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Biomedical subjects

K Martin

Publications and source records attributed to K Martin.

At least 271 records · Page 15Linked to original sources
PubMed1978

Hypomagnesemia and impaired parathyroid hormone secretion in chronic renal disease.

Severe hypocalcemia secondary to magnesium depletion has been described in numerous patients with gastrointestinal disorders. The development of profound hypomagnesemia in chronic renal disease is a rare finding. We studied three patients with advanced renal failure and magnesium depletion. Severe hypocalcemia also was present in these patients. Despite hyperplasia of the parathyroid glands, the levels of immunoreactive parathyroid hormone (PTH) in blood were inappropriately low for the degree of renal insufficiency. After the administration of magnesium there was a significant increase in the levels of circulating i-PTH in serum with a concomitant improvement in the hypocalcemia.

Adult↗
PubMed1977

Degradation of parathyroid hormone and fragment production by the isolated perfused dog kidney. The effect of glomerular filtration rate and perfusate CA++ concentrations.

The renal degradation of intact bovine parathyroid hormone (b-PTH 1-84) was studied with the isolated perfused dog kidney. Disappearance of b-PTH 1-84 from the perfusate occurred concomitantly with the appearance of smaller molecular weight forms of immunoreactive parathyroid hormone (PTH). These smaller molecular weight PTH fragments included both carboxyl and amino terminal regions of the PTH peptide. Perfusate from kidneys with lower glomerular filtration rates (GFR) contained b-PTH 1-84 for longer periods of time than kidneys with higher GFRs, and perfusate from kidneys with lower GFRs demonstrated greater accumulation of carboxyl terminal PTH fragments. Perfusate containing high Ca++ concentrations retarded, and perfusate with low Ca++ concentrations accelerated the rate of degradation of b-PTH 1-84 by the kidney. These studies, therefore document the production of PTH fragments during the course of intact hormone degradation by the kidney. They also demonstrate renal clearance of the PTH fragments produced and define the effects of glomerular filtration rate and calcium concentrations on degradation of intact hormone and the clearance of PTH fragments.

Animals↗
PubMed1977

Hyperphosphatemia.

Serum phosphorus concentrations are maintained within narrow limits in humans. In the extracellular fluid most of the phosphorus is present in the inorganic form and at the level of the glomerulus greater than 90% of PO4 is ultrafilterable. The kidney plays a key role in PO4 homeostasis. Micropuncture experiments have demonstrated that 60 to 70% of the filtered PO4 is reabsorbed in the proximal tubule; however, there is evidence that a significant amount of PO4 is reabsorbed in the distal tubule. Phosphate secretion probably plays a minor role in the overall renal regulation of phosphate. In normal individuals the amount of PO4 ingested plays a key role in the amount that ultimately will be excreted in the urine. The reabsorption of PO4 along the nephron is regulated by a series of factors of which parathyroid hormone is the most important one. Hyperphosphatemia is seen frequently in clinical medicine and by far, the most common cause is a decrease in urinary PO4 excretion secondary to renal failure. From the practical point of view, the most effective way to treat hyperphosphatemia is to decrease PO4 absorption in the GI tract by the use of PO4 binders.

Acromegaly↗
PubMed1976

[Parinaud's syndrome in non-tumorous hydrocephalic intracranial hypertension].

Four cases (3 children and one adolescent) are presented in which Parinaud's syndrome developed in the course of progressive non-tumorous hydrocephalus. The vertical gaze palsy completely disappeared in all cases some days after raised intracranial pressure had been successfully treated. Neuroradiological findings indicate that Parinaud's syndrome can be elicited by a dorsal midbrain compression due to a markedly dilated suprapineal recess. Other contributing factors as distortion and compression of distal branches of the posterior cerebral artery in the cisterna ambiens region and an axial caudal displacement of the oral brain stem may be involved. According to the few cases published in the literature, the vertical gaze palsy seems to occur predominantly in benign connatal aqueduct stenosis and may then be regarded as a relatively early symptom of decompensating hydrocephalic intracranial pressure.

Adult↗
PubMed1976

An irreversible effect of lithium administration to patients.

1 Lithium administration to patients leads to a pronounced inhibition (about 90%) of the choline transport system in erythrocytes. The transport system does not recover when ghosts are prepared from the erythrocytes, thereby removing intracellular as well as extracellular lithium. 2 When a patient is taken off lithium, the choline transport in erythrocytes recovers only very slowly over a period of three months, i.e. at about the same rate at which the erythrocytes that had been exposed to lithium are replaced by new cells. 3 It is concluded that therapeutic concentrations of lithium produce an irreversible inhibition of the choline transport system in human erythrocytes.

Cell Membrane↗
PubMed1976

Selective uptake of intact parathyroid hormone by the liver: differences between hepatic and renal uptake.

Hepatic and renal extraction of immunoreactive parathyroid hormone (i-PTH) was studied in awake dogs with explanted kidneys and chronic indwelling hepatic vein catheters. After a single injection of bovine PTH 1-84 (b-PTH 1-84), hepatic arteriovenous (A-V) differences for immunoreactive PTH (i-PTH) was 39% at 2 min after injection but decreased to 0% by 25 min, despite high levels of i-PTH in the arterial circulation. Gel filtration of arterila and hepatic venous samples obtained when hepatic A-V differences for i-PTH were demonstrable revealed hepatic uptake of the intact hormone and addition of a smaller COOH-terminal fragment, eluting just after the intact hormone, to the hepatic venous blood. Gel filtration of samples obtained 20-30 min after injection of b-PTH was demonstrable) revealed no detectable intact hormone in the circulation. Levels of COOH-terminal fragments of the hormone at the time were identical in arterial and hepatic venous samples. In additional experiemtns no hepatic A-V difference was observed after the injection of the synthetic bovine PTH 1-34 (syn b-PTH 1-34). By comparison there was a demonstrable A-V difference of 20% across the kidney for both intact PTH and COOH-terminal fragments that persisted until i-PTH disappeared from the circulation. The kidney also demonstrated an A-V difference of 22% after injection of syn b-PTH 1-34. These studies demonstrate selective extraction of intact PTH but not of its fragments by the liver. The kidney, on the other hand, extracted the intact hormone and both COOH and NH2 terminal fragments. The studies demonstrate that the kidney was the only organ of those examined that detectably removed the fragments of PTH from the circulation.

Animals↗
PubMed1976

[The role of diastematomyelia in the differential diagnosis and treatment of kyphoscoliotic paraplegia].

By its frequent association with malformative scoliosis and neurological symptoms diastematomyelia has an important place in the diagnostic and treatment of cyphoscoliotic neurological syndromes. In all these cases and even in cases without neurological deficits the diagnosis of disatematomyelia should be done by routine myelography. The indication for operation is often curative in cases with neurological signs and prophylactic in those without.

Adolescent↗
PubMed1976

[Diastematomyelia--its importance in the treatment of congenital scoliosis].

The risk of neurologic complications following corrective surgery in congenital scoliosis is ten times greater than in idiopathic scoliosis, the main reasons being transfixation of the spinal cord by diastematomyelia or by other adhesions of the spinal cord. Therefore preoperative myelography is advisable in congenital scoliosis. The typical findings from 3 cases of diastematomyelia, as shown by myelography and by operation, are presented. The clinical and x-ray features are shown as well as neurological signs, which are easily overlooked.

Child↗
PubMed1972

Extracellular cations and the movement of choline across the erythrocyte membrane.

1. The ability of human erythrocytes to accumulate choline is abolished when external Na is replaced by Cs, Rb, K or Li but is increased when the external cation is Mg or Ca.2. The unidirectional influx of choline is reduced when external Na is replaced by other monovalent cations but is not changed when Na is replaced by Mg or Ca.3. The unidirectional efflux of choline into a choline-free medium is increased when external Na is replaced by other monovalent cations and markedly reduced when Na is replaced by Mg or Ca. When the external medium contains 1 mM choline, changing the external cation has virtually no effect on the rate of choline efflux.4. When the extracellular concentrations of K and Na are similar to that found in the intracellular water, choline appears to become passively distributed across the cell membrane; when the extracellular K is then replaced by Cs a net efflux of choline against a concentration gradient results.5. It is concluded that the choline carrier may be described as a cation carrier with a high affinity for choline and affinities for Cs > Rb > K > Li > Na and that these monovalent cations can cross the membrane on the choline transport system.

Biological Transport, Active↗
PubMed1971

Some properties of an SH group essential for choline transport in human erythrocytes.

1. The choline transport system in human erythrocytes is inhibited by N-ethylmaleimide (NEM), cystamine and p-chloromercuribenzene sulphonic acid (PCMBS).2. External choline increases the rate of inhibition by NEM and cystamine but decreases the rate of inhibition by PCMBS. Intracellular choline has the opposite effect.3. Competitive inhibitors of choline transport that are not themselves transported protect the carrier against all three thiol reagents.4. Some thiol reagents with a very low lipid solubility do not inhibit choline transport.5. The transport inhibition by cystamine is reversed by various reducing agents.6. Cystamine protects the transport system against NEM and PCMBS.7. It is suggested that NEM and cystamine react with an SH group of the transport system and that this SH group is more reactive when the carrier is facing inside. PCMBS penetrates erythrocytes only very slowly and is assumed to react preferentially with the outward facing carrier.8. The reactive SH group seems to be located in a lipophilic environment.

Biological Transport, Active↗