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Biomedical subjects

K Martin

Publications and source records attributed to K Martin.

At least 253 records · Page 14Linked to original sources
PubMed1981

Borderline personality disorder: interrater reliability of the diagnostic interview for borderlines.

Three interviewers, working in pairs and using the Diagnostic Interview for Borderlines (DIB), interviewed three samples of 10 adult psychiatric inpatients. The two members of each interviewer pair alternated in the role of interviewer. Each member of the interviewer pairs completed the interview schedule and scored the protocol according to the instructions provided by the authors of the DIB. Interrater reliability was determined for each interviewer pair using the Kappa statistic. Reliability values were at about the level reported recently by Spitzer, Forman, and Nee (1979) for DSM-III axis I diagnoses in general. Additional statistical analyses were performed to determine whether there were patient sex differences on DIB scores, whether the two male interviewers differed from the female interviewer in their ratings of male or female patients, and whether experience differences among the three interviewers were reflected in their rating of patients. Among the latter analyses, the only significant finding was that in the interviewer pair consisting of a very experienced male psychiatrist and a male first year psychology graduate student, the former rated male patients as less borderline than did the latter. No other difference was found among raters, or between sex of patient and interviewer sex or amount of clinical experience. It was concluded that the DIB is sufficiently reliable for use in clinical research.

Adolescent↗
PubMed1981

Peripheral metabolism of intact parathyroid hormone. Role of liver and kidney and the effect of chronic renal failure.

The plasma disappearance rate (metabolic clearance rate) of administered intact parathyroid hormone (intact PTH) was analyzed in awake dogs with indwelling hepatic and renal vein catheters. The metabolic clearance rate (MCR) of intact PTH was found to be very rapid, 21.6 +/- 3.1 ml/min per kg in 11 normal dogs. The liver accounted for the greatest fraction of the MCR of intact PTH (61 +/- 4%) by virtue of an arterial minus venous (a - v) difference across the liver of 45 +/- 3%. The renal uptake of intact PTH accounted for 31 +/- 3% of the MCR of intact PTH. The renal a - v difference for intact PTH of 29 +/- 2% was significantly greater than the filtration fraction indicating renal uptake of intact PTH at sites independent of glomerular filtration. Together, the hepatic and renal clearances of intact PTH accounted for all but a small fraction of the MCR of intact PTH. The MCR of intact PTH, rendered biologically inactive by oxidation, was markedly decreased to 8.8 +/- 1 ml/min per kg. The a - v difference of oxidized intact PTH was reduced both in the liver and kidney. These data suggested that the high uptake rates of intact PTH are dependent, at least in part, upon sites recognizing only biologically active PTH. Chronic renal failure (CRF) decreased the MCR of intact PTH to 11.3 +/- 1.3 ml/min per kg (n = 10). Both the hepatic and renal a - v differences of intact PTH were reduced in dogs with CRF. This resulted in reductions in the hepatic and renal clearances of intact PTH. These studies identify the liver as a major extrarenal site of PTH metabolism affected by CRF. They suggest that CRF impairs the function of the major uptake sites involved in intact PTH metabolism.

Animals↗
PubMed1980

Long-term effect of lithium on the uptake of 5-hydroxytryptamine by human platelets.

1 The content, uptake and storage of 5-hydroxytryptamine (5-HT) in platelets were determined in eight manic-depressive patients not on lithium (Li); in ten manic-depressive patients on Li; and in ten apparently normal persons as controls. 2 Platelets from the patients, whether or not on Li, contained less 5-HT than platelets from normal people. 3 5-HT uptake and storage by platelets from untreated patients were significantly lower than those of control subjects. 4 When patients had been on Li for 3 months or longer the diminished uptake and storage of 5-HT by their platelets were more than fully reversed. 5 Li added to platelet-rich plasma in vitro had no effect on the uptake of 5-HT by platelets.

Adult↗
PubMed1980

Parathyroid hormone metabolism and its potential as a uremic toxin.

Secondary hyperparathyroidism is a universal complication of chronic renal failure. It has been proposed that the markedly elevated levels of immunoreactive parathyroid hormone (i-PTH) in uremia may represent a "uremic toxin" responsible for many of the abnormalities of the uremic state. Plasma i-PTH consists of a mixture of intact hormone, a single-chain polypeptide of 84 amino acids, and smaller molecular weight hormonal fragments from both the carboxy- and amino-terminal portion of the PTH molecule. The hormonal fragments arise from metabolism of intact PTH by peripheral organs as well as from secretion of fragments from the parathyroid glands. The structural requirements for the known biological actions of PTH reside in the amino-terminal portion of the PTH molecule. Carboxy-terminal fragments, biologically inactive at least in terms of adenylate cyclase activation, hypercalcemia, or phosphaturia, depend on the kidney for their removal from plasma, and thus accumulate in the circulation in chronic renal failure. It is unknown at the present time if other biological effects of these carboxy-terminal fragments may contribute to some of the biochemical alterations observed in uremia. The most significant consequence of increased PTH levels in uremia is the development of bone disease characterized by osteitis fibrosa. In addition, it would appear that PTH plays an important role in some of the abnormal electroencephalographic patterns observed in uremia. This may be due to a potential role of PTH in increasing calcium content of brain. Parathyroid hormone also has been implicated as a pathogenetic factor in many other alterations present in uremia, i.e., peripheral neuropathy, carbohydrate intolerance, hyperlipidemia, and other alterations. Unfortunately, outstanding clinical research is lacking in this field and conclusive experimental data are practically nonexistent. Further studies are necessary if one is to accept the concept of PTH being a significant "uremic toxin."

Animals↗
PubMed1980

Effects of parathyroid hormone on glucose production by the liver.

The present studies demonstrate a stimulatory effect of intact parathyroid hormone on hepatic glucose production in vivo. This increased glucose production was accompanied by augmented alanine uptake by the liver. In addition, PTH increased the conversion of 14C-alanine to 14C-glucose. These results suggest that the increased hepatic release of glucose produced by PTH is mediated in part by increased gluconeogenesis. On the other hand, the synthetic 1-34 amino terminal fragment of PTH, which is not extracted by the liver, did not stimulate hepatic glucose production.

Alanine↗
PubMed1980

Lack of a direct effect of 1,25-dihydroxycholecalciferol on parathyroid hormone secretion by normal bovine parathyroid glands.

Because of differing reports of an effect of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] on parathyroid hormone (PTH) secretion, the present studies were performed in vitro using bovine parathyroid gland slices and isolated parathyroid cells. Both COOH-terminal and NH2-terminal RIAs for PTH were employed. No effect of 1,25(OH)2D3 on PTH secretion was found during a 4-h incubation of parathyroid slices in variable external calcium concentrations. The results from dual RIA measurements also showed no effect of 1,25(OH)2D3 on PTH secretion by isolated parathyroid cells during 90- to 150-min incubations with variable calcium concentrations. In addition, extensive analysis by polyacrylamide gel electrophoresis showed no effect of 1,25(OH)2D3 on cAMP generation. Whereas calcium inhibited and isoproterenol stimulated the production of cAMP, 1,25(OH)2D3 had no effect. We conclude that 1,25(OH)2D3 does not affect parathyroid gland function acutely in vitro.

Animals↗
PubMed1979

Effect of intact parathyroid hormone on hepatic glucose release in the dog.

The liver has been shown to remove parathyroid hormone (PTH) from its arterial circulation by a mechanism that is selective for the intact form of the peptide (PTH 1-84). The present studies demonstrate that PTH has biologic effects on the liver in vivo. Bovine PTH 1-84 stimulated hepatic glucose release in dogs with indwelling hepatic vein catheters from basal values of 31+/-8 to 68+/-9 mg/min per kg after bolus injections of PTH. The effect on hepatic glucose release was apparent by 5 min and persisted for the 80 min of observation. The NH(2)-terminal PTH fragment (syn b-PTH 1-34) had no effect. Bovine PTH 1-84 administered in doses designed to produce circulating levels of immunoreactive PTH similar to the endogenous levels observed in uremic dogs also increased the incorporation of (14)C from infused [(14)C]alanine into glucose, and increased estimated hepatic uptake of both chemical and [(14)C]alanine, while increasing hepatic glucose release. Thus, administration of "physiologic levels" of b-PTH 1-84 stimulated hepatic glucose release in part through increased gluconeogenesis in vivo, whereas syn b-PTH 1-34 had no demonstrable effect. Circulating levels of insulin rose after PTH administration, an increase which presumably represents a secondary response to the rise in glucose release. These results suggest that the liver is a target organ of PTH, and that PTH might potentially alter carbohydrate metabolism during hypersecretion. They also suggest that hepatic uptake of PTH may be related in part to production of a specific biologic effect rather than just simple peptide degradation.

Animals↗