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Biomedical subjects

W M Burch

Publications and source records attributed to W M Burch.

At least 55 records · Page 3Linked to original sources
PubMed1983

Normal menstruation and pregnancy in a patient with Nelson's syndrome.

The patient with Nelson's syndrome in this report represents an unusual case in which regular cyclic menstruation was preserved even though a large ACTH-producing pituitary adenoma was present. Despite normal menses and pregnancy, the radiologic findings of an enlarged sella turcica and an enhanced lesion on CAT scan were identified. This case demonstrates that patients with normal menstruation can have significant pituitary disease, and it exemplifies the need for regular follow-up examination to look for radiologic abnormalities in patients who have had adrenalectomy for treatment of Cushing's disease.

Adenoma↗
PubMed1983

Deficient adenylate cyclase regulatory protein in renal membranes from a patient with pseudohypoparathyroidism.

Recent studies have established that some patients with pseudohypoparathyroidism have a deficiency of the adenylate cyclase regulatory protein (the G unit) in plasma membranes from erythrocytes, platelets, and fibroblasts. We have directly measured the activity of the G unit in renal membranes from a patient with pseudohypoparathyroidism who, in addition to parathyroid hormone resistance, has resistance to thyrotropin and gonadotropins. Erythrocyte membrane G unit activity was 57% that of control erythrocyte membranes. Lubrol PX extracts of renal membranes had only 30% of the G unit activity of control renal membrane extracts, whether assayed with sodium fluoride or guanosine-5'-O-(3-thiotriphosphate) (GTP-gamma-S). In cholate extracts, the G unit activity was 37 and 48% of control with fluoride or GTP-gamma-S, respectively. Cholera toxin-dependent incorporation of [32P]ADP-ribose into the 42,000-Mr subunit of the G unit was decreased in renal membranes from the patient compared with control renal membranes. The data demonstrate that the membrane G unit deficiency in pseudohypoparathyroidism extends to the cells of a clinically relevant parathyroid hormone target tissue.

Adenylyl Cyclases↗
PubMed1983

Hypoparathyroidism after I-131 therapy with subsequent return of parathyroid function.

A 22-year-old woman developed hypoparathyroidism in 1970, 10 months after treatment of hyperthyroidism with I-131. The hypocalcemia was corrected with Vitamin D2 and oral calcium and she remained normocalcemic for 8 yr. In 1979 hypercalcemia was found and Vitamin D2/calcium was discontinued. Because she remained normocalcemic without therapy for 3 yr, we measured the levels of immunoreactive and bioactive PTH in plasma stored since 1970 and in plasma obtained in 1982 to determine whether there had been restoration of parathyroid function. Indeed, PTH levels in 1970 while the patient was hypocalcemic were low. The bioactive PTH was 0.26 pg/ml (normal 1.5-30), whereas--COOH terminal immunoreactive PTH was 620 pg/ml (normal 600-1500) and midmolecule immunoreactive PTH was 433 pg/ml (normal 300-900). In 1982 while normocalcemic the bioactive PTH and immunoreactive PTH were normal (5.18 pg/ml;--COOH, 970 pg/ml; midmolecule, 789 pg/ml, respectively). Thus, an unusual case of hypoparathyroidism after I-131 therapy with return of parathyroid function is documented by measurements of both immunoreactive and bioactive PTH.

Adult↗
PubMed1982

Urine free-cortisol determination. A useful tool in the management of chronic hypoadrenal states.

The clinical value of urine free-cortisol (UFC) determination in the management of hypoadrenal states in patients receiving maintenance glucocorticoid therapy was assessed. Nine patients with primary adrenal insufficiency collected five 24-hour urine specimens while taking their usual oral dose of cortisone acetate or hydrocortisone. Each urine sample was assayed for UFC and creatinine. The range of UFC level for the group was from 9.4 to 43 micrograms/24 hr (10 to 21 micrograms/g of creatinine). However, for each patient the amount of UFC showed little day-to-day variation, with the coefficient of variation ranging from 8% to 26%. The UFC values of the patients with hypoadrenalism who were receiving treatment were well within the values of UFC in the control population (n = 523). Four cases illustrating the usefulness of UFC determination in patients receiving an oral maintenance regimen of hydrocortisone or cortisone are presented. The UFC is a useful biochemical marker that correlated clinically with glucocorticoid deficiency or excess in patients with hypoadrenalism receiving maintenance steroid replacement.

Addison Disease↗
PubMed1982

In vitro stimulation of alkaline phosphatase activity in immature embryonic chick pelvic cartilage by adenosine 3'5'-monophosphate.

Cyclic AMP content in embryonic chick pelvic cartilage increases significantly as the embryo ages from 8 to 10 d. This in ovo elevation in cyclic AMP content precedes maximal cartilage alkaline phosphatase activity by some 24 h. We studied whether this temporal relationship may be causally related, using an in vitro organ culture. Incubation of pelvic cartilage from 9- and 10-d embryos in medium containing monobutyryl cyclic AMP (BtcAMP) resulted in significant increases in alkaline phosphatase activity (220 and 66 percent, respectively) as compared to that of cartilages incubated in medium alone. This stimulation was both concentration- and time-dependent with maximal response at 0.5 mM BtcAMP and 4-h incubation, respectively. Similar incubations of cartilage in medium containing 1-methyl-3-isobutyl xanthine (MIX), 0.25 mM, also resulted in increased alkaline phosphatase activity (114 percent). However, pelvic cartilage from 11-d embryos incubated in medium containing BtcAMP or MIX showed no increase in alkaline phosphatase activity. We postulated that developmental age was the factor responsible for this difference in response and that immature cartilage (that with little or no alkaline phosphatase activity) would respond to BtcAMP whereas mature cartilage (that with significant alkaline phosphatase activity) would not. This was tested by incubating end sections of 11-d cartilage, which have little alkaline phosphatase activity, and center sections, which have significantly alkaline phosphatase activity, with both BtcAMP and MIX. Alkaline phosphatase activity in end sections (immature cartilage) was stimulated by BtcAMP and MIX, whereas it was not stimulated in the center sections. Actinomycin D and cycloheximide inhibited BtcAMP and MIX stimulation of alkaline phosphatase activity. Thus, the in vitro data suggest that cyclic AMP is a mediator for the stimulation of alkaline phosphatase activity in embryonic cartilage.

1-Methyl-3-isobutylxanthine↗
PubMed1982

Triiodothyronine stimulates maturation of porcine growth-plate cartilage in vitro.

We studied the effect of triiodothyronine (T3) on mammalian growth-plate cartilage in vitro. Growth-plate cartilages from fetal pigs scapulae were incubated for 3 to 7 d in serum-free medium alone or medium containing T3. Alkaline phosphatase activity, a marker of hypertrophied chondrocytes, was increased in T3 (10 nM)-treated growth-plate cartilage 152 +/- 36% above that of cartilage incubated in medium alone after 3 d of incubation, and 324 +/- 47% after 7 d of incubation. There was a dose-response increase in alkaline phosphatase activity to T3 over the range of 0.01-10 nM. The rise in alkaline phosphatase activity was specific for T3 since growth-plate cartilage alkaline phosphatase activity was not increased by cortisol, insulin, parathyroid hormone, or 5% fetal calf serum. Histological studies of growth-plate cartilage showed that T3 in a concentration-dependent manner increased the width of the zone of maturation (hypertrophied chondrocytes). Histochemical staining for alkaline phosphatase activity demonstrated that T3 caused the recruitment of new cells into the zone of maturation. T3 also stimulated incorporation of L-[3H]leucine into protein and 35SO4 into proteoglycan in growth-plate cartilage. In contrast, T3 did not increase alkaline phosphatase activity or radiolabeled precursor incorporation into nongrowth-plate scapular cartilage. These studies demonstrate that T3 directly stimulates maturation and, to a lesser degree, growth-related processes in fetal mammalian growth-plate cartilage.

Alkaline Phosphatase↗
PubMed1982

Triiodothyronine stimulation of in vitro growth and maturation of embryonic chick cartilage.

We studied the direct effect of T3 on cartilage growth and maturation in vitro. Pelvic cartilages from 9-day-old chick embryos were incubated in a serum-free organ culture system which supported cartilage growth over a 5-day interval. The addition of T3 (15 nM) to the medium increased cartilage wet weight (approximately 100%), dry weight (77%), length (35%), and total soluble protein (67%) over 3 days compared to cartilage incubated in medium alone. The DNA content was only slightly increased (2%) by T3 over the interval. T3 stimulated the same parameters of growth similarly after 5 days of incubation. In addition, T3 increased the incorporation of [14C]leucine into protein (82%) and 35SO4 into proteoglycan (53%). A dose-dependent increase in cartilage wet weight was seen with T3 (0.0015-15 nM) over 3 days of incubation. Cartilage incubated with T3 demonstrated microscopic changes in maturation, with development of large numbers of hypertrophied chondrocytes, and biochemical evidence of maturation, with increased alkaline phosphatase activity (130%). The dose-response range for T3 stimulation of alkaline phosphatase activity (0.015-0.15 nM) was considerably more restricted than that for stimulation of growth (0.0015-15 nM). These studies demonstrate that T3 in physiological concentrations directly affects cartilage growth and maturation, primarily through stimulating chondrocyte hypertrophy.

Animals↗
PubMed1982

Induction of cellular immunity to Coccidioides immitis after sensitization with dinitrochlorobenzene.

A patient had progressive disseminated coccidioidomycosis and depressed cellular immunity to Coccidioides immitis. He developed a large nasal coccidioidal lesion that was unresponsive to conventional therapy. Application of dinitrochlorobenzene (DNCB) to the nasal lesion was temporally associated with resolution of the lesion and stabilization of the systemic disease. In addition, DNCB application was followed by signs of cellular immunity to C. immitis. These included development of delayed cutaneous hypersensitivity to coccidioidin, as well as lymphokine production and lymphoproliferative responses to coccidioidin. Similar forms of DNCB immunotherapy may prove useful in other patients with fungal disease and depressed cellular immunity.

Adult↗
PubMed1981

Hormonal activation of ornithine decarboxylase in embryonic chick pelvic cartilage.

We assessed whether hormones and metabolic factors known to stimulate anabolic processes in the embryonic chick pelvic cartilage would stimulate ornithine decarboxylase (ODC) activity. In vitro organ culture of these pelvic cartilages in time-course experiments with N(6)-monobutyryl cyclic AMP (BtcAMP), insulin, and 5% rat serum demonstrated maximal stimulation of ODC activity between 4 and 6 h with each factor. However, at 2 h insulin and serum significantly stimulated ODC activity (P less than 0.05) and BtcAMP did not. ODC was stimulated above control (100%) with the following factors: parathyroid hormone (PTH) (555 +/- 15%), BtcAMP (324 +/- 34%), 1-methyl-3-isobutylxanthine (MIX) (223 +/- 6%), prostaglandin E1 (PGE1) (227 +/- 15%), 3,3',5-triiodothyronine (T3) (184 +/- 22%), insulin (182 +/- 14%), multiplication-stimulating activity (MSA) (178 +/- 6%), 5% rat serum (253 +/- 57%). THe increase in ODC activity seen with BtcAMP and insulin was not due to a change in Km or a decreased rate of degradation of the enzyme. Actinomycin D (1 microgram/ml) inhibited stimulation of ODC activity by T3 and the cyclic AMP-mediated factors (PTH, BtcAMP, MIX, PGE1), but had only minimal effects on ODC stimulation by insulin, MSA, or serum. Amanitin inhibited both BtcAMP and T3 stimulation of ODC, but had no effect on insulin stimulation of ODC. Thus, hormones and metabolic factors known to stimulate anabolic processes in chick embryonic pelvic cartilage also increase ODC activity through at least two mechanisms: transcriptional (cyclic AMP-mediated and T3) and posttranscriptional (insulin, serum, MSA).

1-Methyl-3-isobutylxanthine↗
PubMed1981

Adenosine 3',5'-monophosphate: a modulator of embryonic chick cartilage growth.

We tested the hypothesis that cyclic AMP plays a significant role in modulating the growth of embryonic chick cartilage by determining whether cyclic AMP levels change in growing embryonic cartilage and whether cyclic AMP could stimulate embryonic cartilage growth in a long term in vitro organ culture. Cyclic AMP levels were low (0.1 pmol/mg wet wt) in 8-d chick embryo pelvic cartilage, and increased progressively through the 11th d of embryonic development at which time they reached a maximum (1.8 pmol/mg wet weight) and thereafter remained constant. We developed an in vitro organ culture system to determine whether cyclic AMP, a factor known to stimulate radiolabeled precursor incorporation into macromolecules in short-term studies does, in fact, stimulate growth of cartilage. Individual pelvic cartilages were isolated from 9-d chick embryos, placed in serum-free medium (BGJb-FJ modification) and incubated for 3 to 5 d during which time they increased in size (39 and 60% in length, respectively), wet weight (90 and 141%, respectively), and content of total soluble protein (30 and 48%, respectively). N6-monobutyryl cyclic AMP (BtcAMP) added to the medium caused a dose-dependent (0.05 to 1.0 mM) stimulation of growth. After 3 d of incubation, 1.0 mM BtcAMP increased wet weight (125%), [14C]leucine incorporation into protein (75%), and [3H]thymidine incorporation into DNA (48%) compared with control cartilages incubated in medium alone. 1-methyl-3-isobutyl xanthine, a phosphodiesterase inhibitor, also increased cartilage growth above control while sodium butyrate, AMP, and ATP had no effect. Histological examination of cartilage grown in medium was similar to that of cartilage developing in ovo, whereas, cartilage grown in medium containing BtcAMP showed marked hypercellularity with many immature chondrocytes. Our observations are compatible with the hypothesis that cyclic AMP can significantly modulate the growth of embryonic cartilage.

1-Methyl-3-isobutylxanthine↗
PubMed1980

Specific nuclear binding of adenosine 3',5'-monophosphate-binding protein complex with subsequent poly(A) RNA synthesis in embryonic chick cartilage.

We used embryonic chick pelvic cartilage as a model to study the mechanism by which cyclic AMP increases RNA synthesis. Isolated nuclei were incubated with [32P]-8-azidoadenosine 3,5'-monophosphate ([32P]N3cAMP) with no resultant specific nuclear binding. However, in the presence of cytosol proteins, nuclear binding of [32P]N3cAMP was demonstrable that was specific, time dependent, and dependent on a heat-labile cytosol factor. The possible biological significance of the nuclear binding of the cyclic AMP-protein complex was identified by incubating isolating nuclei with either cyclic AMP or cytosol cyclic AMP-binding proteins prepared by batch elution DEAE cellulose chromatography (DEAE peak cytosol protein), or both, in the presence of cold nucleotides and [3H]uridine 5'-triphosphate. Poly(A) RNA production occurred only in nuclei incubated with cyclic AMP and the DEAE peak cytosol protein preparation. Actinomycin D inhibited the incorporation of [3H]uridine 5'-monophosphate into poly(A) RNA. The newly synthesized poly(A) RNA had a sedimentation constant of 23S. Characterization of the cytosol cyclic AMP binding proteins using [32P]N3-cAMP with photoaffinity labeling three major cAMP-binding complexes (41,000, 51,000, and 55,000 daltons). The 51,000 and 55,000 dalton cyclic AMP binding proteins were further purified by DNA-cellulose chromatography. In the presence of cyclic AMP they stimulated poly(A) RNA synthesis in isolated nuclei. The 51,000-dalton cyclic AMP-binding protein was the predominant one that bound to the nuclei. While cyclic AMP-dependent protein kinsae activity was present in the cytosol and DEAE peak cytosol proteins, it was not present in the DNA-cellulose-bound, cyclic AMP-binding proteins. We conclude that one possible mechanism by which cyclic AMP increases RNA synthesis is by complexing to a 51,000-dalton cytosol cyclic AMP-binding protein and being subsequently translocated to the nucleus, where it is specifically bound and associated with induction of poly(A) RNA synthesis.

Animals↗
PubMed1979

Pseudothyrotoxic myopathy: a complication of thionamide therapy in hyperthyroidism.

A hyperthyroid patient treated with methimazole for three weeks developed proximal muscle weakness, myalgia, arthralgia, and fever, and thyrotoxic myopathy was diagnosed. The signs and symptoms spontaneously abated when antithyroid medication was discontinued. This case identified a complication of thionamide treatment mimicking thyrotoxic myopathy and points to the therapeutic necessity of making such a differentiation.

Adult↗