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Biomedical subjects

D Karcher

Publications and source records attributed to D Karcher.

At least 19 recordsLinked to original sources
PubMed1998

Site-selective inhibition of plastid RNA editing by heat shock and antibiotics: a role for plastid translation in RNA editing.

RNA editing in higher plant plastids changes single cytidine residues to uridine through an unknown mechanism. In order to investigate the relation of editing to physiological processes and to other steps in plastid gene expression, we have tested the sensitivity of chloroplast RNA editing to heat shock and antibiotics. We show that heat shock conditions as well as treatment of plants with prokaryotic translational inhibitors can inhibit plastid RNA editing. Surprisingly, this inhibitory effect is confined to a limited number of plastid editing sites suggesting that some site-specific factor(s) but none of the general components of the plastid RNA editing machinery are compromised. Contrary to previous expectations, our results provide evidence for a role of plastid translation in RNA editing.

Anti-Bacterial Agents↗
PubMed1994

Defective measles virus in human subacute sclerosing panencephalitis brain.

Evidence is presented showing that the brain cells of patients with subacute sclerosing panencephalitis (SSPE) contain mutant measles (MV) genomes having the characteristics of 5' copy-back defective interfering (DI) RNAs. Using a polymerase chain reaction-based amplification specific for copy-back DIs, abundant, discrete cDNAs representing different-sized MV defective RNA species were generated from each SSPE brain. The defective genomes were cloned in two portions. The most common of these defective species were sequenced, confirming their MV genome origin and 5' copy-back nature. We deduced that the minimum DI stem length of these species was 95 nucleotides, further delimiting the prerequisite 5' regulatory region sequences specifying MV genomic replication/encapsidation functions. This calculation assumes a precise copy-back mechanism and complete complementarity of the panhandle structure. Since the SSPE-derived viral genome encodes dysfunctional viral envelope proteins, we hypothesize that SSPE brains may lack the high degree of selective pressure encountered in tissue culture MV infections. This allows for the coexistence of numerous replication-competent defective particles in each SSPE brain. A role for viral defective particles as modulators of this persistent measles virus infection of humans is proposed.

Base Sequence↗
PubMed1994

Changing practice patterns in refractive surgery: results of a survey of the American Society of Cataract and Refractive Surgery.

A questionnaire on refractive surgical practice was sent to the entire membership of the American Society of Cataract and Refractive Surgery in 1992. One thousand eight hundred and forty-one (1,841) of the 4,950 members returned the survey for a response rate of 37.2%. The questionnaire was designed to be self-administered and elicited information on types of refractive procedures performed in the survey year and the preceding year, as well as the intent to perform refractive procedures in the future. Surgeons who perform radial keratotomy (RK) increased from 22% in 1991 to 30% in 1992; 45% expected to perform RK in 1993-1994. The following categories of information were requested: characteristics of RK patients, techniques used by the surgeon, characteristics of the surgeon's overall practice, type of RK training, surgical outcome, and prevalence of complications. The results of this survey indicate that the use of RK and astigmatic keratotomy (AK), as well as other refractive procedures, is steadily increasing. Radial keratotomy was mainly performed on patients 20 to 49 years of age who had low to moderate myopia. The majority of surgeons used four to eight radials, centrally directed incisions, and single depth settings. Three quarters of the surveyed RK surgeons used the Casebeer nomogram. The survey results indicated that 42% of surgeons performing photorefractive keratectomy (PRK) did not perform RK or other refractive procedures, suggesting that growth in the practice of PRK following FDA approval may come from both current RK surgeons and novice refractive surgeons.

Adult↗
PubMed1994

Cerebrospinal fluid in multiple sclerosis.

The diagnosis of multiple sclerosis (MS) is a clinical one which should be made by a neurologist. Examination of the cerebrospinal fluid (CSF) [Lowenthal (1991): Neurol Neurosurg 4:914-918], the results of evoked potential studies, and magnetic resonance imaging serve as confirmatory tests. CSF is a window which permits a glimpse into the metabolism of the nervous system. The detailed investigation of the CSF proteins has provided important clues about our understanding of the pathogenesis of MS.

Evoked Potentials↗
PubMed1990

Detection of neuron specific enolase concentrations in cerebrospinal fluid from patients with neurological disorders by means of a sensitive enzyme immunoassay.

An enzyme linked immunosorbent assay (ELISA) for the detection of neuron specific enolase (NSE) in cerebrospinal fluid (CSF) was developed. The sensitivity of the ELISA was less than 1 microgram/ml. This sensitivity is comparable with radioimmunoassays which have the disadvantage that radiolabelled products are used. The developed assay was used to measure cerebrospinal fluid neuron specific enolase (CSF-NSE) levels in 1178 patients with neurological disorders to establish its potential usefulness and clinical application. CSF-NSE levels in this group of patients were independent of sex and no correlation with age was found. CSF-NSE was significantly increased in Creutzfeldt-Jacob disease, meningeal hemorrhage, thrombosis, Guillain-Barré syndrome and in schizophrenia.

Animals↗
PubMed1990

Effects of reduced dietary magnesium on platelet production and function in hamsters.

The increased vulnerability of animals fed a magnesium (Mg)-deficient (MD) diet to ischemia-induced myocardial necrosis has been attributed to changes in myocardial electrolyte metabolism. However, a variety of hematologic changes have also been reported in MD and some of these, such as an increase in platelet aggregability, may contribute to the increased myocardial vulnerability. In the present study, we quantified the effect of MD on platelet and megakaryocyte abundance as well as on platelet aggregability with and without an administered calcium channel blocker (nifedipine). Hamsters were fed either a "minimal Mg" diet, in which the level of Mg was kept just high enough to prevent seizures, or a "preset Mg" diet containing precisely known amounts of Mg. Animals fed the minimum Mg diet showed an initial increase in the platelet count, which returned to control range when the dietary Mg was increased to 9 mmoles/kg. Animals on the preset Mg diet showed an increased platelet count if the Mg level was 10 mmoles/kg or less. In addition to the increase in number, platelets from MD animals were less responsive to the aggregation-inhibiting effect of nifedipine than were platelets from control animals, although MD itself did not result in an increased aggregability under the conditions used here. Animals with an increase in circulating platelets showed decreased megakaryocyte abundance in the femoral marrow, but megakaryocytes that were present were larger than those in control animals. These results indicate a profound effect of dietary Mg deficiency on platelet biology. The observed changes could contribute to the increase in myocardial vulnerability to injury found in MD animals.

Animals↗
PubMed1989

A serum protein involved in aging?

Aging of the brain is characterized, in part, by the appearance of protein anomalies. The proteins deposited within the nervous system structures are hardly soluble. This physiological phenomenon turns out to be pathological, quantitatively at least, and perhaps even qualitatively, in dementia of the Alzheimer's type (DAT). One might wonder whether the brain protein anomalies are related to a general process and, thus, could generate anomalies of the serum proteins. Therefore, we examined, with two-dimensional electrophoresis (2DE), 120 serum samples collected from different neurological patients and 24 serum samples from a control group, and we reached the following conclusion: a protein spot, normally not found and named 10M, corresponding to a molecular weight of 30 kDa with an isoelectric point of +/- 8, is seen in 31% of the patients affected with a neurological disease and in 90% of patients affected with DAT. The frequency of the appearance of this spot, seen after 2DE, increases with age. We wonder whether this protein is playing a role in the formation of the neuropathological lesions observed in DAT.

Adolescent↗
PubMed1989

Effects of WY 47987 (atrial natriuretic factor 102-126) in patients with renal insufficiency: a placebo-controlled, randomised study.

We studied renal, hormonal and cardiovascular effects of ANF 102-126 (WY 47987) in seven patients with chronic renal failure (serum creatinine 25-68 mg/l) and in four normal volunteers. ANF or placebo bolus injections were given at 1, 2, and 3 micrograms/kg i.v. (each dose on separate days). As compared to placebo, ANF did not induce changes of renal excretory parameters, of plasma renin and aldosterone or of blood pressure and heart rate in patients. In healthy volunteers, however, the same dose of ANF increased urinary excretion of sodium, potassium, calcium, chloride and phosphorus as well as water, and creatinine clearances, and decreased plasma aldosterone. The data suggest blunted effectiveness of ANF bolus injections in patients with renal insufficiency.

Aldosterone↗
PubMed1987

Blood and cerebrospinal fluid anomalies in brain ageing and Alzheimer's disease.

The glial fibrillary acidic protein (GFAP), myelin basic protein (MBP), S100 protein (S100), gamma gamma-enolase and neurofilament proteins were determined in the CSF of neurological patients. In Alzheimer's disease (AD), the GFAP values were very often increased but this was not specific to this disease. In 2 cases of familial AD, increases in neurofilament protein were detected. The determination of autoantibodies against neurofilament proteins in blood showed rather low values in AD, although they were higher than in subacute sclerosing panencephalitis (SSPE) and Chagas' disease. Increases were observed in diseases not related to AD such as vascular disorders and Parkinson's disease.

Aging↗
PubMed1986

Anti-neurofilament antibodies in blood of patients with neurological diseases.

A method has been developed to determine quantitatively the level of the anti-neurofilament antibodies in the blood of patients affected with different neurological diseases. In 7 out of the 52 patients, taken as controls and in 33 out of the 208 patients affected with neurological diseases, the antibody levels were increased. The increases were greater in 43 patients with Parkinson dementia and amyotrophic lateral sclerosis who originated from Guam. On the other hand, the levels were very low in 10 patients affected with subacute sclerosing panencephalitis and in 11 cases with Chagas' disease. In 24 cases with dementia of Alzheimer type, the levels were normal.

Alzheimer Disease↗
PubMed1984

Blood-brain barrier in chronic relapsing experimental allergic encephalomyelitis: a correlative study between cerebrospinal fluid protein concentrations and tracer leakage in the central nervous system.

Blood-brain barrier (BBB) permeability in chronic relapsing experimental allergic encephalomyelitis was studied morphologically in tracer studies with horseradish peroxidase (HRP) as well as by quantitative determination of HRP, albumin, and IgG in serum and cerebrospinal fluid (CSF). BBB damage was found to be localized in demyelinating plaques and in blood vessels with vasculitis. Actively demyelinating lesions showed massive increase in BBB permeability, whereas in inactive or remyelinated lesions BBB damage was either minimal or absent. Determination of serum proteins in the CSF of animals with severe disease and a high incidence of actively demyelinating lesions showed evidence of BBB damage (reduction of Q-albumin) and an IgG-index in the normal range. In animals with only inactive lesions the Q-albumin was normal, the IgG index, however, was elevated. This finding indicates intrathecal IgG synthesis. A correlation between morphologically visualized tracer leakage in the central nervous system (CNS) with serum protein concentrations in the CSF revealed that elevated CSF albumin is a reliable indicator for BBB damage in lesions, located near the inner or outer surface of the brain and spinal cord. However, singular focal lesions with BBB damage located in the depth of the CNS parenchyma may not be accompanied by CSF protein alterations. The invariable presence of BBB damage in active inflammatory demyelinating lesions and its absence in inactive plaques or in the unaffected nervous tissue may be important in therapy, not only in experimental allergic encephalomyelitis but also in multiple sclerosis (MS).

Animals↗
PubMed1984

A serum protein affecting the regulation of the immune system.

A thermostable alpha 2 globulin inhibiting the immunoglobulin/anti-immunoglobulin reaction was demonstrated working with subacute sclerosing panencephalitis (SSPE) and control serum IgG. This protein was isolated from SSPE and normal human blood, it inhibits the immunoglobulin/anti-immunoglobulin reaction but no other antigen/antibody reactions when applying different immunochemical methods such as nitrocellulose immunofixation, 2 site immunoradiometric assay, solid phase radioimmunoassay in coated cups. This was demonstrated, working on the one hand with measles virus strain Edmonston or SSPE virus strain D.R. and SSPE serum and on the other hand with IgG from SSPE and control serum. This alpha 2 globulin, an inhibiting protein, appears to be related to "normal immunosuppressive protein".

Alpha-Globulins↗
PubMed1984

Hyperargininemia: the rat as a model for the human disease and the comparative response to enzyme replacement therapy with free arginase and arginase-loaded erythrocytes in vivo.

Rat erythrocytes lack arginase as do the erythrocytes of human homozygote patients with hyperargininemia due to arginase deficiency. The rat has physiological liver arginase activity and plasma arginine and ornithine levels between the homozygotes and the heterozygotes with hyperargininemia. In rats, one injection of free arginase induces a transient exogenous arginase effect which is abolished after 24 hr. One injection of isoionic arginase-loaded erythrocytes provokes an exogenous arginase effect in physiological "hyperargininemic" rats and pathological "hyperargininemic"-made rats for at least 8 and 5 days respectively. The very transient response in vivo to exogenous free arginase can be considerably prolonged by entrapment of the arginase in isoionic prepared erythrocytes.

Amino Acid Metabolism, Inborn Errors↗