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Biomedical subjects

S M Smith

Publications and source records attributed to S M Smith.

At least 325 records · Page 18Linked to original sources
PubMed1987

Calcium transport by permeabilised rabbit small intestinal epithelial cells.

Intestinal epithelial cells isolated from rabbit small intestine and whose plasma membrane had been rendered highly permeable were used to study the role of intracellular structures in Ca2+ buffering. Monitoring free Ca2+ with a selective electrode revealed that the cells could reduce Ca2+ concentration in the medium to a level of 3.6 X 10(-7) M independently, within a certain range, of the initial Ca2+ concentration or amount of cells used. Ca2+ buffering by permeabilised enterocytes was Mg2+- and ATP-dependent and was abolished in the presence of the Ca2+ ionophore A23187. The rapidity of Ca2+ buffering, but not the final Ca2+ level attained, was reduced in the combined presence of the mitochondrial inhibitors azide and oligomycin or in the presence of ruthenium red. Buffering of Ca2+ was abolished in the presence of vanadate, although some uptake was still observed. Complete blocking occurred in the presence of both vanadate and mitochondrial inhibitors. Measurement of initial rates of uptake with radioactive calcium revealed that mitochondrial uptake plays a role at relatively high Ca concentrations but that at the presumably physiological levels most of the uptake is into a non-mitochondrial compartment. Non-differentiated crypt cells seemed to handle intracellular Ca2+ in a similar way as mature villus cells, although they appeared to buffer at a level about 2 X 10(-7) M lower.

Adenosine Triphosphate↗
PubMed1987

Role of neutrophils in hemorrhagic shock-induced gastric mucosal injury in the rat.

Gastric mucosal clearance of 51Cr-labeled red blood cells (51Cr-RBC) was measured in rats during a 30-min control period, a 30-min ischemic period (hemorrhage to 27 mmHg arterial pressure), and a 60-min reperfusion period (reinfusion of shed blood). In untreated (control) rats, a dramatic rise in the leakage of 51Cr-labeled red blood cells into the gastric lumen was observed during the reperfusion period. Treatment with neutrophil antiserum attenuated 51Cr-labeled red blood cell flux into the gastric lumen. Using the radioactive microsphere technique, neutrophil-depleted animals were shown to have higher blood flows in the ischemic period than the untreated rats. Bleeding of untreated rats to a mean arterial pressure of 40 mmHg resulted in blood flows that were not different from those in antiserum-treated rats bled to 27 mmHg and leakage of 51Cr-labeled red blood cells similar to that measured in antiserum-treated rats. The results of this study indicate that neutrophils play an important role in hemorrhagic shock-induced gastric bleeding.

Animals↗
PubMed1987

Gastric mucosal injury in the rat. Role of iron and xanthine oxidase.

Recent studies have implicated oxygen free radicals in ischemia-reperfusion injury to the gastric mucosa. The aims of the present study were to test the hypothesis that the enzyme xanthine oxidase is the source of the oxygen radicals in the ischemic stomach and determine the importance of the iron-catalyzed Haber-Weiss reaction in generating the cytotoxic oxygen radicals. Gastric mucosal clearance of 51Cr-labeled red blood cells was measured during a 30-min control period, a 30-min ischemic period (hemorrhage to 25 mmHg arterial pressure), and a 60-80-min reperfusion period (reinfusion of shed blood). In untreated (control) rats, a dramatic rise (100-fold) in the leakage of 51Cr-labeled red blood cells into the gastric lumen was observed only during the reperfusion period. After the reperfusion period, gastric mucosal damage was further assessed using gross lesion area and histology. Rats were placed on a sodium tungstate diet (to inactivate xanthine oxidase), or treated with either deferoxamine (an iron chelating agent) or superoxide dismutase (a superoxide scavenger). All three interventions substantially reduced 51Cr-labeled red blood cell clearance and gross lesion area relative to untreated rats. However, tissue injury assessed histologically was similar in both treated and untreated animals. The results of this study support the hypothesis that oxygen free radicals mediate the hemorrhagic shock-induced extravasation of red blood cells. The data also indicate that xanthine oxidase is the source of the oxy-radicals and that the iron-catalyzed Haber-Weiss reaction is largely responsible for hydroxyl radical generation in this model.

Animals↗
PubMed1987

Experimental allergic orchitis in mice: IV. Preliminary characterization of the major murine testis specific aspermatogenic autoantigen(s).

Active experimental allergic orchitis (EAO), characterized by inflammation of the testes (autoimmune orchitis), aspermatogenesis, epididymitis and vasitis was induced in mice using a panel of tissue antigens as immunogens. Immunization with allogeneic murine tissue homogenates emulsified in complete Freund's adjuvant (CFA) accompanied by the injection of pertussigen revealed that only adult murine testicular and epididymal homogenates are capable of eliciting murine EAO. All other tissue antigens studied including prepubertal mouse and epididymal homogenates failed to elicit significant disease. Immunization with xenogeneic testicular antigens also failed to elicit significant disease indicating that the major murine aspermatogenic autoantigen(s) is also highly species specific. Sensitization with allogeneic mouse testicular homogenates (MTH) from different disease resistant strains was for the most part no less potent in inducing significant disease than was immunization with mouse testicular homogenates from disease susceptible strains. However, testicular homogenates from NZB/B1NJUnm and MRL/MpJ-/+Unm mice were significantly less potent at inducing autoimmune epididymitis as compared to other strains, indicating possible interstrain differences in the immunogenicity of the aspermatogenic autoantigen(s) relevant to eliciting epididymitis. Attempts at solubilization and purification of the major murine aspermatogenic autoantigen(s) utilizing techniques employed for the purification of aspermatogenic autoantigens such as AP3 from guinea pig (GP) testes were unsuccessful. Additional extraction procedures resulted in solubilization of the relevant autoantigen(s) only after reduction in the presence of 6 M guanidine hydrochloride. These data suggest that: (1) there may be a much more limited number of aspermatogenic autoantigens in murine testes as compared to GP testes; (2) the disease inducing determinant(s) may be expressed as either a sequential antigenic determinant(s) or as an antigenic determinant(s) in the carbohydrate portion of a glycoprotein or glycopeptide; and (3) the disease inducing autoantigen(s) may be present in situ in a highly insoluble form requiring active processing within the target organ in order to generate soluble antigen capable of being seen by immune reactants.

Animals↗
PubMed1987

Experimental allergic orchitis in mice: III. Differential susceptibility and resistance among BALB/c sublines.

Significant differences in susceptibility to the induction of experimental allergic orchitis (EAO) were found to exist among the various substrains of BALB/c mice. Substrains which were susceptible to disease induction include BALB/cKa, BALB/cByJ, BALB/cWtJ, BALB/cCmcCr, BALB/cCrgl, BALB/cHeA, BALB/cAnNCr, BALB/cPt, BALB/cWehiUnm, BALB/cOrnl and BALB/cArg whereas BALB/cJ and BALB/cSki BoyPt were resistant to EAO. Aspermatogenesis and autoimmune vasitis, two additional lesions characteristic of murine EAO, were found to correlate with susceptibility to autoimmune orchitis. Susceptibility and/or disease resistance did not segregate within any of the evolutionary branches of the BALB/c genealogic tree nor did it correlate with any of the previously described allelic differences distinguishing BALB/c substrains. Therefore, differential disease susceptibility may represent the manifestation of mutational and/or retroviral induced genotypic differences in the regulatory genes controlling testicular autoimmunity.

Animals↗
PubMed1987

Nontyphoid salmonella urinary tract infections.

Urinary tract infection caused by nontyphoid salmonella is rare. A case is described in a patient with acquired immunodeficiency syndrome who had multiple recurrences. A review of cases in which salmonella involved the urinary tract indicates that this infection usually occurs in patients who are structurally or immunologically compromised. Recurrence is expected and treatment plan should include an extended course of antibiotic therapy.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Contrasting impairments in IgM and IgG responses of vitamin A-deficient mice.

Mice fed a semipurified, vitamin A-deficient diet (A- mice) and control animals fed the same diet with added retinyl acetate (A+ mice) were used to investigate the effect of vitamin A deficiency on primary immunoglobulin responses to protein antigens. At age 6 weeks, A- mice had serum retinol concentrations that were 46% of A+ controls. When immunized with a single antigen dose, these mice produced an antigen-specific IgM response equivalent to controls, but their IgG1 and IgG3 responses were sharply diminished (less than 30% of A+ controls). At age 8 weeks, A- mice had 20% of A+ serum retinol concentrations and less than 17% of A+ liver retinyl palmitate levels. Responding to a single antigen dose, A- mice produced approximately equal to 70% as much IgM as A+ controls. Their IgG1 response was less than 30% and their IgG3 response less than 3% of A+ controls. The IgG1 response kinetics were identical in A- and A+ mice. Diminished serum antibody responses in A- mice were attributable to fewer immunoglobulin-secreting plasma cells rather than to a decline in IgM or IgG secretion rate per cell. Total serum IgG3 levels, irrespective of antigen specificity, were slightly elevated in A- mice compared to A+ controls. The inefficient clonal expansion of responding B lymphocytes and contrasting impairment of IgM and IgG responses observed in vitamin A-deficient mice are discussed with respect to a possible helper/inducer-T-lymphocyte defect.

Animals↗
PubMed1987

Impaired immunity in vitamin A-deficient mice.

Vitamin A deficiency was produced in mice and was used to investigate the role of vitamin A in immune function. Cellular immunity, as measured by delayed-type hypersensitivity, diminished in early deficiency before weight and appetite changes occurred and declined further as the deficiency progressed. Humoral immunity, as measured by serum immunoglobulin M (IgM) responses to a protein antigen (hemocyanin), also declined. The kinetics of antibody production were unaffected by the deficiency. The T-cell number remained unchanged, but B-cell and macrophage numbers were increased in vitamin A--deficient mice. Surface expression of membrane glycoproteins (Thy-1, Lyt-1, Lyt-2, L3T4, IgM, Mac-1) was unchanged by the deficiency, as were lymphocyte numbers and distribution. The results suggest that vitamin A deficiency is associated with a functional immune system defect.

Animals↗
PubMed1987

Serologic evidence of acute murine typhus infection in a patient with culture-negative endocarditis.

A patient with culture-negative infective endocarditis is presented in whom detailed serological studies were indicative of acute infection with murine typhus. The patient had aortic and mitral regurgitation with congestive heart failure and typical peripheral manifestations of subacute endocarditis, but no documented fever. Aortic and mitral valve replacement surgery and a 6-week course of doxycycline therapy produced a clinical cure in this patient, as well as a diagnostic fall in markedly elevated preoperative typhus indirect fluorescent antibody (IFA) and complement fixation (CF) titers. Serological studies were consistently negative for Q fever.

Acute Disease↗
PubMed1987

Role of polyamines in intestinal adaptation in the rat.

The cellular mechanisms controlling adaptive intestinal mucosal hypo- and hyperplasia are poorly understood but changes in tissue polyamine levels and in the activity of the key enzymes controlling their synthesis (ornithine decarboxylase: ODC) and degradation (diamine oxidase: DAO) have been implicated. Therefore, in two models of adaptive mucosal hyperplasia (pancreatico-biliary diversion, PBD, achieved by surgically transposing the jejunum to lie between pylorus and ampulla of Vater, and 90% small bowel resection, SBR-both studied 8 weeks after surgery) and in one model of hypoplasia (8 days total parenteral nutrition) we measured indices of mucosal mass (wet weight, protein and DNA per 10-cm intestine), the growth-associated polyamines (putrescine, spermidine and spermine per 10-cm intestine and per mg DNA) and DAO activity in the duodenum, five 10-cm segments of jejunum, five 10-cm segments of ileum and in the colon, and compared the results with those found in transected or unoperated controls. The results for the indices of mucosal mass confirmed that TPN led to a modest degree of small bowel mucosal hypoplasia whilst PBD, and particularly 90% SBR, stimulated marked adaptive hyperplasia. There were corresponding changes in the amounts of putrescine and spermidine (but not of spermine)-not only when the results were expressed per unit length but also when calculated per mg mucosal DNA and in the ratio of spermidine:spermine. There was an increasing proximal-to-distal gradient in mucosal DAO per unit length intestine in all experimental groups but when the results were expressed per mg DNA, the ileal DAO levels were significantly reduced in the PBD and resection groups, when compared with the controls. These data support the hypothesis that polyamines play a major, and perhaps a controlling, role in regulating adaptive intestinal mucosal growth.

Amine Oxidase (Copper-Containing)↗
PubMed1987

Caesium ions activate chloride channels in rat cultured spinal cord neurones.

1. Caesium ions (Cs+), applied extracellularly, caused a decrease in the input resistance of cultured spinal cord (s.c.) neurones and depolarized the neurones when they contained 140 mM-CsCl. 2. The reversal potential for Cs+-activated currents shifted 56 mV on average for a 10-fold reduction in the intracellular chloride ion (Cl-) activity, indicating that the Cs+-activated currents were specific to Cl-. 3. The activation of Cl- currents by Cs+ was not due to the depolarization-evoked release of neurotransmitter from presynaptic terminals. We therefore suggest that Cs+ were acting directly on the extracellular surface of the s.c. neurones to activate Cl- currents. 4. Cs+-activated currents showed desensitization in the presence of 140 mM-Cs+. 5. The log-log plot of the dose-response data could be fitted with a straight line with a slope of 1.7 +/- 0.4 (n = 6), indicating that at least 2 Cs+ were needed to activate a single Cl- channel. The KD of the Cs+-induced response was greater than 69 mM. 6. In outside-out patches Cs+ activated single Cl- channels. These channels were not activated by sodium or potassium ions. 7. The Cs+-activated channels displayed a total of five distinct conductance states which had mean conductances of 20, 30, 43, 66 and 92 pS. The 30 and 43 pS states were the most frequently occurring states. 8. The conductance states of the Cs+-activated channel have the same conductances as those reported for gamma-aminobutyric acid (GABA)- and glycine-activated channels in rat s.c. neurones. We therefore conclude that Cs+ activate the same type of Cl- channel as GABA and glycine through an unidentified receptor.

Action Potentials↗
PubMed1987

Evidence for destruction of lung tissues during Pneumocystis carinii infection.

Five cases of Pneumocystis carinii infection with evidence of lung tissue destruction that occurred in patients with the acquired immunodeficiency syndrome were reviewed. None of the patients had a history of cigarette smoking, but all five had either cavitarylike lesions in the lungs or had pneumothorax at the time of presentation to the hospital. All patients had P carinii identified in specimens obtained either from bronchial washings or from open-lung biopsy. In four of the five patients, no other pathogens were involved in the lungs, while the fifth patient had concomitant cytomegalovirus infection. Findings on chest roentgenograms included large thin-walled cavitarylike lesions, multiple cavitary lesions, or pneumothorax. These presentations of the infection have not been previously described, and the mechanisms for lung tissue damage are as yet unknown. Cavitary lung disease found on chest roentgenograms in patients should not exclude the diagnosis of P carinii pneumonia, and patients with the acquired immunodeficiency syndrome presenting with pneumothorax should have the possibility of P carinii infection included in the differential diagnosis.

Adult↗
PubMed1987

Unusual features of arthritis caused by Candida parapsilosis.

A case of arthritis caused by Candida parapsilosis was observed, in which the only manifestation was intermittent knee effusion. The synovial fluid had a normal cell count with a mononuclear cell predominance. A review of such infections substantiates the relative paucity of symptoms seen in septic arthritis caused by this species of Candida, as opposed to other species of Candida that generally cause an acute course with more symptoms.

Adult↗