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Biomedical subjects

L Reik

Publications and source records attributed to L Reik.

At least 19 recordsLinked to original sources
PubMed1999

Disorders that mimic central nervous system infections.

Many noninfectious diseases can cause signs, symptoms, and cerebrospinal fluid (CSF) abnormalities simulating central nervous system (CNS) infection. Infection usually can be excluded in these cases by the judicious use of serologic tests and CSF stains and cultures. Then, the correct diagnosis is typically suggested by the history and the concomitant presence of clinical and laboratory evidence of disease in other organ systems. Occasionally, particularly when such evidence is absent, the distinction requires meningeal or brain biopsy.

Central Nervous System Infections↗
PubMed1996

Induction of the male-specific cytochrome P450 3A2 in female rats by phenytoin.

We previously reported that administration of dexamethasone (DEX) and other selected pharmacological agents to rats resulted in a profound increase in hepatic cytochrome P450 3A1 in both sexes, but male constitutive P450 3A2 was modestly increased (4-fold) in adult males and not detected in either treated or untreated females (Cooper et al., Arch. Biochem. Biophys. 301, 345, 1993). Using a more sensitive Western blot stain, we have now detected in females low but significant induction of P450 3A2 by DEX. Of 10 compounds tested, DEX was the most effective inducer of P450 3A1 in either sex and of P450 3A2 in males. Unexpectedly, the antiepileptic, phenytoin, was the most potent inducer of P450 3A2 in females, resulting in levels up to 30% of those seen in untreated males. Even more striking, phenytoin differentially induces the male-specific P450 3A2 with barely detectable increases in P450 3A1 in either sex. By comparison, when administered to female rats, the other active P450 3A inducers preferentially induce P450 3A1 compared to 3A2 by ratios ranging from 3- to 400-fold. Another male-specific isozyme, P450 2C11, was induced in females by both DEX and phenytoin, but DEX was much more effective than phenytoin. These results suggest that the masculinization of expression of these two sexually dimorphic isozymes of cytochrome P450 may occur by different mechanisms, and that phenytoin is atypical of the other nine compounds we tested. Moreover, of the known inducers of the "steroid inducible" 3A family, phenytoin is unique in its ability to differentially induce P450 3A2 compared to P450 3A1, particularly in the female rat. Also, administration of phenytoin to female rats gave rise to P450 3A2 levels that could be divided into two distinct classes of high and low levels of P450 3A2. Should this prove to be a genetic polymorphism, it could be very useful in studies on the mechanism of P450 3A2 induction.

Animals↗
PubMed1993

Stroke due to Lyme disease.

A 56-year-old Connecticut woman suffered multiple strokes 18 months after antibiotic treatment for early Lyme disease with facial palsy. Pleocytosis, intrathecal synthesis of anti-Borrelia burgdorferi antibody, and the response to antibiotic treatment substantiated the diagnosis of neuroborreliosis. This is the first report of stroke caused by Lyme disease acquired in North America.

Antibodies, Bacterial↗
PubMed1990

Purification and characterization of glycosyl-phosphatidylinositol-specific phospholipase D.

We have developed a simple immunoaffinity chromatography procedure for the purification of a glycosyl-phosphatidylinositol (GPI)-specific phospholipase D (GPI-PLD) from bovine serum. The enzyme was initially purified by a procedure consisting of 9% polyethylene glycol precipitation, Q Sepharose anion-exchange chromatography, S-300 gel filtration, wheat germ lectin-Sepharose, hydroxylapatite agarose, zinc chelate matrix, Mono Q-high performance liquid chromatography (HPLC), and Superose 12 (gel filtration) HPLC. Using this purified material as immunogen, we generated a panel of monoclonal antibodies. A low affinity antibody was selected for the purification of catalytically active GPI-PLD from bovine serum by immunoaffinity chromatography, followed by wheat germ lectin-Sepharose and Mono Q-fast protein liquid chromatography. The latter method provides a simple purification procedure with an overall yield of 26%. The purified enzyme has an apparent molecular weight of about 100,000 by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and a pI of about 5.6 by isoelectric focusing gel analysis. On Superose 12 HPLC, the material purified by the latter method elutes as a single peak with an apparent molecular weight of 200,000 as determined by protein standards. The enzyme activity is inhibited by [ethylenebis(oxyethylenenitrilo)]tetraacetic acid or 1,10-phenanthroline. Phosphatidic acid is the only 3H-labeled product when [3H]myristate-labeled variant surface glycoprotein is hydrolyzed by the purified enzyme. Amino terminal sequence analysis of the intact 100-kDa protein reveals no strong homology to that of any other known protein. Twelve tryptic peptides derived from the intact protein have been subjected to amino acid sequence analysis. Two of them share sequence homology with each other and with the metal ion binding domains of members of the integrin family. Based upon these criteria, it appears that the purified enzyme is distinct from other phospholipases with specificity for inositol phospholipids.

Amino Acid Sequence↗
PubMed1986

Neurologic abnormalities in Lyme disease without erythema chronicum migrans.

The clinical features in eight patients with neurologic abnormalities typical of Lyme disease and elevated titers of antibody to the spirochete, Borrelia burgdorferi, its causative agent, are described. None of the patients had the diagnostic skin lesion, erythema chronicum migrans. Lyme arthritis, the other clinical marker for the disease, developed subsequently in only three. The neurologic abnormalities included aseptic meningitis, encephalitis, cranial neuritis, motor and sensory radiculitis, and myelitis in various combinations. The occurrence of severe encephalitis resulting in dementia in two of these patients and irreversible myelopathy in one enlarges the known spectrum of neurologic abnormalities due to infection with B. burgdorferi. Lyme disease can present with neurologic abnormalities without diagnostic extraneural features, can be suspected on clinical and epidemiologic grounds, and can be diagnosed serologically.

Adult↗
PubMed1986

Disorders that mimic CNS infections.

A variety of inflammatory and neoplastic disorders can cause signs, symptoms, and laboratory abnormalities suggesting CNS infection. The distinction usually can be made through careful consideration of the entire clinical picture and the judicious use of additional laboratory tests.

Acute Disease↗
PubMed1985

Demyelinating encephalopathy in Lyme disease.

A 38-year-old man from southeastern Connecticut developed a diffuse encephalopathy with partial complex seizures, followed weeks later by arthritis, cryoglobulinemia, and increased serum IgM. CT showed confluent low-density lesions in the deep cerebral white matter consistent with demyelination. Neither the encephalopathy nor the CT abnormalities improved. Lyme disease was diagnosed serologically 4 years later.

Adult↗
PubMed1983

The accumulation of distinct mRNAs for the immunochemically related cytochromes P-450c and P-450d in rat liver following 3-methylcholanthrene treatment.

Treatment of rats with 3-methylcholanthrene leads not only to a marked accumulation in the liver of translatable mRNA coding for a 56-kilodalton polypeptide representing cytochrome P-450c, the major 3-methylcholanthrene-induced cytochrome P-450 of rat liver, but also to the accumulation of comparable amounts of mRNA encoding a 52-kilodalton polypeptide which is immunoprecipitated with antibodies prepared against rat liver cytochrome P-450c. Further electrophoretic and immunochemical characterization of the latter translation product demonstrates that it corresponds to cytochrome P-450d, the major isosafrole-induced form of rat liver cytochrome P-450. The mRNAs for cytochromes P-450c and P-450d can be completely separated by electrophoresis in denaturing agarose gels and have chain lengths of approximately 4000 and 2000 nucleotides, respectively. These two mRNAs do not show detectable sequence homology to the mRNAs coding for the major phenobarbital-induced forms of cytochrome P-450 (P-450b and P-450e) since in Northern blotting experiments they fail to hybridize under conditions of low to moderate stringency to cloned probes for the latter mRNAs.

Animals↗
PubMed1983

Granulomatous angiitis presenting as chronic meningitis and ventriculitis.

A 35-year-old woman had a diffuse encephalopathy with increased intracranial pressure and chronic lymphocytic meningitis. Hypoglycorrhachia and ventricular accumulation of tracer on radionuclide brain scanning suggested an infection. Cerebral cortical and leptomeningeal biopsies were done when she failed to improve with antituberculous therapy, but were not diagnostic. Granulomatous angiitis of the nervous system was diagnosed at postmortem examination and should be considered in the differential diagnosis of culture-negative chronic meningitis.

Adult↗
PubMed1982

Multiplicity strain differences, and topology of phenobarbital-induced cytochromes P-450 in rat liver microsomes.

The multiplicity of phenobarbital-induced cytochromes P-450 in live microsomes from male rats was investigated by using two-dimensional gel electrophoresis, peptide fingerprinting, and immunoaffinity chromatography. Two colonies each of Holtzman and Long-Evans rats were studied. Four molecular forms of phenobarbital-induced cytochromes P-450 were distinguished as polypeptides (designated PB3, variant PB3, PB4, and PB5) which showed apparent immunochemical identity and greater than or equal to 95% fingerprint homology. Two of these polypeptides corresponded to cytochrome P-450b [Ryan, D., Thomas, P. E., Korzeniowski, D., & Levin, W. (1979) J. Biol. Chem. 254, 1365-1374] and cytochrome P-450e [Ryan, D., & Levin, W. (1981) Fed. Proc., Fed. Am. Soc. Exp. Biol. 40, 1640] which had been purified from Long-Evans rats (variant PB3 and PB5, respectively). Each rat colony was characterized by unique combinations of two or three of these immunochemically related forms of cytochromes P-450. Cytochrome P-450e was present in rats from all four colonies, but cytochrome P-450b was only found in Long-Evans rats. Polypeptide PB3 was only found in the two colonies of Holtzman rats, whereas polypeptide PB4 was present in one colony each of Holtzman and Long-Evans rats. In addition to these forms of cytochrome P-450, rats from each colony also evidenced three other major phenobarbital-induced polypeptides which gave unique fingerprints, and one of these was identified as representing epoxide hydrolase. Proteolytic digestion studies of intact microsomes demonstrated that the four immunochemically identical forms of cytochrome P-450 were partially exposed on the outer (cytoplasmic) surface of microsomes. However, polypeptide PB3 was characterized by the greatest rate of proteolytic degradation. These results clearly demonstrate that phenobarbital-induced cytochromes P-450 include microheterogeneous proteins which show remarkable variations related to rat strains and/or colony.

Animals↗
PubMed1981

Cryoglobulinemia with encephalopathy: successful treatment by plasma exchange.

A 54-year-old man with essential mixed cryoglobulinemia developed a diffuse and focal encephalopathy while systemic vasculitis was active and serum cryoglobulin was markedly increased. No other cause for his encephalopathy could be determined and the diagnosis of cryoglobulinemic cerebral vasculitis was made. Treatment with plasma exchange, prednisone, and cyclophosphamide resulted in clearing of the encephalopathy and reduction in serum cryoglobulin. The onset of improvement was temporally related to the initiation of plasma exchange. Plasma exchange may have a role in the treatment of other patients with life-threatening immune complex diseases involving the nervous system.

Cryoglobulinemia↗