34)NH2, a selective, high-affinity ligand for characterization of parathyroid hormone receptors.
Photoaffinity radiolabeling techniques have been widely used to characterize the properties of peptide hormone receptors. However, the identity of authentic receptors is often uncertain because many macromolecules are labeled. These ambiguities are due, in part, to the use of a heterogeneous mixture of photoreactive photoligands, many of which have no or low affinity for the relevant hormone receptor. In this report, we describe the synthesis, purification, and structural analysis of the photoreactive parathyroid hormone analog, [Nle8,Lys(N-epsilon-4-azido-2-nitrophenyl)13,Nle18,Tyr34]-bovine parathyroid hormone-(1-34)NH2. The sulfur-free, oxidation-resistant, synthetic analog of bovine parathyroid hormone (PTH), [Nle8,Nle18,Tyr34]bovine PTH-(1-34)NH2 (NlePTH), was reacted with 4-fluoro-3-nitrophenylazide under nonaqueous conditions to yield several derivatives which were separated by reverse-phase high-performance liquid chromatography and analyzed by amino acid compositional analysis, thin-layer chromatography, and ultraviolet and visible absorption spectroscopy. Among the NlePTH derivatives generated, one of the least hydrophobic was shown to retain the highest potency as assessed in the canine renal cortical membrane radioreceptor assay. Sequence analysis of this peptide, after it had been derivatized with 4-fluoro-3-nitro-[2,6-3H]phenylazide and purified to homogeneity, permitted us to determine that the structure of this analog is [Nle8,Lys(N-epsilon-4-azide-2-nitrophenyl)13,Nle18,Tyr34]bovine PTH-(1-34)NH2. We emphasize the importance of using photoreactive ligands which are purified and subjected to detailed chemical and biological analyses for characterizing the properties of parathyroid hormone receptors and receptors for other peptide hormones.
Affinity Labels↗
Angiotensinergic neurons physiologically inhibit prolactin, growth hormone, and thyroid-stimulating hormone, but not adrenocorticoptropic hormone, release in ovariectomized rats.
Angiotensin II (AII)-containing neurons with cell bodies in the rostral medial hypothalamus and axons project to the external layer of the median eminence, so that AII maybe released into the hypophyseal portal vessels for actions on the pituitary gland. Indeed, intrahypothalamic actions of the peptide on the release of hypothalamic hormones and direct actions on the pituitary have been reported. To determine the role of endogenously released AII in hypothalamic-pituitary hormone release, we have determined the effects of central immunoneutralization of AII upon the plasma concentrations of prolactin (PRL), growth hormone (GH), thyroid-stimulating hormone (TSH), and adrenocorticotropic hormone (ACTH). Specific antiserum directed against AII (AB-AII) or normal rabbit serum (NRS), as a control, was microinjected into third ventricular (3 V) cannulae of conscious, ovariectomized (OVX) rats. Immediately before and at various intervals after this procedure, blood samples were withdrawn through previously implanted external jugular catheters. Three hours after injection of the AB-AII, plasma PRL levels diverged from those of the NRS-injected animals and progressively increased from 4 to 24 h after administration of the antiserum. Results were similar with respect to plasma GH, except that the increase in the AB-AII animals above that in the NRS-injected controls from 4 to 6 h was not significant, but was highly significant on measurement 24 h after injection, at which time plasma GH was three times higher than in control rats. Similarly, following injection of AB-AII, plasma TSH values did not diverge significantly from those of the NRS-injected controls until 3 h after injection. From 3 to 5 h they remained constant and significantly elevated above values in the NRS-injected controls with a further nonsignificant increase at 6 h. At 24 h, there was no longer a difference between the values in both groups. In contrast to the significant elevations in plasma hormone levels observed with respect to PRL, GH, and TSH following injection of the antiserum, there was no change in plasma ACTH between the AB-AII-injected and NRS-injected animals throughout the same period of observation. Previous results by others have shown that intraventricular injection of AII has a suppressive action on the release of PRL, GH, and TSH. Consequently, we believe that the antiserum is acting intrahypothalamically to block the action of AII within the hypothalamus, resulting in the elevation of the three hormones mentioned. Therefore, the AII neurons appear to have a physiologically significant suppressive action on the release of hypothalamic neurohormones controlling the release of PRL, GH, and TSH. In contrast, there apparently is no effect of intrahypothalamically released AII on the secretion of corticotropin-releasing factors under these nonstress conditions. We cannot rule out an action of the antiserum at the pituitary level; however, in view of the fact that the actions of AII directly on the gland are to stimulate PRL, GH, TSH, and ACTH release, it appears that the antiserum was acting at the hypothalamic level.
Adrenocorticotropic Hormone↗
Effect of thyrotropin-releasing hormone, triiodothyronine, and chicken growth hormone on plasma concentrations of thyroxine, triiodothyronine, growth hormone, and growth of lymphoid organs and leukocyte populations in immature male chickens.
One-day-old White Leghorn male chicks were fed different levels of Thyrotropin Releasing Hormone (TRH) (1 and 5 ppm) or Triiodothyronine (T3) (.1 and 1 ppm) for an 8-wk period. In a second experiment, chicken growth hormone (cGH) (10 micrograms/kg of BW) was injected (iv) into different birds daily for 7 days starting at 7 wk of age. Different groups of birds received both T3 (.1 and 1 ppm) and cGH. Serum concentrations of thyroxine (T4), T3, and growth hormone (GH), lymphoid organ weights, total circulating white blood cells (WBC), and differential counts were measured following hormone treatments. It was found that T3, cGH, or a combination of both significantly lowered serum T4 concentrations. Triiodothyronine supplementation at 1 ppm, alone or with cGH significantly increased serum T3 concentrations. Chicken GH with T3 (.1 ppm) significantly increased serum GH concentrations. Thyrotropin releasing hormone supplementation did not affect serum concentrations of either T4, T3, or cGH. Relative bursa weights were greater in chicks that received T3 (1 ppm) or TRH (1 or 5 ppm) but not cGH. Relative spleen weights were enhanced in response to cGH alone or with T3 (1 ppm) but not TRH. Total WBC count was significantly increased in response to T3 (1 ppm). Supplementation of T3 (.1 or 1 ppm), TRH (1 ppm), and the combination of cGH and T3 (1 ppm) significantly increased the percentage of lymphocyte cell population. These results demonstrate the impact of feeding hormones on T3, T4, and cGH concentrations in the serum and suggest the involvement of the above hormones in the growth of lymphoid organs as well as the production of lymphocytes.
Animals↗
Difference in the susceptibility of two phenobarbital-inducible forms, P450IIB1 and P450IIB2, to thyroid hormone- and growth hormone-induced suppression in rat liver: phenobarbital-inducible P450IIB2 suppression by thyroid hormone acting directly, but not through the pituitary system.
Suppression of two major phenobarbital-inducible cytochrome P-450s, P450IIB1 and P450IIB2, by thyroid hormone was studied and compared with growth hormone (GH)-induced suppression in rats in vivo and hepatocytes in primary culture in vitro. Treatment of adult male rats with 50 micrograms/kg triiodothyronine (T3) reduced the constitutively expressed amounts of P450IIB1 (up to 1 pmol/mg of protein) and P450IIB2 (2-5 pmol/mg of protein) to 42% and 3% of their levels in nontreated controls. Thyroidectomy increased the hepatic contents of P450IIB2 (to levels of 50-80 pmol/mg of protein) and, to a lesser extent, P450IIB1 (1-5 pmol/mg of protein) in male and female rats. Supplement of T3 to thyroidectomized rats reversed the increased contents to levels similar to those observed in normal rats. Hypophysectomy also increased both P450IIB1 and P450IIB2 protein, and their levels in both sexes were similar to that of P450IIB2 in thyroidectomized rats. Treatment of hypophysectomized rats with T3 as well as human GH suppressed hepatic contents of P450IIB1 and P450IIB2. In a hepatocyte culture including 2 mM phenobarbital, T3 and GH suppressed both P450IIB1 and P450IIB2. Other thyroid hormone derivatives, including thyroxine, D-T3, and reversed T3, also showed suppressive effects, in parallel with the potencies for their stimulatory action that have been reported. These results indicate that thyroid hormone may suppress both P450IIB1 and P450IIB2 by a direct effect on the liver, but not by an indirect effect through the modulation of pituitary GH synthesis. The high susceptibility of hepatic P450IIB2 to thyroid hormone-induced suppression also indicates that constitutive and phenobarbital-induced levels of P450IIB2 are suppressively regulated preferentially by thyroid hormone, in contrast to the high susceptibility to GH of P450IIB1 in rat liver. In addition, a difference in the suppressive mechanisms of thyroid hormone and GH was suggested by the difference in susceptibility to cycloheximide.
Animals↗
Alpha and beta thyroid hormone receptors bind immediately adjacent to the rat growth hormone gene TATA box in a negatively hormone-responsive promoter region.
We report that alpha and beta type rat thyroid hormone receptors bind specifically and with high affinity to the 10-base pair sequence immediately 3' of the rat growth hormone TATA box (positions -25 to -16) in a region of the rat growth hormone promoter which can be negatively hormone responsive (nTRE). The receptors have approximately 7-fold lower affinity in vitro for the nTRE than for the thyroid hormone-responsive enhancer of the rat growth hormone gene (TRE). Proteins extracted with high salt concentration from rat pituitary cell nuclei enhance binding of the receptors to both the TRE and nTRE. A modification of the avidin-biotin complex DNA binding assay which enhances the sensitivity of the assay approximately 100-fold was used in these studies. The immediate proximity of a receptor binding site to the rat growth hormone TATA box suggests that direct interaction between receptor and TFIID (the TATA binding protein) mediates nTRE activity.
Animals↗