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Biomedical subjects

J Herbst

Publications and source records attributed to J Herbst.

34 records · Page 2Linked to original sources
PubMed1981

Impaired beta adrenergic receptor binding and function in cystic fibrosis neutrophils.

Cystic fibrosis (CF), a genetic disease characterized by abnormalities of exocrine gland and mucociliary function, has recently been shown to be associated with abnormal adrenergic and cholinergic physiologic responses in addition to decreased beta adrenergic-induced cyclic AMP generation in human leukocytes. In this study we have attempted to elucidate the nature of this hyporesponsiveness by assessing beta adrenergic receptor number and affinity (KD) in the intact neutrophil using the antagonist ligand [3H] dihydroalprenolol and cyclic AMP responses to isoproterenol in addition to histamine, and prostaglandin E1 in CF subjects, CF obligate heterozygotes (CFH), and normal control subjects. CF patients had significantly less (p less than 0.025) cyclic AMP stimulation above basals levels with isoproterenol (0.1 microM to 0.1 mM), compared with control values, but no consistent differences between groups were noted with histamine or PGE1. CF neutrophils had significantly fewer (p less than 0.005) beta adrenergic receptors per neutrophil (398.0 +/- 54.2 vs. 819.4 +/- 67.2) compared with control neutrophils, but the KD (0.740 +/- 0.11 vs. 0.630 +/- 0.05 nM) did not differ significantly (p greater than 0.05). There was no correlation between clinical severity and either cyclic AMP generation or dihydroalprenolol binding (r = 0.27 and 0.24, respectively, p greater than 0.05). The CFH group had approximately 50% of the cyclic AMP stimulation compared with controls, but the number (909.8 +/- 89.3) and KD (0.710 +/- 0.09 nM) of their beta adrenergic receptors were indistinguishable from control subjects. These findings suggest "down regulation" of the beta receptor in the CF patient. The cause of this remains unknown. Although the etiology of the decreased cyclic AMP responses in CFH was not due to decreased beta adrenergic receptors as assessed by antagonist ligand binding, further studies inthe CFH group to include agonist binding, receptor-adenylate cyclase coupling, intrinsic adenylate cyclase activity, and catecholamine metabolism may help determine the basic cause of beta adrenergic hyperesposiveness in both CFH and CF.

Adolescent↗
PubMed1980

[Addison's disease in pregnancy (author's transl)].

A rare case of Addison's disease in pregnancy in a 20 year old gravida: 2 para: 0 is described. The patient was admitted at 31 weeks gestation with premature labor. The patient was on cortisone therapy for Addison's disease prior to the pregnancy. this was continued. Premature labor was stopped and a 2350 g. male infant was delivered at term. The prenatal and post-natal treatment is described. The seven most important points in treatment of Addition's disease during pregnancy are listed.

Addison Disease↗
PubMed1979

Solitary rectal ulcer progressing to pseudo-cloaca: a case report.

A 57 year old diabetic patient is reported with the progression of a solitary ulcer of the anterior rectal wall which resulted in destruction of the posterior bladder wall, and subsequent pseudocloaca. The patient was successfully treated by colonic and urinary diversion. The etiology of this condition remains obscure. A review of the literature on this uncommon lesion is discussed.

Colostomy↗
PubMed1978

[The evaluation of cortisol in amniotic fluid and in maternal blood as parameter for foetal lung maturity (author's transl)].

The lecithin/sphingomyelin-ratio (L/S-ratio) in amniotic fluid has become established in recent years as a valuable laboratory parameter for determining foetal lung maturity and has thus helped to avoid the neonatal respiratory distress syndrome. Since glucocorticosteroids are a decisive factor in stimulating foetal lung development, we were prompted to investigate whether the determination of cortisol in amniotic fluid or maternal blood could also serve as an indicator of foetal lung maturity. The cortisol concentration was measured by radioimmunoassay in amniotic fluid (n = 91) and in maternal venous plasma (n = 70) from normal and complicated pregnancies and was compared with the L/S-ratio. A significant correlation between gestational age and cortisol in amniotic fluid (r = 0.711) and in maternal venous plasma (r = 0.625) was observed. There was also a significant correlation between the L/S-ratio and amniotic fluid cortisol (r = 0.701). However, compared to the L/S-ratio, measurements of cortisol yielded 10% false positive and 11% false negative results. A significant correlation between the L/S-ratio and the maternal plasma cortisol could also be demonstrated (r = 0.631). Here the comparison with the L/S-ratio gave even poorer results: 16% false positive and 6% false negative. The high percentage of false results, especially false positive results yielded by cortisol estimations in both fluids leads to the conclusion that the L/S-ratio remains the superior diagnostic parameter in determining foetal lung maturity.

Amniocentesis↗
PubMedDate not supplied

A closely linked genetic marker for cystic fibrosis.

Cystic fibrosis is a recessive genetic disorder, characterized clinically by chronic obstructive lung disease, pancreatic insufficiency and elevated sweat electrolytes; affected individuals rarely live past their early twenties. Cystic fibrosis is also one of the most common genetic diseases in the northern European population. The frequency of carriers of mutant alleles in some populations is estimated to be as high as 1 in 20, carrying a concomitant burden of about one affected child in 1,500 births. Because little is known of the essential biochemical defect caused by the mutant gene, a genetic linkage approach based on arbitrary genetic markers and family studies is indicated to determine the chromosomal location of the cystic fibrosis (CF) gene. We have now obtained evidence for tight linkage between the CF locus and a DNA sequence polymorphism at the met oncogene locus. This evidence, combined with the physical localization data for the met locus presented in the accompanying paper, places the CF locus in the middle third of the long arm of chromosome 7, probably between bands q21 and q31.

Chromosome Mapping↗