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Biomedical subjects

R Morecki

Publications and source records attributed to R Morecki.

At least 19 recordsLinked to original sources
PubMed1991

Hepatic pathology in pediatric acquired immunodeficiency syndrome.

In a retrospective study we assessed the hepatic changes in children with the acquired immunodeficiency syndrome by reviewing 12 biopsy specimens and 48 autopsy specimens from 54 children. Hepatopathology differed in biopsy and autopsy material. In biopsy specimens, chronic active hepatitis with predominantly T8 lymphocytes by tissue immunochemistry was common (five of 12 specimens). Fatty degeneration and hepatocellular necrosis were either absent, mild, or patchy. On the other hand, at autopsy, chronic active hepatitis was not observed. The most prominent changes were extensive fatty degeneration, nonspecific portal mononuclear infiltration, portal fibrosis, and confluent (ischemic) necrosis. Opportunistic infections such as Mycobacterium avium-intracellulare (MAI) were noted only at autopsy. In addition, three unusual morphologic characteristics were noted: nodular lymphoplasmacytic portal infiltrate, a pseudosarcomatous variant of Mycobacterium avium-intracellulare infection, and multinucleated giant cells (foreign both type and giant cell transformation of hepatocytes).

Acquired Immunodeficiency Syndrome↗
PubMed1991

Light- and electron-microscopical study of a case of gold salt-induced hepatotoxicity.

A 56-yr-old woman with long-standing rheumatoid arthritis exhibited jaundice, pruritus and abdominal discomfort after 8 yr of periodic gold sodium thiomalate injections amounting to a cumulative dose in excess of 2.5 gm. Histopathological examination of the liver biopsy specimen showed submassive loss of parenchyma, collapse of reticulin and mixed cellular inflammatory infiltrates. Macrophages contained dark granules, which displayed the characteristics of aurosomes when examined by transmission electron microscopy and electron microprobe analysis. It is likely that hepatocellular injury occurred when the lysosomal storage capacity for gold was exceeded.

Arthritis, Rheumatoid↗
PubMed1989

Central nervous system pathology in pediatric AIDS: an autopsy study.

The neuropathologic findings of brains and spinal cords removed at autopsy from 26 infants and children with AIDS is described; in two cases, only the spinal cords were available. The most common finding in the brains was dystrophic calcification of blood vessels of all calibers in the basal ganglia and deep cerebral white matter (21 og 24 cases). The next most frequent finding was subacute encephalitis (SE) (15 of 24 cases) with microglial nodules and multinulceated giant cells. Immunocytochemical and in situ hybridization studies showed HIV antigen or genetic sequences only in the brains of cases with SE. Multinucleated giants cells (MGC) were the most frequent cells with reaction products. MGC were labeled with ricinus lectin (RCA), but not with leukocyte common antigen (LCA) or glial fibrillary acidic protein. Many cells in microglial nodules were labeled with RCA, but not LCA; cells in the perivascular compartment were labeled with LCA, but not RCA. Corticospinal tract degeneration was noted in 15 of 20 spinal cords. In six cases tract degeneration was consistent with delayed myelination, and the remaining cases had axonal injury consistent with Wallerian degeneration. Opportunistic infections were rare (three cases). Central nervous system lymphoma occurred in three children and was the most common mass lesion. In two cases lymphoma occurred in the setting of a systemic polyclonal immunoproliferation possibly related to Epstein-Barr virus infection. Cerebrovascular accidents were noted in seven cases. Two cases had hemorrhage associated with immune thrombocytopenia; one hemorrhage was catastrophic. Two children had large vessel arteriopathy with multiple encephalomalacias. Two children had a necrotizing encephalopathy with encephalomalacia and vascular changes suggestive of a mitochondrial cytopathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Acquired Immunodeficiency Syndrome↗
PubMed1989

Atenolol-associated cholestasis.

Atenolol, a beta 1-selective beta-adrenergic receptor-blocking agent, is frequently used for the treatment of hypertension and angina pectoris. We report our experience with a patient who developed cholestatic hepatitis related to the initiation of therapy with atenolol with prompt resolution of symptoms and biochemical abnormalities upon discontinuation of this medication. A review of the literature failed to demonstrate any prior report of atenolol-associated hepatic injury. Although rare, because of the common use of atenolol, clinicians should be aware of this potential adverse effect.

Aged↗
PubMed1988

Pulmonary disease in infants and children.

Pulmonary diseases contribute significantly to the morbidity and mortality in children infected with the human immunodeficiency virus. The wide array of lung diseases spans from early acute bacterial infections, to the lymphoid interstitial pneumonitis/pulmonary lymphoid hyperplasia complex, to opportunistic infections. The unique clinical and histopathologic features of these diseases are reviewed.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Immunoglobulin A stimulates growth of the extrahepatic bile duct in BALB/c mice.

BALB/c mice injected with seven 0.15-ml samples of whole rabbit serum over a 2-week period developed nonneoplastic proliferation of the extrahepatic bile duct epithelium and glandular components. Sera from other animals, including bovines, humans, pigs, goats, and chickens as well as non-serum-containing secretions such as human breast milk and bile also produced this effect. Partial purification utilizing gel filtration and affinity chromatography of the active 33-65% saturated ammonium sulfate precipitate of whole serum indicated that the distribution and characteristics of this glycoprotein showed some similarities with those of IgA. Chromatographically purified human IgA was administered to BALB/c mice and was found to induce bile duct proliferation identical to that seen with whole human serum. Purified human IgG and IgM had no activity. Since IgA-containing serum from BALB/c mice was inactive, it appears that heterologous IgA functions as a specific extrahepatic bile duct growth factor (BDGF) in BALB/c mice. Murine susceptibility to the growth-stimulating effect of serum was strain specific; genetic studies utilizing crosses of susceptible (BALB/c) and resistant (C57BL/10) strains of mice revealed that the ability to respond to the infusion of BDGF is inherited in a polygenic fashion.

Animals↗
PubMed1986

Pulmonary disease in children with acquired immune deficiency syndrome and AIDS-related complex.

Two major pulmonary diseases were defined on the basis of lung biopsies in 15 children with acquired immune deficiency syndrome (AIDS) or AIDS-related complex. Pneumocystis carinii pneumonia was observed in eight children, and pulmonary lymphoid hyperplasia in six. One child had nonspecific interstitial pneumonitis. Children with P. carinii pneumonia had more severe hypoxemia, with higher alveolar-arterial oxygen gradients, and higher isomorphic elevations of serum lactate dehydrogenase. Clinically, children with pulmonary lymphoid hyperplasia were older, and had digital clubbing, parotid gland enlargement, and elevated serum IgG levels. Results of serologic assays and lung tissue analysis were suggestive of persistent Epstein-Barr virus infection exclusively in patients with pulmonary lymphoid hyperplasia. Recognition of the clinical and laboratory findings characteristic of each entity may assist in the differential diagnosis without the need of surgical biopsy.

Acquired Immunodeficiency Syndrome↗
PubMed1979

Chemodectoma in the mid-thyroid region.

A chemodectoma (non-chromafin paraganglioma), which presented as a neck mass in the mid-thyroid region, is reported in a 36 year old female. Clinically, it resembled a thyroglossal duct cyst and on frozen section it looked like a thyroid adenoma.

Adult↗
PubMed1977

Hydration of arene and alkene oxides by epoxide hydrase in human liver microsomes.

The comparative hydration of styrene 7,8-oxide, octene 1,2-oxide, naphthalene 1,2-oxide, phenanthrene 9,10-oxide, benzo[a]anthracene 5,6-oxide, 3-methylcholanthrene 11,12-oxide, dibenzo[a,h]anthracene 5,6-oxide, and benzo[a, 7,8-, 9,10-, and 11,12-oxides to their respective dihydrodiols was investigated in microsomes from nine human autopsy livers. The substrate specificity of the epoxide hydrase in human liver microsomes was very similar to that of the epoxide hydrase in rat liver microsomes. Phenanthrene 9,10-oxide was the best substrate for the human and rat epoxide hydrases and dibenzo[a,h]anthracene 5,6-oxide and benzo[a-a)pyrene 11, 12-oxide were the poorest substrates. Plotting epoxide hydrase activity obtained with one substrate against epoxide hydrase activity for another substrate for each of the nine human livers revealed excellent correlations for all combinations of the 11 substrates studied (r = 0.87 to 0.99). The data suggest the presence in human liver of a single epoxide hydrase with broad substrate specificity. However, the results do not exclude the possible presence in human liver of several epoxide hydrases that are under similar regulatory control. These results suggest the need for further investigation to determine whether there is a safe epoxide of a drug whose in vivo metabolism is predictive of the capacity of different individuals to metabolize a wide variety of epoxides of drugs and environmental chemicals.

Alkenes↗
PubMed1977

Idiopathic proctitis. I. The morphology of proximal colonic mucosa and its clinical significance.

A group of 31 patients with idiopathic proctitis were colonoscoped while they were symptomatic. Multiple mucosal biopsies were taken from the transverse, descending, and sigmoid colon and from the rectum. While visualization by colonoscopy revealed abnormalities limited to the most distal 18-20 cm of the colon, microscopic abnormalities were frequently seen in more proximal locations. Analysis of clinicopathological data indicates that there is good correlation between the extent of microscopic mucosal abnormalities and the clinical course. Patients with abnormalities limited to the rectum generally responded well to conventional treatment while patients with more proximal involvement were refractory to such therapy.

Adult↗
PubMed1976

Congenital hemophagocytic reticulosis.

A fatal case of an apparently congenital form of hemophagocytic reticulosis is reported. The onset was manifested by hyperbilirubinemia and hepatosplenomegaly which were present at birth and persisted throughout life. Fever, anemia and pancytopenia developed at 1 month of age and became progressively worse. A splenectomy was performed at the age of 3 months, but the child died one day later with disseminated intravascular coagulation and pulmonary hemorrhage. The literature is reviewed with regard to the relationship of this case to (familial) hemophagocytic reticulosis and malignant histiocytosis (histiocytic medullary reticulosis). It is suggested that congenital hemophagocytic reticulosis, as described here, (familial) hemophagocytic reticulosis in infants, and malignant histiocytosis in adults all represent the same basic disorder with different ages of onset and clinicopathologic manifestations.

Autopsy↗
PubMed1976

Hypophosphatasia: a cytochemical study of phosphatase activities.

Skeletal abnormalities with defective formation of mature calcified bone are the most prominent clinical features of hypophosphatasia. Low concentrations of serum and tissue alkaline phosphatase and elevated plasma and urinary levels of phosphorylethanolamine (PEA) are also present. Although PEA is hydrolyzed by serum alkaline phosphatase, the relationship between PEA and the deficiency is unclear. PEA has not previously been tested as a cytochemical substrate for the in situ demonstration of human alkaline phosphatase activity. We have studied alkaline phosphatase activity in hypophosphatasia in tissue sections, utilizing PEA and adenosinetriphosphate (ATP) as well as the usual beta-glycerophosphate and naphthol phosphate substrates. Neutral and acid phosphatase activities were also examined. Our results demonstrate that PEA is a substrate for the localization of alkaline phosphatase in normal human tissue, but is not hydrolyzed in hypophosphatasia in the liver, brain or costochondral junction under alkaline conditions. In the kidney in hypophosphatasia only the straight segments of proximal tubules that rim the medullary rays are reactive with PEA. Similar results in hypophosphatasia were obtained at an alkaline pH with ATP, beta-glycerophosphate, and naphthol phosphate. However, the defect in hypophosphatasia is not a generalized deficiency of membrane-associated phosphatases because membranes that were deficient in alkaline phosphatase activity demonstrated normal reactivity with ATP at neutral pH. In addition, thiamine pyrophosphate was also split by Golgi membranes within the cytoplasm. Acid hydrolysis of beta-glycerophosphate by lysosomes was normal.

Alkaline Phosphatase↗