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H Baker

Publications and source records attributed to H Baker.

At least 127 records · Page 7Linked to original sources

Localization of tyrosine hydroxylase and olfactory marker protein immunoreactivities in the human and macaque olfactory bulb.

These studies utilized specific antisera to examine the distribution and characteristics of tyrosine hydroxylase and olfactory marker protein in the olfactory bulb of the human and macaque monkey. The macaque displayed immunoreactive profiles to both antisera comparable to those described previously for other mammals. Olfactory marker protein antiserum labeled the olfactory nerve layer and glomeruli. Within the glomeruli, labeled processes were interdigitated with unlabeled processes believed to be the postsynaptic dendrites of olfactory bulb neurons. Tyrosine hydroxylase antisera labeled somata surrounding the glomeruli as well as putative dendritic processes with the glomerular neuropil. It appeared that only a subset of juxtaglomerular neurons were immunoreactive. A similar pattern was observed in the human for both antibodies. Fascicles of olfactory marker protein immunoreactive olfactory nerves often coursed long distances into the olfactory bulb prior to arborizing within a glomerulus. The data suggest that olfactory receptor cell axons destined for specific glomeruli fasciculate into bundles prior to reaching the target glomeruli. The immunoreactivity in the human to tyrosine hydroxylase was qualitatively similar to the macaque and other mammals although the number of labeled somata and intraglomerular processes appeared lower. As in the macaque, it appeared that only a subset of juxtaglomerular neurons were labeled.

Adult↗

Species-specific distribution of aromatic L-amino acid decarboxylase in the rodent adrenal gland, cerebellum, and olfactory bulb.

Aromatic L-amino acid decarboxylase (AADC), the enzyme that converts L-dopa to dopamine, displayed species-specific differences in both activity and immunoreactivity in the cerebellum, olfactory bulb, and adrenal glands of three rodent species, the hamster, rat, and mouse. Specifically, in the hamster but not the rat or mouse, AADC immunoreactive cells were observed in the cerebellum and adrenal cortex. The unusual distribution of the enzyme was confirmed biochemically. AADC activity was greater in the adrenal gland and the cerebellum in the hamster than in the mouse or rat. In addition, by Western blot analysis, one band of appropriate molecular weight was observed both in the hamster adrenal gland and cerebellum. The rat adrenal gland displayed a similar immunoreactive protein on the Western blot; however, the protein could not be detected in the rat cerebellum by the technique utilized. Tyrosine hydroxylase (TH) immunoreactivity in these same tissues did not differ among the species. In the main olfactory bulb of the mouse, juxtaglomerular cells exhibited very limited immunoreactivity for AADC, but TH-immunoreactivity in these cells was robust. In contrast, juxtaglomerular cells in the rat displayed a similar intensity of immunostaining for both AADC and TH. AADC activity in the mouse, consistent with the reduced immunostaining for the enzyme, was 50% of that in the rat and the hamster. These data demonstrate that AADC protein, which is contained in cells of diverse function, also displays qualitative and quantitative species specific variations in both distribution and amount.

Adrenal Glands↗

Vitamin and micronutrient concentrations in cyclosporine-induced renal tumor from diabetic rats.

Concentrations of vitamins, biopterin, free inositol and acid-soluble carnitine were determined in cyclosporine A induced renal adenocarcinoma and uninvaded renal tissue from streptozotocin diabetic rats. Vitamin B6, thiamin, riboflavin, nicotinate, free inositol and acid-soluble carnitine were significantly decreased in tumor than nontumor tissue. Concentrations of folic acid, B12, biotin, pantothenate and biopterin were similar in both tissues. These studies suggest that renal adenocarcinoma affects concentrations of only certain vitamins and micronutrients.

Adenocarcinoma↗

Role of 5'-deoxy-5'-methylthioadenosine in growth of several microbial B12 requirers.

5'-Deoxy-5'-Methylthioadenosine (MTA) figures in cellular methionine and polyamine syntheses. It replaces B12 for growth of the chrysomonad protozoan Poteriochromonas malhamensis at a ratio of MTA:B12 of approximatly 10,000,000:1 (by weight). MTA does not replace B12 for other B12-requirers, e.g.: Euglena gracilis, Lactobacillus leichmannii, and Escherichia coli 113-3. The methionine synergism for P. malhamensis growth is also negated when B12 activity is annulled by alkali treatment; MTA is not inactivated by such treatment. The growth promoting activity of various deoxynucloesides and deoxynucloetides for P. malhamensis and other B12-requirers is reported here due to contamination by cobalamins. Ethionine antagonizes the growth-enhancing effect of MTA, methionine, and B12, individually and collectively -evidence that MTA plays a role in supplying methionine for P. malhamensis growth. MTA concentrations in body fluids and mammalian tissues are too low to interfere with the use of P. malhamensis for estimating only metabolically active B12.

Adenosine↗

Characterization of recombinant bovine phenylethanolamine N-methyltransferase expressed in a mouse C127 cell line.

Bovine phenylethanolamine N-methyltransferase (PNMT) cDNA was inserted into a bovine papilloma virus-based expression vector and used to transfect a mouse C127 cell line. The resultant recombinant bovine PNMT was characterized biochemically and immunochemically. Recombinant bovine PNMT activity, like the native bovine enzyme, was enhanced by phosphate ion in a concentration-dependent manner. Their molecular weights were shown to be identical by Western blot analysis. Antibodies raised against native bovine adrenal PNMT equally immunoprecipitated the activity of the recombinant and native enzymes. In addition, double immunodiffusion analysis showed a single precipitin line of confluence with both enzyme preparations, indicating immunological identity of native and recombinant bovine PNMT. These antibodies immunostained the recombinant enzyme protein in transfected cells and in their neurite-like processes. In addition, in situ hybridization with the bovine PNMT cDNA probe resulted in a labelling pattern similar to the immunostaining. The recombinant bovine PNMT as the native bovine enzyme exist in multiple-charge forms, but only one form is predominant. Taken together, our results suggest that recombinant bovine PNMT, expressed from bovine PNMT cDNA in a mouse cell line is enzymatically active and shares many common features with native bovine adrenal PNMT.

Adrenal Glands↗

Effect of short- and long-term diabetes on carnitine and myo-inositol in rats.

1. The effect of short- (2 wk) and long-term (20 wk) streptozotocin diabetes was studied on urine, blood, liver, heart, brain, skeletal muscle, pancreas and kidney concentrations of acid-soluble carnitine and free myo-inositol. 2. Short-term diabetic rats excreted significantly higher concentrations of carnitine as well as myoinositol than normal rats. Blood carnitine and myo-inositol were not different between normal and diabetic rats. Diabetes caused a decrease in liver, brain and pancreatic carnitine, but not in heart, skeletal muscle and kidney. Myo-inositol concentration was decreased in liver, heart and kidney but not in brain, pancreas and skeletal muscle. 3. Long-term diabetic rats had higher urinary excretions of both carnitine and myo-inositol. Blood carnitine did not change; however, myo-inositol was higher in diabetic than in normal rats. Diabetes caused a significant increase in liver and a decrease in heart, brain, skeletal muscle and pancreatic content of carnitine; no difference in kidney carnitine was noted. Myo-inositol content was elevated only in liver of diabetic rats. 4. We suggest that carnitine and myo-inositol concentrations are influenced both by short- and long-term diabetes through changes in tissue metabolism.

Acute Disease↗

Differential spatial and temporal expression of two type III intermediate filament proteins in olfactory receptor neurons.

Olfactory receptor neurons (ORNs) do not express the typical neuronal intermediate filament proteins (IFPs), the neurofilament triplet proteins. Immunocytochemical evidence shows that ORNs coexpress vimentin and peripherin but distribute them differently. Specifically, ORNs contain vimentin in dendrites, cell bodies, and axons, but not in terminals in glomeruli; peripherin is present in axons, but excluded from dendrites, cell bodies, and terminal glomeruli. In adult rats, ORN axon fascicles are variably stained with antisera for peripherin; in juvenile rats, staining of fascicles is uniform. Staining with antibody to vimentin is uniform in both adult and juvenile ORN axon fascicles. The unusual pattern of IFP expression and intracellular sorting may have implications for the unique plastic and regenerative capacities of these neurons.

Age Factors↗

Hypovitaminosis C in patients treated with high-dose interleukin 2 and lymphokine-activated killer cells.

Patients (n = 15) with metastatic malignant melanoma, hypernephroma, and colon carcinoma received a three-phase adoptive immunotherapy protocol: phase 1, 10(5) units (high-dose) interleukin-2 (IL-2) iv every 8 h or 1 mg/m2 continuous intravenous infusion; phase 2, 6.5 d rest + leukapheresis; phase 3, 4 d of high-dose IL-2 plus three infusions of autologous lymphokine-activated killer cells. Toxicities of treatment included fever, chills, tachycardia, hypotension, vomiting, diarrhea, and fluid retention. Patients entering the trial were not malnourished, and mean plasma ascorbic acid concentrations before therapy were normal (36.3 +/- 14.2 mumol/L). Mean concentrations dropped by 80% after the first phase of treatment with high-dose IL-2 alone (to 7.4 +/- 4.5 mumol/L). Mean plasma ascorbic acid concentrations remained severely depleted (between 4.5 and 7.4 mumol/L) throughout the remainder of the 15-d treatment. Ascorbic acid concentrations became undetectable (less than 2.8 mumol/L) in 12/15 patients during this time. Blood pantothenate and plasma vitamin E concentrations remained within normal limits in all patients tested throughout the phases of therapy.

Adult↗

Evaluation of species-specific biochemical variation as a means for assessing homology in neuronal populations.

The phylogenetic history of neurons, as derived from the establishment of homologies, has been thought to be useful for furthering the understanding of nervous system function and behavior. The sensitivity of current biochemical and molecular techniques has been heralded as the ultimate means to establish neuronal phenotype and, thus in, turn to assess neuronal homology among species. Studies delineated in this review define the caveats associated with over reliance on such an approach, even when an in-depth understanding of the biochemical and genetic makeup of homologous neuronal populations is available.

Animals↗

Branched-chain amino acids overcome cycloleucine growth inhibition in B12 and non-B12-requiring microorganisms.

Because cycloleucine (CL) inhibits methionine, and probably B12, we studied CL activity in some B12 or methionine dependent microorganisms to determine whether methionine or other amino acids are targeted by CL. We found that branched-chain amino acids, valine in particular, effectively annulled CL growth inhibition, whereas B12 was ineffective. alpha-Ketoisovalerate was the only intermediate in pathways of branched-chain amino acids catabolism that overcome CL toxicity; propionate, methylmalonate, succinate, alpha-ketoisocaproate and alpha-ketoglutarate were inactive by themselves or in combination. This study suggests that CL antagonizes the action of not only B12 and methionine but also branched-chain amino acids. Results seem comparable to those with B12-deficient fruit bats having neurologic involvement.

Amino Acids↗

Localization of p62c-yes protein in mammalian neural tissues.

Expression of the c-yes proto-oncogene in mammalian brain, retina and adrenal gland was studied by immunohistochemistry and immune assays with affinity-purified anti-yes IgG. Immunohistochemical staining with anti-yes IgG showed that in the central nervous system p62c-yes is highly expressed in mitral cells of the olfactory bulb, Purkinje cells of the cerebellum, hippocampal neurons and granule neurons of the dentate gyrus and ependymal cells lining central nervous system ventricles. Less intense labeling by anti-yes IgG was observed in most neuronal cell bodies in the brain. In addition, we observed intense c-yes immunoreactivity in the ganglion cells of the retina, the inner segment layer of rods and cones and medullary cells of the adrenal gland. Mapping p62c-yes expression to specific areas of mammalian neural tissues points to attractive experimental systems which could be used to investigate the function of the proto-oncogene product in neural processes.

Adrenal Glands↗

The expression of the neuronal intermediate filament protein peripherin in the rat embryo.

The expression of the neuronal type III intermediate filament protein peripherin was examined in the rat embryo during and following neuronogenesis in the spinal cord and the peripheral nervous system. In situ hybridization analysis reveals that peripherin mRNA is found in the mid-gestational rat embryo in ventral and lateral motoneurons in the spinal cord, and in neurons of all peripheral ganglia examined, including spinal, sympathetic, and enteric ganglia. Peripherin mRNA is seen only in post-migratory motoneurons or neuronal cells in aggregating ganglia, indicating that precursor cells do not express peripherin. To examine the expression of the protein, an affinity-purified antibody (anti-per) specific for a bacterially produced peripherin fusion protein was generated. Anti-per specifically recognizes a 58 kDa, cytoskeletal-enriched, nerve growth factor (NGF)-inducible protein of the expected tissue distribution. Immunocytodetection with anti-per shows that the initiation of peripherin protein synthesis is coincident with the morphological differentiation of neurons. In development, peripherin is one constituent of a program of gene expression activated at terminal neuronal differentiation.

Animals↗

Calcitonin gene-related peptide in the developing mouse olfactory system.

The development of calcitonin gene-related peptide (CGRP) was investigated in the mouse olfactory system. The peptide was not found in olfactory receptor neurons in embryos examined from gestational day 13 (E13) to E18 but was present in other brain regions and in peripheral tissues. At E18, CGRP-immunoreactive fibers, presumably of trigeminal, not olfactory receptor cell, origin were observed within the lamina propria. These data suggest that in vivo CGRP does not act through olfactory receptor neurons to regulate phenotypic expression in the olfactory bulb.

Animals↗

Region-specific consequences of PCD gene expression in the olfactory system.

These studies investigated the response of olfactory bulb juxtaglomerular dopamine neurons to the loss of mitral cells in 6-7-month-old Purkinje cell degeneration (PCD) mice. Previous studies in normal mice, with tyrosine hydroxylase (TH) enzyme as a marker, demonstrated that following peripheral olfactory afferent denervation the juxtaglomerular dopamine neurons exhibited a large reduction in TH activity and immunoreactivity. These intrinsic dopamine neurons also receive afferent input via dendrodendritic contacts with mitral cells. In contrast to the deficits produced by peripheral denervation, following mitral cell degeneration in homozygous recessive PCD mice, TH activity and immunoreactivity were unaltered as compared to normal heterozygous littermates. Moreover, TH activity in the substantia nigra also was unchanged, thus suggesting that the dopamine phenotype is resistant to the influences of the pcd gene. Despite the absence of a well-defined effect of the pcd gene on neurons bearing the TH phenotype, the expression of this mutation within the olfactory system is not limited to mitral cell degeneration. The current studies also demonstrate the absence of the anterior commissure, especially pars anterior, in homozygous recessive PCD mice at 6-7 months postnatal. Whether or not the loss of the anterior commissure is a primary effect or one that is secondary to mitral cell degeneration, this structural alteration provides evidence that the pcd gene exerts more widespread effects within the olfactory system that previously appreciated. The neuronal specificity of those effects remains apparent as indicated by the lack of change in TH expression.

Animals↗

An in-frame insertion in the prion protein gene in familial Creutzfeldt-Jakob disease.

In a pedigree with Creutzfeldt-Jakob disease we identified a 144-bp insertion in the open reading frame of the prion protein (PrP) gene. The insertion is in-frame and codes for 6 extra uninterrupted octapeptide repeats in addition to the 5 that are normally present in the N-terminal region of the protein. The possibility that this mutation may prove relevant to elucidating the mechanism of horizontal transmission of the spongiform encephalopathies is discussed.

Amino Acid Sequence↗