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Biomedical subjects

R Morecki

Publications and source records attributed to R Morecki.

At least 37 records · Page 2Linked to original sources
PubMed1980

The association of kernicterus with bacterial infection in the newborn.

A total population of 29,395 neonates cared for in the six-year period from 1971 to 1976 was reviewed for evidence of autopsy-proven kernicterus. A total of 327 neonates died and 232 were autopsied. The only cases of kernicterus occurred in four near-term infants with antemortem proven sepsis. All four of these infants weighed more than 2,200 gm and were delivered after gestations of either 36 or 37 weeks. These cases of kernicterus occurred during a period when more aggressive management of hyperbilirubinemia in low-birth-weight infants had apparently eliminated immaturity as a predisposing factor in the development of kernicterus, uncovering bacterial infection as the major remaining etiologic co-factor.

Bacterial Infections↗
PubMed1980

Comparative studies of biliary atresia in the human newborn and reovirus-induced cholangitis in weanling mice.

The hepatobiliary histologic lesions of human newborns with biliary atresia have been compared to those induced in weanling mice by reovirus type III. Although the obliterative fibrotic lesions, the hallmark of human disease, are only transient or segmental in the mouse and therefore do not result in permanent or complete obstruction of bile flow, many of the inflammatory stages of the disease are identical in humans and in the mouse. Prompted by these similarities, antibodies to reovirus type III were sought in sera of human newborns with biliary atresia. Two of 12 babies had elevated and rising neutralizing titers to reovirus type III during the course of their illness. Using recobinant reoviruses which contain some genes from a nonpathogenic reovirus type I and other genes from the pathogenic parental reovirus type III, we have shown that hepatobiliary murine pathology is not the property of a single viral gene.

Animals↗
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↗