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H Baker

Publications and source records attributed to H Baker.

At least 145 records · Page 8Linked to original sources
PubMed1990

Decrease in tyrosine hydroxylase, but not aromatic L-amino acid decarboxylase, messenger RNA in rat olfactory bulb following neonatal, unilateral odor deprivation.

Unilateral naris cauterization in rats results in occlusion of the affected naris and blockade of odorant access to ipsilateral olfactory receptor cells in the olfactory epithelium. These receptor cells project exclusively to the olfactory bulb (OB) and appear to regulate expression of the dopaminergic phenotype in a population of OB juxtaglomerular neurons. Unilateral odor deprivation results in a loss of normal stimulatory input to the OB and a marked and specific decrease in ipsilateral OB tyrosine hydroxylase (TH) expression. The expression of co-localized aromatic L-amino acid decarboxylase (AADC) is not similarly affected. We have used this procedure in neonatal rats to examine the effect of stimulus deprivation on OB TH and AADC mRNA levels. Both Northern blot and in situ hybridization analyses revealed a pronounced decrease in ipsilateral as compared to contralateral OB TH mRNA levels 40 days after naris closure. In contrast, the levels of OB AADC mRNA were unaltered by naris closure. By in situ hybridization histochemistry, both TH and AADC mRNAs were localized to OB juxtaglomerular neurons. Odor deprivation was associated with an apparent region-specific reduction in TH mRNA within the ipsilateral OB glomerular layer. By densitometric analysis, the loss of TH-specific message was quantitatively consistent with the decrease in TH activity, suggesting that the observed plasticity of OB dopaminergic neurons following functional deafferentation can be attributed to a selective, transneuronally-mediated down regulation of TH gene transcription.

Animals↗
PubMed1990

Transneuronal regulation of neuronal specific gene expression in the mouse olfactory bulb.

Peripheral afferent denervation (deafferentation) of the rodent main olfactory bulb produces a marked decrease in tyrosine hydroxylase (TH) activity and immunoreactivity in a population of juxtaglomerular dopaminergic neurons. Preservation of activity and immunostaining for aromatic L-amino acid decarboxylase implies that these cells do not die, but change phenotype. We now report that the steady-state level of TH mRNA markedly decreases in the adult mouse olfactory bulb in response to deafferentation. This reduction is permanent following intranasal irrigation with 0.17 M zinc sulphate (ZnSO4) but reversible following deafferentation produced by intranasal irrigation with 0.7% Triton X-100. The initial declines in TH activity, protein and mRNA of dopaminergic juxtaglomerular neurons observed after Triton X-100 treatment are all reversible as the steady-state level of TH mRNA gradually returns to control levels. Steady-state levels of mRNA for olfactory marker protein (OMP), a protein found in high concentrations in olfactory receptor neurons and their processes which innervate the olfactory bulb, were also monitored following deafferentation. Following treatment with either ZnSO4 or Triton X-100, the pattern of changes in steady-state levels of OMP mRNA was similar to that observed for TH. The steady-state level of PEP19 mRNA, a peptide previously localized to granule cells in the olfactory bulb, was not altered by deafferentation. These data indicate selective and parallel regulation of TH and OMP message and protein levels following deafferentation.

Afferent Pathways↗
PubMed1990

Unilateral, neonatal olfactory deprivation alters tyrosine hydroxylase expression but not aromatic amino acid decarboxylase or GABA immunoreactivity.

Recent publications have demonstrated an important role for olfactory afferent innervation in maintenance of the dopamine phenotype of olfactory bulb target neurons. The mechanisms underlying the control of phenotypic expression in this system are not known. These studies employed the model of unilateral neonatal olfactory deprivation to investigate the effects of lack of odorant stimulation on dopamine expression in the rat. Immunoreactivity of tyrosine hydroxylase, the first and rate-limiting enzyme in dopamine biosynthesis, used as a marker of the dopamine system, exhibited a large decrease both 40 and 70 days following olfactory deprivation. The losses were region specific suggesting that the deprivation was not complete. The number of immunoreactive GABAergic neurons was not reduced. The number of neurons containing aromatic L-amino acid decarboxylase (the second enzyme in the dopamine biosynthetic pathway) was also not decreased. Olfactory marker protein immunoreactivity in the glomeruli, a marker for afferent innervation, was not significantly altered indicating that the olfactory bulb was not denervated. These data demonstrate that neonatal deprivation, and the resulting lack of odorant stimulation, produces a transneuronal alteration in dopamine expression without neuronal loss. The studies also suggest that neuronal activity or the activity-dependent release of a trophic factor is necessary for the expression of the dopamine phenotype.

Animals↗
PubMed1990

Excess vitamin A injures the liver.

Chronic vitamin A intoxication in a 56-year-old female is reported. Some abnormal blood chemistries included elevated transaminase and alkaline phosphatase, increased cerebrospinal fluid and portal pressure, and elevated vitamin A in blood and liver. A liver biopsy indicated histologic evidence of perisinusoidal collagen deposition and noncoalescent fat droplets in Ito cells. Caution against the misdiagnosis of alcoholic cirrhosis for vitamin A intoxication is recommended.

Diagnosis, Differential↗
PubMed1990

Effect of genetic diabetes and alcohol on tissue carnitine and inositol concentrations in mice.

Concentrations of acid-soluble L-carnitine and inositol were determined in heart, kidney, muscle, pancreas, liver, brain and blood of genetically diabetic obese db/db and their nondiabetic control C57BL/6J (CBL) mice. Results were compared to a group of diabetic and CBL mice fed ethanol (ETOH) 4 g/kg daily for 58-64 days. In CBL and db/db mice, heart muscle was found to have the greatest and brain the least content of carnitine. Diabetes caused a significant decrease in hepatic concentration of carnitine but did not affect carnitine concentration of heart, kidney, skeletal muscle, brain and pancreas. ETOH intake had no effect on carnitine content of any of the tissues studied. Free inositol content was highest in brain and lowest in skeletal muscle of CBL and db/db mice; diabetes or ETOH intake did not affect tissue inositol content. Except for liver, neither diabetes nor ETOH intake affects tissue carnitine or inositol concentration.

Alcohol Drinking↗
PubMed1990

Micronutrient status and human immunodeficiency virus (HIV) infection.

This study surveyed serum concentrations of vitamins, electrolytes, and trace elements in subjects seropositive for HIV-1 by ELISA and confirmatory Western blot. Thirty subjects (26 males, 4 females) were recruited at a hospital clinic. Seventeen were classified as having mild or severe ARC (AIDS-related complex), 7 had AIDS, and 6 were asymptomatic. Eight had experienced weight loss of 10 pounds or more in the past 6 months. Most (93%) were anergic to skin test antigens. Percentages of subjects with below normal plasma concentrations include: zinc-30%, calcium-27%, magnesium-30%, carotenes-31%, total choline-50%, and ascorbate-27%. Eighty-seven percent of the subjects had at least one abnormally low value. Percentages with above normal values include: folate-37% and carnitine-37%. Some subjects with above normal values for plasma vitamins reported self-supplementation, usually with large doses. The results suggest that one or more abnormally low concentrations of the plasma micronutrients studied here are likely to be present in the majority of HIV seropositive patients.

AIDS-Related Complex↗
PubMed1990

Riboflavin excretion in normal and diabetic rats.

Twenty-four hour urinary excretion of riboflavin was determined in normal and short-term and long-term streptozotocin diabetic rats. Compared to non-diabetic rats (controls), short-term (1 week) diabetic rats had no increased urinary riboflavin. In contrast, long-term (20 week) diabetic rats excreted significantly elevated levels of urinary riboflavin. Results suggest that the reported riboflavin deficiency seen in chronic diabetes may be related to augmented urinary excretion of riboflavin.

Animals↗
PubMed1989

Interleukin-2 enhances biopterins and catecholamines production during adoptive immunotherapy for various cancers.

Biopterins production during three different protocols for adoptive immunotherapy for human cancer was investigated. Adoptive immunotherapy treatment with interleukin-2 (IL-2) was carried out for 13 patients with malignant melanoma; eight with metastatic renal cell carcinoma; and three with metastatic colon cancer. The authors estimated total biopterins in plasma and lymphokine (IL-2)-activated killer cells (LAK) from these patients before and during various treatment phases to determine if increased biopterins production reflects leukocyte activation by IL-2 or antitumor activity. They noted an increased synthesis of total "biopterins," i.e., biopterin; 7,8-dehydrobiopterin; and L-neopterin in LAK cells and plasma which correlated with IL-2 exposure. Mean plasma biopterins were normal (1.2 +/- 0.5 ng/ml) before therapy; in contrast, biopterins increased significantly to 3.4 +/- 1.9 ng/ml and 3.9 +/- 1.9 ng/ml during IL-2 and IL-2 + LAK treatment each, respectively. Similar biopterin elevations were noted irrespective of the different adoptive immunotherapy protocols used. Elevated biopterins decreased to normal levels (1.2 +/- 0.7 ng/ml) when IL-2 treatment was omitted. Tumor regression with adoptive immunotherapy did not correlate with increased plasma biopterins. Increased biopterins production was also associated with increase in plasma catecholamine after IL-2 treatment during adoptive immunotherapy. Conceivably increased biopterins, induced by IL-2 activation of a leukocyte population, is a cell-mediated consequence not necessarily serving as a signal for the antitumor effect associated with adoptive immunotherapy.

Adult↗
PubMed1989

Biochemical and immunocytochemical characterization of olfactory marker protein in the rodent central nervous system.

Olfactory marker protein (OMP), previously thought to be expressed only by olfactory receptor neurons and their processes, was localized anatomically with immunocytochemical techniques to a number of brain regions in three rodent species, the mouse, rat, and hamster. In addition, the amount of antigen was quantified by radioimmunoassay (RIA) and characterized by an immunoblot procedure. In all three species the antigen could be detected immunocytochemically in the preoptic region and hypothalamus. The rat did not exhibit immunostaining in any other brain region. However, in the mouse neuronal labelling was observed throughout the neural axis, including cellular labelling in the bed nucleus of the anterior commissure, the median preoptic nucleus, the bed nucleus of the stria terminalis, the periventricular region, the anterior parvicellular subnucleus of the paraventricular nucleus, around the dorsomedial hypothalamic nucleus (pars compacta), the subincertal region, the arcuate nucleus, the anterior cortical nucleus of the amygdala, the suprageniculate nucleus, the lateral lemniscal nuclei, the lateraldorsal and lateralventral central gray, the posterior aspects of the commissural and marginal nuclei of the inferior colliculus, the paragenule nucleus, the A-5 region, the area postrema, the ventromedial nucleus of the solitary tract, area X, the spinal trigeminal nucleus (pars zonale), and superficial laminae of the spinal cord. The hamster displayed a different pattern of labelling including cells in the periventricular gray, the pontine reticular tegmental nucleus, the A-5 region, the medial vestibular complex, the prepositus hypoglossal nucleus, the parvicellular reticular nucleus, the lateral paragigantocellular nucleus, the raphe obscuras, the lateral reticular nucleus, and the lateral nucleus of the cerebellum. Immunostaining was seen in fibers within the red nucleus and within mossy fibers of the cerebellum. OMP levels could only be quantified by radioimmunoassay in the olfactory bulb of the three species and in the hamster cerebellum where they were 1/1,000 of those determined in the olfactory bulb. The authenticity of OMP measured in the RIA and detected immunocytochemically was verified by a double-antibody immunoisolation/immunodetection procedure, which confirmed that the antigen being visualized had the molecular properties expected for OMP. In summary, these experiments demonstrate that authentic OMP exists in small groups of neurons in many areas of the central nervous system.

Animals↗
PubMed1989

Squamous cell carcinoma radioimmunoassay in squamous cell carcinoma of the head and neck.

Tumor-associated antigen has shown promise as a clinical aid in the detection and monitoring of uterine cervical squamous cell carcinoma. Antigen levels have been shown to reflect the extent of disease and response to treatment. These findings have suggested that measurements of tumor-associated antigen may be useful in monitoring other squamous cell carcinomas. To test this hypothesis, we measured tumor-associated antigen using the squamous cell carcinoma radioimmunoassay in 103 patients with previously treated squamous cell head and neck tumors and 28 patients with known squamous cell carcinoma of the head and neck. Increased squamous cell carcinoma antigen levels were found in 39 percent of patients with known tumors and in 19 percent of the patients with previous curative resection. The sensitivity of the assay limited its usefulness in predicting the presence of new and recurrent tumors.

Adult↗
PubMed1989

Experience with combinations containing mitoxantrone in the treatment of adult acute leukemias.

Thirty cases of acute leukemia in patients over 15 years of age (18 males and 12 females) were treated with combinations containing mitoxantrone between January 1986 and August 1987 at the Kuwait Cancer Control Center. Acute nonlymphoblastic leukemia (ANLL) cases received mitoxantrone 10 mg/m2/day, days 1-3, cytosine arabinoside (Ara-C) 100 mg/m2 continuous daily infusion, days 1-5, and 6-thioguanine 100 mg/m2/day, days 1-5. Cases of acute lymphoblastic leukemia (ALL) received mitoxantrone 10 mg/m2/day, days 1-3, vincristine 1.4 mg/m2 days 1, 8, 15 and 22 and prednisone 40 mg/m2/day, days 1-22, then tapered down over one week. There were 16 cases of newly diagnosed ANLL, 9 cases of newly diagnosed ALL and 5 cases of relapsing leukemias. The 30 patients received 59 courses of therapy. The main toxicity was pancytopenia which occurred following all courses. It started following 75% of courses on day 8, lasted between 8-10 days and then rapidly recovered. In cases of ALL, the platelet count was much less affected in subsequent courses. Nausea and vomiting was a minor problem and occurred following 19% of courses, and in the majority was mild. Mucositis occurred following 30% of courses, and was mainly of moderate degree starting one week following the start of the course, and lasted about one week. Alopecia in the 25 newly diagnosed cases occurred in 18 cases (9 partial and 9 complete).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1989

The efficacy of L-tryptophan in the reduction of sleep disturbance and depressive state in alcoholic patients.

Alcoholic male inpatients (N = 76) served as subjects in this study which examined the effect of L-tryptophan on depressive state and sleep disturbance. All subjects were residents of a 6-week alcohol treatment program at a Veterans Administration Medical Center. Subjects' degree of depression (Zung's Depression Scale) and sleep satisfaction (Webb's Post-Sleep Inventory) were measured four times during the study, just prior to and following ingestion of a substance that was either 3 gms L-tryptophan or 3 gms of an identical-appearing placebo. Subjects in the L-tryptophan/placebo condition received the active substance for 4 days followed by the placebo with a 4-day washout period in between. A second group of subjects received the same regimen of reverse order and a third received placebos on both occasions. There were two additional control groups that received no substances. All subjects in the study reported decreased levels of depression due to nonspecific treatment effects. The subjects who took L-tryptophan in either sequence reported even lower levels of depression. Sleep disturbance was not affected by L-tryptophan since it was barely present when the study began. A phenomenon referred to as the interval effect is discussed and an alternative explanation for this effect is offered.

Adult↗
PubMed1989

Pyridoxal phosphate annuls acetaldehyde inhibition of uridine uptake by hepatocytes.

Methods were evaluated for depressing the acetaldehyde (AcH) inhibition of uridine uptake by Chang liver cells and isolated autologous liver cells, obtained by percutaneous liver biopsy from cases of alcoholic hepatitis. Hepatocytes so obtained were significantly more susceptible to AcH-induced inhibition of uridine uptake than hepatocytes from normal liver, alcoholic fatty liver, stable alcoholic cirrhosis and acute viral hepatitis. Benzylamine (an aldehyde buffer) and pyridoxal-5' phosphate (PLP) counteracted the inhibition of uridine uptake by AcH in vitro. We suggest that benzylamine neutralizes AcH toxicity through a Schiff-base condensation with AcH thus taking AcH out of the field of action. PLP protects against AcH-induced inhibition of uridine uptake by probably forming a Schiff base with cellular amino acids thus blocking further condensation of these amino groups with AcH. In this manner, uridine uptake by liver cells for RNA synthesis can proceed without interference by AcH.

Acetaldehyde↗
PubMed1989

Pharmacodynamics and pharmacokinetics of the oral antispastic agent tizanidine in patients with spinal cord injury.

The efficiency and duration of action of a single oral dose (8 mg) of tizanidine in patients with spinal cord injuries were determined by studying its antispastic, cardiovascular and sedative effects along with its pharmacokinetic profile in five tetraplegic and five paraplegic patients. After the administration of tizanidine, there was a reduction in spasticity in both groups within half an hour, with the effects lasting for 3 to 4 hours. There was no rebound increase in blood pressure. There was a greater increase in sedation in the tetraplegics than in the paraplegics. Plasma tizanidine levels rose within half an hour after dosing and peaked at one hour. The levels had fallen to 15 percent by 6 hours. The plasma half-life was 2.7 +/- 0.06 hours. We conclude that oral tizanidine has antispastic effects in patients with spinal cord injuries without affecting the power of non-involved muscle groups. It has minimal effects on blood pressure and it lowers heart rate. Side effects include sedation and dryness of mouth.

Administration, Oral↗
PubMed1988

Vitamins and other metabolites in various sera commonly used for cell culturing.

Many cell culture media use different sera to enhance growth. We assayed vitamins and some related metabolites in different sera and identified the concentration of: thiamin, biotin, folates, riboflavin, pantothenates, nicotinates, vitamins B6, B12, A, E, C, and carotenes and some related metabolites: biopterins, free inositol, free and total choline, total carnitines in chicken, horse, rabbit, goat, pig, calf, newborn calf, fetal calf and human sera. Results indicate that vitamin and metabolite content of different sera vary. Such variations could produce fluctuant effects on cell culturings if the metabolite content of the serum is not documented.

Animals↗
PubMed1988

Differential afferent regulation of dopaminergic and GABAergic neurons in the mouse main olfactory bulb.

Peripheral deafferentation of the mouse main olfactory bulb following intranasal irrigation with ZnSO4 produced profound decreases in tyrosine hydroxylase activity and immunoreactivity in intrinsic dopamine neurons normally localized to the juxtaglomerular region of the bulb. In contrast, only modest alterations in GABA-immunoreactivity and glutamic acid decarboxylase (GAD) activity were observed in the same region. In fact, when GAD activity was expressed per mg tissue, a reflection of enzyme concentration, no changes in activity were observed 3 weeks postlesion and only relatively modest decreases in specific activity were found following long survival times (4 months). When the data were expressed per bulb, as an indication of the total amount of enzyme present, GAD activity and bulb weight exhibited similar reductions. Olfactory marker protein levels, determined as an indication of the completeness of the deafferentation, were at or below the limits of detection in all lesioned mice. These data indicate that afferent regulation of transmitter expression in the juxtaglomerular neurons of the olfactory system is phenotype specific.

Afferent Pathways↗
PubMed1988

Biotin supplementation improves glucose and insulin tolerances in genetically diabetic KK mice.

Because biotin treatment may lower blood glucose in insulin-dependent diabetes, we chose to study such an effect in non-insulin dependent diabetes. Twenty-six diabetic KK mice, moderately hyperglycemic and insulin resistant, were treated for 10 weeks: 9 animals with 2 mg of biotin/Kg, 8 with 4 mg of biotin/Kg, and 9 with saline (controls). Blood glucose levels, oral glucose tolerance, insulin response to oral glucose, and blood glucose decrease in response to insulin were quantitated. Compared to controls, biotin treatment lowered post-prandial glucose levels, and improved tolerance to glucose and insulin resistance. Serum immunoreactive insulin levels in biotin-treated mice were like the controls.

Animals↗