An externally powered, multichannel, implantable stimulator for versatile control of paralyzed muscle.
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Biomedical subjects
Publications and source records attributed to B Smith.
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We have evaluated the use of an intravascular ion-selective electrode for continuous plasma potassium monitoring in patients during and after cardiac surgery. Potassium estimations from the indwelling electrode provided a rapid and sensitive, but only moderately reliable, indicator of potassium as confirmed by blood samples. Several significant changes in the plasma potassium were found to occur in the period studied and using this continuous monitor, the precise time course of these changes was recorded.
Autoimmune hemolytic anemia (AIHA) caused by warm-reacting IgM autoantibodies is rare. We report a fatal case of primary AIHA with a warm-reacting IgM autoantibody. Recurrent episodes of intravascular hemolysis, unresponsive to all therapy and progressive hepatic dysfunction characterized the patient's clinical course. Despite corticosteroid therapy, splenectomy and multiple blood transfusions, the patient died from liver failure. The IgM autoantibody caused autoagglutination of the patient's red cells at 37 degrees C. Eluates prepared from the patient's red cells agglutinated saline-suspended test cells without the addition of antiglobulin reagent. We propose that warm-reacting IgM antibodies may lead to in vivo autoagglutination and may be associated with hepatic failure.
To evaluate the relationship between ELC density and pulmonary malignancies, as reported in previous investigations, we examined the nonsun-exposed epidermis of 18 patients with pulmonary cancer (CA) not receiving immunosuppressive therapy, 20 patients with chronic obstructive pulmonary disease (COPD-S), and 10 patients with COPD receiving glucocorticosteroid (GCS) therapy (COPD + S). The ELC density was not significantly different between lung tumor patients (1024 +/- 167) and COPD-S (1072 +/- 200, p less than 0.4) control patients, and we found no significant correlation between ELC density and tumor cell type, presence or absence of metastases, tumor stage, or present smoking status. Although we did detect that systemic GCS therapy significantly reduced the ELC density in COPD + S patients (910 +/- 211, p less than 0.05); use of inhaled or chronic low dose (less than or equal to 20 mg daily) GCS did not appear to significantly alter ELC density. In addition, anergy to epicutaneous dinitrochlorobenzene in CA and COPD + S patients positively correlated with a reduction in ELC density, suggesting a possible functional deficit arising from the numerical change. Further investigation is needed to elucidate whether factor(s) other than a reduction in ELC density are involved in the anergic state.
To determine the effect on new connective tissue attachment of citric acid conditioning and fibronectin-laminin application in treating naturally occurring periodontitis, all 4 quadrants in each of 2 Beagle dogs were used. Each quadrant included: P2, P3, P4, and M1 teeth. 2 treatment modalities were employed and comparatively analyzed for differences in histological healing respponses at 120 days after surgery. The treatments were: (1) surgery (mucoperiosteal flaps) plus citric acid; (2) surgery plus citric acid followed by fibronectin-laminin application. After scaling and root planing, coronal and root surface reference notches were placed for histometric measurements. Following each of the randomly assigned treatments, flaps were sutured. After sacrifice, tissue blocks of treated areas were decalcified and serially cut, obtaining bucco-lingual and mesiodistal sections. Using a Filar micrometer, 5 distances were masured on the buccal aspect: (1) from root surface notch to alveolar bone crest; (2) from root surface notch to coronal extent of the cementum; (3) from root surface notch to apical extent of the junctional epithelium; 84) from free gingival margin to apical extent of junctional epithelium; (5) from the coronal notch to the alveolar bone crest. Results showed no differences among the 5 measurements between the 2 treatments tested. On mesio-distal sections, surface area determinations were made in the furcations, evaluating the space occupied by new connective tissue, with or without bone, or by epithelium. For this, images were digitized using a Zeiss IBAS Image analysis system with a 4mB of array processor memory coupled to a Newvicon TV camera and a microcomputer.(ABSTRACT TRUNCATED AT 250 WORDS)
The anterior pituitary (AP) grafted, adrenalectomized, steroid hormone-replaced male rat is characterized by hyperprolactinemia and hypercalciuria. To determine the origin of the hypercalciuria, clearance experiments were performed under Inactin anesthesia in adrenalectomized Fischer rats 8-10 wk after implantation of extra AP glands under the kidney capsule. Glomerular filtration rate, ultrafilterable calcium, and fractional sodium excretion were comparable in the AP and control groups. However, fractional calcium excretion was significantly higher in the AP-implanted rats, P less than 0.05, resulting in a marked dissociation of the calcium/sodium clearance ratio. Because filtered calcium load did not change, these results clearly demonstrate that AP-implanted animals have a defect in tubular calcium reabsorption. The dissociation of calcium transport from sodium transport suggests the distal tubule as a likely site of action. Parathyroidectomy did not alter the calciuric response to AP implantation. To test whether hyperprolactinemia was responsible for decreased calcium reabsorption in AP-implanted rats, purified rat prolactin was infused into normal rats to achieve high blood prolactin levels, or was injected into normal rats daily for 8 days. Changes in fractional calcium excretion and the ratio of calcium to sodium clearance were identical in animals receiving prolactin or control infusions. Thus, hypercalciuria in the AP-implanted rat may be attributed to an unidentified factor, perhaps secreted from the implanted anterior pituitaries, rather than to prolactin excess.
To explain the transient anemia and poikilocytosis seen during infancy in hereditary elliptocytosis (HE), we resealed erythrocyte (RBC) ghosts from affected children or their elliptocytic parents with 2,3-diphosphoglycerate (DPG) (0-8 mM), a compound that dissociates membrane skeletons, then measured ghost mechanical stability in the ektacytometer. Without added 2,3-DPG, ghost mechanical stability was subnormal in infantile poikilocytosis (IP) and HE but was even more abnormal in hereditary pyropoikilocytosis (HPP). Addition of 2,3-DPG (2.55 mM) to IP or HE ghosts, decreased their stability to that of HPP ghosts (without 2,3-DPG). Nonphysiological 2,3-DPG levels (6-8 mM) were required to elicit a similar effect in normal ghosts. The data suggest that free 2,3-DPG, present in neonatal RBC as a consequence of diminished binding to HbF, may render HE susceptible to in vivo fragmentation. The developmental switch from fetal to adult hemoglobin, by diminishing available free 2,3-DPG, may explain the abatement of poikilocytosis and hemolytic anemia that accompanies maturation.
Since 1980, many data have been published concerning the pathophysiology of acute myocardial infarction and its effect on mortality. Research has been directed at developing a means of interrupting the evolution of transmural infarction and normalizing blood flow through the infarct-related vessel. Intracoronary delivery of thrombolytic agents has proved to be an effective, albeit logistically limited, means of reperfusion. The use of intravenous agents has broadened the applicability of thrombolytic therapy without severely compromising its efficacy. The recent availability of clot-selective agents has produced the potential of safely interrupting the infarction process at the earliest possible moment. This article reviews the research that has led to our use of thrombolytic agents and proposes a reasonable program of patient management in acute myocardial infarction.
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Hospitalized and domiciliary patients were studied to determine the incidence of the endemic nematode Strongyloides stercoralls in stool samples. Strongyloides was found in 14 (6.1%) of 229 hospitalized patients and in nine (2.6%) of 346 domiciliary patients. Clinical symptoms, laboratory data, and underlying diseases were compared for stool-positive and stool-negative patients. Infected patients were more likely to complain of abdominal bloating. They had a higher incidence of eosinophilia and guaiac-positive stools. They were more likely to have been treated with corticosteroids, cimetidine, and antacids. Efficacy of treatment with thiabendazole was studied in all stool-positive patients; a relapse rate of 15% was noted with standard thiabendazole therapy.
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Five patients with traumatic colobomas of the eyelid secondary to human bites were surgically repaired with retrieved autogenous tissue. All patients were treated with prophylactic intravenous antibiotics. Surgical repair consisted of debridement of the autograft, meticulous layered closure of the autograft to the wound, and placement of a lid margin suture. In two of the patients, mild upper eyelid retraction was noted, and two patients had loss of cilia.
We report two patients with systemic lupus erythematosus who subsequently developed thrombotic thrombocytopenic purpura. In each case the coexistence of these two conditions was confirmed by pathological findings. Both patients responded to treatment, but one eventually died. A review of the literature suggests a possible relationship between the two disorders.
Chronic renal failure is a common complication of spinal cord injury. When end-stage renal disease supervenes in the spinal cord injured patient, hemodialysis has almost exclusively been selected for its long-term management. Though a number of theoretical concerns exist which might dissuade one from the active use of peritoneal dialysis, in practice, this dialytic modality can be safely and effectively employed in this patient population. Herein we discuss the successful long-term use of peritoneal dialysis in two spinal cord injured patients.
Although thromboxane A2 is a potent platelet agonist and vasoconstrictor in vitro, our knowledge of its pathophysiologic importance in human disease is limited. To facilitate the elucidation of its role in vivo, we sought to define a human syndrome in which pharmacologic interventions designed to inhibit the biosynthesis or biologic actions of thromboxane A2 might be appropriately assessed. Patients with severe peripheral vascular disease were selected on the basis of elevated plasma beta-thromboglobulin and circulating platelet aggregates and compared with healthy, age-matched control subjects. In addition to the platelet indexes, their bleeding time was shorter and excretion of 2,3-dinor-thromboxane B2, a noninvasive index of thromboxane formation in vivo, and 2,3-dinor-6-keto-prostaglandin F 1 alpha, the major urinary metabolite of prostacyclin, was markedly increased. A selective inhibitor of thromboxane synthase, imidazo (1,5-2) pyridine-5-hexanoic acid, was administered to these patients under randomized, double-blind, controlled conditions. Platelet aggregation ex vivo, the circulating platelet aggregate ratio, and the bleeding time were all unaltered, despite almost maximal inhibition of platelet thromboxane formation 1 hr after dosing. By contrast, pronounced inhibition of aggregation was observed when platelet cyclooxygenase was inhibited by aspirin. During long-term dosing with the synthetic inhibitor, inhibition of thromboxane biosynthesis was incomplete, which would permit continued thromboxane-dependent platelet aggregation to occur. However, the failure of enzyme blockade to influence platelet function at the time of maximal drug action, despite efficient inhibition of serum thromboxane B2, suggests that accumulation of proaggregatory endoperoxides is also likely to have contributed to the persistence of platelet activation. We have characterized a human preparation in which platelet activation coexists with increased thromboxane biosynthesis. In this setting, platelet activation persists despite long-term administration of a thromboxane synthase inhibitor in a dosing regimen representative of that employed in clinical trials. Prolongation of drug action and combination with antagonists of the shared endoperoxide/thromboxane A2 receptor may be necessary to assess the potential of selective inhibition of thromboxane synthase as a therapeutic strategy in man.
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