Kuldeep Teja
University of Virginia
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Journal of the American College of Cardiology | 1988
Mark W. Keller; William P. Glasheen; Kuldeep Teja; Adrian R. L. Gear; Sanjiv Kaul
All agents used for myocardial contrast echocardiography to date produce adverse hemodynamic effects and alter coronary blood flow. It was hypothesized that because 5% human albumin, when sonicated for use as a contrast agent, is neither hyperosmolar nor a calcium chelator, it would not have significant effects on coronary blood flow, left ventricular function or systemic hemodynamics. Albumin microbubbles of two distinct sizes (mean size 2.9 and 5.8 micron) were produced and compared with nonsonicated albumin, nonsonicated Renografin, sonicated Renografin and hand-agitated Renografin for their effects on hemodynamics, coronary blood flow and regional left ventricular systolic thickening in 15 open chest anesthetized dogs. None of the albumin solutions significantly altered left atrial, left ventricular systolic and end-diastolic and mean aortic pressures. These agents did not cause a coronary hyperemic response or alter left ventricular systolic thickening, but slightly lowered the peak positive left ventricular maximal rate of rise in pressure (dP/dt) (-4.1 +/- 5.4%, p less than 0.01). In contrast, all the Renografin solutions caused significant changes in all these variables (p less than 0.02). In six dogs. albumin solutions did not alter these variables even in the presence of critical coronary stenosis. The contrast opacification produced by 5.8 micron albumin microbubbles was equivalent to that produced by sonicated Renografin. Compared with an equivalent amount of saline and nonsonicated albumin solutions, 10 ml of sonicated albumin did not produce any evidence of infarction, embolization or hemorrhage in the myocardium, brain or kidneys of rabbits.(ABSTRACT TRUNCATED AT 250 WORDS)
Human Pathology | 1982
Frank A. Mitros; Michael D. Schuffler; Kuldeep Teja; Sinn Anuras
Familial visceral myopathy is the most common cause of chronic primary (idiopathic) intestinal pseudo-obstruction. We studied four family groups with this disease and found that it has a characteristic morphologic appearance. Grossly, there is segmental dilatation of the alimentary tract, often involving multiple sites and most commonly producing a megaduodenum. Microscopically, the involved areas show a characteristic change consisting of degenerating muscle cells and fibrosis, which may involve the full thickness of the muscularis propria but is often more prominent in or limited to the external layer. Degenerating muscle cells appear pale, poorly defined, and fragmented. As residual thread-like remnants become surrounded by collagen or as muscle cells are destroyed, leaving apparent spaces surrounded by collagen, the longitudinal and circular muscles take on a vacuolated appearance easily recognized at low magnifications. Recognition of this change is greatly facilitated by use of a trichrome stain, and mild lesions may be recognized only with such stains. The nondilated segments of intestine show similar changes but of a less severe degree. Neural and vascular structures are apparently normal. Although the lesion most closely resembles progressive systemic sclerosis, the degenerating muscle cells and vacuolated appearance of the muscle serve to distinguish familial visceral myopathy from the latter entity.
The New England Journal of Medicine | 1981
Kuldeep Teja; Philip H. Cooper; Jerry E. Squires; Patricia T. Schnatterly
PULMONARY alveolar proteinosis (PAP) is a distinctive pathologic lesion in which alveoli are filled with periodic acid–Schiffpositive proteinaceous material. It is usually idiopathic, but it has be...
Journal of Pediatric Surgery | 1981
Kuldeep Teja; P. Schnatterly; A. Shaw
This paper describes the clinical and pathologic features of a rare case of multiple intestinal atresias and attempts to offer a concept for the pathogenesis of this rare type.
American Journal of Surgery | 1979
Stacey E. Mills; Kuldeep Teja; Ivan K. Crosby; Benjamin C. Sturgill
During the eleven year period from 1965 to 1976, aortic dissection was diagnosed in seventy-eight patients treated at the University of Virginia Medical Center. The seventy-four cases that comprise the present report were confirmed by aortography, surgery, or autopsy. Forty patients (54 per cent) were surgically treated by interruption of the origin of dissection and insertion of a Dacron prosthesis. The remaining thirty-four (46 per cent) were treated according to the Wheat regimen or by nonspecific supportive measures. The overall survival at one year was 28 per cent. One year survival for patients with type I dissections treated surgically was 19 per cent compared with 8 per cent one year survival for nonsurgically treated patients. Sixty per cent of patients with type II dissections treated surgically were alive at the end of one year, whereas no patients with type II dissection treated nonsurgically survived beyond one year. Half the patients with type III dissections treated surgically were alive at one year compared with 35 per cent of those nonsurgically treated. These data suggest that surgery is the treatment of choice for all types of aortic dissections, but particularly for type II. Patients with type I dissections have a very poor prognosis regardless of therapy.
Human Pathology | 1981
Kuldeep Teja; Hernan Sabio; David R. Langdon; Ann J. Johanson
A 27 month old white male infant clinically suspected of having histiocytosis X had an enlarged hard hypofunctioning thyroid. A needle biopsy of the thyroid showed disruption of the thyroid architecture by an infiltrate consisting of large histiocytes admixed with eosinophils, neutrophils, and lymphocytes, confirming the clinical diagnosis of histiocytosis X.
Journal of Pediatric Surgery | 1975
Edwin W. Shearburn; Kuldeep Teja; Luis M. Botero; Anthony Shaw
A 2-mo-old female with congenital fibrosarcoma causing duodenal obstruction had a pancreaticoduodenectomy. She is doing well with the aid of oral pancreatic enzyme supplements 14 mo after her pancreaticoduodenectomy with no evidence of tumor recurrence or pancreatic endocrine dysfunction.
Journal of Pediatric Surgery | 1981
Kuldeep Teja; Philip H. Cooper
Accessory tragus is a frequently misdiagnosed entity. A brother and sister with this lesion are reported. Clinical and pathologic features are described which should help to make a correct preoperative diagnosis.
Cancer | 1982
H. Branch Coslett; Kuldeep Teja; Thomas Sutula
An unusual case is described of pure meningeal carcinomatosis in the absence of other evidence of tumor occurring 21 years after lobectomy for a localized bronchiolo‐alveolar carcinoma. The metastatic disease was confined to the leptomeninges and was documented only by a cisternal cerebrospinal fluid (CSF) examination. Four previous lumbar punctures had shown hypoglycorrachia as the only CSF abnormality.
The Journal of Pediatrics | 1982
Anthony Shaw; Kuldeep Teja
1. Fukuyama Y, Osawa M, and Suzuki H: Congenital progressive muscular dystrophy of the Fukuyama type---clinical, genetic and pathological considerations, Brain Dev 3:1, 1981. 2. Nonaka I, and Chou SM: Congenital muscular dystrophy, in Vinken P J, and Bruyn GW, editors: Handbook of clinical neurology, vol 41, Amsterdam, 1979, North Holland Publishing Company, pp 27-50. 3. Yoshioka M, Takehiko O, Ito M, et al: Congenital muscular dystrophy (Fukuyama type), repeated CT studies in 19 children, Comput Tomogr 5:81, 1981. 4. Yoshioka M, Okuno T, Honda Y, and Nakano Y: Central nervous system involvement in progressive muscular dystrophy, Arch Dis Child 55:589, 1980. 5. Kamoshita S, Konishi Y, Segawa M, and Fukuyama Y: Congenital muscular dystrophy as a disease of the central nervous system, Arch Neurol 33:513, 1976. 6. Fowler M, and Manson JT: Congenital muscular dystrophy with malformation of central nervous system, in Kakulas BA, editor: Clinical studies in myology. Proceedings of the Second International Congress of Muscle Diseases, Perth, 1971, Amsterdam, 1973, Excerpta Medica, pp 192-197. 7. Krijgsman JB, Barth PG, Stam FC, Slooff JL, and Jaspar HHJ: Congenital muscular dystrophy and cerebral dysgenesis in a Dutch family, Neuropaediatrie 11:108, 1980. 8. Jervis GA: Progressive muscular dystrophy with extensive demyelination of the brain, J Neuropathol Exp Neurol 14:376, 1955. 9. Bernier JP, Brooke MH, Naidich TP, and Carroll JE: Myoencephalopathy: Cerebral hypomyelination revealed by CT scan of the head in a muscle disease, Trans Am Neurol Assoc 104:244, 1979. 10. Nogen AG: Congenital muscle disease and abnormal findings on computed tomography, Dev Med Child Neurol 22:658, 1980. 11. McMenamin JB, Becker LE, and Murphy EG: Congenital muscular dystrophy: A clinicopathologic report of 24 cases, J PEDIATR 100:692, I982. 12. Lazaro RP, Fenichel GM, and Kilroy AW: Congenital muscular dystrophy: Case reports and reappraisal, Muscle Nerve 2:349, 1979. 13. Donner M, Rapola J, and Somer H: Congenital muscular dystrophy: A clinicopathological and follow up study of 15 patients, Neuropaediatrie 6:239, 1975. 14. Misugi N: Light and electron microscopic studies of congenital muscular dystrophy, Brain Dev 2:191, 1980.