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Biomedical subjects

R M Shah

Publications and source records attributed to R M Shah.

At least 19 recordsLinked to original sources
PubMed1995

Superior vena cava syndrome caused by aneurysm of the innominate artery.

Isolated aneurysms or ruptures of the innominate artery are rare causes of the superior vena cava syndrome. We report on a patient who suffered an isolated acute expansion and rupture of an innominate artery aneurysm that precipitated a dramatic superior vena cava syndrome. Immediate repair using modern surgical techniques, cardiopulmonary bypass, profound hypothermia, circulatory arrest, and a Dacron graft rapidly cured the patient of this deadly syndrome.

Aged↗
PubMed1995

Analysis of cell proliferation kinetics during the secondary palate development in quail.

A study was undertaken to analyze the spatio-temporal pattern of mesenchymal cell proliferation in the developing palate of quail. Quail embryos were grown in shell-less culture. The developing palates were labelled with 3H-thymidine between culture days 2-6 (which corresponded in vivo incubation days 5-9), and processed for light microscopic autoradiography. Percent labelled mesenchymal cells were determined. The data showed that, as in mammals, a high rate of random cell proliferation in mesenchyme was a major component of early palate development in quail. As the palate morphogenesis advanced, the rate of cell proliferation declined. Segmental analysis, however, indicated that, in contrast to mammals, the mesenchymal cell proliferation rates continually changed in various regions of quail palate during morphogenesis. It was suggested that the spatio-temporal changes in the distribution of dividing cells may reflect differences in the timings of cell cycles between various segments, thus resulting in a heterogeneous population of cells in the developing palate of quail. Further, the differences in the segmental pattern of cell proliferation between birds and mammals may form the basis for differences in the morphogenesis of their palates.

Animals↗
PubMed1994

Effects of 5-fluorouracil on macromolecular synthesis during secondary palate development in quail.

A study was undertaken to examine the growth of normal and 5-fluorouracil-treated quail secondary palate during embryogenesis. The rates of DNA, RNA, and protein synthesis were measured in the developing quail palate by liquid scintillation counting of radiolabelled thymidine, uridine, or leucine. In addition, shelf volume was determined morphometrically. The results showed that in control palates the shelf volume increased rapidly between days 5 and 7 of incubation. Drug treatment on day 4 did not alter the shelf volume until day 9 of incubation, at which time the treated shelves were smaller than controls. In control palates, the rate of DNA synthesis decreased steadily between days 5 and 9 of incubation. A burst in RNA synthesis on day 7 of incubation was followed by an increase in protein synthesis. Administration of FU seems to exert its effect via disturbing the synthesis of RNA and protein, instead of disruption of DNA synthesis, to ultimately affect the shelf area, and thus palate morphogenesis in quail. Comparison of avian and mammalian data indicated that differences in their palate morphogenesis are also reflected in the different temporal patterns of various macromolecular synthesis.

Animals↗
PubMed1994

A comparative study on the effects of 5-fluorouracil on glycosaminoglycan synthesis during palate development in quail and hamster.

A comparative study was undertaken to investigate the effects of 5-fluorouracil (FU) on glycosaminoglycans (GAG) synthesis during morphogenesis of the secondary palate in birds (where, unlike mammals, palate morphogenesis begins in a horizontal direction ad initium and lacks mammalian-type shelf reorientation) and mammal. Previous studies have shown that FU induces cleft palate in both birds and mammals. Air sacs of quail eggs were injected with 100 micrograms FU in 0.1 ml saline or 0.1 ml saline only. Hamsters were given intramuscular injection of 81 mg/kg FU in 1 ml saline or 1 ml saline only. Total GAG synthesis was measured by incorporation of 3H-glucosamine. Sulfated and non-sulfated GAGs were identified by Alcian Blue histochemistry combined with the use of GAG-degrading enzymes. The results indicated that a continuous synthesis of GAG at a steady rate was associated with normal palate morphogenesis in both quail and hamster. The amount of GAG synthesized in hamster palate was four-fold higher than in quail palate. In contrast to the developing hamster palate where the predominant GAG was hyaluronate, the major GAGs present during quail palate development were sulfated and were concentrated on the nasal side. FU treatment did not affect the rate of GAG synthesis in the developing palate of quail. In contrast, FU administration altered the rates of GAG synthesis, and affected hyaluronate accumulation, during palate morphogenesis in hamster.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcian Blue↗
PubMed1992

Donor iliac angioplasty and crossover femorofemoral bypass.

We reviewed our experience with 99 patients who had 111 femorofemoral bypass grafts placed over a 10-year period. Mean follow-up was 36 +/- 28 months (range: 1 to 120 months). Bypass alone was performed in 89 cases (group 1). Preoperative donor iliac angioplasty was utilized in 22 cases (group 2). Overall graft failure was 21 of 89 in group 1 and 2 of 22 in group 2 (difference was not significant by chi 2: p greater than 0.05). Clinical success as calculated by life-table analysis was 95%, 83%, 75%, and 67% at 1, 3, 5, and 7 years, respectively, for group 1. Clinical success was 100% and 91% at 1 and 3 years, respectively, and 91% at 42 months for group 2. The success rates were not different for the two groups when analyzed by the log-rank test at 42 months (p greater than 0.30). We conclude that donor iliac angioplasty and femorofemoral bypass is an excellent option for patients with severe occlusive disease of one iliac artery and contralateral disease amenable to angioplasty.

Anastomosis, Surgical↗
PubMed1991

Pathogenesis of bromodeoxyuridine-induced cleft palate in hamster.

In the present study, the morphological, histochemical, biochemical, and cellular aspects of the pathogenesis of bromodeoxyuridine (BrdU)-induced cleft palate in hamster fetuses were analyzed. Morphological observations indicated that BrdU interferes with the growth of the vertical shelves and thus induces cleft palate. At an ultrastructural level, BrdU-induced changes were first seen in the mesenchymal cells. Eighteen hours after drug administration, the initial alterations were characterized by swelling of the nuclear membrane and the appearance of lysosomes in the mesenchymal cells of the roof of the oronasal cavity. During the next 6 hr, as the palatal primordia developed, lysosomes were also seen in the overlying epithelial cells. The appearance of lysosomal activity, which was verified by acid phosphatase histochemistry, was temporally abnormal and was interpreted as a sublethal response to BrdU treatment. Later the cellular alterations subsided; 48 hr after BrdU treatment, they were absent in both the epithelial and mesenchymal cells of the vertically developing palatal shelves. Subsequently, unlike controls (in which the palatal shelves undergo reorientation and fusion), the BrdU-treated shelves remained vertical until term. Biochemical determination of DNA synthesis indicated that although there was an inhibition of DNA synthesis at the time of appearance of palatal primordia, a catch-up growth during the ensuing 12 hr may have restored the number of cells available for the formation of a vertical palatal shelf. It was suggested that BrdU affected cytodifferentiation in the palatal tissues during the critical phase of early vertical development to induce a cleft palate.

Acid Phosphatase↗
PubMed1991

Genesis of hadacidin-induced cleft palate in hamster: morphogenesis, electron microscopy, and determination of DNA synthesis, cAMP, and enzyme acid phosphatase.

A morphological, electron microscopic, and biochemical study was undertaken to analyze the genesis of hadacidin-induced cleft palate in hamster fetuses. Gross and light microscopic observations indicated that hadacidin affected the growth of vertical palatal shelves to induce cleft palate. Electron microscopic observations showed that initial hadacidin-induced changes were seen in the mesenchymal cells. Within 12 hr of drug administration, the perinuclear space was swollen and a lysosomal response injury was evident in the mesenchymal cells. Subsequently, 24 hr after hadacidin treatment, lysosomes appeared in the epithelial cells; changes were also seen in the basal lamina which included separation of the lamina densa from the basal cells, duplication of lamina densa, and complete loss of basal lamina. Between 36 and 42 hr post-treatment, the cellular and basal lamina changes subsided, and the epithelium of vertical shelves underwent stratification. Biochemical determination of enzyme acid phosphatase indicated that the levels of enzyme activity in both the control and treated palatal tissues corresponded to the appearance of lysosomes. Measurement of cAMP levels suggested that the peak activity of cAMP corresponded to that of enzyme acid phosphatase and cell injury. The cAMP activity in hadacidin-injured cells, however, was significantly lower in comparison to that of the dying cells of control palates. Hadacidin treatment also affected DNA synthesis in the developing primordia of the palate. It was suggested that hadacidin injures the precursor cells of the palate prior to the appearance of the primordia, and subsequently affects their proliferative behavior, stunting the vertical growth of the palatal shelves and inducing a cleft palate.

Acid Phosphatase↗
PubMed1991

Dioxin contamination and growth and development in great blue heron embryos.

A great blue heron colony located near a pulp mill in British Columbia failed to fledge young in 1987, with a concurrent sharp increase in polychlorinated dibenzo-p-dioxin (PCDD) and polychlorinated dibenzofuran (PCDF) levels in their eggs. In 1988 we tested the hypothesis that the PCDD and PCDF contamination caused reproductive failure by increasing mortality of the heron embryos in ovo. Pairs of great blue heron eggs were collected from three British Columbia colonies with low, intermediate, and high levels of dioxin contamination: Nicomekl, Vancouver, and Crofton, respectively. One egg of each pair was incubated under laboratory conditions at the University of British Columbia (UBC) while the other egg was analyzed for PCDDs and PCDFs. All incubated eggs were fertile. All eggs from the Nicomekl colony hatched, while 13 of 14 eggs from Vancouver and 12 of 13 eggs from Crofton hatched. Subcutaneous edema was observed in 4 of 12 chicks from Crofton and 2 of 13 chicks from Vancouver. No edema was seen in the chicks from Nicomekl. There was a small, but significant, negative regression of plasma calcium concentration, yolk-free body weight, tibia length, wet, dry, and ash weight, beak length, and kidney and stomach weight of the hatched chicks on the tetrachlorodibenzo-p-dioxin (TCDD) level of the paired eggs. Fewer down follicles were present on the heads of TCDD-contaminated chicks. Hence while dioxins did not cause mortality of the heron embryos in ovo, the depression of growth and the presence of edema are suggestive that dioxins at the levels found in the environment have an adverse effect on the development of great blue heron embryos.

Animals↗
PubMed1991

Pulmonary function tests in bronchopleural fistula.

A 53-year-old white man underwent a left pneumonectomy for alveolar cell carcinoma. His postoperative course was complicated by pneumonia. At a follow-up clinic visit, the patient complained of a "roaring sound" during respiration. A follow-up PFT did not show the expected loss of volume (nitrogen washout) from a preoperative PFT, suggesting a bronchopleural fistula. A chest x-ray film and xenon lung scan confirmed the diagnosis. The fistula was surgically repaired.

Bronchial Fistula↗
PubMed1990

Differentiation of cyclophosphamide-treated hamster secondary palate: ultrastructural and biochemical observations.

A study was undertaken to analyze the ultrastructural aspects and the enzyme acid phosphatase cytochemistry and biochemistry of the pathogenesis of cyclophosphamide (CP)-induced cleft palate in hamster fetuses. The initial CP-induced alterations were the appearance of lysosomes in the mesenchymal cells of the vertically developing palatal primordia within 8 hr of drug administration. The mesenchymal lysosomal activity, which increased during the next 16 hr, was abnormal and interpreted as a sub-lethal response to CP treatment. Subsequently, the lysosomal activity in the mesenchyme diminished gradually and, 48 hr after CP treatment, was absent. At this time, lysosomes were seen in the epithelial cells of the vertical palate. Fifty-six hours after CP treatment, unlike controls where palatal shelves were already fused, lysosomal activity subsided in the epithelial cells. Changes, however, continued to be seen at the epithelial-mesenchymal interface. These changes were characterized by discontinuity in the basal lamina, and by epithelial-mesenchymal contacts. They persisted for 8 hr but were absent thereafter. Sixty-four hours after CP administration, the vertical shelves became horizontal and remained so until term. Following analysis of data, both from the literature and from the present study, it was suggested that CP first affected mesenchymal cell proliferation, and then its cytodifferentiation, during the critical phase of early vertical development; consequently the reorientation of the shelves to a horizontal plane was delayed, inducing cleft palate.

Acid Phosphatase↗
PubMed1990

Toward the origin of the secondary palate. A possible homologue in the embryo of fish, Onchorhynchus kisutch, with description of changes in the basement membrane area.

The oral cavity of embryos and larvae of the teleost Onchorhynchus kisutch was examined. Tissues were obtained at different ages prior to and after hatching and processed for transmission and scanning electron microscopy. A bilaterally symmetrical bulge developed from the superolateral aspect of the oral cavity and projected toward its floor, along the sides of the tongue. The bulge extended from behind the primary palate to a position midway below the eye, anterior to the gill arches, and it is suggested to be the homologue of the secondary palate of higher vertebrates. Ultrastructurally, the epithelium differentiated as the stratified squamous type and it contained mucous cells. However, the features of programmed cell death seen during palatogenesis in mammals were absent in fish. The fish palate mesenchyme, unlike that of higher vertebrates, was chondrified. Also in contrast to higher vertebrates, alterations were seen in the fish palatal basement membrane. A transient appearance of adepidermal granules in the lamina lucida region was followed by organization of collagen fibrils, first into an orthogonal pattern and then into a herring-bone arrangement, in the lamina reticularis region. There was no further advancement in the morphogenesis of fish palate. It is suggested that the differences in the morphogenesis and structure of the secondary palates of various vertebrates may reflect environmentally enforced adaptation, resulting in different programming of cells.

Animals↗
PubMed1989

Growth of the secondary palate in the hamster following hydrocortisone treatment: shelf area, cell number, and DNA synthesis.

The contribution made by mesenchymal cells during the later stages of palatal development was examined in control and hydrocortisone-treated hamster embryos. Cross-sectional area of the palatal shelf was measured, and the numbers of both epithelial and mesenchymal cells were counted. DNA synthesis was measured by 3H-thymidine incorporation and was used as an index of growth by cell proliferation. The observations in controls indicated that, unlike development during the initial 24 hr, the later period of vertical palate development, followed by reorientation of shelves and their closure, was characterized by a steady level of mesenchymal cell number and palatal shelf area. An absence of corresponding growth in the epithelial cell number suggests that the cells may accommodate the growth either by increasing their size and/or by stretching along the basal lamina. Hydrocortisone treatment did not alter the growth pattern of cell numbers or shelf area. However, it prevented the fusion between the opposing shelves, perhaps by affecting the cytodifferentiation of the palatal tissues. Although a continuous increase in the number of mesenchymal cells during the latter half of vertical shelf development, i.e., between days 11:00 and 12:00 of gestation, is not required for reorientation and fusion of the shelves, it is not clear from the data from the present study whether a critical number of cells and/or cell density is essential for reorientation and fusion of the palate. It was suggested that, for normal palatal development, information on cell cycle and positioning of mesenchymal cells within the shelf during the vertical development may be crucial for further understanding of subsequent events of palatogenesis.

Animals↗
PubMed1989

Palatal shelf reorientation in hamster embryos following treatment with 5-fluorouracil.

A study was undertaken to examine the issue of whether achieving a critical mass of cells and/or palatal shelf volume during vertical development of shelf is essential for reorientation to occur. In control and 5-fluorouracil (5FU)-treated hamster embryos' palatal shelves, at different times during gestation, the numbers of both epithelial and mesenchymal cells were counted and cross-sectional area was measured. DNA synthesis was measured by 3H-thymidine incorporation and was used as an index of growth by cell proliferation. The control data indicated that, unlike development during initial 24 hours, the later period of vertical palatal development was characterized by a steady level of mesenchymal and epithelial cell numbers and palatal shelf area. Following 5FU treatment all the measurements were reduced, and until they reached the equivalent of control values, the palatal shelves did not reorient. The density of mesenchymal cells in the developing palate did not seem to affect cell number. On the basis of the analysis of results of the present study, along with those reported in the literature, it is suggested that, in hamsters, acquisition and maintenance of both a specified number of mesenchymal cells and shelf area, at least 24 hours prior to reorientation, may be critical for ensuing mesenchymal differentiation to enforce palatal shelf reorientation on schedule. 5FU affected these features to delay reorientation of the palatal shelf.

Abnormalities, Drug-Induced↗
PubMed1989

Effects of cyclophosphamide on the secondary palate development in golden Syrian hamster: teratology, morphology, and morphometry.

Cyclophosphamide (CP), when injected in hamster mother between days 9 and 11 of pregnancy, was teratogenic in fetuses. On the basis of a morphological study it was deduced that CP delayed the reorientation of hamster palatal shelves by 16-20 h. In a subsequent experiment, in both control and CP-treated palatal shelves, the numbers of epithelial and mesenchymal cells were counted and cross-sectional area was measured. DNA synthesis, measured by 3H-thymidine incorporation, was used as an index of growth by cell proliferation. The results showed that during the vertical development of palatal shelves, the mesenchymal cells reached their peak number during the initial 24 hours, i.e., at the end of the second peak in DNA synthesis, and remained unchanged thereafter throughout reorientation. The shelf area also showed rapid increase during the initial 24 h followed by a spurt 2 h prior to reorientation. Cyclophosphamide prolonged the acquisition of these features by affecting the mesenchymal cells and consequently delayed the reorientation of the vertical shelves until such time that the number of healthy mesenchymal cells and shelf area were restored to the control values. The data lend further support to the hypothesis that the acquisition of a specific number of cells and shelf volume, during vertical palatal development, may be essential for palatal shelf reorientation.

Abnormalities, Drug-Induced↗
PubMed1988

Gross and cellular analysis of 6-mercaptopurine-induced cleft palate in hamster.

The present study analyzes the morphological, histochemical, and ultrastructural aspects of the pathogenesis of 6-mercaptopurine (6MP)-induced cleft palate in hamster fetuses. Gross and light microscopic observations indicated that 6MP stunts the growth of vertical palatal shelves and thus induces cleft palate. Ultrastructural analysis showed that, in contrast to controls, 6MP-induced alterations were first seen in the mesenchymal cells 24 hr after drug administration. The initial alterations were characterized by swelling of the nuclear membrane. During the next 12 hr, lysosomes were seen first in the mesenchymal cells and then in the cells of the medial edge epithelium (MEE) of the developing palatal primordia. The appearance of lysosomes was temporally abnormal and was interpreted as a sublethal response to 6MP treatment. Subsequently, the nuclear alterations and the lysosomes diminished; and 48 hr after 6MP administration, they were absent from the palatal tissues. Ninety hours after 6MP administration, unlike the controls (in which the palatal shelves were already fused), changes were seen at the epithelial-mesenchymal interface in the developing cleft palatal shelves. These changes were characterized by breakdown of the basal lamina and epithelial-mesenchymal contacts. Eventually, at term, the MEE of the vertical shelf stratified. It was suggested that 6MP affected cytodifferentiation in the palatal tissues during the critical phase of early vertical shelf development and thereby induced cleft palate.

Acid Phosphatase↗
PubMed1988

Vertical development of the secondary palate in hamster embryos following exposure to 6-mercaptopurine.

Cellular aspects of vertical development of the secondary palate were examined in control and 6-mercaptopurine (6MP)-treated hamster embryos. Cross-sectional area of the palatal shelf was measured and the numbers of both epithelial and mesenchymal cells counted. Also, in 6MP-treated palates the damaged mesenchymal cells, characterized by the presence of dense bodies, were counted. DNA synthesis in both control and treated fetuses was measured by 3H-thymidine incorporation. The results indicated that both the shelf area and cell numbers increased with age in control and 6MP-treated palates. However, in controls the mesenchymal cell density and DNA synthesis showed two peaks that were absent following 6MP treatment. Unlike controls, in treated embryos the damage to mesenchymal cells became increasingly pronounced between days 10:00 and 10:12 but subsided by day 11:00 of gestation. It is suggested that a major force in the development of the initial primordia and early vertical development of the palatal shelf may be provided by a spurt of DNA synthesis in the mesenchymal cells resulting in their increased number. After 6MP treatment, depression of DNA synthesis and consequent reduction in the mesenchymal cell number and density followed by cell damage lead to retardation in the vertical development of the palatal shelves.

Animals↗