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Biomedical subjects

R Friedman

Publications and source records attributed to R Friedman.

At least 145 records · Page 8Linked to original sources
PubMed1987

Antibodies to the neuronal cytoskeleton are elicited by Alzheimer paired helical filament fractions.

Antibodies were raised to paired helical filament (PHF) enriched fractions obtained from brains of individuals with Alzheimer disease by extraction with ionic detergent followed by sucrose gradient centrifugation. Electron microscopic examination showed that the fractions were enriched in Alzheimer PHF but contained also lipofuscin, amyloid, granular material and membranous elements. Analysis of these fractions with SDS-PAGE stained with Coomassie blue showed only a faint band at approximately 60 kDa while most of the material was excluded from the stacking gel. BALB/c mice were injected weekly with 100 or 200 micrograms of these fractions or corresponding fractions from age-matched control brains. The 3 mice injected with Alzheimer brain, but not the 5 mice injected with control brain fractions, produced antibodies that reacted with central and peripheral nervous system axons, Alzheimer neurofibrillary tangles in intact tissue as well as with isolated, SDS-treated paired helical filaments. In gel strips antibodies from all 3 mice injected with Alzheimer brain fractions reacted with the 200-kDa and 168-kDa but not the 68-kDa neurofilament subunits. The 3 antisera reacted also with some forms of the microtubule-associated protein tau. Adsorptions with the insoluble fraction from Alzheimer but not from control brains blocked staining of axons and NFT by all 3 antisera. Adsorption with highly purified neurofilament proteins or with a preparation containing the 200-kDa and 168-kDa neurofilament subunits blocked axon and NFT immunostaining only in one antiserum. Adsorptions with microtubule protein, heat-stable microtubule-associated protein, or a preparation of tau did not completely block immunostaining by any of the 3 antisera. These results demonstrate that fractions enriched with Alzheimer paired helical filaments contain insoluble neurofilament, tau and other yet unidentified antigens.

Aged↗
PubMed1987

Ubiquitin is detected in neurofibrillary tangles and senile plaque neurites of Alzheimer disease brains.

Neurofibrillary tangles (NFT) and neurites associated with senile plaques (SP) in Alzheimer disease-affected brain tissues were specifically immunostained with affinity-purified antibody preparations directed against ubiquitin. In addition, a class of neurites seen in brain regions containing NFT and SP were also specifically stained. Cross-reactivity of the ubiquitin antisera for tau protein, neurofilament proteins, and high molecular weight microtubule-associated proteins (MAPs) were ruled out by (i) the inability of the ubiquitin antisera to stain these proteins in immunoblotting experiments and (ii) the inability of tau, neurofilament, and MAP preparations, when preincubated with the ubiquitin antisera, to inhibit the selective neurofibrillar staining observed. Our results are consistent with the suggestion that ubiquitin is covalently associated with the insoluble neurofibrillary material of NFT and SP. We propose that the ubiquitin-mediated degradative pathway may be ineffective in removing these fibrillar structures in Alzheimer disease brain.

Aged↗
PubMed1987

Family satisfaction with psychiatric evaluations.

In the current study, psychiatric patient, family, and evaluator satisfaction with initial treatment recommendations was examined in relation to patient compliance with treatment methods and clinical improvement. Only family satisfaction was positively correlated with both compliance and improvement. This finding challenges the predominant view that families play negative roles in psychiatric illness by exacerbating symptomatology and, instead, stresses the positive facilitating role of the family. Implications for involving families in treatment evaluations and social work practice are discussed.

Consumer Behavior↗
PubMed1987

Filaments of Pick's bodies contain altered cytoskeletal elements.

Pick's disease, a form of progressive senile dementia, is distinguished by the presence of neuronal inclusions known as Pick's bodies. The Pick's body consists mostly of sparse 10-20-nm straight filaments admixed with other cytoplasmic elements. This ultrastructural study was undertaken to establish which components of the Pick's body share epitopes with the normal neuronal cytoskeleton and with Alzheimer's paired helical filaments. Vibratome sections from postmortem brains of patients afflicted with Pick's disease were immunostained by means of polyclonal and monoclonal antibodies to neurofilaments, an antiserum to microtubule proteins not cross-reacting with neurofilaments, and an antiserum to Alzheimer's paired helical filaments. All the antibodies have been shown previously to react with Alzheimer's paired helical filaments. The peroxidase-antiperoxidase or indirect immunogold procedure was used for immunostaining. In addition, we used Bodian's silver stain, which has a high affinity for neurofilaments. At the electron-microscopic level the antibodies and Bodian's silver reacted with the straight filaments and some amorphous elements contained within the Pick's body. The following preadsorptions blocked the immunoreaction: neurofilament antibodies with neurofilaments; microtubule antibodies with microtubule protein or a preparation of the microtubule associate protein, tau; antibodies to paired helical filaments with Alzheimer's brain tissue. Treatment of brain tissue containing Pick's bodies with sodium dodecyl sulfate, a solvent of the normal neuronal cytoskeleton, did not dissolve straight 12-nm filaments. The detergent extracted filaments contained the same isotopes as the Pick's filaments in intact tissue. These results demonstrate that the straight filament components of the Pick's body contain the same neurofilament and microtubule epitopes as the Alzheimer's paired helical filaments and that the filaments share insolubility characteristics similar to those of the paired helical filaments. It is proposed that these two structures are related and are derived at least in part from altered components of the normal neuronal cytoskeleton.

Antibodies, Monoclonal↗
PubMed1987

Sudden death following white cell transfusion in a premature infant.

A 1,700-g, 31 weeks' gestational age infant developed early onset Group B streptococcal septicemia associated with shock and respiratory distress. The infant was treated with antibiotics, exchange transfusion, and white cell transfusion. The infant improved, and then acutely deteriorated following the third white cell transfusion. Cause of death was presumed to be pulmonary sequestration of white cells or anaphylaxis.

Anaphylaxis↗
PubMed1986

Pre- and neonatal exposure of the Dahl rat to NaCl: development and regional distribution of myocardial alpha 1-adrenergic and cholinergic receptor sites.

The prenatal and/or postweaning effects of a hypertensinogenic high NaCl-containing diet (8.0% NaCl, w/w) on (1) the regional distribution of alpha 1-adrenoceptors and muscarinic cholinergic receptor sites in the heart and (2) the predisposition/resistance to hypertension (HT) were assessed in the inbred Dahl HT-sensitive (S/JR) and HT-resistant (R/JR) rat. The density of alpha 1-adrenoceptors was reduced in the left ventricle but not consistently affected in the ventricular septum, right ventricle, or atria of S/JR offspring with NaCl-induced HT. Both normotensive and hypertensive S/JR rats also displayed a significantly greater density of cholinergic receptor sites in the atria but few consistent alterations in other regions of the heart, compared to R/JR rats. Maternal diet had no effect on the predisposition/resistance to salt-induced HT and little effect on the regional development of alpha 1-adrenoceptors and cholinergic receptor sites. The results of this study suggest that the reduced density of ventricular alpha 1-adrenoceptors in the S/JR strain is a consequence of HT while the elevated density of cholinergic receptors in the atria may be related to the genetic predisposition/resistance to HT.

Animals↗
PubMed1986

Presence and identification of polyamines in xylem and Phloem exudates of plants.

Polyamines were identified by high performance liquid chromatography (benzoylation) and by thin layer chromatography (dansylation) in xylem exudates from stems of sunflowers (Helianthus annuus [L.]), mung bean (Vigna radiata [L.] Wilczek), grapevine (Vitis vinifera [L.] cv Grenache), and orange (Citrus sinensis [L.] Osbeck, cv Valencia), as well as in phloem sap (using elution into EDTA) of sunflower and mung bean plants. Putrescine was the major polyamine detected, ranging in concentrations of 150 to 9200 picomoles per milliliter exudate, whereas only trace amounts of spermine were detected. High amounts of putrescine and spermidine were found in EDTA eluates (possibly phloem sap) as compared with elution into water. Concentrations of putrescine and spermidine in xylem exudates were related to the physiological conditions of the plants prior to exudate collection. More putrescine was found in exudates of older than in younger sunflower plants, and salt stress applied to sunflower plants resulted in a higher concentration of putrescine and spermidine in the exudate. The presence and abundance of putrescine and spermidine in xylem and phloem exudates indicate that polyamines may be translocated in plants. This long-distance translocation further supports the hypothesis that polyamines have a regulatory role in plant growth and response to stress.

Journal Article↗
PubMed1986

North American brugian filariasis: report of nine infections of humans.

Nine people living in Rhode Island, New York, Pennsylvania, Florida, or California acquired autochthonous brugian filariasis. Each patient had an enlarged lymph node containing a single worm or, in one patient, a pair of worms. Most worms were in lymphatic vessels within the node, but two worms were in the substance of the node. Ten worms were studied, seven female and three male. Female worms contained paired uteri that occupied most of the body cavity of the worm, and male worms contained a single reproductive tract. No worms were gravid. The diameter of the worms was small, 30 micron to 75 micron. The usual diameter of female worms was 65 micron to 75 micron, and 45 micron to 50 micron for male worms. The morphologic features of these worms, their anatomical location, and their geographic distribution are all characteristic of infection with a North American Brugia species.

Adult↗
PubMed1986

Development of a radioimmunoassay for the fibrinogen-derived peptide B beta 1-42.

The peptide B beta 1-42 is the initial cleavage product of plasmin-mediated proteolysis of the NH2-terminal region of fibrinogen or fibrin I, while beta 15-42 is the major fragment released by plasmin degradation of fibrin II. Numerous studies have described the measurement of plasma B beta 1-42 levels as an index of plasmin activity. Previous assays were indirect and included quantitation of thrombin-increasable fibrinopeptide B immunoreactivity (TIFPB) or measurement of beta 15-42 with an antiserum (132) which cross-reacted with B beta 1-42. We report on a new antiserum (R142) directed against B beta 1-42 which does not cross-react with beta 15-42 or fibrinopeptide B. Employing this antiserum, a specific assay for B beta 1-42 was developed. This assay was used to measure plasmin-mediated B beta 1-42 release from fibrinogen and its subsequent proteolysis by thrombin. The selectivity constant (Kcat/Km) for thrombin cleavage of the B beta 14-15 bond of B beta 1-42 was 10(5)-fold less than that for proteolysis of the same bond in the intact fibrinogen molecule, thus explaining the stability of this peptide in the presence of thrombin activity in the blood. Similarly, the selectivity constant for plasmin cleavage of the B beta 21-22 bond of B beta 1-42 was 140-fold less than that for proteolysis of the B beta 42-43 bond of fibrinogen, indicating that secondary plasmin attack of the B beta 1-42 molecule is not physiologically important. The specific B beta 1-42 assay provided excellent recovery of peptide added to blood or plasma. Comparison of B beta 1-42 levels with TIFPB values in 37 patient samples yielded good correlation over a wide range of levels (r2 = 0.91). The median plasma B beta 1-42 level in 15 normal individuals was 1.2 pmol/mL. This is similar to the previously reported normal range for TIFPB (1 to 4 pmol/mL) but is higher than the normal level of 0.4 pmol/mL reported with the assay employing antiserum 132. This discrepancy reflects rapid removal of Arg (B beta 42) by plasma carboxypeptidase activity resulting in 50% loss of B beta 1-42 immunoreactivity with antiserum 132 but no loss with R142. To circumvent this problem, we have developed a beta 15-42 antiserum (R154) which, like antiserum 132, cross-reacts with B beta 1-42. However, B beta 1-42/beta 15-42 immunoreactivity with R154 is stable in the presence of carboxypeptidase activity.(ABSTRACT TRUNCATED AT 400 WORDS)

Drug Stability↗
PubMed1985

The effect of pertussis toxin on alpha-2-adrenoceptor-mediated pigment migration in fish melanophores.

The aggregation of melanin-granules within fish pigment cells (melanophores) can be elicited either by electrical stimulation of intrinsic nerves or by the addition of adrenergic agonists. The pigment aggregation seems to be mediated by alpha-2-adrenoceptors. In this investigation we have used various agonists and antagonists (noradrenaline, (+)- and (-)-adrenaline, isoprenaline, yohimbine and prazosin) to further characterize the pigment-aggregating receptor of Labrus ossifagus. All the results obtained support the notion of alpha-2-adrenoceptor-mediated pigment aggregation. The pertussis toxin, islet-activating protein (IAP), is known to inhibit the alpha-2-adrenoceptor-mediated signal transduction in mammals. We have used IAP to investigated whether fish melanophore alpha-2-adrenoceptors are also inhibited by this toxin. We found that IAP inactivated the alpha-2-adrenoceptor-mediated pigment aggregation in a dose-dependent manner. The inhibitory IAP-effect had a remarkably short onset-time in the melanophores (maximal effect was obtained within 10 min of incubation). Interestingly, binding of an agonist (noradrenaline) to the receptors prevented IAP from exerting its inhibitory action, whereas binding of an antagonist (yohimbine) gave no protection against the IAP-inactivation. In conclusion, the pigment-aggregating receptors of melanophores of L. ossifagus are very similar to the mammalian alpha-2-adrenoceptors. It is possible to inactivate the melanophore receptor system with IAP and this inactivation has a remarkably short onset-time. Stimulation of the alpha-2-adrenoceptors prevents IAP from inactivating the receptor system.

Adrenergic alpha-Agonists↗
PubMed1985

Cellular activation of diaziquone [2,5-diaziridinyl-3,6-bis (carboethoxyamino)-1,4-benzoquinone] to its free radical species.

Human leukemic cell lines K562 and HL60, and the murine leukemic cell line L1210, reduce Diaziquone (AZQ) (NCS182986) to its free radical anion. With all cell lines, the free radical was observed immediately in both aerobic and anaerobic cell suspensions. The steady-state concentration of AZQ free radicals was approximately 1% of the total AZQ concentration. L1210 cells treated with azide reduced AZQ, but cells treated with diamide and N-ethylmaleimide did not. NADPH and L-cysteine reduced AZQ. The latter did so under anaerobic conditions; the former did so under both anaerobic and aerobic conditions.

Animals↗