Laparoscopic cholangiography: a new technique for difficult cannulation.

Laparoscopic surgery has become accepted in the United States as the surgical procedure of choice for treatment of symptomatic cholelithiasis. The general surgeon is now presented with a vast array of instrumentation and new techniques that have rapidly developed since the introduction of laparoendoscopic surgery. Much of this new technology is designed for easier and less expensive laparoscopic cholangiography.

Assessment and rehabilitation of children with special needs.

Evaluating the visual functioning of children with multiple impairments has long been a source of frustration for many eye care practitioners. A reflection of this difficulty is seen in the number of persons with multiple handicaps, especially children who are labeled "untestable" or "blind" by eye care specialists, but whose parents, teachers, and other caregivers know have some residual vision. These children with special needs may not be responsive to standard testing procedures for a variety of reasons.

beta-Amyloid1-40 increases expression of beta-amyloid precursor protein in neuronal hybrid cells.

Studies of cell injury and death in Alzheimer's disease have suggested a prominent role for beta-amyloid peptide (beta-AP), a 40-43-amino-acid peptide derived from a larger membrane glycoprotein, beta-amyloid precursor protein (beta-APP). Previous experiments have demonstrated that beta-AP induces cytotoxicity in a neuronal hybrid cell line (MES 23.5) in vitro.

Prognosis of amyotrophic lateral sclerosis and the effect of referral selection.

We followed two cohorts of Amyotrophic Lateral Sclerosis (ALS) patients to examine the survival and prognostic factors of ALS and the impact of selective referral on prognosis of ALS. The first cohort consisted of population-based incident ALS cases from Harris County, Texas, first diagnosed between 1985 and 1988. The second was a clinical series from a tertiary care center in Houston, Texas, diagnosed between 1977 and 1989.

Alpha-1 subunits of voltage gated Ca2+ channels in the mesencephalon x neuroblastoma hybrid cell line MES23.5.

The identity of alpha 1 subunits from voltage operated Ca2+ channels was determined in the rat/mouse mesencephalon x N18TG2 hybridoma cell line MES23.5, by sequence analysis of reverse transcription-polymerase chain reaction products and antagonist binding. Sequences were derived from the L-(alpha 1D), Q-(alpha 1A) and omega-conotoxin GVIA sensitive N-type (alpha 1B) Ca2+ channel alpha 1 subunits.

Modelling of the pharmacodynamic interaction of an A1 adenosine receptor agonist and antagonist in vivo: N6-cyclopentyladenosine and 8-cyclopentyltheophylline.

1. The purpose of this investigation was to develop a pharmacokinetic-pharmacodynamic model for the interaction between an adenosine A1 receptor agonist and antagonist in vivo. The adenosine A1 receptor agonist, N6-cyclopentyladenosine (CPA) and the antagonist, 8-cyclopentyltheophylline (CPT) were used as model drugs.

Cell death induced by beta-amyloid 1-40 in MES 23.5 hybrid clone: the role of nitric oxide and NMDA-gated channel activation leading to apoptosis.

The molecular events associated with beta-amyloid-induced neuronal injury remain incompletely characterized. Using a substantia nigra/neuroblastoma hybrid cell line (MES 23.5) synthetic beta-amyloid 1-40 induced a time and dose-dependent apoptotic cell death which was characterized by cell shrinkage and fragmentation of DNA, and was inhibited by aurintricarboxylic acid (ATA), and cycloheximide (CHX).

Lack of interaction between fluvastatin and oral hypoglycemic agents in healthy subjects and in patients with non-insulin-dependent diabetes mellitus.

Human drug interaction studies in vivo are conducted when in vitro and/or animal interactions suggest clinical relevance. Studies in vitro have indicated that the new, entirely synthetic 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor fluvastatin affects the metabolism of the nonsteroidal anti-inflammatory drug diclofenac and the oral hypoglycemic tolbutamide. Diclofenac and tolbutamide are both model substrates of the CYP2C isozymes, suggesting that this enzyme could be involved in the underlying mechanism of interaction.

Hemorrhagic shock-induced alterations in circulating and bronchoalveolar macrophage nitric oxide production.

Local and systemic host immune functions are markedly altered after trauma. Activated macrophages (M phi) are the major effector cells of protective immunity, mediated in part by nitric oxide (NO). This study was undertaken to determine the effects of hemorrhage (HEM) on M phi cytotoxic function as measured by NO production.

Antibodies to calcium channels from ALS patients passively transferred to mice selectively increase intracellular calcium and induce ultrastructural changes in motoneurons.

Antibodies to Ca channels in ALS patients IgG can be demonstrated to enhance Ca current and cause cell injury and death in a motoneuron cell line in vitro. To determine whether these antibodies can alter neuronal calcium homeostasis in vivo IgG fractions from six ALS patients were injected intraperitoneally into mice, and neurons assayed by ultrastructural techniques for calcium content. After 24 h, all six ALS IgG by (40 mg/animal) increased vesicle number in spinal motoneuron axon terminals, and in boutons synapsing on spinal motoneurons.

Altered muscle calcium channel binding kinetics in autoimmune motoneuron disease.

While skeletal muscle is not apparently affected directly in amyotrophic lateral sclerosis (ALS), immunoglobulin G fractions purified from patients with ALS (ALS IgG) bind dihydropyridine (DHP)-sensitive L-type voltage-gated calcium channel (VGCC) antigen isolated from skeletal muscle in ELISA and Western immunoblot, and alter VGCC function in vitro. To determine whether muscle VGCC properties are altered in ALS, VGCC-enriched subsarcolemmal membrane fractions were prepared from biopsied quadriceps muscle of patients with ALS, with other neurologic diseases, or without apparent muscle disease, and tested for DHP binding with [3H]PN200-110. ALS muscle VGCCs possessed eightfold higher binding affinities for [3H]PN200-110 than did VGCCs from muscle fractions of most other patients, independent of denervation-induced increases in DHP binding site number.

Natural history of amyotrophic lateral sclerosis in a database population. Validation of a scoring system and a model for survival prediction.

Over 1200 patients with motor neuron disease have been carefully diagnosed, followed, and included in a detailed database delineating characteristics of the disease. Of these patients, 831 were identified as exhibiting typical, sporadic amyotrophic lateral sclerosis (ALS). The progression of the disease in these patients has been followed with our scoring system, and the ALS score was verified as a significant covariate of survival.

Experimental autoimmune nigral damage in guinea pigs.

An animal model of experimental autoimmune nigral damage (EAND) has been developed in guinea pigs by immunization with hybrid dopaminergic cells (MES 23.5). In such animals, loss of 40% of the substantia nigra (SN) neurons and damage to an additional 10% of SN neurons was associated with a 37-43% decrease of tyrosine hydroxylase (TH) activity and a 36% decrease of dopamine (DA) content in the nigral-striatum.

Increased intracellular calcium triggered by immune mechanisms in amyotrophic lateral sclerosis.

Although the causes of motor neuron degeneration and death in amyotrophic lateral sclerosis (ALS) is unknown, recent evidence suggests a prominent role for increased intracellular calcium, possibly triggered by autoimmune mechanisms. The presence in ALS patients of paraproteinemias, lymphomas, lymphoid cells in the central nervous system (CNS) and the availability of animal models of immune-mediated motor neuron disease provide circumstantial evidence for autoimmunity. Direct evidence derives from the demonstration that ALS IgGs bind to voltage-gated calcium channels in 75% of sporadic cases, but not in familial ALS cases, and that ALS IgGs increase N-type and P-type calcium currents in neuronal cells and in lipid bilayers.

Amyotrophic lateral sclerosis immunoglobulins increase Ca2+ currents in a motoneuron cell line.

The sporadic form of amyotrophic lateral sclerosis (ALS) is an idiopathic and eventually lethal disorder causing progressive degeneration of cortical and spinal motoneurons. Recent studies have shown that the majority of patients with sporadic ALS have serum antibodies that bind to purified L-type voltage-gated calcium channels and that antibody titer correlates with the rate of disease progression. Furthermore, antibodies purified from ALS patient sera have been found to alter the physiologic function of voltage-gated calcium channels in nonmotoneuron cell types.

Neurotoxicity of A beta amyloid protein in vitro is not altered by calcium channel blockade.

In cortical cultures, A beta protein destabilizes calcium homeostasis, but direct neurotoxicity of A beta is not observed. In hippocampal cultures, we and others find treatment with A beta protein decreases neuronal survival, but the mechanism of neurotoxicity is unknown. We have used low-density, serum-free cultures of hippocampal neurons to determine whether the neurotoxicity of A beta protein in vitro can be altered by voltage- or ligand-gated calcium channel antagonists or cyclic nucleotides.

Molecular approaches to amyotrophic lateral sclerosis.

New discoveries are expanding our knowledge of mechanisms involved in amyotrophic lateral sclerosis (ALS) pathogenesis. Some recent advances in our understanding of motoneuron death in familial ALS (fALS) and sporadic ALS (sALS) are reviewed, with emphasis on molecular similarities that may further unite these phenotypically linked diseases.

The role of calcium-binding proteins in selective motoneuron vulnerability in amyotrophic lateral sclerosis.

The factors contributing to selective motoneuron loss in amyotrophic lateral sclerosis (ALS) remain undefined. To investigate whether calcium-binding proteins contribute to selective motoneuron vulnerability in ALS, we compared calbindin-D28K and parvalbumin immunoreactivity in motoneuron populations in human ALS, and in a ventral spinal cord hybrid cell line selectively vulnerable to the cytotoxic effects of ALS IgG. In human autopsy specimens, immunoreactive calbindin-D28k and parvalbumin were absent in motoneuron populations lost early in ALS (i.

Apoptotic cell death of a hybrid motoneuron cell line induced by immunoglobulins from patients with amyotrophic lateral sclerosis.

Apoptotic cell death has recently been implicated in diseases involving nonproliferating, terminally differentiated cells such as neurons. Previous experiments have documented that immunoglobulins from patients with amyotrophic lateral sclerosis (ALS) can kill motoneuron-neuroblastoma hybrid cells [ventral spinal cord 4.1 (VSC 4.

The effect of verapamil calcium antagonist on autonomic imbalance in migraine: evaluation by spectral analysis of beat-to-beat heart rate fluctuations.

Abnormalities in autonomic control have been documented in migraine even during the headache-free interval. It has long been recognized that spectral analysis of heart rate (HR) fluctuations can reflect the autonomic function, especially the sympathetic to parasympathetic balance. This technique is the basis for a quantitative approach to the investigation of migraine applied in the present study.

Decremental motor responses to repetitive nerve stimulation in ALS.

Repetitive nerve stimulation (RNS) of the trapezius muscle at slow rates was performed on 192 patients with amyotrophic lateral sclerosis (ALS). Fifty-six patients (29%) showed classical neuromuscular decrement of 10-43% (mean 16.8%) while 44 patients (23%) had a borderline decrement of 5-9%.