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Biomedical subjects

R H Shikes

Publications and source records attributed to R H Shikes.

33 records · Page 2Linked to original sources
PubMed1982

A surgical approach to the treatment of fetal hydrocephalus.

Untreated fetal hydrocephalus results in gross cranial and facial abnormalities and profound brain damage. In an attempt to prevent both, a ventriculoamniotic shunt was implanted in a fetus with probable X-linked aqueductal stenosis and hydrocephalus. Performed at 24 weeks' gestation, the procedure used techniques similar to those used for intrauterine transfusion. After shunt placement, the fetal head size grew normally until after the 32d week, when the shunt failed. A cesarean delivery was performed at 34 weeks' gestation. The infant received a standard ventriculoperitoneal shunt after delivery, and his neonatal course has been evaluated through the first three months of life. In selected cases, the ventriculoamniotic shunt may be an acceptable treatment for fetal hydrocephalus.

Adult↗
PubMed1979

Determinants of survival after Kasai's operation for biliary atresia using actuarial analysis.

Survival after Kasai's operation for "noncorrectable" biliary atresia is influenced by (1) age, (2) large bile ducts, and (3) concentration of the bile bilirubin. Critical values are: age less than 10.5 wk, any evidence of a large bile duct, and a bile bilirubin concentration greater than 8.8 mg/100 ml. Using these 3 factors, a predictive model is able to identify a favorable group with an 89% expected 4 yr survival.

Actuarial Analysis↗
PubMed1977

Glutaric aciduria: biochemical and morphologic considerations.

Biochemical and morphologic studies on a patient with glutaric aciduria are presented. Generalized aminoaciduria, alpha-aminoadipic aciduria, and saccharopinuria were noted just prior to death, as well as glutaconic aciduria greater than beta-hydroxyglutaric aciduria. Mutant liver mitochondria did not oxidize glutaryl-CoA to glutaconyl-CoA, indicating deficiency of glytaryl-CoA dehydrogenase. Autopsy revealed cerebral edema, ischemic neuronal changes, and striatal degeneration in the brain with fatty changes in liver, kidney, and myocardium.

Amino Acid Metabolism, Inborn Errors↗
PubMed1976

Segmental lung resection in the first year of life.

Segmental lung resection was performed in 5 infants with congenital lung disease. The lesions were cystic adenomatoid malformation in 2, congenital cystic disease in 2, and congenital lobar emphysema in 1. A higher than expected incidence of major segmental bronchovascular anomalies was encountered (3 of 5 patients). Other than prolonged air leak in 1 patient, complications were negligible. All patients were well from one to six and one-half years after operation. Segmentectomy is a sensible operation for congenital pulmonary disease and ultimately may have as its greatest virtue the preservation of normal lung tissue.

Bronchi↗
PubMed1976

The decline and early fall of neonatal pulmonary hemorrhage.

Seven years' experience (1965-1972) with neonatal pulmonary hemorrhage at the University of Colorado was reviewed. Pulmonary hemorrhage still occurs frequently as a preterminal event in hyaline membrane disease. As an isolated "pure" entity, however, pulmonary hemorrhage has shown a marked decline. This phenomenon is probably related to advances in neonatal intensive care. The radiographic pattern of "pure" pulmonary hemorrhage in the newborn is most commonly a diffuse alveolar infiltrate. Since pure hemorrhage is now an uncommon entity, the radiologist can reasonably suggest this diagnosis on rare occasions only, in the clinical setting of profound hypoxia.

Hemorrhage↗
PubMed1970

Distribution of labeled chromatin. I. M 1 and M 2 anaphases of diploid and tetraploid cultured mammalian cells.

The question of whether distribution of chromatids to daughter cells in mitosis is a random or nonrandom process was investigated by study of the distribution of labeled chromatin in anaphase pairs at M(1) and M(2) after a pulse of tritiated thymidine. Diploid and tetraploid rat and diploid human fibroblast-like cells in serial monlayer culture were synchronized by two different methods to "purify" M(1) and M(2) anaphases: metaphase shake, and FUdR block to DNA synthesis followed by exogenous thymidine. Exposed grains of NTB-2 emulsion were counted over M(1) and M(2) anaphase pairs. An analysis (by pair) of diploid M(2) anaphase grain counts showed two discrete populations of daughters with less and with more radioactivity. A similar analysis of diploid M(1) and tetrapolid M(2) anaphases showed a single grain-count distribution. These findings may support a nonrandom model of chromatid segregation for diploid mammalian cells but do not rule out random segregation until sound mathematical models are formulated for expected random grain distributions in M(2) anaphases of cells with differing numbers of chromosomes.

Analysis of Variance↗
PubMedDate not supplied

Relationship of pretransplant hepatobiliary disease to bile duct damage occurring in the liver allograft.

Histopathological features of nonsuppurative destructive cholangitis have been described in primary biliary cirrhosis, chronic graft-vs-host disease, and chronic rejection of human liver allografts. To determine whether or not susceptibility to injury of interlobular bile ducts was related to the original hepatobiliary disease requiring transplantation, we compared the histopathology of allografts transplanted into two groups of patients. The first group consisted of patients whose original hepatobiliary diseases primarily affect bile ducts: primary biliary cirrhosis, sclerosing cholangitis, and biliary atresia. The second group consisted of patients whose original hepatobiliary diseases do not result in injury to interlobular bile ducts. In 32 liver allografts studied histopathologically, the original disease did not recur. Interlobular bile duct damage occurred, however, in 17 of the 32 and resembled that seen in primary biliary cirrhosis. The spectrum of bile duct injury included mononuclear inflammation of the bile duct epithelium, destruction of the bile duct epithelium, and dissolution of the bile duct. There was no relationship between the frequency or severity of bile duct damage and original hepatobiliary disease, age, sex, duration of allograft survival, or cause of death. We conclude that nonsuppurative destructive cholangitis occurs frequently in liver allografts and represents one component of allograft rejection. This lesion resembles, in many respects, that seen in primary biliary cirrhosis so that histopathological differentiation may be difficult.

Adolescent↗
PubMedDate not supplied

Ultrastructure of congenital cystic adenomatoid malformation of the lung.

Four cases of congenital cystic adenomatoid malformation of the lung are presented with ultrastructural analysis. In some of the cases the ultrastructure is similar to that described in normal fetal airways during the early embryonic phase of lung development. Varying degrees of differentiation are noted, confirming what has previously been observed ultrastructurally in this lesion. One new finding is the presence of tonofilaments in one of our cases, which may represent a metaplastic change. Although the exact nature of the insult is unknown, there may be a developmental defect affecting epithelial differentiation as well as the interaction between the developing pulmonary mesenchyme and distal respiratory units.

Cell Membrane↗
PubMedDate not supplied

Pulmonary hypertension in congenital heart disease: irreversible vascular changes in young infants.

Among 280 infants under 1 year of age with congenital heart disease autopsied at the University of Colorado Health Sciences Center between 1959 and 1978, there were six instances of grade IV1 pulmonary artery hypertension. Five were patients with ventricular septal defect (four associated with other cardiovascular malformations). The sixth was a patient with atrioventricular canal. The youngest was 2 1/2 months of age. Advanced degrees of pulmonary hypertensive arteriopathy (grade IV or more) have been said to be rare in infants, especially under the age of 1 year. The fact that all of these cases occurred within the last few years of the study suggests the possibility of improved supportive care leading to the prolonged survival of infants who might otherwise have died prior to developing severe disease. In addition, the role of altitude in accelerating the arteriopathy must be considered in the present series. In any case, this unexpected increase in the frequency of severe pulmonary hypertensive arteriopathy should stimulate consideration of early surgical correction of the underlying cardiovascular malformation, especially in areas of relatively high altitude.

Altitude↗
PubMedDate not supplied

X-linked myotubular myopathy: a case report of prenatal and perinatal aspects.

Nine families have been reported in which male newborns presented with X-linked myotubular (centronuclear) myopathy. Little is known about the biochemical basis of this disorder or about its natural history in utero. We report a family in which an infant with myotubular myopathy presented in utero with polyhydramnios, poor fetal movement, and fetal cardiac arrhythmias. Shortly after birth the infant died from severe respiratory insufficiency. Gas chromatography-mass spectrophotometry for serum organic acids showed a large octanoic acid peak, but total acyl-CoA dehydrogenase activities in liver were normal. The maternal family history was significant for two perinatal male deaths. Postmortem examination revealed generalized muscle wasting, cardiac enlargement, cryptorchidism, and flexion contractures. Examination of muscle showed numerous fibers that had enlarged, centrally located nuclei and perinuclear clear zones. The muscle fibers were hypotrophic and predominantly of type I. Biopsy specimens of the muscles of the mother and maternal aunt had increased numbers of centrally located nuclei. Neurologic examination was normal. The case demonstrates the typical clinical course, pathology, and family history of severe X-linked myotubular myopathy. In addition, it confirms the reported detection of fetal cardiac arrhythmias and documents what may be an abnormality in fatty acid oxidation.

Family↗