Biomedical subjects

Ravi Kumar Kurup

Publications and source records attributed to Ravi Kumar Kurup.

At least 55 records · Page 3Linked to original sources

PubMed2003

Hypothalamic digoxin, hemispheric chemical dominance, and mesenteric artery occlusion.

The role of the isoprenoid pathway in vascular thrombosis, especially mesenteric artery occlusion and its relation to hemispheric dominance, was assessed in this study. The following parameters were measured in patients with mesenteric artery occlusion and individuals with right hemispheric, left hemispheric, and bihemispheric dominance: (1) plasma HMG CoA reductase, digoxin, dolichol, ubiquinone, and magnesium levels; (2) tryptophan/tyrosine catabolic patterns; (3) free radical metabolism; (4) glycoconjugate metabolism; and (5) membrane composition. In patients with mesenteric artery occlusion there was elevated digoxin synthesis, increased dolichol and glycoconjugate levels, low ubiquinone, and elevated free radical levels. The RBC membrane Na(+)-K+ ATPase activity and serum magnesium were decreased. There was also an increase in tryptophan catabolites and reduction in tyrosine catabolites in the serum. There was an increase in cholesterol:phospholipid ratio and a reduction in glycoconjugate level of RBC membrane in these patients. The biochemical patterns obtained in mesenteric artery occlusion is similar to those obtained in left-handed/right hemispheric dominant individuals by the dichotic listening test. But all the patients with mesenteric artery occlusion were right-handed/left hemispheric dominant by the dichotic listening test. Hemispheric chemical dominance has no correlation with handedness or the dichotic listening test. Mesenteric artery occlusion occurs in right hemispheric chemically dominant individuals and is a reflection of altered brain function. Hemispheric chemical dominance may thus control the risk for developing vascular thrombosis in individuals.

Aged↗

PubMed2003

Schizoid neurochemical pathology-induced membrane Na(+)-K+ ATPase inhibition in relation to neurological disorders.

Psychiatric abnormalities have been described in primary neurological disorders like multiple sclerosis, primary generalized epilepsy, Parkinson's disease, subacute sclerosing panencephalitis (SSPE), central nervous system glioma, and syndrome X with vascular dementia. It was therefore considered pertinent to compare monoamine neurotransmitter pattern in schizophrenia with those in the disorders described above. The end result of neurotransmission is changes in membrane Na(+)-K+ ATPase activity. Membrane Na(+)-K+ ATPase inhibition can lead to magnesium depletion, which can lead to an upregulated isoprenoid pathway. The isoprenoid pathway produces three important metabolites--digoxin, an endogenous membrane Na(+) -K+ ATPase inhibitor; ubiquinone, a membrane antioxidant and component of mitochondrial electron transport chain; and dolichol, important in N-glycosylation of protein. The serum/plasma levels of digoxin, dolichol, ubiquinone, magnesium, HMG CoA reductase activity, and RBC Na(+)-K+ ATPase activity were estimated in all these disorders. The result showed that the concentration of serum tryptophan and serotonin was high and serum tyrosine, dopamine, adrenaline, and noradrenaline low in all the disorders studied. The plasma HMG CoA reductase activity, serum digoxin, and serum dolichol levels were high and serum ubiquinone levels, serum magnesium, and RBC Na(+)-K+ ATPase activity were low in all the disorders studied. The significance of these changes in the pathogenesis of syndrome X, multiple sclerosis, primary generalized epilepsy, schizophrenia, SSPE, and Parkinson's disease is discussed in the setting of the interrelationship between these disorders documented in literature.

Adult↗

PubMed2003

Hypothalamic digoxin, hemispheric chemical dominance, and addictive behavior.

The isoprenoid pathway produces an endogenous membrane sodium-potassium ATPase inhibitor, digoxin. Digoxin can regulate neurotransmitter transport in the brain with upregulation of tryptophan transport over tyrosine. The pathway was assessed in individuals with addiction, as well as in those with differing hemispheric dominance. The isoprenoid pathway was upregulated with increased digoxin synthesis in addiction. There was an increase in tryptophan catabolites--quinolinic acid, serotonin, nicotine, and strychnine--in patients with addiction, and a reduction in tyrosine catabolites--dopamine, noradrenatine, and morphine. The pattern seen in addiction individuals was similar to that in right hemispheric chemical dominance. Addiction represents a state of right hemispheric chemical dominance, hyperdigoxinemia, and endogenous morphine deficiency state.

Behavior, Addictive↗

PubMed2003

Endogenous digoxin, hemispheric dominance and family bonding behavior.

The isoprenoid pathway produces endogenous digoxin which can regulate neurotransmitter and amino acid transport. Digoxin synthesis and neurotransmitter patterns were assessed in individuals with differing family bonding patterns. The patterns were compared in those with right hemispheric and left hemispheric dominance. Digoxin synthesis was increased with upregulated tryptophan catabolism (increased levels of serotonin, strychnine and nicotine) and down regulated tyrosine catabolism (decreased levels of dopamine, noradrenaline and morphine) in those with reduced family bonding and right hemispheric chemical dominance. Digoxin synthesis was reduced with down regulated tryptophan catabolism (decreased levels of serotonin, strychnine and nicotine) and upregulated tyrosine catabolism (increased levels of dopamine, noradrenaline and morphine) in those with increased family bonding and left hemispheric chemical dominance. Hypothalamic digoxin plays a central role in the regulation of family bonding behavior. Hemispheric chemical dominance in relation to digoxin status is also crucial.

Adult↗

PubMed2003

Hypothalamic digoxin, hemispheric chemical dominance and syndrome X with multiple lacunar state. A hypothesis.

This study assessed the changes in digoxin and some other metabolites of the isoprenoid pathway in metabolic syndrome X presenting with multiple lacunar state. The isoprenoid pathway and digoxin status was also studied for comparison in individuals of differing hemispheric dominance to find out the role of cerebral dominance in the genesis of syndrome X. There was an increase in plasma HMG CoA reductase activity with a consequent increase in serum digoxin, which caused a reduction in RBC membrane Na(+)-K+ ATPase activity. There was an increase in serum tryptophan and its metabolites and a decrease in tyrosine and its metabolites. Serum magnesium was decreased with consequent alteration in the metabolism of glycosaminoglycans and glycolipids. Increase in dolichol, another product of the isoprenoid pathway, resulted in alteration in glycoprotein metabolism. Changes in the composition of membrane glycosaminoglycans, glycoproteins and cholesterol: phospholipid ratio were also observed in this disorder leading to decreased lysosomal stability. Decrease in ubiquinone, another isoprenoid metabolite, resulted in alteration in the free radical generation. Membrane Na(+)-K+ ATPase inhibition due to digoxin, altered membrane structure, increased tryptophan catabolites and decreased tyrosine catabolites can lead to increased intracellular calcium and reduced intracellular magnesium which can account for the symptoms of syndrome X. The biochemical patterns including hyperdigoxinemia observed in syndrome X correlated with those obtained in right hemispheric chemical dominance. Right hemispheric chemical dominance is a predisposing factor for syndrome X with multiple lacunar state.

Analysis of Variance↗

PubMed2002

Detection of endogenous lithium in neuropsychiatric disorders--a model for biological transmutation.

The human hypothalamus produces an endogenous membrane Na(+)-K(+) ATPase inhibitor, digoxin. A digoxin induced model of cellular/neuronal quantal state and perception has been described by the authors. Biological transmutation has been described in microbial systems in the quantal state. The study focuses on the plasma levels of digoxin, RBC membrane Na(+)-K(+) ATPase activity, plasma levels of magnesium and lithium in neuropsychiatric and systemic disorders. Inhibition of RBC membrane Na(+)-K(+) ATPase activity was observed in most cases along with an increase in the levels of serum digoxin and lithium and a decrease in the level of serum Mg(++). The generation of endogenous lithium would obviously occur due to biological transmutation from magnesium. Digoxin and lithium together can produce added membrane Na(+)-K(+) ATPase inhibition. The role of membrane Na(+)-K(+) ATPase inhibition in the pathogenesis of neuropsychiatric and systemic disorders is discussed. The inhibition of membrane Na(+)-K(+) ATPase can contribute to an increase in intracellular calcium and a decrease in magnesium, which can result in a defective neurotransmitter transport mechanism, mitochondrial dysfunction and apoptosis, defective golgi body function and protein processing dysfunction, immune dysfunction and oncogenesis.

Adult↗

PubMed2002

Hypothalamic digoxin related membrane Na+-K+ ATPase inhibition and familial basal ganglia calcification.

The isoprenoid pathway produces three key metabolites-digoxin (membrane sodium-potassium ATPase inhibitor and regulator of intracellular calcium-magnesium ratios), dolichol (regulator of N-glycosylation of proteins) and ubiquinone (free radical scavenger). The pathway was assessed in a rare and specific type of familial basal ganglia calcification described. The family had a coexistence of basal ganglia calcification (six out of 10 cases), schizophrenia, Parkinson's disease, Alzheimer's disease, rheumatoid arthritis, systemic tumours and syndrome X and were all right hemispheric dominant. The isoprenoid pathway was also studied for comparison in right hemispheric dominant, bihemispheric dominant and left hemispheric dominant individuals. The isoprenoid pathway was upregulated with increased digoxin synthesis in familial basal ganglia calcification. Membrane sodium-potassium ATPase inhibition can lead on to increase in intracellular calcium and calcification of the basal ganglia. There was increase in tryptophan catabolites and a reduction in tyrosine catabolites. There was also an increase in dolichol and glycoconjugate levels with reduced lysosomal stability in these patients. The ubiquinone levels were low and free radical levels increased. The cholesterol-phospholipid ratio was increased and glycoconjugate level of the RBC membrane reduced in these group of patients. No significance difference was noted in family members with and without basal ganglia calcification. This findings were correlated with the pathogenesis of syndrome X, immune mediated diseases, degenerations, tumours and psychiatric disorders noted in the familial basal ganglia calcification described. The biochemical patterns obtained in familial basal ganglia calcification correlated with those in right hemispheric dominance.

Adult↗

PubMed2002

Hypothalamic digoxin, hemispheric dominance, and neuroimmune integration.

The isoprenoid pathway produces three key metabolites--digoxin (membrane Na(+)-K+ ATPase inhibitor, regulator of neurotransmitter transport, and immunomodulatory agent), dolichol (regulatory of N-glycosylation of proteins), and ubiquinone (free-radical scavenger). The pathway was assessed in systemic lupus erythematosis with neuropsychiatric manifestations, slow viral diseases (subacute sclerosing panencephalitis [SSPE], and Creutzfeldt-Jakob disease [CJD]) and patients with recurrent respiratory infections. This was also studied for comparison in patients with right hemispheric and left hemispheric dominance. The isoprenoid pathway was upregulated with increased digoxin synthesis in patients with neurolupus, SSPE, and CJD, and in those with right hemispheric dominance. The tryptophan catabolites were increased and the tyrosine catabolites reduced. In these patients the dolichol and glycoconjugate levels were elevated and lysosomal stability was reduced. The ubiquinone levels were low and free-radical levels increased in these patients. The membrane cholesterol:phospholipid ratios were increased and membrane glycoconjugates reduced. On the other hand, in patients with recurrent respiratory infection and left hemispheric dominance, the reverse patterns and hypodigoxinemia with a downregulated isoprenoid pathway were noticed. The isoprenoid pathway is important in the pathogenesis of neurolupus, CJD, SSPE, and recurrent respiratory infections. Hypothalamic digoxin and chemical hemispheric dominance play an important role in the regulation of immunity.

Creutzfeldt-Jakob Syndrome↗

PubMed2002

Central role of hypothalamic digoxin in conscious perception, neuroimmunoendocrine integration, and coordination of cellular function: relation to hemispheric dominance.

Alteration in the isoprenoid metabolites--digoxin, ubiquinone, and dolichol--have been reported in neuronal degeneration (Parkinson's disease), oncogenesis (central nervous system glioma), functional neuropsychiatric disorders (schizophrenia and epilepsy), and immune-mediated disorders (multiple sclerosis). The coexistence of these disorders has been documented in literature and a central dysfunction related to digoxin and the isoprenoid pathway may underlie all these disorders. A family with a high prevalence of Parkinson's disease, schizophrenia, neoplasms, syndrome X, rheumatoid arthritis, and epilepsy has been described. The psychological behavioral patterns of the family were: creativity and high IQ, hypersexual behavior, reduced appetite and eating behavior, insomnia and reduced sleep patterns, increased tendency for spirituality, increased tendency for addiction, less bonding and affectionate behavior, and left handedness/right hemispheric dominance. Digoxin, an endogenous Na(+)-K+ ATPase inhibitor secreted by the hypothalamus, was found to be elevated and red blood cell (RBC) membrane Na(+)-K+ ATPase activity was found to be reduced in all the disorders and in the indexed family studied. Hypothalamic digoxin can modulate conscious perception and its dysfunction may lead to schizophrenia. Digoxin can also preferentially upregulate tryptophan transport over tyrosine, resulting in increased levels of depolarizng tryptophan catabolites, serotonin, quinolinic acid, strychnine, and nicotine, and decreased levels of hyperpolarizing tyrosine catabolites, dopamine, noradrenaline, and morphine, contributing to membrane Na(+)-K+ ATPase inhibition in all the above disorders and the indexed family. Digoxin-induced membrane Na(+)-K+ ATPase inhibition can result in increased intracellular Ca2+ and reduced Mg2+ levels, leading on to glutamate excitotoxicity, oncogene activation, and immune activation. Digoxin-induced altered Ca2+/Mg2+ ratios, reduced ubiquinone, and increased dolichol can affect glycoconjugate metabolism, membrane formation and structure, and mitochondrial function, leading to the diverse disorders described above, including those in the indexed family. The isoprenoid pathway and neurotransmitter patterns were compared in right-handed/LH dominant and left-handed/RH dominant individuals. The left-handed/RH dominant individuals compared to right-handed/LH dominant individuals had elevated hydroxymethylglutarylcoenzyme A reductase activity, with increased serum digoxin and dolichol levels. The serum ubiquinone, serum Mg2+ and RBC Na(+)-K+ ATPase activity were reduced in left-handed/RH dominant individuals. The left-handed/RH dominant individuals compared to right-handed/LH dominant individuals had elevated levels of serum tryptophan, quinolinic acid, serotonin, nicotine, and strychnine. The levels of tyrosine, dopamine, noradrenaline, and morphine were low in left-handed/RH dominant compared to right-handed/LH dominant individuals. The hyperdigoxinemic state indicates right hemispheric dominance. Hypothalamic digoxin can thus function as the master conductor of the neuroimmunoendocrine orchestra and coordinate the functions of various cellular organelles.

Brain Diseases↗

PubMed2002

Hypothalamic digoxin deficiency in obsessive compulsive disorder and la Tourette's syndrome.

The isoprenoid pathway related cascade was assessed in 15 patients with obsessive compulsive disorder (OCD) and la Tourette's syndrome (TS). The pathway was also assessed in right hemispheric dominant, left hemispheric dominant, and bihemispheric dominant individuals to assess whether hemispheric dominance has any correlation with these disease states. The levels of serum digoxin, HMG CoA reductase activity, and dolichol were found to be decreased in OCD and la Tourette's syndrome as well as in left hemispheric dominant individuals with a corresponding increase in RBC Na(+)-K+ ATPase activity, serum ubiquinone, and magnesium levels. There was an increase in tyrosine and its catabolites, and a reduction in tryptophan and its catabolites in the serum. The total and individual glycosaminoglycan (GAG) fractions, carbohydrate residues of glycoproteins, and the concentration of glycolipids decreased in the serum. The activity of GAG degrading enzymes and glycohydrolases were decreased. The RBC membrane glycoconjugates were increased while the membrane cholesterol:phospholipid ratio was decreased. The activity of free radical scavenging enzymes increased while the concentration of free radicals decreased significantly. On the other hand, there was hyperdigoxinemia and the reverse biochemical patterns in those with right hemispheric dominance. Membrane Na(+)-K+ ATPase stimulation can result in decreased intracellular Ca2+ and increased magnesium levels. Increased levels of dopamine can lead to a tic syndrome, while reduced levels of serotonin and increased dopamine can both lead to obsessive compulsive disorder. Decrease in fucose and sialo-ligands, increased immunosuppressive morphine levels, decreased T-cell calcineurin signal transduction related to decreased intracellular calcium, reduced free radical production, and altered presentation of bacterial glycoconjugate antigens can lead to a hypoimmune response and recurrent respiratory infection in OCD patients. OCD and la Tourette's syndrome are associated with left hemispheric chemical dominance.

Cholesterol↗

PubMed2002

Endogenous strychnine: description of hypo- and hyperstrychninergic state in relation to neuropsychiatric diseases.

Previous work from our laboratory has demonstrated the presence of endogenous strychnine in the mammalian brain and human serum samples. The present study examines the role of strychnine in neuropsychiatric disorders. Strychnine is synthesized from tryptophan. The blood levels of tyrosine, tryptophan, and strychnine were studied as also RBC membrane Na(+)-K+ ATPase activity. It was found that serum tyrosine levels were reduced and that tryptophan levels were elevated in all neuropsychiatric disorders studied with a reduction in RBC Na(+)-K+ ATPase activity. Strychnine was present in significant amounts in the serum of patients with epilepsy, Parkinson's disease, and manic depressive psychosis. The presence of strychnine in significant amounts could be related to elevated tryptophan levels, suggesting the synthesis of these alkaloids from tryptophan. Na(+)-K+ ATPase inhibition present in most of the disorders could be related to increased depolarizing strychninergic transmission. The role of strychnine in the pathogenesis of these disorders, in the setting of membrane Na(+)-K+ ATPase inhibition, is discussed.

Adult↗

PubMed2002

Hypothalamic digoxin, cerebral dominance, and mitochondrial function/free radical metabolism.

The present study assessed the biochemical differences of free radical metabolism and mitochondrial function between right hemispheric dominant and left hemispheric dominant individuals. The following parameters were measured: (1) plasma HMG CoA reductase activity, (2) isoprenoid metabolites--digoxin and ubiquinone, (3) plasma magnesium and RBC membrane Na(+)-K+ ATPase activity; (4) lipid peroxidation products--malondialdehyde, hydroperoxides and conjugated dienes, and NO, (5) reduced glutathione, and (6) activity of superoxide dismutase, catalase, GSH peroxidase, and GSH reductase. The results showed that right hemispheric dominant individuals had (i) increased plasma HMG CoA reductase activity and elevated digoxin levels, (ii) decreased plasma magnesium and RBC membrane Na(+)-K+ ATPase activity, (iii) reduced ubiquinone levels, (iv) with increased levels of lipid peroxidation products and NO, (v) decreased levels of reduced glutathione and free radical scavenging enzymes, and (vi) increased tryptophan and reduced tyrosine levels. Left hemispheric dominant individuals had the opposite patterns. Right hemispheric dominance represents a hyperdigoxinemic state with membrane sodium-potassium ATPase inhibition and increased lipid peroxidation. Left hemispheric dominance represents the reverse pattern with hypodigoxinemic/membrane sodium-potassium ATPase stimulation and decreased lipid peroxidation. Cerebral dominance can regulate mitochondrial function and free radical metabolism.

Acoustic Stimulation↗

PubMed2002

Hypothalamic digoxin, hemispheric chemical dominance, and endocrine/metabolic/cellular regulation.

The hypothalamus produces an endogenous membrane Na(+)-K+ ATPase inhibitor and regulator of neurotransmission, digoxin. Digoxin, a steroidal glycoside, is synthesized by the isoprenoid pathway. In view of the reports of elevated digoxin levels in metabolic syndrome X with high body mass index, the isoprenoid-mediated pathway biochemical cascade was assessed in individuals with high and low body mass index. It was also assessed in individuals with differing hemispheric dominance to find out the relationship among digoxin status, body mass index, and hemispheric dominance. The isoprenoid pathway metabolites, tryptophan/tyrosine catabolic patterns, glycoconjugate, and free radical metabolism, as well as membrane composition, were assessed. In individuals with high body mass index, an upregulated isoprenoid pathway with increased digoxin levels, increased glycoconjugates, and dolichol levels, reduced lysosomal stability, low ubiquinone levels with increased free radical generation, and increased membrane cholesterol:phospholipid ratio were observed. The reverse patterns were seen in individuals with a low body mass index. The patterns in individuals with a high body mass index and low body mass index correlated with right hemispheric dominance and left hemispheric dominance, respectively. Hemispheric dominance and digoxin status regulated the differential metabolic pattern observed in individuals with high and low body mass index. Hypothalamic digoxin/cerebral dominance can regulate the metabolic/endocrine function, as well as the structure/function of cellular organalle.

Adult↗

PubMed2002

Hypothalamic digoxin, cerebral dominance, and membrane biochemistry.

The present study assessed the biochemical differences in membrane composition/function between right hemispheric dominant and left hemispheric dominant individuals. The HMG CoA reductase activity, serum isoprenoid metabolite--digoxin--serum magnesium, and the RBC membrane composition/Na(+)-K+ ATPase activity were studied. The results showed that right hemispheric dominant individuals had (i) increased HMG CoA reductase activity and elevated digoxin levels, (ii) decreased RBC membrane Na(+)-K+ ATPase activity and serum magnesium levels, and (iii) increased cholesterol:phospholipid ratio of RBC membranes with reduced membrane glycoconjugates. Left hemispheric dominant individuals had the opposite patterns. Right hemispheric dominance represents a hyperdigoxinemic state with membrane sodium-potassium ATPase inhibition. Left hemispheric dominance represents the reverse pattern with hypodigoxinemia and membrane sodium-potassium ATPase stimulation. Cerebral dominance can regulate membrane structure/function.

Adult↗

PubMed2002

Hypothalamic digoxin, cerebral dominance, and Golgi body/lysosomal function.

The present study assessed the biochemical differences of glycoconjugate metabolism between right hemispheric dominant and left hemispheric dominant individuals. The isoprenoid metabolites--digoxin and dolichol, glycoconjugates, and lysosomal enzymes--were studied. The results showed that right hemispheric dominant individuals had increased (i) HMG CoA reductase activity and elevated digoxin levels, and (ii) increased dolichol and glycoconjugate levels with reduced lysosomal stability. Left hemispheric dominant individuals had the opposite patterns. Right hemispheric dominance represents a hyperdigoxinemic state with membrane sodium-potassium ATPase inhibition. Left hemispheric dominance represents the reverse pattern with hypodigoxinemia and membrane sodium-potassium ATPase stimulation. Cerebral dominance can regulate glycoconjugate metabolism (golgi body/lysosomal function).

Adult↗

PubMed2002

Hypothalamic digoxin-mediated model for subacute sclerosing panencephalitis.

The isoprenoid pathway including endogenous digoxin was assessed in subacute sclerosing panencephalitis (SSPE). This was also studied for comparison in patients with right hemispheric and left hemispheric dominance. The following parameters were measured in patients with SSPE and in individuals with right hemispheric, left hemispheric and bihemispheric dominance-(a) plasma HMG CoA reductase, digoxin, dolichol, ubiquinone, and magnesium levels; (b) tryptophan/tyrosine catabolic patterns; (c) free-radical metabolism; (d) glycoconjugate metabolism; and (e) membrane composition and RBC membrane Na(+)-K(+) ATPase activity. The isoprenoid pathway was upregulated with increased digoxin synthesis in patients with SSPE and in those with right hemispheric dominance. In this group of patients: (a) the tryptophan catabolites were increased and the tyrosine catabolites reduced; (b) the dolichol and glycoconjugate levels were elevated; (c) lysosomal stability was reduced; (d) ubiquinone levels were low and free-radical levels increased; and (e) the membrane cholesterol:phospholipid ratios were increased and membrane glycoconjugates reduced. On the other hand, in patients with left hemispheric dominance the reverse patterns were obtained. The upregulated isoprenoid pathway and hypothalamic digoxin are involved in the pathogenesis of SSPE. SSPE occurs in right hemispheric chemically dominant individuals and a pathogenetic model for SSPE implicating hypothalamic digoxin is proposed.

Adolescent↗

PubMedDate not supplied

The isoprenoid pathway and the pathogenesis of Reye's syndrome.

UNLABELLED: The isoprenoid pathway produces three key metabolites: endogenous digoxin (regulator of neurotransmitter uptake), dolichol, and ubiquinone (free radical scavenger). Because a mitochondrial dysfunction has been described in Reye's syndrome, we thought it pertinent to assess the pathway in this disease. Since endogenous digoxin can regulate neurotransmitter transport, the pathway also was assessed in patients with right hemispheric, left hemispheric, and bihemispheric dominance to find out the role of hemispheric dominance in its pathogenesis. The plasma/serum activity of HMG CoA reductase, magnesium, digoxin, dolichol, ubiquinone, tryptophan/tyrosine catabolic patterns, free radical, and lipid levels as well as (red blood cell) RBC Na(+)-K(+) ATPase activity were measured in the above mentioned groups. RESULTS: In the patient group as well as in individuals with right hemispheric dominance similar patterns were obtained. There was elevated digoxin and dolichol levels with low levels of ubiquinone in patients with Reye's syndrome as well as in those with right hemispheric dominance. The serum magnesium and RBC Na(+)-K(+) ATPase activity were reduced. There also was an increase in tryptophan catabolites and a reduction in tyrosine catabolites as well as increased free radical levels. Reye's syndrome is associated with an upregulated isoprenoid pathway, elevated hypothalamic digoxin secretion, and right hemispheric chemical dominance.

Adolescent↗

PubMedDate not supplied

Hypothalamic digoxin-mediated model for trisomy 21.

The isoprenoid pathway related cascade was assessed in trisomy 21. Membrane Na+, K(+)-ATPase activity, serum magnesium, and ubiquinone were decreased while hydroxy methyl glutaryl CoA (HMG) coenzyme A (CoA) reductase activity, serum digoxin, and dolichol levels were increased in trisomy 21. There were increased levels of tryptophan catabolites--nicotine, strychnine, quinolinic acid, and serotonin--and decreased levels of tyrosine catabolites--dopamine, noradrenaline, and morphine in trisomy 21. There was an increase in dolichol levels, carbohydrate residues of glycoproteins, glycolipids, total/individual glycosaminoglycan (GAG) fractions, and lysosomal enzymes in trisomy 21. Reduced levels of ubiquinone, reduced glutathione, and free radical scavenging enzymes as well as increased lipid peroxidation products and nitric oxide were noticed in trisomy 21. Hypothalamic digoxin and a disordered isoprenoid pathway are important in the pathogenesis of trisomy 21.

Alkaloids↗