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Biomedical subjects

T R Wells

Publications and source records attributed to T R Wells.

At least 19 recordsLinked to original sources
PubMed1997

The ratio of progesterone receptor isoforms changes in the monkey corpus luteum during the luteal phase of the menstrual cycle.

Recent evidence suggests that progesterone is required for ovulation, luteinization, and the maintenance of luteal structure and function in primates. Progesterone action is mediated by intracellular progesterone receptors (PRs), and PRs are detectable by immunocytochemistry in the monkey corpus luteum. However, changes in total luteal PR and PR isoform expression have not been quantitated in the corpus luteum during its life span in the menstrual cycle. This study was initiated to identify and quantify PR isoforms in the macaque corpus luteum throughout the luteal phase of the natural cycle by means of Western blotting. Several antibodies generated against the human PR recognized two bands of consistent molecular weights in monkey tissues, and these bands comigrated with PR-A and PR-B from human T47D cells. Taken together, these data suggest that the two proteins identified were macaque PR-A and PR-B. The estimated molecular weights of monkey PR-A and PR-B were approximately 90,000 and 120,000, respectively. PRs were detected in a variety of macaque tissues, including the endometrium, whole ovary, and decidua, but not in spleen, which is PR-negative by other techniques. Whereas PR-A was the predominant isoform observed in endometrium and decidua, PR-B predominated in the ovary without a dominant follicle or corpus luteum as well as in the corpus luteum. In luteal tissue, PR-A levels decreased (p < 0.05) over the course of the luteal phase, while PR-B levels were unchanged. Hence the ratio of PR-B to PR-A (PR-B:PR-A) increased (p < 0.05) from early to very late luteal phase. Since PR-B:PR-A can alter gene expression in response to progestins and antiprogestins in vitro, the temporal changes in PR-B:PR-A in the monkey corpus luteum may contribute to functional differences in luteal responses to progesterone and other steroids in vivo.

Animals↗
PubMed1991

The question of parallax-effect on radiographic assessment of short trachea in infants and children.

Disproportionately short trachea, can be recognized in AP chest radiographs of infants and older children taken during quiet respiration and showing an evaluable air tracheobronchogram, by the thoracic vertebral level of the carina (normally at T4 in neonates and infants, and at T5 in children two years of age or older). To establish the extent to which a parallax-effect of differing angles of X-ray beam relative to the patient can influence the radiologic assessment of carinal level, we measured the tracheal-vertebral distance at the carina in 29 lateral radiographs of neonates, infants and children, prepared diagrams of the loci of carinal beam intercept of the vertebral column for different angles of beam to body, from tracings of lateral radiographs of two 2-week-old infants, one with trachea of normal length and one with short trachea; of a nine-year-old child with short trachea, and of a ten-year-old with normal trachea, and made radiographs of a postmortem tracheobronchogram of a two-day-old infant at different beam angles. We conclude that tube-body angles of the order of 10-15 degrees from vertical at 27 inches (68.6 cm) or at 40 inches (101.6 cm) FFD do not significantly affect the apparent thoracic vertebral level of the carina in AP chest radiographs, and that a beam angle of 20 degrees or more from vertical is necessary to change the apparent level of tracheal bifurcation by one vertebral body, depending on the patient's age and on whether the patient's position relative to the X-ray beam is lordotic or anti-lordotic.(ABSTRACT TRUNCATED AT 250 WORDS)

Child↗
PubMed1990

Diagnostic aspects and syndromal associations of short trachea with bronchial intubation.

Conditions with disproportionately short trachea, with a reduced number of tracheal cartilage rings and a high level of tracheal bifurcation, have been reported. We have seen accidental bronchial intubation in nine patients with short trachea. This risk can be reduced by recognition of conditions associated with short trachea, by awareness that methods for calculating endotracheal tube length from body length can overpredict tube length for patients with short trachea, and when feasible, by use of preintubation chest roentgenograms showing air bronchograms to establish the thoracic level of tracheal bifurcation. Twelve patients with short trachea, four with bronchial intubation, and six conditions not previously associated with short trachea, are reported. Three of the patients also had laryngeal hypoplasia.

Child↗
PubMed1990

Serial section-reconstruction of anomalous tracheobronchial branching patterns from CT scan images: bridging bronchus associated with sling left pulmonary artery.

The use of the technique of wax-plate serial section-reconstruction, based on contiguous axial plane CT images of the upper thorax, to prepare a replica of the central air-way (trachea and major bronchi) of an infant with sling left pulmonary artery type 2B, with bridging bronchus, abortive right main bronchus, and tracheal stenosis due to absence of the tracheal pars membranacea with "ring" tracheal cartilages is described. The technique is applicable to demonstration of the anatomic features of other abnormalities of branching pattern or caliber of the trachea and major bronchi.

Bronchi↗
PubMed1990

Morphometric studies of cystic and tubulointerstitial kidney diseases with hepatic fibrosis in children.

Portal tract fibrosis with biliary ductular enlargement or proliferation occurs in a number of genetic diseases that have cystic or tubulointerstitial renal lesions. These include some with renal cystic disease such as autosomal recessive diseases (e.g., infantile polycystic disease, juvenile polycystic disease, and Meckel's syndrome), autosomal dominant diseases (e.g., adult polycystic disease) and, rarely, tuberose sclerosis and dominant glomerulocystic disease. Portal tract fibrosis with biliary enlargement and proliferation occurs also with tubulointerstitial kidney diseases. These probably include at least three disorders in the category nephronophthisis-congenital hepatic fibrosis (one autosomal recessive disease and two either autosomal or X-linked recessive diseases) plus Jeune's syndrome (the tubulointerstitial diseases Fanconi's familial nephronophthisis and anti-tubular membrane antibody disease do not regularly cause hepatic fibrosis). Morphometric data on ratios of bile ductules to connective tissue in hepatic portal tracts show high values for infantile polycystic disease (mean, 0.616) compared to lower values for juvenile polycystic disease (mean, 0.286). That the cystic renal lesions of the first two diseases differ in type and time course is known. Similar data on ratios of glomeruli plus tubules to connective tissue in renal cortices and of tubules to connective tissue in outer medullary zones of kidneys, respectively, are as follows: for Fanconi's nephronophthisis, 0.445 and 0.197; for anti-tubular basement membrane antibody disease, 0.585 and 0.164; and for the three types of nephronophthisis-congenital hepatic fibrosis studied, 0.668 and 0.446, 1.39 and 0.921, and 1.18 and 0.12. These data support clinical impressions that the category nephrophthisis-congenital hepatic fibrosis includes more than one disease entity.

Bile Ducts, Intrahepatic↗
PubMed1990

Acrocephalospondylosyndactyly--a possible new syndrome: analysis of the vertebral and intervertebral components.

Apert-Crouzon syndrome (formerly ACS type 2; 10130) is now considered a subset of autosomal dominant Apert acrocephalosyndactyly type 1 (10120), with features of craniosynostoisis, syndactyly of all extremities, maxillary hypoplasia, "parrot-beaked" nose, hypertelorism, exophthalmos, external strabismus, and short upper lip. We report a 3 1/2-month-old infant with features of Apert syndrome, plus thoracic vertebral anomalies radiographically similar to those seen in spondylothoracic dysplasia, a condition in which block thoracic vertebrae with widely open neural arches and a fan-shaped thoracic cage are found. Our patient also had flared metaphyseal ends of humeri, dislocated radii with immobile elbows, an unusual tail-like protuberance in the coccygeal area, and a solid cartilaginous tracheal wall. To date, in ongoing reviews of radiographs of other patients with acrocephalosyndactyly or acrocephalopolysyndactyly complexes and of relevant literature, we have not identified other patients with these findings. The vertebrae and intervertebral discs of the patient in this report, three patients with Jarcho-Levin syndrome, and one with Apert syndrome were measured from anteroposterior chest radiographs; the findings clearly distinguish the condition in our patient from Jarcho-Levin syndrome or Apert syndrome.

Abnormalities, Multiple↗
PubMed1989

Short trachea, a hazard in tracheal intubation of neonates and infants: syndromal associations.

Short trachea results from reduction in number of tracheal cartilage rings to 15 or fewer from normal mean of 17 rings in infants. In a review of radiologic and pathologic data, the thoracic vertebral level of tracheal bifurcation as seen in anteroposterior chest radiographs of infants with congenital malformations, cardiovascular anomalies, and skeletal dysplasias, was compared with numbers of tracheal cartilage rings demonstrated in postmortem specimens. Increased frequency of short trachea was seen in patients with DiGeorge anomaly (77%), skeletal dysplasias (55%), brevicollis (57%), diaplacental rubella (40%), and patients with congenital heart disease who did not have DiGeorge anomaly (36%, with range 25-83% for different types, the highest, 83%, being interrupted aortic arch). Preintubation high kilovoltage chest radiographs to establish the level of tracheal bifurcation in patients with increased risk of short trachea can be helpful in avoiding bronchial intubation and its complications. Postintubation chest films to assure the level of the endotracheal tube tip should be considered for such patients. Growth in length of the trachea with age is accomplished both by increase in size of tracheal cartilage rings and interring membranes, and by increase in ring number.

Bronchi↗
PubMed1989

Renal lesions and clinical findings in thalassemia major and other chronic anemias with hemosiderosis.

Renal lesions found in 21 autopsied patients with hemosiderosis, 18 with beta-thalassemia, two with Blackfan-Diamond anemia, and one with aplastic anemia included: cellular glomeruli with increased mesangial matrix; hemosiderin deposit in visceral and parietal glomerular epithelial cells; greater hemosiderin deposit in terminal straight portions of proximal convoluted tubules and distal convoluted tubules than in connecting segments, or collecting tubules, connective tissue ferrugination; lipofuscin in tubular epithelium and vascular smooth muscle; infrequently, intimal or medial arterial thickening, and, in one patient with thalassemia, an infarct resulting from arterial thrombus. The progression of these lesions over the course of disease, and possible effects on the various lesions of high transfusion regimen, oral pancreatin, vitamin E supplementation, or treatment with intramuscular, subcutaneous, or intravenous desferrioxamine were evaluated. The results of urine and renal function studies of 4 of the autopsied patients (3 thalassemia, 1 Blackfan-Diamond anemia), and 14 patients with thalassemia and 4 with Blackfan-Diamond anemia who were not autopsied, are presented. Rarely significant until preterminal stages, the renal functional changes reflect distal more than proximal tubule dysfunction.

Adolescent↗
PubMed1988

Reconsideration of the anatomy of sling left pulmonary artery: the association of one form with bridging bronchus and imperforate anus. Anatomic and diagnostic aspects.

In sling (retrotracheal) left pulmonary artery (SLPA), the tracheobronchial pattern is generally considered basically normal. Analysis of dissected specimens and/or bronchograms and other preparations from five studied and 32 reported patients suggests that there are two different forms of SLPA: (1) types 1A and B, with normal TB pattern [with (A) or without (B) a right pre-eparterial (tracheal bronchus)], and the aberrant left pulmonary artery causing TB compression. The tracheal bifurcation in type 1 SLPA is usually demonstrable at the fourth to fifth thoracic vertebral level; (2A) SLPA type 2A, with bridging bronchus (BB), in which condition the right main bronchus supplies the right upper lobe, but the bronchus supplying the right middle and lower lobes (the bridging bronchus) arises from the left main bronchus (LMB), posterior to which the SLPA courses; (2B) SLPA type 2B, with absence of the right bronchial tree, and the right lung (usually hypoplastic) supplied by a BB from the LMB, posterior to which the SLPA courses. SLPA types 2A and B have in common varying degrees of tracheal stenosis with abnormal cartilage rings and absent tracheal pars membranacea, abnormally low tracheal "bifurcation" (pseudocarina) at average level T6, increased bronchial angles with "inverted T" pattern, and lower level of anterior esophageal indentation by the SLPA than SLPA type 1. Imperforate anus occurred in 8/58 (14%) of patients with SLPA types 2A or B, but possibly in none with SLPA type 1. SLPA type 2 is the predominant form of SLPA, with the incidence of type 2B being twice that of type 2A.(ABSTRACT TRUNCATED AT 250 WORDS)

Abnormalities, Multiple↗
PubMed1987

Embryologic and other developmental considerations of thirty-eight possible variants of the DiGeorge anomaly.

The DiGeorge anomaly (DGA) represents a polytopic developmental field defect that can be caused by a number of different chromosomal, mendelian, toxic, or metabolic factors operating in early embryonic life. If the affected field is thought to be focused on either the fourth branchial arch or the third branchial pouch, with variable cephalad or caudad extension, 38 different combinations of malformations can include DiGeorge anomalies, 24 complete and 14 partial DGA, with the constraints that the field defect must be contiguous (involvement of more than one branchial arch or pouch requires involvement of all intervening arches or pouches) and complete (all derivatives of an affected branchial arch or pouch are deficient). The types and relative frequencies of abnormalities of structures other than the thymus and parathyroid glands in these possible "subsets" of DGA are discussed, and the need for more data on their occurrence in patients diagnosed as having DGA is emphasized.

Branchial Region↗
PubMed1987

Demonstration of myenteric plexus abnormalities in genetic diseases by a microdissection technique: preliminary studies.

Eighty-eight specimens of esophagus, small intestine, or colon from 45 patients, predominantly infants and children, with 30 different genetic diseases were analyzed by a microdissection technique for the following abnormalities of the Auerbach (myenteric) plexus: (1) abnormality of the pattern of the nervous network of the plexus, (2) abnormal fraction of neural tissue in the plane of the plexus, (3) abnormal size or appearance of the cytoplasm of the neurons of the plexus, and (4) abnormal number of neurons in the ganglia of the plexus. Seven of 8 specimens of esophagus from patients with neuronal storage diseases (infantile Niemann-Pick disease, Jansky-Bielschowsky disease, etc.) showed an increased fraction of neural tissue in the plane of the plexus, whereas 2 of 3 patients with Cockayne syndrome showed a reduced fraction, with abnormally slender interganglionic fibers. The fraction of neural tissue in the plane of the plexus was also abnormal at one or more levels in patients with adrenoleukodystrophy, ataxia telangiectasia, Krabbe disease, and juvenile metachromatic leukodystrophy. Abnormality of neuron size and cytology was seen in several neuronal lipidoses, including Jansky-Bielschowsky and Sandhoff diseases and juvenile GM2 gangliosidosis, with the most striking neuronal enlargement noted in infantile Niemann-Pick disease. Abnormalities of plexus mass or pattern, as well as those of neuronal cytoplasm and neuron number, offer improved insight into possible mechanisms producing gastrointestinal tract dysfunction (swallowing difficulty, gastroesophageal reflux, constipation, etc) in patients with genetic disorders.

Child↗
PubMed1986

Abnormal Auerbach plexus in the esophagus and stomach of patients with esophageal atresia and tracheoesophageal fistula.

The Auerbach plexus of the upper gastrointestinal tract of five patients with esophageal atresia and tracheoesophageal fistula (EA-TEF) who had not had surgical reconstruction of the esophagus was studied by a microdissection technique to investigate the etiology of dysphagia, gastroesophageal reflux, and delayed gastric emptying; common findings in patients with repaired EA-TEF. All five patients showed a looser than normal Auerbach plexus in the distal esophagus, and to a lesser degree in the proximal esophagus, confirmed by point-count morphometric studies. The Auerbach plexus of the gastric fundus of all the patients was also abnormal. These findings suggest the existence of congenital functional impairment of the upper gastrointestinal tract in patients with EA-TEF, due to abnormal development of the myenteric plexus.

Esophageal Atresia↗
PubMed1986

Abnormal tracheal innervation in patients with esophageal atresia and tracheoesophageal fistula: study of the intrinsic tracheal nerve plexuses by a microdissection technique.

The automatic nervous plexus of the trachea of patients with esophageal atresia and tracheoesophageal fistula (EA-TEF) was examined by a microdissection method. Of 28 autopsied patients with EA-TEF, four patients who had not had esophageal anastomosis were selected, to exclude any changes secondary to anastomosis. The plexus of the pars membranacea of the trachea was hypoplastic in all four patients, and severely so in one. An extra plexus, similar to the myenteric plexus of the esophagus, was present in three of the patients, and an abnormal muscle bundle was seen in the fibroelastic tissue dorsal to the pars membranacea of the trachea in two patients. These findings are suggestive of abnormal separation of the trachea from the esophagus. An abnormal extrachondral plexus was also observed in two patients. These congenital abnormalities of the intrinsic tracheal nervous plexus may be related to tracheal dysfunction and respiratory symptoms in patients who survive EA-TEF.

Adult↗
PubMed1986

Ossification centre of the hyoid bone in DiGeorge syndrome and tetralogy of Fallot.

The incidence of radiographic visibility of the ossification centre of the body of the hyoid bone in radiographs taken during the first month of life was analysed for 34 autopsied infants: 16 with DiGeorge syndrome (DGS), 14 with tetralogy of Fallot (TOF), four with interrupted aortic arch (IAA) and a further 13, surviving infants with non-DGS TOF or non-DGS IAA. The incidence of visible hyoid ossification centre (HOC) was 75.7% in a control series of infants with neither congenital heart disease (CHD) nor DGS. Autopsied patients with DGS, TOF without DGS, and IAA without DGS showed a significantly low incidence of visible HOC. Infants with TOF (and possibly those with IAA) who did not have DGS and who did not die during infancy showed a normal incidence of visible HOC in radiographs taken during the first post-natal month. Radiological visibility of the HOC in the first post-natal month appears useful in the diagnosis of DGS and forms of CHD often seen in association with DGS and in assessing prognosis of neonates with certain types of CHD.

Age Factors↗
PubMed1986

Ossification centre of the hyoid bone in complete transposition of great vessels, Ivemark asplenia syndrome, and Down's syndrome with congenital heart disease: correlation with the humeral capital epiphysis.

The incidence of radiographic visibility of the ossification centres of the body of the hyoid bone and of the humeral capital epiphysis in antero-posterior or lateral chest radiographs taken during the first month of life of 63 autopsied infants were analysed. The group comprised patients with Down's syndrome (DS) with congenital heart disease, 15; complete transposition of the great vessels (TGV), 10; Ivemark asplenia syndrome (IS), 17; and a control group of infants with congenital heart disease (CHD) who had none of the above conditions, nor tetralogy of Fallot, interrupted aortic arch, DiGeorge syndrome or hypoplastic left-heart complex, 31. The incidence of radiographically visible hyoid ossification centre (HOC) in the control group was 71% and of humeral capital epiphysis (HE), 16.1%. Autopsied infants with TGV, IS or DS with CHD showed increased visibility of HOC (100%); the incidence of visible HE was increased in neonates with IS (71.4%) and with TGV (50%). The differences in the incidence of radiographic visibility of HOC and HE in neonates with CHD, in this study and in others in the literature, appear to have diagnostic value.

Age Factors↗
PubMed1986

Abnormal growth of the thyroid cartilage in the DiGeorge syndrome.

Larynges from 17 patients with DiGeorge syndrome (DGS) and from 14 patients with tetralogy of Fallot (TOF) (11 non-DGS and 3 possible but unproven DGS) were dissected, measured, and compared to a control population of comparable body length. The patients with DGS and the 3 patients with TOF suspected of having DGS showed the following: small thyroid cartilages with increased anterior angle, abnormally short superior cornua, low ratio of mean superior cornual length to distance between superior cornual tips, and delayed time of maximal rate of increase in superior cornual length relative to increase in body length. The hypoplasia, delayed maximal growth rate and persistent fetal shape of the thyroid cartilage (predominantly a derivative of the fourth branchial arch) in DGS, indicates that the causative process in the syndrome affects not only the third and fourth branchial pouches, but also, by a contiguous field defect, other derivatives than great vessels of the fourth-sixth branchial arches.

DiGeorge Syndrome↗