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C Langston

Publications and source records attributed to C Langston.

At least 73 records · Page 4Linked to original sources
PubMed1989

Comparison of the D-xylose and polyethylene glycol absorption tests as indicators of mucosal damage in infants with chronic diarrhea.

The determination of serum levels of D-xylose and the urinary excretion of an orally administered mixture of low-molecular-weight polyethylene glycol were compared to assess their sensitivity to predict small-bowel mucosal damage. Eighteen infants with severe diarrhea and villus atrophy were observed. Results of the D-xylose and polyethylene glycol tests were compared with the villus-to-crypt ratios that were determined from biopsy specimens. The D-xylose test predicted accurately 12 (67%) of the 18 small-bowel biopsy results, while the polyethylene glycol test predicted 14 (78%). However, the McNemar test indicated that the two tests did not differ significantly in their ability to predict an abnormal small-bowel biopsy. We conclude that neither the D-xylose nor the polyethylene glycol test is a reliable indicator of small intestinal mucosal damage in infants with chronic diarrhea.

Atrophy↗
PubMed1989

Long-term consequences of compensatory lung growth.

Left pneumonectomy or left nephrectomy was performed on 10-wk-old littermate male New Zealand White rabbits, and they were killed at 30 wk of age. Thirty-week-old male littermates served as controls. Nephrectomy was done to produce major tissue loss and trauma and to assess blood somatomedin C. At the end of the experiment, the right lungs of the pneumonectomy animals had a greater lung volume, weight, gas-exchanging surface area, and alveolar number than the nephrectomy animals and the controls, and their air spaces were the same size. When compared with both lungs of the nephrectomy group and the controls, lung weight was the same; lung volume, alveolar number, and protein were not significantly less in the pneumonectomy group, but gas-exchanging area (compared with controls only), DNA, and RNA were. After left nephrectomy, the right kidney increased in weight; nephrectomy had no effect on lung size or structure. We conclude that pneumonectomy at age 10 wk in male rabbits results in significant compensatory lung growth, including alveolar multiplication, and this persists to age 30 wk. Compensatory lung growth, however, was incomplete; that is, it did not reconstitute (equal) in all respects that of both lungs of the nephrectomy animals or the controls.

Animals↗
PubMed1989

Epidemiologic aspects of childhood mesothelioma.

Our calculation provides the first population-based incidence rate of childhood mesothelioma in the United States. Based on these data and on our pathology review, we conclude that mesothelioma occurs rarely in children and that this diagnosis is difficult to establish. A more systematic approach to identifying mesothelioma cases in children, as well as adults, will be facilitated by increasing state surveillance of cancer incidence and by the proposed addition of a unique code for mesothelioma in the Tenth Revision of the ICD. There is a critical need for histopathological verification of mesothelioma cases. The increased use of a uniform, reproducible histopathologic classification and mesothelioma panels should address this problem. A thorough microscopic study of individual cases needs to be supplemented by a careful assessment of the clinical findings and environmental factors. The available data thus far do not support an association between childhood mesothelioma and asbestos exposure. However, the ubiquitous nature of asbestos exposures, the known association of asbestos with adult mesothelioma, the unreliability of the diagnosis, and the lack of adequate data regarding asbestos exposures, all indicate that asbestos involvement cannot be categorically ruled out, especially in older children with the potential for a longer duration of exposure and a plausible induction period. Mesothelioma in children, as well as in adults, is likely to have a multifactorial etiology. Radiation, prenatal medications, and genetic factors are all possible etiologic agents in childhood mesothelioma. In addition, other, as of yet unspecified environmental factors may play a role in this disease. When cases are diagnosed, the physician should inquire about the history of exposure to asbestos or other hazardous materials in the patient's environment, prior radiation exposure, medication exposure pre- and postnatally, prior cancer diagnoses, and a family history of cancer. An interdisciplinary approach, combining the diagnostic skills of the pathologist and the analytic skills of the epidemiologist, will be of value and of special relevance in the study of mesotheliomas.

Adolescent↗
PubMed1989

Prostaglandin E1-associated pathology of pulmonary microvasculature in newborn pups: similarity to findings in prostaglandin E1-treated human newborns.

Prostaglandin E1 (PGE1) administration is a useful therapeutic measure for short-term maintenance of ductal patency in patients with obstructions to pulmonary or systemic blood flow. Such treatment is not without complications, however, and a report of three infants from our institution with abnormalities of the pulmonary microvasculature after varying periods of PGE1 therapy was recently published (Heffelfinger et al., Pediatr Pathol 1987;7:165-73). The vascular abnormalities appeared to be temporally related to the PGE1 administration. To test this hypothesis, we investigated the effects of PGE1 in newborn beagles by infusing PGE1 for periods of up to 21 days in four experimental pups. Two control pups were infused with saline for the same period of time. Five of the animals developed respiratory infection during the course of the infusions. One PGE1-treated pup was not infected. Both the PGE1- and saline-treated pups had bronchopneumonias of similar severity; however, pulmonary arteritis occurred only in the PGE1-treated pups. The severity of the arteritis varied with the amount of pulmonary parenchymal inflammation and not with the duration of PGE1 administration. Inflammatory and vascular lesions were found in organs other than the lung only in two pups receiving longer courses of PGE1 treatment. We conclude that systemic PGE1 infusion at therapeutic levels plays a role in the development of arterial lesions in small muscular arteries and that this is potentiated by the presence of infection.

Alprostadil↗
PubMed1988

Teratogenic effects of nitrofen on cellular and functional maturation of the rat lung.

The herbicide nitrofen was administered to pregnant Sprague-Dawley and Fischer-344 rats on Days 10-13 of gestation (po, 20 or 40 mg/kg daily) and the effects of maturation of the perinatal lung were evaluated. Nitrofen interfered with the ontogenetic acquisition of lung cells as DNA, RNA, and protein content were subnormal. The hypoplastic lungs in the newborns were associated with structural deficits, resulting in a profound reduction of surface area available for gas exchange and depressed lung compliance. Other factors which influence pulmonary function and systemic delivery of oxygen were also considered. Adrenal catecholamines, which play an important role in surfactant production and fluid resorption in the lung during the transition to air-breathing, were markedly reduced. In addition, red blood cell concentration was significantly diminished. Taken together, these results suggest that the neonatal mortality observed in the nitrofen-treated rats is likely associated with respiratory distress caused by a number of cellular and functional aberrations. These include (a) hypoplasia and structural defects in the lung leading to deficient pulmonary function, (b) deficits in adrenal catecholamines potentially impeding the transition of the lung to air-breathing, and (c) impaired systemic delivery of oxygen due to reduced hemoglobin concentration.

Adrenal Medulla↗
PubMed1988

Mesothelioma of childhood.

Malignant mesothelioma (MM) of childhood is a rare but important neoplasm. Eighty children with a previous diagnosis of MM were identified. Four of the 80 children had exposure to known risk factors (two had history of exposure to asbestos, one had received radiation therapy, and one had been exposed in utero to isoniazid). Tissue slides were available for independent and joint review by a panel of three pathologists in 22 of the cases. Ten were accepted as MM, nine were reclassified as other malignancies, and three were considered tumors of uncertain nature. Six of the ten children with MM were boys, and four were girls. Eight had pleural tumors, and two had peritoneal tumors. Four died at 7, 8, 18, and 48 months after diagnosis; three remained alive at 19, 20, and 59 months; and three had no follow-up. This review suggests that MM of childhood is a valid entity with a grave prognosis. The tissue diagnosis is difficult and is best made by a panel of pathologists. The available evidence does not support a causal relationship between MM and asbestos, radiation, or isoniazid.

Adolescent↗
PubMed1988

The effect of age on postpneumonectomy growth in rabbits.

To assess the effect which age at pneumonectomy has on pulmonary compensatory growth, male New Zealand white rabbits underwent left pneumonectomy or sham thoracotomy at 10, 18, or 26 weeks of age. Morphometric and biochemical evaluation of the remaining lungs was carried out four weeks later. There was significant compensatory growth in terms of lung volume, weight, DNA, RNA, and protein in all three age groups. Lung volume response was incomplete, i.e., right lung volume of the experimental animals did not match the volume of both lungs of controls; other variables were not significantly different between the right lung of experimentals and both lungs of the controls. An unchanged surface area per unit volume accompanied by a stable mean linear intercept indicated that alveolar multiplication occurred in the 10 and 18 week age groups. The oldest group had significantly decreased surface area per unit volume and significantly increased mean linear intercept, suggesting an increase in the size of existing alveoli at 26 weeks of age.

Adaptation, Physiological↗
PubMed1987

Severe cardiopathy in branching enzyme deficiency.

A 7 1/2-year-old girl had exercise intolerance and exertional dyspnea. Four months later, congestive heart failure developed, with recurrent chylous pleural effusions, and she died at age 8 1/2 years. Endomyocardial biopsy tissue showed abundant PAS-positive, diastase-resistant cytoplasmic deposits. Similar inclusions were seen in muscle, skin, and liver specimens. Postmortem studies showed that the abnormal polysaccharide was especially abundant in heart and muscle, but was also present in all other tissues, including the central nervous system. Glycogen isolated from heart, muscle, and spinal cord showed a shift of the iodine spectrum toward higher than normal wavelengths. Branching enzyme activity was lacking in the muscle biopsy specimen and in all postmortem tissues; glycogenolytic enzymes had normal activities. These studies show that cardiomyopathy can be the first symptom of generalized branching enzyme deficiency and that the degree of accumulation of the abnormal polysaccharide may vary in different tissues.

Biopsy↗
PubMed1987

Pulmonary vascular changes associated with prolonged prostaglandin E1 treatment.

Prostaglandin E's (PGEs) are used therapeutically in newborn infants to maintain an open ductus arteriosus when there is obstruction to systemic or pulmonary arterial blood flow. These prostaglandins have been shown to have other systemic physiologic effects, such as vasodilation, inhibition of platelet aggregation, and enhancement of chemotactic-factor-mediated polymorphonuclear leukocyte infiltration, with resultant loss of lysosomal granules and possibly the generation of free radicals. We have recently seen previously unreported vascular lesions in 3 infants with hypoplastic left heart syndrome treated with usual therapeutic doses of PGE1 for prolonged periods. At autopsy, pulmonary vascular changes reflecting increased flow were present in each infant. One infant had a necrotizing vasculitis, sometimes associated with infarcts, in the lungs and in small muscular arteries in other organs. The form and severity of the vascular changes appear to be related to the duration of PGE1 administration.

Alprostadil↗
PubMed1987

A mouse model of chronic pulmonary infection with Pseudomonas aeruginosa and Pseudomonas cepacia.

A mouse model of chronic pulmonary infection with either Pseudomonas aeruginosa or Pseudomonas cepacia was developed to compare bacteriologic and pathologic features of these infections. Experimental pneumonia was established in Swiss mice by transoral intratracheal inoculation of 10(3)-10(4) colony-forming units of mucoid P. aeruginosa or P. cepacia enmeshed in agarose beads. Unilateral infection with either strain was tolerated without morbidity. By 10 days postinoculation, the mean colony-forming units per infected lung was 3.8 X 10(5) for P. aeruginosa and 1.0 X 10(5) for P. cepacia. Bacterial counts remained stable through 21 days with no significant difference between organisms. Acute and chronic inflammatory histopathologic changes similar to many found in the lungs of cystic fibrosis patients were present in 95% of lung specimens. The changes occurred with both organisms but were more extensive with mucoid P. aeruginosa. This model represents an important tool for study of the contribution of complement, antibody, and adoptive transfer of T cell-mediated immunity to the pathogenesis of chronic pneumonia with Pseudomonas species, and represents the first successful model of chronic pulmonary infection with P. cepacia.

Animals↗
PubMed1987

Pulmonary vascular lipid deposition after administration of intravenous fat to infants.

The incidence of pulmonary vascular lipid deposits in infants who did or did not receive intravenous lipid emulsion was determined through a review of the pulmonary histopathology and clinical course of 39 neonates who died during a two-year period. The relationship between pulmonary vascular lipid deposits and the duration and amount of administered intravenous fat emulsion was assessed. In addition, the effect of monitored serum triglyceride levels on the development of pulmonary vascular lipid deposits was evaluated. The incidence of pulmonary vascular lipid deposits was greater in the group that received intravenous fat emulsion (P less than .02). Both the amount (grams per kilogram per day) and duration (days) of intravenous fat emulsion infusion were correlated positively with severity (P less than .05) in infants who had pulmonary vascular lipid deposits. No relationship was seen between peak serum triglyceride levels, the frequency of elevated triglycerides, and pulmonary vascular lipid deposits. Although administered fat emulsion was a risk factor for the development of pulmonary vascular deposits, two of 13 infants who had not received intravenous fat emulsion had such deposits.

Fat Emulsions, Intravenous↗
PubMed1984

Human lung growth in late gestation and in the neonate.

We studied the lungs of 42 infants dying of obstetrical accidents, acute infections, and trauma, who ranged in age from 19 wk gestation to 3 wk postpartum at 42 wk gestation. The earliest lungs (19 to 20 wk gestation) had smooth-walled respiratory channels lined by cuboidal epithelium. Between 22 and 24 wk gestation with further development of the acinus, these channels took on a wavy internal configuration. After 28 wk gestation the air spaces (saccules) of the developing acinus became subdivided by secondary crests. Alveolar development began in some infants as early as 32 wk and was uniformly present by 36 wk. Respiratory bronchioles were not present in any of our cases, including those in the immediate postnatal period. Quantitative studies showed a rapid increase in lung volume and alveolar surface area beginning at about 28 wk gestation (crown-rump length, 25 cm) coinciding with increasing complexity of the saccules. Surface area, lung volume, and total number of alveoli showed an exponential relationship to gestational age and crown-rump length. Air-space wall thickness showed a rapid decline starting at 28 wk gestation and is best related exponentially to age and crown-rump length. Volume proportions of air spaces increased steadily throughout gestation. The increase in bronchial and bronchiolar air and air-space dimensions correlated relatively poorly with age, and nonparenchyma remained a relatively constant volume proportion, regardless of age.(ABSTRACT TRUNCATED AT 250 WORDS)

Body Weight↗
PubMed1984

Pulmonary veno-occlusive disease as a cause of sudden infant death.

Clinical and gross autopsy findings on a 3-month-old infant were consistent with the sudden infant death syndrome. However, on histologic examination pulmonary veno-occlusive disease was found. Five previous cases of pulmonary veno-occlusive disease appearing in infancy are reviewed. In infants, the disease is initially observed as feeding difficulty and/or failure to thrive, often accompanied by mild respiratory distress. Two of the infants died suddenly. While neither cause nor pathogenesis can be determined, it is important to recognize the process and include it among the possible causes of sudden infant death.

Humans↗
PubMed1982

Morphologic and functional effects of Clostridium difficile enterotoxin in tissue culture.

The effects of the Clostridium difficile toxin were examined in HeLa and mouse adrenal tumor (MAT) cells. Cytotoxicity was evaluated by vital dye exclusion and 51Cr release. In both HeLa and MAT cells, C. difficile toxin caused rounding of virtually 100% of cells. This rounding was distinguishable from rounding produced by the Escherichia coli heat-labile enterotoxin (LT): (1) LT was inactive in HeLa cells; (2) in MAT cells, C. difficile toxin produced uniformly rounded cells, while LT-rounded cells usually had cytoplasmic extensions and a regular background of flattened cells. In C. difficile toxin affected HeLa cells, there were less than mitotic figures per 1000 cells compared with 15-18 in controls. Clostridium difficile toxin treated HeLa cells showed less than 10% cytotoxicity in 24 h and no more than 30% by 74 h, similar to control cells. However, paralleling the suppression of mitotic figures, cell multiplication was inhibited in C. difficile toxin treated cells when subcultured in a short-term (72 h) assay compared with up to a 500% increase in control cells. This inhibition was also seen in a 6-week cloning assay in which C. difficile toxin treated cells had a cloning efficiency of less than 1% compared with approximately 10% in controls. We conclude that the major effect of the C. difficile toxin is inhibition of growth rather than immediate cell death. The relationship of this growth inhibition to colitis remains to be elucidated.

Adrenal Gland Neoplasms↗