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Biomedical subjects

L D Recht

Publications and source records attributed to L D Recht.

At least 37 records · Page 2Linked to original sources
PubMed1992

The preponderance of posterior circulatory events is independent of the route of cardiac catheterization.

BACKGROUND AND PURPOSE: Central nervous system complications of cardiac catheterization are most often attributed to embolic events that occur at the time of catheter manipulation. Nevertheless, the reason that over 50% of these events are localized to the posterior circulation remains unexplained. One potential explanation offered for this preponderance is the use of the brachial artery approach. In this report, we examined the relation between the route of catheterization and central nervous system complications. SUMMARY OF REPORT: We retrospectively analyzed all central nervous system complications that occurred after cardiac catheterization through a femoral route at our institution over a 3 1/2-year period. Thirteen patients were identified as having central nervous system complications. Using defined criteria, posterior circulatory events still accounted for at least 54% of central nervous system complications. CONCLUSIONS: The preponderance of posterior circulatory events is apparently independent of the route of catheterization. Furthermore, given the array of neurological symptoms and their often complete resolution, we feel it is unlikely that embolism is the sole pathophysiological mechanism involved in these events.

Aged↗
PubMed1991

Coexistence of Lambert-Eaton myasthenic syndrome and subacute cerebellar degeneration: differential effects of treatment.

A 61-year-old woman presented with two paraneoplastic neurologic disorders--Lambert-Eaton myasthenic syndrome (LEMS) and subacute cerebellar degeneration (SCD)--that antedated the diagnosis of small-cell carcinoma of the lung by 15 months. Plasmapheresis initiated before the identification of the tumor had a beneficial effect on LEMS but did not affect the SCD. Chemotherapy administered for treatment of the primary tumor was also associated with improvement of LEMS but, like plasmapheresis, had no effect on SCD. While the pathogenesis of both LEMS and SCD is thought to be mediated predominantly by humoral immune factors, a differential therapeutic response indicates that mechanisms of tissue damage or susceptibility to tissue injury, or both, differ in these two disorders.

Female↗
PubMed1991

Neurologic complications of systemic lymphoma.

Lymphoma denotes a heterogeneous group of neoplasms derived from lymphoreticular tissues. It can cause neurologic symptoms by infiltrating into the meninges or brain parenchyma. Alternatively, lymphomas may metastasize to bone or infiltrate into the epidural space via intervertebral foramina to cause neurologic dysfunction by compressing adjacent CNS structures. These direct effects can occur at any time during the disease process; most distressingly, meningeal infiltration may be the initial site of relapse after a complete remission. Diffuse and more undifferentiated lymphomas are much more likely to be responsible for producing either meningeal infiltration or intraparenchymal lesions. Direct CNS invasion by lymphoma is associated with significant patient morbidity and short survival despite intensive therapy; whether this manifestation of lymphoma can be prevented by prophylactic CNS treatment remains uncertain. CNS complications may also occur as a result of indirect effects of lymphoma. Therefore, CNS dysfunction may develop as a result of infections that occur secondary to immunosuppression, as a result of antineoplastic therapies, or as a result of true paraneoplastic syndromes. It is important to distinguish between these indirect effects and tumor progression because their recognition permits frequently available appropriate treatment modalities to be administered.

Brain Neoplasms↗
PubMed1991

Neuromuscular complications of systemic cancer.

In patients with cancer, neuromuscular dysfunction often develops as a result of some combination of direct effects of the cancer, from complications of therapy, or from paraneoplastic syndromes. Direct effects include leptomeningeal involvement by tumors (most frequently of the breast and lung) causing polyradiculopathy and compressive brachial and lumbar plexopathies that produce distinctive and typically painful syndromes. The differentiation between radiation and tumor-associated brachial plexopathies may be difficult, however. Peripheral neuropathy is an important dose-limiting toxic side effect of two commonly utilized agents, vincristine and cisplatin. Recent studies have suggested that this complication may be ameliorated or even prevented by prophylactic administration of protective agents. Finally, cancer can cause neuromuscular dysfunction through more remote effects and can produce a variety of paraneoplastic syndromes that include subacute sensory neuropathy. Lambert-Eaton myasthenic syndrome, and the neuropathy associated with paraproteinemia. In some syndromes, the presence of specific antibodies that cross-react with both neuromuscular tissues and primary tumors strongly suggests an immune-mediated pathogenesis. In some patients, immunosuppressive therapies and plasmapheresis may relieve symptoms.

Humans↗
PubMed1990

Potent cytotoxicity of an antihuman transferrin receptor-ricin A-chain immunotoxin on human glioma cells in vitro.

The cytotoxic effects of an antihuman transferrin receptor monoclonal antibody-ricin A-chain conjugate (anti-TfR-A) immunotoxin on glioma cells were assessed in vitro. Five human glioma cell lines were studied; three were derived from surgical explants (MG-1, MG-2, MG-3) and two were well characterized established glioma cells (U-87 MG, U-373 MG). The C6 rat glioma line served as a nonhuman control. One of six lines (U-373) expressed glial fibrillary acidic protein, as assessed by immunohistochemistry. All five human lines expressed human transferrin receptor, as assessed by flow cytometry; no human transferrin receptor was demonstrable on rat C6 cells. Potent inhibition of protein synthesis was found after an 18-h incubation with anti-TfR-A. Fifty % inhibitory concentration (IC50) values for human glioma cells ranged from 1.9 X 10(-9) to 1.8 X 10(-8) M. In contrast, no significant inhibition of leucine incorporation was observed when anti-TfR-A was tested on rat cells (IC50 greater than 10(-7) M) or when a control immunotoxin directed against carcinoembryonic antigen was substituted for anti-TfR-A on human glioma cells (IC50 greater than 10(-7) M). Coincubation with the carboxylic ionophore monensin (10(-7) M) decreased the IC50 of anti-TfR-A against human glioma lines from 16- to 842-fold (range, 7.0 X 10(-12) to 1.5 X 10(-10) M). In contrast, an IC50 of greater than 10(-7) M was obtained when C6 cells were incubated with anti-TfR-A and monensin. Anti-TfR-A immunotoxins potentiated by monensin are extremely potent in vitro cytotoxins for human glioma cells.

Antibodies, Monoclonal↗
PubMed1989

Brain tumor presenting as an acute pure motor hemiparesis.

Acute pure motor hemiparesis is a clinical syndrome of isolated hemiparesis usually related to lacunar infarction, although other etiologies have been described. We recently encountered three patients with the abrupt onset of pure motor hemiparesis as the initial manifestation of primary or metastatic brain tumor. In each patient, early computed tomography demonstrated a nonhemorrhagic, right frontal, enhancing mass lesion. While the mechanism whereby brain tumor may present abruptly and simulate a stroke remains uncertain, these cases illustrate that pure motor hemiparesis can be the initial symptom of intracranial tumor. Early computed tomography or magnetic resonance imaging is suggested for all patients who present acutely with pure motor hemiparesis.

Acute Disease↗
PubMed1989

Tumor-associated aphasia in left hemisphere primary brain tumors: the importance of age and tumor grade.

Although one-quarter of patients with primary brain tumors have language disturbances at the time of initial presentation, the factors contributing to their aphasia are not clear. A group of 32 patients with primary tumors of the left hemisphere was collected retrospectively and the relationship between clinical, radiographic, and pathologic factors and tumor-associated aphasia was examined. We assessed language function before beginning any treatment including steroids. The factor that best predicted language disturbance was greater patient age; the only other significant factor was tumor grade. Tumor size made a nearly significant impact, but tumor location within the left hemisphere did not correlate with aphasia.

Adult↗
PubMed1987

Effects of beta-funaltrexamine on radiolabeled opioid binding.

beta-Funaltrexamine (beta-FNA) potently competed with the binding of a series of radiolabeled opiates and opioid peptides in standard binding assays with IC50 values under 10 nM. In addition, higher concentrations of beta-FNA produced an irreversible inhibition of binding which was relatively selective for mu receptors; delta binding was not affected much. The production of irreversible inhibition of [3H]dihydromorphine binding required concentrations of beta-FNA over 10-fold higher than beta-FNA concentrations needed in standard competition studies. Both mu 1 and mu 2 sites were irreversibly inhibited by beta-FNA, but mu 1 sites were more sensitive. The reversible and irreversible inhibition in these in vitro binding assays by beta-FNA were quite similar to naloxonazine. However, the activity of beta-FNA in the guinea-pig ileum suggests that it may not distinguish between mu 1 and mu 2 receptors as effectively as naloxonazine in bioassays and in vivo.

Animals↗
PubMed1986

Synchronous occurrence of glioblastoma multiforme in a husband and wife.

Glioblastomas developed within two years of each other in an otherwise unrelated married couple in their fifties. There was a daughter who died of Hodgkin's disease but no other unusual incidence of cancer in either siblings, parents or other children. No clear etiology of risk factors for brain tumor were identified. The development of such conjugal tumors, although apparently rare, raises important etiologic questions.

Brain Neoplasms↗
PubMed1986

Neuropeptides and their role in nociception and analgesia.

The authors highlight the potential importance of neuropeptides as clinical tools in the study and treatment of pain. Although many questions remain unanswered, it is encouraging that several clinical and experimental advances have shed new light on the neuropharmacology of nociception and have prompted new hope for more effective treatments of such diverse problems as chronic intractable pain, migraine, and drug dependency. Within the next few years, it is anticipated that further work in this area will lead to better basic and clinical understanding of these important clinical problems.

Animals↗
PubMed1985

Quantitative autoradiography of the development of mu opiate binding sites in rat brain.

The regional developmental appearance of mu binding sites in rat brain was examined by quantitative autoradiography of 3H-dihydromorphine binding in rats 2, 14, 21, and 28 days old. Labeling with 3H-dihydromorphine was heterogeneous in adult rat brains, as previously reported by other laboratories. Levels of 3H-dihydromorphine binding ranged from approximately 250 nCi/g tissue in the interpeduncular nucleus and 100 nCi/g tissue in the habenula to 40 nCi/g tissue in the hypothalamus and periaqueductal gray. Some areas, particularly white matter regions, had no detectable specific binding. The density of 3H-dihydromorphine binding increased in all regions between 2 and 28 days of age. The increases in 3H-dihydromorphine binding in various regions of rat brain developed at different rates. Maximal densities were seen by 14 days of age in most regions examined, including the caudate, hippocampus, amygdala, and hypothalamus. Binding in the medial thalamus and quadrigeminal plate, however, did not reach maximal levels until 21 days. Although quantitative autoradiography offers major advantages in the examination of the regional distribution of opiate binding sites, variability both between sections from the same brain and between sections from different brains demonstrate some of the difficulties associated with this type of experimental approach.

Aging↗
PubMed1984

Biochemical characterization of high-affinity 3H-opioid binding. Further evidence for Mu1 sites.

In saturation studies with [3H]dihydromorphine, unlabeled D-Ala2-D-Leu5-enkephalin (1 nM) inhibited the high-affinity binding component far more potently than the lower-affinity one. Similarly, morphine (1 nM) inhibited the higher-affinity binding of 3H-D-Ala2-D-Leu5-enkephalin to a greater extent than its lower-affinity binding component, consistent with a common high-affinity binding site for opiates and enkephalins. Treatment of tissue with either trypsin (1 microgram/ml) or N-ethylmaleimide (25 microM) effectively eliminated the high-affinity binding component of a series of 3H-opiates and opioid peptides. Competition studies following both treatments were consistent with a common high-affinity binding site. Both treatments also eliminated the ability of low morphine concentrations (less than 1 nM) to inhibit 3H-D-Ala2-D-Leu5-enkephalin binding and of low D-Ala2-D-Leu5-enkephalin concentrations (less than 1 nM) to inhibit [3H]dihydromorphine binding. Protection experiments examining N-ethylmaleimide (25 microM) inhibition of [3H]dihydromorphine binding showed significant protection (p less than 0.002) by both unlabeled D-Ala2-D-Leu5-enkephalin and morphine (both at 1 nM). When studied together, both naloxonazine and N-ethylmaleimide inhibited [3H]dihydromorphine binding to a similar extent. Equally important, tissue previously treated with naloxonazine was far less sensitive to N-ethylmaleimide than was untreated control tissue, consistent with the possibility that both treatments affected the same site. Together, these results support the concept of a common high-affinity binding site for opiates and opioid peptides.

Animals↗
PubMed1983

Biochemical and pharmacological evidence for opioid receptor multiplicity in the central nervous system.

Evidence from a variety of experimental models has suggested the existence of mu 1, mu 2 and delta binding sites for morphine and the enkephalins in the central nervous system. Additional biochemical experiments now support this concept of a common high affinity site for opiates and opioid peptides. Mu sites have now been implicated in a number of pharmacological actions, including supraspinal analgesia, prolactin release, and catalepsy, but not in others (spinal analgesia, respiratory depression, and the guinea pig ileum). The hypothesis of mu 1 sites was supported by the unique opioid meptazinol, which selectively bound to mu 1 sites. As expected from its mu 1 binding selectivity, its analgesic actions in the mouse, localized supraspinally, were antagonized by the selective mu 1 antagonist naloxonazine and it had no respiratory depressant actions. Other binding studies suggested the presence of discrete SKF10,047-selective (KD approximately 5 nM) binding sites in rat brain which differed from both kappa sites and the previously reported PCP-binding sigma sites. Additional binding and autoradiographical studies have also implied the presence of beta-endorphin, or epsilon, sites in the CNS.

Analgesia↗
PubMed1982

Blastomycosis in immunosuppressed patients.

Of 78 patients with blastomycosis, 3 patients had received glucocorticoid therapy prior to diagnosis and 3 others had an underlying hematologic malignancy (chronic lymphocytic leukemia, chronic myelogenous leukemia, multiple myeloma). The clinical picture in these 6 patients was similar to blastomycosis in nonimmunosuppressed patients (in contrast to histoplasmosis or coccidioidomycosis in immunosuppressed patients in whom a distinct clinical syndrome is often seen). The patients presented with chronic pulmonary infiltrates or with isolated skin ulcers. The response to therapy was good if the diagnosis was made early. Blastomycosis can occur in immunosuppressed patients. However, the spectrum of underlying illness is not that seen in opportunistic histoplasmosis or coccidioidomycosis, where patients with T-cell defects predominate. Possible explanations for the rarity of blastomycosis in more classically T-cell-immunosuppressed patients are discussed.

Adult↗
PubMed1981

Vasopressin concentrations in hypophysial portal plasma: insignificant reduction following removal of the posterior pituitary gland.

This study was designed to determine the relative contribution of vasopressin-secreting nerve terminals in the median eminence compared to those in posterior pituitary to the high concentrations of the hormone in hypophysial portal blood. Vasopressin was measured by radioimmunoassay in plasma obtained by microcannulation of individual long portal veins of 8 intact male Long-Evans rats (2.0 +/- 0.44 ng/ml SEM), and in 8 in which the posterior pituitary was removed just prior to collection (1.5 +/- 0.3 ng/ml SEM). Since there was no significant difference /p = 0.23, NS) in the concentration of vasopressin in portal plasma after removal of the posterior pituitary gland, these results suggest that the direct vasopressin pathway to the median eminence is the major source of vasopressin in portal blood of the rat.

Animals↗
PubMed1979

Self-limited blastomycosis: a report of thirteen cases.

Blastomycosis is not generally recognized to be a self-limited pulmonary infection. We report 13 patients with blastomycosis who followed a self-limited course. Presenting complaints were usually those of an acute pulmonary infection with fever, productive cough, and pleurtiic chest pain. The duration of symtpoms before diagnosis was usuallms were variable and not diagnostic. The blastomycin skin test and complement-fixing serologies to blastomycin were generally not helpful. In all patients the diagnosis was made by either cultural or visual identification of the organism from sputum, bronchial washings, or pleural fluid. All patients were improving both clinically and by chest roentgenograms by the time the diagnosis was reached, and thus therapy was withheld. Follow-up of these 13 patients ranged from 5 months to 8 yr (mean, 43 months), and in no instance has there been any evidence of reactivation of the illness.

Adolescent↗