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Biomedical subjects

G Baker

Publications and source records attributed to G Baker.

At least 91 records · Page 5Linked to original sources
PubMed1987

In vitro LH release from the hypothalamus-pars tuberalis; effects of gonadotropin-releasing hormone (GnRH), beta-endorphin and biogenic amines.

Immunoreactive and bioactive luteinizing hormone (LH) has been shown to be widely distributed in the rodent central nervous system (CNS), particularly in the hypothalamus. Subcellular localization of this LH in fractions rich in synaptosomes and in vitro release by potassium-induced depolarization suggests that this peptide may act in trans-synaptic neuromodulatory roles. Furthermore, a variety of experiments have proved that this brain-based LH is not of pituitary origin. In the in vitro studies reported here characterization of brain-based LH release, in response to gonadotropin-releasing hormone (GnRH), beta-endorphin, and biogenic amines, was examined. Adult male rats were sacrificed by decapitation, hypothalami removed, quartered, and incubated in Krebs Ringer's Bicarbonate (KRB). High potassium concentration and GnRH induced release of LH from these hypothalamic explants in short-term culture and serotonin significantly inhibited release of LH from these explants. In contrast, however, beta-endorphin, norepinephrine, dopamine, and acetylcholine, agents known to modulate pituitary LH release, had no effect on the release of LH from hypothalamic tissues in vitro. Furthermore, beta-endorphin did not alter potassium-induced release of LH from the hypothalamus. Whereas there are some similarities between LH release from the pituitary and from the CNS, the differences reported here suggest that hypothalamic LH does not simply serve as a supplemental source for LH in the general circulation but more likely subserves an entirely different role(s) than its pituitary counterpart, presumably acting in a neuromodulatory fashion within the brain.

Animals↗
PubMed1987

Alterations in selected serum biochemical constituents in equids after induced hepatic disease.

Effects of induced cholestasis and hepatocellular necrosis and of fasting on serum biochemical constituents including bile acids, IgA, bilirubin, alkaline phosphatase, gamma-glutamyltransferase (GGT), arginase, and the clearance of sodium sulfobromophthalein were studied in 4 groups of equids. The reference value for serum bile acids, as determined by an enzymatic colorimetric procedure for horses and ponies was 5.94 +/- 2.72 mumol/L, there being no statistical difference for horses and ponies. Sample collection at time of feeding had no effect on serum bile acid concentration. Seemingly, serum bile acids, arginase, and GGT were the most sensitive indicators of cholestasis and/or hepatocellular necrosis and would form an essential minimum effective battery of tests to diagnose and prognose hepatic disease in equids. These tests provided a measure of hepatobiliary transport function (bile acids), cell necrosis (arginase), and cholestasis (GGT and bile acids).

Alkaline Phosphatase↗
PubMed1987

Regulation of thrombopoiesis: effects of the degree of thrombocytopenia on megakaryocyte ploidy and platelet volume.

We have established a murine model and techniques with which to serially study thrombocytopoiesis after induction of experimental immune thrombocytopenia of variable severity and duration. Bone marrow megakaryocyte ploidy distribution was determined by using unfractionated bone marrow, a polyclonal megakaryocyte-specific probe, and two-color, fluorescence-activated flow cytometry. With these techniques, the modal megakaryocyte ploidy class in normal murine bone marrow was 16N. Serial studies of bone marrow megakaryocyte ploidy after the induction of acute, severe thrombocytopenia (platelet count, less than 0.05 X 10(6) microL) demonstrated no detectable change in the ploidy distribution at 12, 24, and 36 hours after the onset of thrombocytopenia. At 48 hours, the modal ploidy class shifted from 16N to 32N, and the 64N class increased significantly (P less than .001). The ploidy distribution returned to normal 120 hours after the onset of thrombocytopenia. A lesser degree of thrombocytopenia (platelet count reduction to 0.100 to 0.200 X 10(6)/microL) delayed the modal ploidy class shift from 16N to 32N until 72 hours after the onset of thrombocytopenia. Chronic, severe thrombocytopenia (platelet count, less than 0.05 X 10(6)/microL for seven days) resulted in a modal ploidy class shift from 16N to 32N during the thrombocytopenic phase and an enhanced increase in the 64N megakaryocyte class during the recovery phase. Mean platelet volume (MPV) was simultaneously measured on isolated total platelet populations after induction of thrombocytopenia. MPV was significantly increased (P less than .001) as early as eight hours after the onset of acute, severe thrombocytopenia, 40 hours before a shift in the ploidy distribution. Mild thrombocytopenia (platelet count reduction to 0.400 X 10(6)/microL) was not associated with a ploidy shift but did result in a significantly increased MPV (P less than .001). These studies demonstrate that the temporal relationship and magnitude of the effects of thrombocytopenia upon megakaryocyte ploidy distribution are dependent upon the degree and the duration of the thrombocytopenic stimulus and that the effects of experimental thrombocytopenia on platelet volume and megakaryocyte ploidy are dissociated.

Acute Disease↗
PubMed1985

Brain thyroid-stimulating hormone: effects of endocrine manipulations.

We have previously described the presence of and the immunologic, chromatographic and biologic characteristics of a thyroid-stimulating hormone (TSH)-like peptide, widely distributed in the rat and monkey central nervous system (CNS). In order to test the hypothesis that brain TSH, specifically hypothalamic TSH, participates in the turnover of pituitary TSH, we have assessed the effect on hypothalamic TSH of two endocrine manipulations, castration and adrenalectomy, known to significantly decrease pituitary and/or serum TSH in the rat. Orchidectomy led to a significant decline of pituitary and serum TSH while a significant increase in hypothalamic TSH concentrations was seen. Adrenalectomy also led to decreased pituitary concentration of TSH linked with a significant increase in hypothalamic TSH levels. Neither manipulation led to changes in TSH in the extrahypothalamic brain. The inverse relationship wherein serum and/or pituitary TSH decrease is accompanied by an increase in hypothalamic TSH is compatible with a role for hypothalamic TSH in pituitary TSH regulation. The possible significance of these findings in terms of TSH triiodothyronine interactions in the CNS is discussed.

Adrenal Cortex Hormones↗
PubMed1985

Isolation, experimental transmission, and characterization of causative agent of Potomac horse fever.

Potomac horse fever, a disease characterized by fever, anorexia, leukopenia, and occasional diarrhea, is fatal in approximately 30 percent of affected animals. The seasonal occurrence of the disease (June to October) and evidence of antibodies to the rickettsia Ehrlichia sennetsu in the serum of convalescing horses suggested that a related rickettsia might be the causative agent. Such an agent was isolated in cultured blood monocytes from an experimentally infected pony. This intracytoplasmic organism was adapted to growth in primary cultures of canine blood monocytes. A healthy pony inoculated with these infected monocytes also developed the disease. The organism was reisolated from this animal which, at autopsy, had pathological manifestations typical of Potomac horse fever. Cross serologic reactions between the newly isolated agent and antisera to 15 rickettsiae revealed that it is related to certain members of the genus Ehrlichia, particularly to Ehrlichia sennetsu. Since the disease occurs in other parts of the United States as well as in the vicinity of the Potomac River, and since it has also been reported in Europe, the name equine monocytic ehrlichiosis is proposed as being more descriptive.

Animals↗
PubMed1985

The impact of aging on luteinizing hormone (LH) and thyroid-stimulating hormone (TSH) in the rat brain.

Immunoreactive and bioactive luteinizing hormone (LH), thyroid-stimulating hormone (TSH) and growth hormone (GH) have been described by this and other laboratories to be present in discrete areas of the rodent and primate brain. In the present studies, LH and TSH concentrations in serum, pituitary, hypothalamus, brainstem, cerebellum, cerebral cortex and hippocampus were measured in male Sprague-Dawley rats at 2.5 months of age, when 11-12 months old and at 24 months of age. There was a significant decrease in hypothalamic TSH concentrations in the 11-12-month-old rats compared to younger animals (672 +/- 127 ng/mg vs 86 +/- 17 ng/mg, P less than 0.001). This was unaccompanied by any changes in TSH levels in serum, anterior pituitary, or in any of the extrahypothalamic brain areas that were examined. In contrast, there was a significant 50% drop in LH concentrations in the anterior pituitary gland of 11-12-month-old animals when compared with young controls (72 +/- 58 micrograms/mg vs 137.2 +/- 27 micrograms/mg, P less than 0.05) without any noted change in serum or brain LH concentrations. Similar decreases in LH concentration were also seen in the anterior pituitary glands of two-year-old animals. These discordant profiles between pituitary and brain LH and TSH provide additional circumstantial evidence that these brain peptides do not represent contaminants from the anterior pituitary. Further, these significant changes in TSH and LH concentrations that develop with aging may implicate these particular peptides in the development of certain features of senescence.

Aging↗
PubMed1984

Release of immunoreactive luteinizing hormone (LH) from rat hypothalamus-pars tuberalis explants.

A luteinizing hormone (LH)-like molecule has been described in the rodent central nervous system and has been shown to have immunologic, chromatographic, and biologic activity similar to that of pituitary LH. In this communication we report that a depolarizing stimulus, high potassium concentration in the presence of calcium, causes in vitro release of LH from hypothalamic explants containing the pars tuberalis. Release from other brain areas containing LH was not seen nor was release of LH, in vitro, significantly provoked from dorsal segments of the hypothalamus, thus suggesting that most, if not all, of the releasable LH from intact hypothalamic explants may come from cells of the pars tuberalis.

Animals↗
PubMed1984

Standard electromotive force of the H2-AgCl;Ag cell in 30, 40, and 50 mass% dimethyl sulfoxide/water from -20 to 25 degrees C: pK2 and pH values for a standard "Bicine" buffer solution at subzero temperatures.

The establishment of the pH (designated pH*) of a standard buffer solution suitable as a pH reference in 30, 40, and 50 mass% dimethyl sulfoxide (DMSO)/H2O mixtures at temperatures in the range -20 to 0 degrees C is reported. The buffer material selected was the ampholyte Bicine (N,N-bis(2-hydroxyethyl)glycine), and the reference standard consists of equal molal quantities of Bicine and its sodium salt. The assignment of pH* values rests on measurements of the emf of cells without liquid junction, Pt;H2(g, 1 atm) [Bicine, Na Bicinate, NaCl [AgCl;Ag, and the pH* was derived from a determination of K2, the equilibrium constant for the dissociation process (Bicine) +/- in equilibrium (Bicinate)- + H+. The standard emf in the DMSO/H2O solvents at subzero temperatures was determined from emf measurements of the cell with solutions of HCl replacing the buffer-chloride mixture.

Buffers↗
PubMed1983

Immunoreactive thyroid stimulating hormone (TSH)(: association with synaptosomally-rich fractions in the rat hypothalamus.

The subcellular compartmentalization of brain thyroid stimulating hormone (TSH) in the hypothalamus of the rat was investigated using differential and discontinuous sucrose density gradient centrifugation. When the mitochondrial fraction (P2) was layered on a discontinuous sucrose density gradient (0.32-1.4 M) and centrifuged for 60 min at 72,000 g, TSH recovered from the gradient was found, by double antibody radioimmunoassay, to be associated preferentially with the synaptosomally-rich layers. The separation was monitored by electron microscopic examination of all fractions obtained throughout the procedure. The addition of a large excess of either [125I]-labeled or unlabeled pituitary TSH at the time of homogenization did not influence the amount of immunoreactive TSH associated with the synaptosome-rich fractions, and both the unlabeled and labeled hormone were recoverable in the final supernatant indicating that the simple addition of peptide to hypothalamic homogenates did not result in any preferential association to any particular subcellular fraction. The apparent association of this brain-based pituitary peptide was not, therefore, an artifact of the homogenization process. It is concluded that an association exists between immunoassayable TSH and brain-based synaptosomes in homogenates of the rodent hypothalamus.

Animals↗
PubMed1983

Extrahypothalamic brain luteinizing hormone: characterization by radioimmunoassay, chromatography, radioligand assay and bioassay.

We have recently reported that luteinizing hormone (LH) is present in the hypothalamus of rats. It has chromatographic and biologic characteristics similar to pituitary LH. In this report we focus on extrahypothalamic LH that is widely distributed in the rodent central nervous system. This material has a chromatographic profile similar to that of pituitary LH. Serial dilution of this material is parallel with dilutions of rat pituitary LH in the immunoassay. Brain extracts are active in the testis LH radioligand receptor assay and in the rat interstitial cell testosterone secretion bioassay. Prior incubation of extract with LH antibody significantly attenuated both of these activities. Thus, extrahypothalamic LH has immunologic, chromatographic, and biologic characteristics similar to hypothalamic and pituitary LH.

Animals↗
PubMed1982

Growth hormone (GH) immunoreactivity in the rodent and primate CNS: distribution, characterization and presence posthypophysectomy.

Using a specific sensitive radioimmunoassay, the distribution of growth hormone (GH) immunoreactivity in the rodent and primate central nervous system (CNS) was determined. Highest levels of extractable growth hormone-like materials were obtained from the rat amygdaloid nucleus, although other areas including cortex, hippocampus and the thalamus, contained immunoreactive material. Primate hypothalamus showed the highest levels of growth hormone immunoreactivity but it was also detectable in all regions examined. Forty-eight days posthypophysectomy, levels of GH immunoreactivity did not change in most rodent CNS areas studied. Moreover, levels in the amygdaloid nucleus and hypothalamus, although demonstrating an initial fall, actually rose above control levels several weeks following hypophysectomy. Dispersed CNS cells from both intact and hypophysectomized rats continuously released a GH-like material into the growth medium during a 20-day period of tissue culture. This phenomenon was suppressed with the addition of somatostatin to the growth medium. Characterization of this readily extractable GH-like material using column chromatography, parallel displacement curves, and biologic assay in the hypophysectomized rat showed a similarity between the CNS growth hormone-like material and its pituitary counterpart. The blood-brain barrier was found to be most likely intact to circulating pituitary growth hormone lending further support to the CNS origin of this biologically active and immunoreactive GH-like material in the brain.

Amygdala↗
PubMed1982

Growth hormone (GH), thyroid-stimulating hormone (TSH), and luteinizing hormone (LH)-like peptides in the rodent brain: non-parallel ontogenetic development with pituitary counterparts.

Brain and anterior pituitary growth hormone (GH), thyroid-stimulating hormone (TSH) and luteinizing hormone (LH) were measured during fetal, neonatal, and pubertal life and into adulthood. Immunoassayable GH and TSH could be found in the fetal whole brain before their detection in the fetal pituitary. Developmental patterns of pituitary and brain hormones differed in that pituitary hormones showed a gradual rise in levels from birth to puberty at approximately 20 days of age. Biochemically similar, brain-based peptides demonstrated a remarkable preparturitional surge in concentrations that was limited to a few days immediately preceding birth. Twenty-four hours after birth, brain GH, TSH, and LH had dropped to levels equal to or less than concentrations in the neonatal pituitary and subsequently rose to adult levels around the time of puberty. In these studies it could be shown that both the placental-fetal barrier and the neonatal blood-brain barrier were intact. These observations indicate the presence of two biochemically and immunologically similar but topographically distinct pools of peptides present in the developing brain and in the anterior pituitary gland.

Aging↗