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Biomedical subjects

J Ludwig

Publications and source records attributed to J Ludwig.

At least 217 records · Page 12Linked to original sources
PubMed1987

Thyrocalcitonin-containing cells in the Di George anomaly.

The Di George syndrome is an anomaly characterized by the complete or partial absence of derivatives of the third and fourth pharyngeal pouches often associated with defective development of the third, fourth, and sixth aortic arches leading to absence or hypoplasia of the thymus and parathyroid glands and to cardiovascular anomalies. The fifth pharyngeal pouch, often considered a part of the fourth pouch, gives rise to the ultimobranchial body (UB), which becomes incorporated into the thyroid gland and is thought to be the source of thyroid C cells. Robinson suggested that complete or partial absence of the UB should be considered a part of the Di George anomaly. To substantiate this theory, the thyroid glands of 11 patients with the Di George syndrome and 11 age-matched control infants were examined immunohistochemically using the immunoperoxidase technique for presence or absence of thyrocalcitonin (TC)-containing cells. Only three of 11 patients with the Di George syndrome had TC-containing cells in their thyroid glands (27 per cent), and nine of 11 control infants had these cells (82 per cent). It is concluded that thyroid C cell deficiency is present in most patients with Di George anomaly, suggesting a relationship between these cells and development of derivatives of the third through fifth visceral pouches. Furthermore, there is a spectrum of deficiency of thyroid C cells in these individuals comparable with the spectrum of partial to complete absence of third and fourth pharyngeal pouch derivatives regarding thymus and parathyroid glands. Immunostaining for TC of the lungs of all infants with the Di George syndrome and control infants revealed similar numbers of thyrocalcitonin-containing cells in both groups. Asynchronous development of thyroid and lung thyrocalcitonin-containing cells in those with the Di George syndrome favors the theory that the latter develop independently of derivatives of the third through fifth visceral pouches. This study further supports a neural crest origin of the Di George anomaly and strengthens the concept that the Di George anomaly is a neurocristopathy.

Calcitonin↗
PubMed1987

Coexistent pulmonary and portal hypertension: morphologic and clinical features.

Patients with portal hypertension of varying etiology may develop pulmonary artery hypertension. In the present autopsy study, pulmonary and hepatic tissue was studied in 12 patients in whom pulmonary and portal hypertension coexisted. Plexogenic pulmonary arteriopathy was present in 10 patients, 7 of whom had coexistent thromboembolic lesions. One patient had isolated medial hypertrophy, which may be an early stage in the plexogenic category, whereas isolated thromboembolic pulmonary vascular disease was observed in one subject. Hepatic disease was consistent with alcoholic cirrhosis in seven patients, cryptogenic cirrhosis in four and extrahepatic portal hypertension without cirrhosis in one. Thrombocytopenia was present in all 10 patients whose platelet count was determined. This study suggests that pulmonary hypertension associated with portal hypertension commonly has a plexogenic appearance on histologic examination. However, thrombosis (whether embolic or in situ) may also contribute to vascular obstruction.

Collateral Circulation↗
PubMed1987

Immunohistologic labeling as an indicator of liver allograft rejection.

Monoclonal antibodies were used to identify T-helper cells (TH) and T-suppressor/cytotoxic cells (TS/C) in biopsy specimens obtained 7, 21, 90, 180, and 365 days postoperatively, and during episodes of graft dysfunction, from 34 consecutive liver transplant patients treated with cyclosporine and steroids. Rejection was diagnosed by the presence of appropriate laboratory and light microscopic findings and at least 8 weeks of follow-up to exclude other causes of graft dysfunction. Four immunohistologic patterns were seen--no labeled cells (No), only lobular TS/C, only portal TH, and a portal mixture of TH and TS/C (mix). Of 36 specimens with the No or only lobular TS/C pattern, 29 were not associated with rejection. Of the 39 specimens with the portal TH or portal Mix pattern, 33 were associated with a rejection episode. In addition, in nine specimens from patients with no biochemical or routine histologic evidence of rejection, the presence of portal TH or a portal mix indicated immunologic rejection 5 days to 5 weeks before biochemical and routine histologic evidence of it was manifested. Immunohistologic labeling appears to be an early indicator of liver allograft rejection.

Antibodies, Monoclonal↗
PubMed1987

Assessing the autopsy.

This study outlines the role of autopsies in medical practice and health policy, details the nature and reason for declining rates, including those in Rochester, Minnesota, and suggests possible remedial measures to halt or reverse this trend. It is concluded that one of the principal impediments to reversing the declining rate of autopsies is what is referred to in Economics as "market failure." In particular, the nature of the spatial and temporal distribution of costs and benefits has precluded the existence of an incentive structure which can lead to a realization of the major net social benefits from the autopsy. Ultimately, it is only the explicit recognition by the medical profession, government agencies, corporate insurers, and the general public of the nature and significance of this market failure and foregone benefits which can lead to remediation.

Age Factors↗
PubMed1986

The effect of partial inhibition of monoamine oxidase on the steady-state rate of deamination of 3H-catecholamines in two metabolizing systems.

Two different "deaminating systems" were compared (i.e., intact tissues in which an uptake process translocates the 3H-catecholamine from the extracellular space to the intracellular MAO): the adrenergic nerve endings of the rat vas deferens exposed to 10 nmol/l 3H-(-)-noradrenaline, and the extraneuronal deaminating system of the rat heart perfused with 50 nmol/l 3H-(-)-adrenaline. Vesicular uptake and COMT were inhibited. In both systems MAO was partially inhibited by pargyline, and the steady-state tissue content of the 3H-catecholamine was determined as well as the steady-state rate of deamination. Rat vas deferens (preincubated with 10-40 nmol/l pargyline for 30 min). Inhibition of neuronal MAO caused not more than a moderate decrease of the steady-state rate of deamination of 3H-(-)-noradrenaline, but the steady-state tissue content was greatly increased. Determinations of the activity of MAO in homogenates of vasa deferentia showed that preincubation with 10 and 20 nmol/l pargyline inhibited the enzyme by 80 to 95%. Rat heart (of animals pretreated with 1 to 30 mg/kg pargyline). Inhibition of extraneuronal MAO caused a steep decline of the steady-state rate of deamination of 3H-(-)-adrenaline, but only a small rise in the steady-state tissue content. The decisive difference between the two deaminating systems lies in the fact that the ratio "kmao/kout" (where the two k-values characterize the activity of the unsaturated intracellular MAO and the ability of the 3H-catecholamine to leave the relevant cells, respectively) is much higher for the neuronal deaminating system exposed to 3H-(-)-noradrenaline than for the extraneuronal deaminating system exposed to 3H-(-)-adrenaline.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Inhibition by K+ of uptake2 of 3H-(+/-)-isoprenaline in the perfused rat heart.

The kinetics of the inhibitory effect of extracellular K+ on uptake2 of 3H-(+/-)-isoprenaline were determined in isolated hearts obtained from reserpine-pretreated rats; catechol-O-methyl transferase was inhibited. Initial rates of uptake2 of a very low concentration of 3H-(+/-)-isoprenaline (10 nmol/l) were determined in the presence of various extracellular concentrations of K+ (2.7 to 60 mmol/l). The inhibitory effect of K+ was concentration-dependent with an IC50 of about 20 mmol/l. - In these experiments KCl was added to the perfusion solution, and some hypertonicity resulted. In some experiments NaCl was added to a solution containing 5 mmol/l K+ to result in the same degree of hypertonicity as that obtained for 60 mmol/l K+; hypertonicity increased the initial rate of uptake2 of 3H-(+/-)-isoprenaline. Thus, the inhibitory effect of K+ had been slightly underestimated. In subsequent experiments the increase of the concentration of K+ in the perfusion fluid to 30 mmol/l was compensated for by a corresponding reduction of Na+. Initial rates of uptake2 of 10 nmol/l 3H-(+/-)-isoprenaline were determined in the absence and presence of various concentrations of unlabelled (+/-)-isoprenaline. At 30 mmol/l K+ the IC50 (= Km for uptake2) did not significantly differ from that determined in an earlier study at 2.7 mmol/l K+ (Grohmann and Trendelenburg 1984). Finally, the Vmax for uptake2 of 3H-(+/-)-isoprenaline was determined at either 2.7 or 30 mmol/l K+. At 30 mmol/l K+ the Vmax was only about 1/4 of that observed at 2.7 mmol/l K+.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Frequency and significance of antimitochondrial antibodies in severe chronic active hepatitis.

Of 187 patients with severe chronic active hepatitis, 37 (20%) had antimitochondrial antibodies, usually of low titer (less than or equal to 1:40). To assess the significance of this finding and to identify differentiating features from primary biliary cirrhosis, 24 of these patients were compared to two groups of matched counterparts of which one lacked antimitochondrial antibodies and one had the antibodies together with typical primary biliary cirrhosis. Higher serum levels of alkaline phosphatase and an increased frequency of stainable hepatic copper were the only features that distinguished these patients from those without antimitochondrial antibodies. The response to corticosteroids was not influenced by antibody status. Histologic interpretation differentiated primary biliary cirrhosis from antibody-positive chronic active hepatitis in 91% of instances. High antibody levels (greater than or equal to 1:160), immunoglobulin M concentrations (greater than or equal to 6.0 mg/ml), alkaline phosphatase activity (greater than or equal to fourfold normal), and cholesterol elevations (greater than or equal to 300 mg/dl) separated the syndromes in 82% of instances. Patients with laboratory features of primary biliary cirrhosis but histologic findings of chronic active hepatitis responded to corticosteroids. We conclude that low titers of antimitochondrial antibodies are common in chronic active hepatitis, and the presence of these antibodies does not preclude a satisfactory response to corticosteroids. Histologic features are more reliable than biochemical findings in differentiating the syndromes and should be the basis for diagnosis and treatment.

Adrenal Cortex Hormones↗
PubMed1986

Fulminant Wilson's disease treated with postdilution hemofiltration and orthotopic liver transplantation.

A 22-yr-old woman presented with fulminant Wilson's disease. The diagnosis was suspected clinically and was later confirmed with chemical and pathologic studies. She presented with acute hepatic failure, hemolysis, and acute anuric renal failure. Postdilution hemofiltration and continuous arteriovenous hemofiltration with oral D-penicillamine allowed removal of a total of 95,700 micrograms of copper; 78,665 micrograms of the total were removed via postdilution hemofiltration alone. On the 57th day, the patient received successful liver and renal transplants. We found that the determination of serum copper was instrumental in the diagnosis of fulminant Wilson's disease, that postdilution hemofiltration allowed a rapid removal of copper in the presence of renal failure, and that, finally, orthotopic liver transplantation should be performed early in the clinical course of these patients. This patient is the longest survivor of this serious condition.

Acute Disease↗
PubMed1986

[Postnatal development of the sympathoadrenergic system in premature and newborn infants].

Autonomic regulatory mechanisms and some metabolic functions are predominantly influenced by the sympathetic nervous system. Premature and mature newborns show a high variability and a low adaptability of the sympathetic nervous system. In order to investigate whether sympathetic systems are completely developed at birth or underly a postnatal maturation process we have determined plasma levels of adrenaline and noradrenaline as well as the density and affinity of alpha- and beta-adrenoceptors on thrombocytes and lymphocytes in pre- and mature newborns and adults. Catecholamines were determined by means of a radioenzymatic method, number and affinity of adrenoceptors by use of the radioactive labelled antagonists 3-H-Yohimbine and 125-I-Cyano-Pindolol. Beta-adrenoceptor responsiveness was assessed by measurement of cyclic AMP in lymphocytes before and after stimulation of beta-adrenoceptors by isoprenaline. A linear relationship occurred between the gestational age and the number of adrenoceptors on lymphocytes, whereas the alpha-adrenoceptors on thrombocytes showed no age dependency. The basal content of cyclic AMP and the accumulation in response to beta-adrenoceptor stimulation by isoprenaline was significantly lower in newborns than in adults. Since noradrenaline and adrenaline plasma levels were not significantly different in newborns and adults it is assumed that the low density of beta-adrenoceptors in premature and mature newborns is due to a postnatal maturation and not to a "down regulation" by circulating catecholamines. Our results suggest that an immaturity of beta-adrenoceptors is involved in the poorly developed adaptive control in newborns.

Adult↗
PubMed1985

Trial of penicillamine in advanced primary biliary cirrhosis.

A total of 227 patients with histologically advanced primary biliary cirrhosis entered a double-blind, randomized, controlled trial to determine whether penicillamine (1 g per day) was therapeutically effective; 111 patients received the drug, and 116 received placebo. The two groups were highly comparable at entry with regard to clinical, biochemical, and histologic features. Penicillamine therapy did not result in an overall improvement in survival as compared with placebo. Clinical symptoms and serial hepatic laboratory values reflected the progressive nature of the disease and were similar in both groups. There were no substantial differences between treatment groups in the morphologic features of sequential biopsy specimens. The development of major side effects led to permanent discontinuation of penicillamine in 22 per cent of the patients taking the drug. We conclude that penicillamine is not useful for patients with histologically advanced primary biliary cirrhosis. The trial is being continued in patients with early histologic disease whose better prognosis necessitates longer follow-up.

Clinical Trials as Topic↗