Biochemical abnormalities in an infant with sudanophilic leukodystrophy

1982 ◽  
Vol 5 (S1) ◽  
pp. 33-34
Author(s):  
R. Sengers ◽  
J. Bakkeren ◽  
W. Ruitenbeek ◽  
F. Trijbels ◽  
J. Rotteveel ◽  
...  
Keyword(s):  
Sudanophilic Leukodystrophy ◽  
Biochemical Abnormalities

Cerebrospinal fluid γ-aminobutyric acid levels in dogs with chronic portosystemic encephalopathy

1986 ◽  
Vol 71 (6) ◽  
pp. 749-753 ◽  
Author(s):  
J. E. Maddison ◽  
D. Yau ◽  
P. Stewart ◽  
G. C. Farrell
Keyword(s):  
Cerebrospinal Fluid ◽  
Aminobutyric Acid ◽  
Plasma Ammonia ◽  
Portosystemic Encephalopathy ◽  
Dog Model ◽  
Csf Levels ◽  
Neurological Features ◽  
The Brain ◽  
Biochemical Abnormalities

1. Cerebrospinal fluid (CSF) γ-aminobutyric acid (GABA) levels were measured in a dog model of spontaneous chronic portosystemic encephalopathy. 2. Dogs with congenital portacaval shunts (intra- or extra-hepatic) develop neurological features of abnormal psychomotor behaviour and depressed consciousness that are consistent with the symptoms of chronic portosystemic encephalopathy in humans. In the five dogs studied, plasma ammonia was elevated, as was CSF tryptophan, both usual biochemical abnormalities in portosystemic encephalopathy. 3. CSF levels of GABA in five dogs with portosystemic encephalopathy (100 ± 13 pmol/ml) were not significantly different from those in five control dogs (96 ± 14 pmol/ml). CSF levels of GABA were not altered after ammonia infusion. 4. If enhanced GABA-ergic neurotransmission, due to influx of gut-derived GABA into the brain, is responsible for the pathophysiology of chronic portosystemic encephalopathy in this model, it is not reflected by increased levels of GABA in CSF.

Biochemical Abnormalities of Platelets in Renal Failure

1981 ◽  
Vol 1 (1) ◽  
pp. 17-23 ◽  
Author(s):  
Garabed Eknoyan ◽  
Clarence H. Brown, III
Keyword(s):  
Renal Failure ◽  
Biochemical Abnormalities

Can Biochemical Abnormalities Predict Symptomatology in Patients with Primary Hyperparathyroidism?

2011 ◽  
Vol 213 (3) ◽  
pp. 410-414 ◽  
Author(s):  
Anna E. Bargren ◽  
Daniel Repplinger ◽  
Herbert Chen ◽  
Rebecca S. Sippel
Keyword(s):  
Primary Hyperparathyroidism ◽  
Biochemical Abnormalities

Inborn Errors of Metabolism

1980 ◽  
Vol 2 (6) ◽  
pp. 175-181
Author(s):  
George M. Komrower
Keyword(s):  
Neurospora Crassa ◽  
Inborn Error ◽  
Inborn Errors Of Metabolism ◽  
Metabolic Disorders ◽  
Homogentisic Acid ◽  
Turn Of The Century ◽  
Inborn Errors ◽  
The Family ◽  
The One ◽  
Biochemical Abnormalities

Around the turn of the century Garrard established the concept of an inborn error of metabolism using his study on alcaptonuria to exemplify his hypothesis that a considerable number of metabolic disorders with clearly defined clinical, pathologic, and biochemical abnormalities arise because an enzyme governing a single metabolic step is either reduced in activity or missing altogether. He pointed out the familial distribution of alcaptonuria and later showed that the inheritance could be explained on mendelian principles, ie, the affected individual was homozygous for the abnormal gene and that the inheritance was recessive, both parents being heterozygous for the disorder. He suggested that the accumulation of homogentisic acid in alcaptonuria was evidence that this substance is a normal metabolite in the degradation of tyrosine and attributed this accumulation to a failure of oxidation of homogentisic acid. In addition to alcaptonuria he described cystinunia, pentosuria, and albinism. This work was the forerunner of the classic studies of Beadle and Tatum on mutants of Neurospora crassa which led to the one gene-one enzyme concept. DETECTION Different groups require special attention: the family at risk because of previously affected individuals, those with unusual features suggestive of metabolic disorders, and sick newborns. Screening of normal newborns requires a different approach.

Contractile behavior of rat myocardium after reversal of hypertensive hypertrophy

1982 ◽  
Vol 242 (5) ◽  
pp. H882-H889 ◽  
Author(s):  
J. M. Capasso ◽  
J. E. Strobeck ◽  
A. Malhotra ◽  
J. Scheuer ◽  
E. H. Sonnenblick
Keyword(s):  
Myocardial Hypertrophy ◽  
Applied Pressure ◽  
Pressure Overload ◽  
Heart Weight ◽  
Biochemical Alterations ◽  
Time To Peak ◽  
Velocity Of Shortening ◽  
Significant Depression ◽  
Contractile Performance ◽  
Biochemical Abnormalities

The effects of renovascular hypertension and its reversal on the contractile performance of papillary muscles from rats has been examined. Hypertension of 10 wk duration caused a 48% increase in heart weight and significant prolongations of isometric time to peak tension (TPT), time to half relaxation, and time to peak shortening (TPS). A significant depression in the velocity of shortening was observed in the 10-wk group. However, muscles from hypertensive rats were still able to maintain normal levels of peak isometric developed tension and peak shortening; this may be due to the observed prolongation of TPT and TPS, respectively. In addition, calcium-activated actomyosin ATPase activity was depressed in hearts of hypertensive animals. Reversal of hypertension was studied at 20 wk after the onset of hypertension (10 wk of hypertension followed by 10 wk of normotension). Contractile and biochemical alterations observed in hypertensive animals were reversed in rats undergoing this regime. Thus reversal of a gradually applied pressure overload resulted in the regression of mechanical and biochemical abnormalities associated with the pressure overload myocardial hypertrophy.

DRD2/ANKK1 TaqI A1 polymorphism associates with overconsumption of unhealthy foods and biochemical abnormalities in a Mexican population

2018 ◽  
Vol 24 (5) ◽  
pp. 835-844 ◽  
Author(s):  
Ingrid Rivera-Iñiguez ◽  
Arturo Panduro ◽  
Omar Ramos-Lopez ◽  
Sergio Javier Villaseñor-Bayardo ◽  
Sonia Roman
Keyword(s):  
Mexican Population ◽  
Biochemical Abnormalities
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