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Biomedical subjects

T R Wells

Publications and source records attributed to T R Wells.

At least 37 records · Page 2Linked to original sources
PubMed1986

Intestinal plexuses in Crohn's disease and ulcerative colitis in children: pathologic and microdissection studies.

The relative fraction of neural tissue in the plane of the myenteric (Auerbach) plexus (MEP) of ileum and colon of patients with Crohn's disease and ulcerative colitis was analyzed by point-count morphometric analysis of microdissected flat-mount ("circuit diagram") preparations of the plexus. Increase in the relative fraction of neural tissue (myenteric plexus hyperplasia) was seen in the MEP of some patients in both ileum and colon in both diseases. The frequency of ulceration or inflammation extending into the bowel wall deep enough to injure the various levels of the intestinal plexus system (mucosal plexus of Cajal; upper submucosal plexus of Meissner; deeper submucosal plexus of Henle; intermuscular plexus of Auerbach; outer muscular/serosal plexus of Stöhr) was analyzed for small intestine, appendix, and colon for patients with both diseases. As expected, Crohn's disease tends to produce deeper intestinal wall damage in ileum versus colon, and ulcerative colitis the reverse. The effect of such injury on local and more distal motor control of the intestine and on integrative functions of the intestinal plexus system appears not to have been considered previously. Since injury deep enough to damage any given plexus necessarily damages all overlying plexus levels, analysis of such effects appears a fruitful field for study.

Adolescent↗
PubMed1986

Microdissection study of the incidence of branched eccrine sweat glands and the number of eccrine glands per unit area of infants' and childrens' skin.

That branched eccrine sweat glands occur has rarely been mentioned in the literature, and their incidence has never been determined. All eccrine glands in 0.5-cm2 pieces of anterior trunk skin of 59 children were microdissected, and the total number of glands and the number of branched eccrine glands determined. One-hundred fourteen of 17,539 (0.65%) were branched, 90% in the middermis and 10% at the epidermis. The apparently normal anatomic property that almost 1% of eccrine sweat glands are branched has not hitherto been appreciated. One doubly branched gland was found. Patients with leukemia (11 in the study) possibly had more branched glands than nonleukemic patients of the same body size. The best statistical relation of the number of sweat glands per unit area of skin (GUA) to surface area (SA) or age in children was the natural logarithm of GUA versus the reciprocal of surface area: LnGUA = (0.2205 X 1/SA) + 5.42. This result is consistent with the classical proposition that there is no important degree of formation of new eccrine glands, nor of loss, after birth, the density of glands per unit area of skin reducing as SA rises with growth during childhood.

Child↗
PubMed1986

Microdissection demonstration of the lesion of the endocrine kidney in children.

Microdissection of nephrons of kidneys of children showing advanced ischemic tubular atrophy, and removed for control of hypertension, demonstrates marked proximal convoluted tubular atrophy, with formation of multiple small proximal tubular diverticula. These diverticula presumably contribute to the microscopic appearance of large numbers of small tubules lined by low epithelial cells with pale or clear cytoplasm, adjacent to glomeruli in the cortices of kidneys showing ischemic tubular atrophy (endocrine kidney). Segmentation of such atrophic tubules leads to formation of blind segments (microcysts), as demonstrated in this study and by Oliver. The distinctive microscopic appearance of the endocrine kidney, a not infrequent finding in kidneys of children with chronic renal insufficiency who require nephrectomy for control of hypertension, has not hitherto been emphasized in the literature on pediatric renal disease.

Adolescent↗
PubMed1985

Association of common origin of the carotid arteries with anomalous origin of the left coronary artery from the pulmonary artery.

Common origin of the carotid arteries (COCA) is a common pattern of aortic arch vessels and is the single most common cause of tracheobronchial compression by a congenital cardiovascular anomaly. By no means all affected patients are symptomatic. Symptoms may range from recurrent pulmonary infections and "noisy respiration" to stridor and apneic spells. In our study of patients with anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) we found a highly significant association of COCA with ALCAPA (85%), although no patient with ALCAPA in this study had evidence of tracheal stenosis documented in the hospital chart. As COCA is easily correctable, we suggest consideration of COCA during evaluation and surgery of patients with ALCAPA so that, if the patient also has symptoms possibly related to COCA, the artery can be suspended from the posterior wall of the sternum.

Aorta, Thoracic↗
PubMed1985

Short trachea, with reduced number of cartilage rings--a hitherto unrecognized feature of DiGeorge syndrome.

Adequate tracheas from 6 of 14 patients with DiGeorge syndrome (2 complete and 4 partial forms) were available for tracheal ring study. The number of tracheal rings in these patients was significantly low (mean +/- SD 14.7 +/- 1.4). This is consistent with an effect of deficient blood supply to the fetal cervical region, a mechanism that has been proposed to explain the defective development of thymus and parathyroid glands in DiGeorge syndrome. To our knowledge this lesion has not been described as one of the malformations found in the syndrome. In 8 of 14 (57%) patients with DiGeorge syndrome, common origin of the carotid arteries was found, and 4 of these 8 patients showed minor tracheal compression. These findings support the proposal that abnormal blood supply to the region of the third and fourth pharyngeal arches may play a role in the pathogenesis of DiGeorge syndrome.

Adolescent↗
PubMed1985

Structural abnormalities of the myenteric (Auerbach's) plexus in familial dysautonomia (Riley-Day syndrome) as demonstrated by flat-mount preparation of the esophagus and stomach.

The esophageal and gastric myenteric (Auerbach's) plexus were studied by a flat-mount preparation in 3 patients with familial dysautonomia. In 1 patient a typical esophageal network was found in the stomach. In another patient both esophageal and gastric plexus patterns were significantly different from normal. These changes, by producing abnormal nervous stimulation, may explain disturbed motility of the esophagus and stomach in familial dysautonomia.

Child↗
PubMed1985

Congenital hypernephronic nephromegaly with tubular dysgenesis: a distinctive inherited renal anomaly.

This paper describes a distinct, apparently inherited renal disorder we call congenital hypernephronic nephromegaly with tubular dysgenesis. The disorder is characterized by oligohydramnios, the Potter phenotype, and enlarged nonfunctional kidneys. Light microscopy demonstrates increased numbers of glomeruli, undifferentiated tubules, and interstitial fibrosis. Microdissection reveals short, immature nephrons that lack proximal convolutions, and abnormal vascularization of the glomerulus. Morphometric analysis demonstrates increased glomerular mass, primarily in the region of the corticomedullary junction, increased interstitial mass, and decreased tubular mass. The parameters that define this anomaly are presented, and the possible mechanisms of pathogenesis are discussed in relation to pathologic observations and current concepts concerning renal embryogenesis and differentiation. The recurrence of this anomaly in the male children of a consanguineous couple suggests an X-linked recessive mode of inheritance, although an autosomal-recessive mode of inheritance cannot be ruled out. This condition indicates that not all cases of the Potter phenotype can be considered to be sporadic.

Amniotic Fluid↗
PubMed1985

Time course of the intrahepatic lesion of extrahepatic biliary atresia: a morphometric study.

The time course of the intrahepatic lesions of untreated extrahepatic biliary atresia was evaluated by morphometric analysis of 49 specimens from 27 patients. The data show an early phase of rapid bile ductular proliferation, with peak in this material at 205 days, followed by rapid duct regression to approximately 400 days, and slower progressive intrahepatic duct loss thereafter. The ratio of ducts to connective tissue in portal tracts follows a similar course. Connective tissue in portal tracts rises on a slower course and continues to increase after maximum duct regression is reached, so the ratio of parenchyma to fibrous septa falls over the later course of the process. Although duct and connective tissue proliferation in hepatic portal tracts is associated in many liver diseases, the data of this study demonstrate dissociability of the relationships, with the fibrosis in the later stages of the intrahepatic process in extrahepatic biliary atresia apparently neither responsive to nor inducing biliary ductular proliferation.

Bile Ducts↗
PubMed1985

Preferentially longer survival of males than of females with untreated extrahepatic biliary atresia: correlations with time course of intrahepatic lesions and suggestion of possible ethnic influences.

Males with untreated or unsuccessfully treated extrahepatic biliary atresia show statistically significantly longer survival than females. Females show a greater degree of intrahepatic biliary ductular proliferation than males in the early phase of the process (to age approximately 200 days) and greater duct regression and more rapid connective tissue proliferation than males from approximately 200 to 400 days. Females also show greater frequency of statistically significant hepatomegaly than males over the first year. The black and Hispanic patients in this series tended to show a less marked degree of bile ductule proliferation in the early phase of the process than other patients, but the numbers of such patients available for study were not enough for statistical significance. This point, and its possible clinical correlates, will require further analysis, as will possible biochemical explanations for the differences between males and females in the time course of the intrahepatic lesions of extrahepatic biliary atresia.

Black or African American↗
PubMed1984

The renal lesion of congenital hepatic fibrosis: pathologic and morphometric analysis, with comparison to the renal lesion of infantile polycystic disease.

The renal lesion of congenital hepatic fibrosis (CHF = Blyth and Ockenden's juvenile polycystic disease of liver and kidneys) was analyzed from 6 specimens from patients aged 3 3/12 to 19 3/12 years and compared with that of 5 patients with infantile polycystic disease (IPCD) aged 6 months to 14 4/12 years. Pathologic, microdissection, injection, and morphometric studies show that the predominantly medullary cystic lesion of CHF shows different distribution in medullary, cortico-medullary, and cortical zones of kidney from the lesion of IPCD, and shows a different time course, from early life to renal insufficiency, from that of IPCD. The renal cysts in CHF affect deep or central collecting tubules, in contrast to the involvement of more peripheral orders of collecting tubules in IPCD. Papillary pore counts, performed for 1 patient, gave significantly low values, in contrast to normal values reported for IPCD. The findings support the previously published conclusion, based on differences in the hepatic lesions of the two conditions, that CHF and IPCD are difference diseases, rather than different permissible manifestations of a single disease.

Adolescent↗
PubMed1980

Morphometric analysis of liver lesions in cystic diseases of childhood.

Morphometric analysis of the liver lesions in patients with various forms of cystic disease of the liver in childhood demonstrates that the entities called the congenital, perinatal, and infantile forms of polycystic disease produce the same liver lesion. The data suggest that these entities are actually the same disorder, for which the name infantile polycystic disease (of the liver and kidneys) is recommended. In all patients with this autosomal recessive disorder there is involvement of both the liver and the kidneys, and patients present with hepatonephromegaly at birth or in early infancy. Similarly, the entity called the juvenile form of polycystic disease produces the same liver lesion as does the disease to which the term congenital hepatic fibrosis has been applied to describe patients presenting in later childhood with portal hypertension. The latter name is recommended to distinguish this condition from infantile polycystic disease. Nephromegaly is not a feature of this also autosomal recessive disease, but renal insufficiency, progressing slowly through later childhood and adolescence, is. The hepatic lesions of infantile polycystic disease and congenital hepatic fibrosis differ from those of other disorders causing cystic lesions of the liver and kidneys, either regularly (Meckel's syndrome, Jeune's syndrome) or variably (vaginal atresia syndrome, tuberous sclerosis, medullary cystic disease).

Adolescent↗