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Biomedical subjects

N Baker

Publications and source records attributed to N Baker.

At least 55 records · Page 3Linked to original sources
PubMed1991

Model development to describe the heterogeneous kinetics of apolipoprotein B and triglyceride in hypertriglyceridemic subjects.

The heterogeneous nature of very low density lipoprotein (VLDL) metabolism in hypertriglyceridemia gives rise to complex kinetics when labeled VLDL are traced. Analysis of such systems benefits from the simultaneous study of several metabolically discrete subfractions which are then integrated. We have studied the kinetics of VLDL and intermediate density lipoprotein (IDL) apoprotein B and triglyceride simultaneously by injecting homologous 125I-labeled VLDL1 and 131I-labeled VLDL2 and [2-3H]glycerol intravenously in three diverse type IV hyperlipoproteinemic subjects. An additional type IV subject received only [2-3H]glycerol. Specific radioactivities were measured in: VLDL1-triglyceride and -apoB, VLDL2-triglyceride and -apoB, and in each corresponding subfraction after further separation into heparin-Sepharose-bound and -unbound fractions. ApoB and triglyceride specific radioactivities were also measured in IDL. Analysis of the kinetics of apoB in the unbound fractions in VLDL1 and VLDL2 showed the presence of two pools of particles, one of which turned over rapidly. The kinetics of apoB in the bound fractions in VLDL1 and VLDL2 were, in contrast, dominated by a large slowly turning over pool of particles that resembled the kinetics of whole VLDL. Evidence of a partial precursor-product relationship between the unbound and bound fractions suggested that the former was richer in nascent-like particles, while the latter contained more remnant particles. However, triglyceride specific radioactivity curves for both unbound and bound fractions showed initial rapid rises and broad peaks, indicating that the bound fraction also contained a substantial proportion of nascent-like particles. Using multicompartmental analysis, a model was constructed to account for the kinetics of both apoB and triglyceride in all fractions of VLDL and in IDL. The model comprises two parallel delipidation pathways that supply a common remnant pool with these features: 1) multiple direct inputs of particles into plasma at VLDL2 and IDL levels; 2) heterogeneous triglyceride precursor pools leading to different rates of labeling of VLDL1 and VLDL2; 3) very substantial delipidation of VLDL2 particles prior to conversion to IDL and; 5) triglyceride production rates somewhat higher than previously reported. The inclusion in the model of the rapidly turning over pool of triglyceride-rich particles, identified in the heparin-unbound fraction, suggests that values for triglyceride production in man have been underestimated.

Aged↗
PubMed1990

Reduced suppression of plasma saturated fatty acid mobilization and oxidation by feeding in lymphoma-bearing mice.

Lymphoma-bearing mice have a circulating lipid-mobilizing factor, but increased plasma free fatty acid (FFA) turnover has not been demonstrable in earlier studies using postabsorptive tumor-bearing mice. We hypothesized that FFA mobilization in lymphoma-bearing mice is only elevated in fed mice and may best be observed at night (dark, reversed light cycle). AKR mice with early and advanced tumors (10(6) SL-3 lymphoma cells, i.p.) and controls were fed ad libitum (reversed light cycle, dark) or fasted 4 h (daylight, regular cycle), given injections of [14C]bicarbonate of [1-14C]palmitate-mouse serum albumin, i.v., and plasma [14C]FFA disappearance and/or breath 14CO2 were monitored. Plasma FFA mobilization, estimated by multicompartmental analysis (SAAM) of the oxidation rate was lower in fasted mice with advanced tumors [tumor, 9.5 +/- 6.0% (%SE); controls, 14 +/- 4.4% micrograms-atoms fatty acid-carbon/min/30 g body weight, n = 3 to 6 mice/time point/group]. Feeding reduced these rates 90% in control mice and 53% in mice with early tumors, but only 14% in mice with advanced tumors. Plasma FFA fractional catabolic rates were 2.5 times faster in fed mice with advanced tumors than in controls. Diminished suppression of fatty acid mobilization in fed tumor-bearing mice (at night) probably accounts partially for the body fat loss.

Adipose Tissue↗
PubMed1990

Sensory physiology and catecholamines in schizophrenia and mania.

Hypersensitivity to sensory stimulation is a prominent characteristic of both schizophrenia and mania. Neurophysiological recordings suggest a common deficit in a central neuronal sensory gating mechanism which regulates sensitivity to repeated auditory stimuli. Dopamine and norepinephrine are hypothesized to have major roles in these illnesses, but their role in aberrant sensory processing has not yet been proved. Presumptive evidence for effects of catecholamines on sensory processing comes from psychophysiological studies of normal subjects challenged with stimulants who show decreased sensory gating, and studies of psychotic patients treated with neuroleptics who show improved function. Studies of similar phenomena in animals show comparable effects of catecholamines on sensory processing, both behaviorally and at the single neuron level. In this study, gating of auditory evoked potentials (EPs) during treatment of both illnesses was compared with plasma dopamine and norepinephrine metabolites. Comparisons of medicated and unmedicated states showed that schizophrenic patients have a fixed deficit in sensory gating, which is a familial trait, unchanged by medication. During acute illness, they have an additional transient hypersensitivity to stimuli, manifested as smaller EPs, which seems to be mediated by dopamine. Manic patients have only the deficit in sensory gating, which is transient and seems to be mediated by norepinephrine. Thus, similar neurophysiological deficits in the two psychoses are associated with different biochemical abnormalities, which may explain similarities in acute symptoms and differences in other aspects of the illnesses, such as their response to treatment.

Adult↗
PubMed1990

Glycosphingolipid receptors for Pseudomonas aeruginosa.

The binding of Pseudomonas aeruginosa to glycosphingolipids and to buccal and bronchial epithelial cells was analyzed. Three independently expressed specificities were found by bacterial binding to glycosphingolipids separated by thin-layer chromatography. All strains bound gangliotria- and gangliotetrasylceramide. All but one of the strains bound sialic acid-containing glycosphingolipids and lactosylceramide. The latter two specificities could be separated in that the lactosylceramide binding was retained and the sialic acid binding was suppressed when bovine serum albumin was used as a blocking agent in the thin-layer chromatography assay. The attachment to buccal epithelial cells, like the binding to sialylated compounds and lactosylceramide, was abolished by Formalin treatment of the bacteria, suggesting the importance of these specificities for cell adherence. In contrast, the binding to gangliotria- and gangliotetraosylceramide was retained by nonattaching Formalin-treated bacteria.

Antigens, CD↗
PubMed1990

The influence of properties encoded by the Yersinia virulence plasmid on adhesion of Yersinia enterocolitica to ileal brush border membrane vesicles.

The influence of plasmid-associated cell surface structures on the ability of Yersinia enterocolitica to bind to ileal brush border membrane vesicles (BBVs) was investigated. Rabbit or human BBVs were immobilized on polystyrene microtiter plates and adhesion of radiolabeled cells of Y. enterocolitica was determined. Strains of pathogenic serotypes carrying the Yersinia virulence plasmid (pYV+), as well as their isogenic plasmid cured derivatives (pYV-), adhered to immobilized BBVs, but adhesion of pYV+ organisms was markedly greater than that of pYV- ones. Strains belonging to non-pathogenic serotypes did not adhere significantly. The pYV+ strain Ye0301P+ did not express specific adhesion to glycolipids, nor was adhesion to BBVs reduced in the presence of various monosaccharides. Proteolytic digestion of surface structures on strain Ye0301P+ markedly reduced adhesion. pYV+ strains also demonstrated greater adhesion to a non-biological surface (polystyrene) and showed a higher degree of hydrophobicity than pYV- organisms as evaluated in a two-phase partitioning system. It is therefore likely that the plasmid-associated adhesion of Y. enterocolitica is promoted by one or more outer membrane proteins, that confer hydrophobicity to the bacterial surface.

Animals↗
PubMed1989

Increased platelet intracellular calcium concentration in patients with bipolar affective disorders.

Using the fluorescent indicator Fura 2, we measured the free intracellular calcium ion concentration in blood platelets of patients with untreated mania, bipolar depression, and unipolar depression; patients who had recovered from bipolar depression or mania; and age- and sex-matched controls. The baseline intracellular calcium ion concentration was significantly increased in platelets from patients with mania compared with controls. The free intracellular calcium ion concentration after stimulation with platelet-activating factor and thrombin was significantly higher in platelets of manic and bipolar depressed patients than in all other groups. The degree to which intracellular calcium ion concentration increased over baseline after stimulation was significantly lower in unipolar than in bipolar patients. These findings suggest that platelets of manic and depressed bipolar patients have a similar enhancement of intracellular calcium ion activity that is distinctly different from the decreased ability of platelets of unipolar patients to mobilize intracellular calcium in response to stimulation.

Adult↗
PubMed1989

Turnover and fate of plasma free fatty acids in briefly-fasted lymphoma-bearing mice.

Body fat loss during tumor growth may be due to increased mobilization of adipose triglycerides. Earlier work from this laboratory suggested that (i) lymphoma-bearing AKR mice have a circulating lipid mobilizing factor (LMF) which caused body fat loss during cancer growth; that (ii) fatty acids (FA) mobilized in these tumor-bearing (TB) mice were not oxidized to CO2 as in starved mice that lose their body fat; and that (iii) instead, the mobilized FA were sequestered by the lymphoma. We tested these hypotheses by injecting [1-14C]palmitate-albumin into lymphoma-bearing and control mice. We measured turnover of plasma FFA for 24 hr and predicted the cumulative conversion of tracer into breath 14CO2 (at 85 min) in the TB mice. Plasma FFA were mobilized more slowly in briefly fasted tumor-bearing mice than in controls with the same plasma FFA pool sizes. The fractional catabolic rate (FCR) (min-1) of plasma FFA turnover in both groups decreased during the night when the mice ate: postabsorptive controls, 1.07 (+/- 5.6%); fed controls, 0.25 (+/- 13%); postabsorptive TB, 0.53 (+/- 4.6%); fed TB, 0.29 (+/- 7.3%). Virtually all of the plasma FFA irreversible disposal in TB mice was accounted for as breath 14CO2 (30 to 40% I.D.), not as tumor lipids (1.1 +/- 0.22% I.D.). Thus, FFA oxidation to CO2 is the major fate of plasma FFA turnover in TB mice, and sequestration of FFA (palmitate) by tumor cells is a quantitatively minor process. The putative circulating LMF did not cause increased FFA mobilization in these lymphoma-bearing mice in the post-absorptive state.

Animals↗
PubMed1989

Binding specificities of wild-type and cloned Escherichia coli strains that recognize globo-A.

In this study we compared the specificity for the globoseries of glycolipids of Escherichia coli expressing the O-negative, A-positive (ONAP) adhesin and clones transformed with the pap-like (prs or pap-2) gene cluster. Receptor-active glycolipids were identified by the ability of radiolabeled bacteria to bind to the glycolipids on thin-layer chromatogram plates. The ONAP adhesin and pap-like clones bound with high affinity to the globo-A and Forssman glycolipids. The ONAP strains did not recognize other glycolipids of the globoseries. In contrast, the pap-like clones also showed weak binding to globotriaosylceramide and reacted weakly with Gal alpha 1----4 Gal beta-latex beads. We suggest that the pap-like and ONAP adhesins recognize an epitope shared by the globo-A and Forssman structures, e.g., terminal GalNAc alpha 1----3 bound to Gal alpha 1----4Gal beta-containing glycolipids.

Adhesins, Escherichia coli↗
PubMed1988

Globo-A--a new receptor specificity for attaching Escherichia coli.

Uropathogenic Escherichia coli strains designated as ONAP, based on their O negative A positive agglutination of human P1 erythrocytes, were shown to prefer the globo-A glycolipid as a receptor structure. The dependence on both the A terminal and the globoseries chain was confirmed by agglutination of human AP1, but not Ap or OP1 erythrocytes and by binding to the globo-A glycolipid on TLC plates. Neither Gal alpha 1----4Gal beta nor the A trisaccharide GalNAc alpha 1----3(Fuc alpha 1----2)Gal beta alone functioned as receptors. The bacteria thus appeared to recognize an epitope resulting from the combination of the terminal and internal structures.

Animals↗
PubMed1988

Fat pad triacylglycerol fatty acid loss and oxidation as indices of total body triacylglycerol fatty acid mobilization and oxidation in starving mice.

We tested our hypothesis that, kinetically, triacylglycerol fatty acids in heterogeneously labeled adipocytes behave similarly to the whole fat pad triacylglycerol fatty acid during starvation in mice. Adipose triacylglycerol fatty acids were labeled with [1-14C]palmitate (complexed to albumin) by injection of a small bolus (2-5 microliter) into either epididymal or inguinal fat pads. Both 14C-labeled triacylglycerol fatty acid spec. act. and breath 14CO2 spec. act. were monitored 30 min after tracer injection and after 24-72 h starvation. Adipose triacylglycerol fatty acid spec. act. remained approximately constant during fasting, i.e., tracer and mass disappeared at similar rates. Negligible translocation of labeled triacylglycerol fatty acid from the injection site to other parts of the same fat pad or to distant fat pads occurred. Triacylglycerol fatty acid was mobilized more slowly from epididymal than from inguinal fat pads in two of three studies. Triacylglycerol fatty acid disappearance (loss) from inguinal fat pads was more replicable than from epididymal fat pads and more closely reflected the fall in whole body total lipid during starvation. The estimated percent of breath CO2-carbon derived from adipose triacylglycerol fatty acid increased from an average of approx. 32% in the postabsorptive state to about 77% after 48 h starvation. The data help to validate the direct tracer injection technique as a means of studying adipose triacylglycerol fatty acid turnover and oxidation. This approach should be particularly useful for studying the fate of adipose triacylglycerol fatty acid when it is mobilized. e.g., during states of inanition and starvation and in response to hormones and cancer-induced cachexia.

Adipose Tissue↗
PubMed1988

Cerebral coenurosis in a cat.

Coenurus serialis, the intermediate stage of Taenia serialis, was the cause of progressive, fatal, intracranial disease in a 5-year-old cat. X-Ray computed tomographic findings were identical to those associated with intracranial parasitic cysts in people, in whom x-ray computed tomographic features are considered pathognomonic and superior to those of other diagnostic methods. The presumed source of the coenurus was the owner's dog.

Animals↗
PubMed1987

Neurophysiological assessment of sensory gating in psychiatric inpatients: comparison between schizophrenia and other diagnoses.

Gating of auditory sensory responsiveness was examined in 75 psychiatric inpatients using a conditioning-testing paradigm with the P50 wave of the auditory evoked response, in which pairs of stimuli are presented to the subject. In previous studies, most schizophrenics did not decrement the second response to the extent seen in normals. Acutely ill patients, who were representative of patients admitted to a public university teaching service and a proprietary hospital, were used to examine the extent to which diminished sensory gating is found in diagnoses other than schizophrenia. About half of these patients showed diminished sensory gating that correlated with measures of severity of illness. The data, taken together with that from other studies using this paradigm, suggest that diminished sensory gating, like several other psychophysiological abnormalities, is a trait deficit in schizophrenia, but a state deficit in many other mental illnesses.

Adjustment Disorders↗
PubMed1987

Neurobiological studies of sensory gating in schizophrenia.

The sensory disturbance in schizophrenia is often described as an inability to filter out extraneous noise from meaningful sensory inputs. The neurobiological basis of this inability to filter has been examined using auditory evoked potentials, which are computerized averages of the brain's electrical response to sound. The sounds are presented in pairs to test the ability of the brain to inhibit, or gate, its response to a repeated stimulus. Schizophrenic patients lack the ability to gate the neuronal response shown by a particular wave, the P50 wave. The measurement of this deficit in human subjects and the exploration of its neurobiology in animals has produced evidence about several issues in the pathophysiology of schizophrenia: (1) the role of dopamine in improvement of sensory function in schizophrenic patients treated with neuroleptic drugs, (2) the interaction between familial or genetic deficits in sensory functioning in schizophrenic patients and possible abnormalities in dopamine metabolism, and (3) a mechanism by which noradrenergic hyperactivity in mania and other psychiatric illnesses might mimic some pathophysiological deficits in schizophrenia.

Antipsychotic Agents↗
PubMed1987

Delayed recycling of plasma FFA in mice: revised model of turnover and oxidation.

We have reexamined the concept of the irreversible disposal rate (IDR) or fractional catabolic rate (FCR) in relation to the oxidation of a major metabolic fuel, plasma free fatty acids (FFA), in mice. We measured the disappearance of intravenously injected [1-14C]palmitate complexed to mouse serum albumin from the circulation of normal mice fed ad libitum and fasted approximately 4 h before tracer injection. We also measured the appearance of expired 14CO2 in the breath. Using multicompartmental analyses (SAAM) we found that, in contrast to earlier studies in this and other mammals where the estimated IDR has always been two to three times greater than the oxidative rate, the IDR (FCR) corresponded closely to the fractional rate of plasma FFA oxidation to CO2. This rate could be estimated accurately in a study of 10- to 15-min duration. In an extended study (5-h duration) we obtained kinetic evidence of a major transport pathway that involves delayed recycling of FFA through at least several unidentified relatively slowly turning compartments.

Animals↗
PubMed1987

Transport and metabolism of extracellular free fatty acids in adipose tissue of fed and fasted mice.

We used a new tracer technique, direct tracer injection of [1-14C]palmitate-serum albumin into extracellular fluid (ECF) of epididymal fat pads, to study relative transport rates of ECF-free fatty acids (FFA) to cell-FFA and subsequent esterification to diglyceride fatty acid (DGFA) and triglyceride fatty acid (TGFA) in adipose tissue versus movement of ECF- and cell-FFA into the circulation of mice fed ad libitum or fasted 48 hr. Radioactivity was measured in the following fractions at varying times (for 1 hr): ECF-FFA, cell-FFA, cell-DGFA, cell-TGFA, plasma-FFA (total lipids), and breath CO2. Pool sizes of ECF-FFA, cell-FFA, cell-TGFA, and plasma-FFA were determined. Analysis by multicompartmental methods (SAAM) indicates that the ECF-FFA compartment of epididymal fat pads is in a relatively rapid exchange with a cellular-FFA compartment, but neither is in direct, nor appreciably rapid, communication with circulating FFA. FFA is rapidly esterified in adipocytes of fed mice, but esterification is significantly inhibited in mice fasted for 48 hr. In both dietary states, essentially all labeled FFA appearing in the circulation was derived from ECF-FFA that were first transferred to the cell, esterified to TGFA, then hydrolyzed to FFA before being transported to the circulation.

Adipose Tissue↗