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Biomedical subjects

N L Banik

Publications and source records attributed to N L Banik.

At least 91 records · Page 5Linked to original sources
PubMed1984

Changes in myelin and axonal proteins in CaCl2-induced myelopathy in rat spinal cord.

Calcium-induced myelopathy was produced in rats by dripping 1.0 ml of a 10% solution of CaCl2 at pH 7.4 upon exposed spinal cord. Changes in spinal cord proteins were examined following application of calcium. Analysis of proteins by SDS-PAGE revealed progressive losses of neurofilament, microtubular, and glial filament proteins over a period of 8 hours to 5 days. Large losses of myelin proteins were also evident. The protein alterations observed correlate well with ultrastructural changes and resemble those previously found with physical trauma. These observations indicate that Ca2+ plays a pivotal role, possibly by activating proteinase(s), in the degeneration of axons and myelin sheath in both Ca2+-induced myelopathy and spinal cord injury.

Animals↗
PubMed1983

Purification of a calcium-activated neutral proteinase from bovine brain.

A calcium-activated neutral proteinase (CANP) resolved into three components has been partially purified from bovine brain. The method of isolation has resulted in 22,000, 7,100, and 8,000-fold purification for CANP I, II and III respectively. All three fractions require Ca2+ for activation. The characterization of the purified CANP I has shown that it is activated by 250 microM Ca2+ and the enzyme loses its activity when incubated in the presence of Ca2+ without substrate. Mg2+ is ineffective. The enzyme degrades neurofilament triplet proteins, tubulin and casein efficiently. The myelin basic protein is hydrolyzed after longer incubation. Bovine serum albumin and histones are unaffected. The enzyme is active at pH 5.5 to 9.0 with optimum between pH 7.5 and 8.5. It has a Km of 1.8 X 10(-7) M for the 69,000 dalton neurofilament protein. The enzyme is inhibited by sulphydryl blocking reagents and also by EGTA, leupeptin and E-64c. The SDS-PAGE analysis of the enzyme fractions has shown a major band at 66-68,000 daltons and two minor bands at 60,000 and 48-50,000 daltons for CANP I; a major band at 48-50,000 daltons and a minor band at 30-32,000 daltons for CANP II and a predominant doublet at 30-32,000 daltons with a minor band at 48-50,000 daltons for CANP III. The degradation of neurofilament proteins suggests that the CANP(s) may be involved in the turnover of these proteins.

Animals↗
PubMed1982

Degradation of cytoskeletal proteins in experimental spinal cord injury.

Spinal cord injury was produced in rats by dropping a 10 g weight from 30 cm upon dura-invested exposed spinal cord. Examination of the fine structure of the traumatic lesion (15 min to 30 min) revealed granular degeneration of axons and occasional loosening of myelin lamellae. Older lesions (4 to 72 hours) showed degeneration of axons and vesiculation of myelin. At 15 minutes there is more loss of neurofilament proteins than of myelin proteins. Substantial decreases in the neurofilament and myelin proteins were observed at 30 minutes and the losses were even greater 2-72 hours after injury. This indicates that degeneration of axons may precede degradation of the myelin sheath and also that increased proteinase(s) activity, possibly activated by calcium, mediates the traumatic axonolysis and myelinolysis in experimental spinal cord trauma.

Animals↗
PubMed1981

Ca2+-accumulation in experimental spinal cord trauma.

Quantitative measurements of the time course of calcium levels in experimental spinal cord trauma have been made. The injury was produced in rats by dropping a 10 g weight from 30 cm upon exposed dura-invested spinal cord. Lumbar sections of traumatized spinal cord and internal controls from remote cervical cord were excised and analyzed for calcium using atomic absorption spectroscopy. Total calcium levels in the lesioned cord were significantly elevated over control values within 45 min post-trauma (P less than 0.005), with maximal increase at 8 h. The increased levels of calcium in the lesion tissue confirm the previous morphologic finding of calcium deposits within axons in the lesion.

Animals↗
PubMed1980

The effects of spinal cord trauma on myelin.

Experimental spinal cord trauma was produced in rats by dropping a 10-g weight from a height of 30 cm upon exposed spinal cord. The histological lesion consisted of edema, necrosis, and hemorrhage. The fine structure of the early traumatic lesion (4 to 12 hours) included granular dissolution of axons and a characteristic vesiculation of myelin. The predominant ultrastructural features of older lesions (12 to 72 hours) were intra-axonal calcification and lipid-laden macrophages. The yield of myelin and the activity of adenosine 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNP) were reduced by approximately 15% at 4 hours and by 60% at 72 hours. Losses in all myelin proteins were observed, but were most severe and occurred earliest in the basic proteins. The ultrastructural and biochemical alterations observed in this study indicate that proteinase activity is increased and may be partially responsible for the traumatic myelinolysis in experimental spinal cord trauma.

Animals↗
PubMed1979

Activity of 2',3'-cyclic nucleotide 3'-phosphohydrolase in human cerebrospinal fluid.

Activity of the myelin marker enzyme 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNP) was assayed in cerebrospinal fluid samples obtained from patients with multiple sclerosis (MS) and other neurological diseases. The enzyme activity was found to be elevated in acute cases of MS and reduced during remission. It was present in other demyelinating diseases, and no activity was detected in normal CSF. CNP may be released into CSF from any insult to myelin. The level of activity appears to reflect demyelination and the rate of breakdown of the myelin sheath.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1979

Adrenoleukodystrophy brain cholesteryl esters and other neutral lipids.

Further examination of the neutral lipid fractions derived from brain tissue of two patients afflicted with adrenoleukodystrophy has demonstrated the presence not only of free cholesterol and cholesteryl ester, but also of appreciable free fatty acid and triglyceride. Using a gas--liquid chromatographic system normally employed for the analysis of long-chain fatty acids of galactolipids and spingomyelin, it was possible to establish the presence of long-chain (greater than C20) fatty acids in the cholesteryl ester, free fatty acid and triglyceride fractions. Long-chain fatty acids were most abundant in the cholesteryl esters. Fatty acids identified by gas--liquid chromatography and gas chromatography--mass spectroscopy included normal saturated and monounsaturated fatty acids as large as C34. Several unknown fatty acyl compounds, of as yet undetermined structure, were also observed. All investigations thus far would indicate that the pathogenesis of adrenoleukodystrophy is closely related to the aberrant metabolism of these long-chain fatty acids.

Adrenal Gland Diseases↗
PubMed1977

Protein determinants of myelination in different regions of developing rat central nervous system.

Measurements of several different protein determinants correlated with the time and rate of myelination in five areas of the central nervous system are presented. The deposition of protein in the subcellular fraction corresponding to the density of adult myelin, the appearance of basic protein characteristic myelin, the change in proportions of the individual myelin proteins, the appearance and distribution of the myelin marker 2':3'-cyclic nucleotide3'-phosphohydrolase, and the results of morphological studies of purified myelin are compared. According to these various criteria, and in agreement with the morphological observations of others, myelin appears earliest in the spinal cord, then in the brain stem, and latest in the cerebral hemispheres. Multilamellar myelin was observed in the rat brain stem and spinal cord as early as 5 days of age. The relative proportion of the individual myelin proteins changed with myelin maturation in all areas, with the larger basic protein decreasing reciprocally with increase of the smaller basic protein. The proportion of Wolfgram protein also decreased with maturation. Larger proportions of the enzyme 2':3'-cyclic nucleotide 3'-phosphohydrolase were located in the microsomal fraction at early ages. During development the enzyme activity gradually became associated more with a fraction of a density corresponding to adult myelin, suggesting the presence of precursor membrane fragments in microsomal fractions in the early stages of myelination before compact myelin formation. A significant proportion of the total nucleotide phosphohydrolase activity of the homogenate could not be recovered in subcellular fraction at early ages, but the recovers of the enzyme increased with maturation and the activity was found more in the myelin fraction.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1977

Galactolipid fatty acid composition in adrenoleukodystrophy.

The non-hydroxy and hydroxy fatty acids of the major brain galactosphingolipids, cerebroside and sulphatide, have been isolated from white matter, gray matter and myelin of 2 children with adrenoleukodystrophy and from a corresponding control. In addition, cerebroside fatty acids were recovered from a myelin-related fraction on 1 patient. In comparison to control observations, myelin and the myelin-related fraction cerebroside demonstrate a loss of C24:1 and C24h:o fatty acids from normal and hydroxy fatty acid fractions, respectively. White and gray matter galactolipids isolated from 1 patient indicated a signficant increase in short chain (C16, C18 and C18:1) non-hydroxy fatty acids. In the isolated diseased myelin, the ratio of cerebroside hydroxy to non-hydroxy fatty acids was elevated about 1.5 times above the value for normal myelin, whereas the ratio derived for the myelin-related fraction was about two-thirds the values for the control myelin cerebroside.

Adrenal Insufficiency↗
PubMed1977

Fatty acid composition of myelin isolated from the brain of a patient with cellular deficiency of co-enzyme forms of vitamin B12.

Myelin fractionation and subsequent lipid isolation have been carried out on a brain from a patient who suffered from a cellular deficiency of the adenosylcobalamin and methylcobalamin co-enzyme forms of vitamin B12. Examination of the fatty acid composition of choline and ethanolamine glycerophospholipids indicated a relative enrichment of odd-chain fatty acids which were identified by gas-liquid chromatography-mass spectroscopy as C15, C15:1, C17 and C17:1. A mixture of methyl branched C17 fatty acids was also identified. Odd-chain fatty acids accounted for 9.8% of the total fatty acid in the myelin choline phospholipid conpared to control values of 1.2%. The affected brain myelin phospholipids had a lower unsaturated fatty acid content. Examination of the myelin sphingolipids, sphingomyelin, cerebroside and sulfatide, yielded abnormal fatty acid profiles. The sphingomyelin contained only small amounts of C24:1 fatty acid. Both normal and hydroxy fatty acid containing cerebroside and sulfatide had reduced levels of C24 fatty acid. Determination of the relative hydroxy and normal fatty acid content of the galactolipids indicated an abnormally high hydroxy fatty acid level. Abnormal fatty acid profiles of brain cerebral sphingolipids have not been previously described in cases of vitamin B12 deficiency. Whether or not these alterations are characteristic will only be established by estimating sphingolipids in other such cases.

Brain Chemistry↗
PubMed1976

Neurochemical findings in adreno-leukodystrophy.

The results of neurochemical examination of brain tissue derived from 2 cases of adreno-leukodystrophy have been presented. Both white and grey matter contained suadanophilic material. Although free fatty acid was also present, cholesteryl ester accounted for the bulk of the sudanophilic material. Total cholesterol, galactolipid and phospholipid content was reduced in both white and grey matter. The lipid loss was particularly severe from white matter indicative of considerable demyelination. Cholesterol was found to be the only major sterol present in white or grey matter. Subcellular fractionation of the diseased white matter resulted in myelin and two related fractions, one of which was very fatty and was rich in steryl ester. Morphological examination of myelin indicated loosely-packed lamellae. All of 3 fractions had adenosine 2',6'-cyclic nucleotide-3'-phosphohydrolase activity. Myein and the fraction not rich in cholesteryl ester had discernable basic protein bands when examined by polyacrylamide gel electrophoresis. Analysis of the fatty acid composition of choline and ethanolamine glycerophospholipids indicated a general increase of saturated fatty acids, relative to control values and a decrease in long-chain fatty acids. Examination of sphingomyelin fatty acids also demonstrated a loss of long-chain fatty acids. The fatty acid composition of the cholesteryl esters from white and grey matter differed. The findings indicate generalized damage to the brain, both of white and grey matter, with the damage to the white matter being much more severe. No abnormal sterol or other lipid was isolated.

Adrenal Insufficiency↗
PubMed1976

Neurochemical findings in a perinatal sudanophilic leukodystrophy rich in steryl ester.

Neurochemical and neuropathological studies have been made of a 10-day-old child who suffered from a sudanophilic leukodystrophy. The brain white matter contained abundant sudanophilic material. The patient's grey matter total cholesterol content was 30% higher than whole brain tissue derived from a comparable control. White matter cholesterol content was more than double the control value. Nearly 80% of the white matter cholesterol was esterified. Subcellular fractionation of the white matter resulted in a "floating fraction" rich in cholesteryl ester. The steryl ester fatty acid composition was not typical of control tissue or demyelinating tissue. Patient phospholipid fatty acid composition patterns differed from control, but white matter galactolipid fatty acid composition appeared normal. Cholesteryl ester hydrolase activity appeared normal. Myelin and myelin-like fractions, isolated from diseased and normal brain tissue, were of a primitive developing nature but appeared to be comparable. The findings indicate a neonatal sudanophilic leukodystrophy which doubtless began in prenatal life and which was rich in cholesteryl ester. The aetiology of the leukodystrophy is unknown.

Brain↗
PubMed1976

The action of snake venom, phospholipase A and trypsin on purified myelin in vitro.

1. Purified myelin was incubated with snake venom or phospholipase A in the presence of or absence of trypsin at 37 degrees C, pH7.4, for different times. 2. Analysis of the myelin pellet obtained after centrifugation of the myelin sample incubated with snake venom or phospholipase A alone showed conversion of phosphatidylcholine, phosphatidylethanolamine and phosphatidylserine into their corresponding lyso compounds. No significant loss of myelin protein was observed in these samples. 3. A marked digestion of basic proteins and proteolipid protein was observed from the myelin pellet when trypsin was present in the incubation mixture. 4. The digestion of basic protein and particularly of proteolipid from myelin suggest that phospholipases may make protein more exposed to proteolytic enzyme for its digestion. 5. The relevance of the co-operative effect of phospholipases and proteinases as a model system of the mechanism of myelin breakdown in degenerative brain diseases is discussed.

3',5'-Cyclic-AMP Phosphodiesterases↗