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Biomedical subjects

S J Fishman

Publications and source records attributed to S J Fishman.

At least 19 recordsLinked to original sources
PubMed1999

Allergic colitis: a mimic of Hirschsprung disease.

BACKGROUND: Allergy to cow milk protein is a common cause of gastrointestinal symptoms in infancy. Milk allergy is usually a clinical diagnosis, and thus there have been few reports of the radiographic findings. OBJECTIVE: To describe the barium enema findings of allergic colitis and differentiate them from Hirschsprung disease. Materials and methods. Four infants (age range 7 days-5 weeks) with constipation underwent barium enema to exclude Hirschsprung disease. Radiographic findings were correlated with the pathologic specimens from suction rectal biopsy. RESULTS: All enemas revealed irregular narrowing of the rectum and a transition zone. Rectal biopsies in each case demonstrated ganglion cells and evidence of an allergic colitis, with inflammatory infiltrates in the lamina propria. A diagnosis of milk allergy colitis was made and symptoms resolved after removal of milk from the diet. CONCLUSIONS: Milk allergy is common in infancy. The rectum is a primary target organ, with allergic colitis often diagnosed on clinical grounds alone. However, a child with allergic colitis may be referred to radiology for barium enema, especially if constipation is present. The radiologist should be aware of the unique imaging findings of allergic colitis, so as to avoid confusion with Hirschsprung disease and perhaps an unnecessary rectal biopsy.

Animals↗
PubMed1998

Fetal carotid blood flow during videofetoscopy.

BACKGROUND/PURPOSE: Intracranial bleeding has been reported as one of the complications of both open and minimally invasive fetal surgery and putatively attributed to intraoperative fluctuations of carotid blood flow. The aim of this study was to look at fetal carotid blood flow and its relationship with umbilical blood flow, blood pressure, oxygen delivery, and acid-base status in the fetus at various intraamniotic pressures with both liquid and gas media during fetoscopic surgery. METHODS: Six 115- to 130-day-gestation ewes underwent continuous invasive systemic blood pressure monitoring in the descending aorta. A hysterotomy was performed. A 6-mm ultrasonic blood flow probe was placed around the common umbilical artery at its origin from the fetal aorta. This was followed by placement of a double-lumen, 4F catheter in the fetal descending aorta through a femoral artery. A 4-mm ultrasonic blood flow probe was then placed around the fetal left common carotid artery. A pressure-monitoring, multiperforated catheter was placed inside the amniotic cavity. The fetus was repositioned inside the uterus, which was then closed. The abdominal wall was closed loosely. No further manipulation was performed for 1 hour. Intraamniotic pressure was raised from 0 to 30 mm Hg at 5-mm Hg intervals by infusing either warmed saline or medical air. Common umbilical artery and left carotid artery blood flows, blood pressure, blood gases, bicarbonate, sodium, and hematocrit were recorded in all fetuses at each 5-mm Hg interval. Maternal systemic blood pressure, O2 saturation, and temperature were kept constant. RESULTS: Carotid blood flow remained stable within the intra-amniotic pressure range studied (0 to 30 mm Hg), despite the significant drop in common umbilical artery blood flow uniformly observed above 20 mm Hg when saline was infused and above 15 mm Hg when air was infused. There was fetal hypoxemia and hypercarbia concomitant with decreased common umbilical artery blood flow (however, without fetal acidosis, because of compensatory elevation of bicarbonate). Within the intraamniotic pressure range studied, fetal aortic blood pressure, sodium, and hematocrit did not vary significantly, even when there was decreased umbilical blood flow. CONCLUSIONS: Fetal carotid blood flow is protected, possibly autoregulated, remaining stable even after umbilical blood flow decreases as a consequence of elevated intrauterine pressures up to 30 mm Hg during videofetoscopy. These data suggests that perioperative intracranial bleeding related to videofetoscopic surgery is caused by factors other than fluctuations of cerebral blood flow.

Amniotic Fluid↗
PubMed1998

Videofetoscopically assisted fetal tissue engineering: bladder augmentation.

BACKGROUND/PURPOSE: Treatment of several congenital anomalies is frequently hindered by lack of enough tissue for surgical reconstruction in the neonatal period. Minimally invasive harvest of fetal tissue, which is then processed through tissue engineering techniques in vitro while pregnancy is allowed to continue so that at delivery a newborn with a prenatally diagnosed congenital anomaly can benefit from having autologous, expanded tissue promptly available for surgical reconstruction at birth. This concept was applied to a bladder defect. METHODS: Bladder exstrophy was surgically created in ten 90- to 95-day gestation fetal lambs, which were divided in two groups. In group I, a small fetal bladder specimen was harvested through a minimally invasive technique (videofetoscopy). Urothelial and smooth muscle cells were then separately cultivated and expanded in vitro for 55 to 60 days, resulting in a total of approximately 200 million cells. Seven to 10 days before delivery, the cells were seeded in two layers in a 16- to 20-cm2, 3-mm thick biodegradable polyglycolic acid polymer matrix. One to 4 days after delivery, autologous engineered tissue was used for surgical augmentation of the exstrophic bladder. In group II, no harvest was performed, and the bladder exstrophy was primarily closed after delivery. In both groups, a catheter was left inside the bladder for 3 weeks, at which time a cystogram was performed and the catheter then removed. In all animals, at 60 days, another cystogram was performed and urodynamic studies of the bladder were performed. The bladder was then removed for histological analysis. RESULTS: Fetal survival rate was 100%. One newborn died immediately after the implantation of the engineered bladder from an anesthetic accident. The other nine (four in group I and five in group II) survived. One of the animals from group I lost its bladder catheter prematurely and had a urinary leak detected only at the time of death. There were no other complications. The engineered bladders were more compliant (P < .05) and had greater capacity pressures greater than 20 mm Hg (P < .05) than those closed primarily. Histological analysis of the engineered tissue showed a multilayered urothelial lining on the luminal side and overlying layers of smooth muscle cells surrounded by connective tissue. CONCLUSIONS: Videofetoscopically assisted fetal bladder engineering may be a viable alternative for prompt bladder reconstruction at birth. The architecture of autologous engineered fetal bladder tissue resembles that of native bladder. This concept may prove useful for the treatment of certain human neonatal conditions such as bladder and cloacal exstrophies.

Animals↗
PubMed1998

Videofetoscopically assisted fetal tissue engineering: skin replacement.

BACKGROUND/PURPOSE: Treatment of several congenital anomalies is frequently hindered by lack of enough tissue for surgical reconstruction in the neonatal period. The purposes of this study were (1) introduction of a novel concept in perinatal surgery, involving minimally invasive harvest of fetal tissue, which is then processed through tissue engineering techniques in vitro while pregnancy is allowed to continue, so that, at delivery, the newborn can benefit from having autologous, expanded tissue promptly available for surgical implantation at birth; (2) analysis of the progress of an engineered fetal skin graft with time, after implantation in the neonate; and (3) study of the effects of current tissue engineering techniques on fetal keratinocytes and fetal dermal fibroblasts. METHODS: Ten 90- to 95-day-gestation fetal lambs underwent surgical creation of two large paramedian excisional skin defects on the posterior body wall. Subsequently, fetal skin specimens no larger than 1.5 x 1.5 cm were videofetoscopically harvested. Fetal keratinocytes and dermal fibroblasts were then separately cultivated and expanded in vitro for 45 to 50 days, resulting in a total of approximately 250 to 300 million cells. Seven to 10 days before fetal delivery, all cells were seeded in two layers on a 16 to 20-cm2, 3-mm thick biodegradable polyglycolic acid polymer matrix. One to 4 days after delivery, the autologous engineered skin was implanted over one of two previously created skin defects. The second skin defect region received an absorbable polymer scaffold without cells as a control. If necessary, the original skin wounds were further amplified before implantation. Each animal provided at least one time-point for histological analysis of both types of repair through excisional biopsies performed at weekly intervals, up to 8 weeks postimplantation. Normal skin specimens were also used as controls. RESULTS: Fetal and neonatal survival rates were 100%. Based on previous postnatal skin engineering studies, fetal dermal fibroblasts multiplied significantly faster in vitro (approximately fivefold) than expected. Fetal keratinocytes multiplied at expected postnatal rates. The engineered grafts induced faster epithelization of the wound (partial at 1 week and complete between 2 and 3 weeks postoperatively) than did the acellular ones (partial at 3 weeks and complete between 3 and 4 weeks postoperatively). Analysis of skin architecture showed a higher level of epidermal organization and less dermal scarring in the wounds that received the engineered, cell-implanted polymer scaffold. CONCLUSIONS: (1) Videofetoscopically assisted fetal tissue engineering is a viable method for obtaining expanded autologous tissue for prompt surgical reconstruction at birth. (2) Fetal skin can be expanded and engineered in vitro at faster rates than expected postnatally, with current tissue engineering techniques. (3) Engineered autologous fetal skin induces a faster and more organized healing of neonatal skin defects than that observed with second intention. This concept may prove useful for the treatment of certain human neonatal conditions such as giant neoplasias, ectopia cordis, and other body wall defects.

Animals↗
PubMed1998

Gastrointestinal manifestations of vascular anomalies in childhood: varied etiologies require multiple therapeutic modalities.

BACKGROUND/PURPOSE: Vascular anomalies, including hemangiomas and vascular malformations afford complex diagnostic and therapeutic challenges when gastrointestinal (GI) manifestations are present. METHODS: Twenty-one patients evaluated or treated in our Vascular Anomalies Program from 1993 through 1997 were reviewed retrospectively with regard to presentation, treatment modalities, and outcome. RESULTS: Four patients had hemangiomas, and 17 had various vascular malformations. GI symptoms began in infancy or early childhood in all patients. Manifestations included GI bleeding (n = 15), obstruction (n = 2), diarrhea (n = 2), ascites (n = 2), pain (n = 1), emesis (n = 1), ileo-ileal intussusception (n = 1), protein-losing enteropathy (n = 1), and hypersplenism (n = 1). Four patients had proven portal hypertension. Fourteen had associated musculoskeletal or cutaneous lesions. Congestive heart failure, partial anomalous pulmonary venous return, pulmonary edema, and pleural or pericardial effusion occurred in one patient each. Bleeding was the most common symptom of both hemangiomas and malformations. Of four patients with hemangiomas, three were treated with corticosteroids or interferon. Endoscopic banding and embolization of an associated arterioportal hepatic shunt were each used in one patient. One patient died. The malformations were treated with resection (n = 8), endoscopic banding or sclerosis (n = 7), percutaneous or intraoperative sclerosis (n = 5), embolization or device interruption (n = 3), and portosystemic shunt (n = 2). GI symptoms were ameliorated in 12 patients with malformation, improved in two, unchanged in two, and one died after prolonged palliation. CONCLUSIONS: Vascular anomalies with gastrointestinal manifestations are heterogeneous in their presentation and type. Although bleeding is the most common symptom of both hemangiomas and vascular malformations, treatment differs. Pharmacological angiogenesis inhibition is the mainstay of hemangioma therapy. Resection, endoscopic or radiologic vascular obliteration, and portal decompression are important in treating vascular malformations. An individualized and interdisciplinary approach is often required to successfully diagnose and treat these complex lesions.

Adolescent↗
PubMed1998

Vascular anomalies. A primer for pediatricians.

The future is bright for children with vascular anomalies. Children with vascular anomalies no longer have to languish in the interface between various medical specialties. Vascular anomalies centers are available for consultation. Not only are specialists focusing on the conditions, but basic science has brought us to the horizon of new insights into etiology and thus the possibility for new treatment. For children with vascular tumors, newer antiangiogenic agents are already in clinical trials. For children with vascular malformations, research in molecular genetics has begun to uncover the genes responsible for normal fetal vasculogenesis and angiogenesis. Molecular studies of familial vascular malformative syndromes are just beginning to pinpoint causative mutations. Next, animal models of vascular abnormalities will be engineered to elucidate pathogenesis, and these studies, in turn, should lead to development of novel therapies.

Blood Vessels↗
PubMed1997

Serum basic fibroblast growth factor in pediatric Crohn's disease. Implications for wound healing.

Basic fibroblast growth factor is a heparin-binding protein known to stimulate angiogenesis and promote wound healing in tissues. Since Crohn's disease is characterized in part by submucosal vascular proliferation, we sought to determine whether serum basic fibroblast growth factor is elevated in children with Crohn's disease and whether serum levels reflect disease activity. Sera were obtained from 64 children with Crohn's disease, 44 children with ulcerative colitis, 20 children with functional abdominal pain, and 29 from children with documented inflammatory disease evaluated in our gastroenterology program. Disease activity indices and clinical data were gathered prospectively for the inflammatory bowel disease patients. Serum basic fibroblast growth factor levels were measured by enzyme-linked immunosorbent assay. Although the mean basic fibroblast growth factor level did not significantly differ between children with Crohn's disease and other conditions, there was a strong (r = 0.53, P < 0.001) correlation between basic fibroblast growth factor level and disease activity. The relationship of basic fibroblast growth factor with disease activity persisted even after adjusting for other covariates (including age, sex, hematocrit, albumin, and sedimentation rate) in a multivariate linear regression model. There was also a statistically significant, although less strong correlation (r = 0.33, P = 0.03) between basic fibroblast growth factor level and disease activity in ulcerative colitis. While basic fibroblast growth factor is not a specific marker for Crohn's disease, serum levels reflect disease activity. Therefore, basic fibroblast growth factor release may be important in mediating the angiogenesis and wound healing seen in Crohn's disease.

Adolescent↗
PubMed1996

The effects of Carmeda Bioactive Surface on human blood components during simulated extracorporeal circulation.

Postoperative morbidity after cardiopulmonary bypass most commonly manifests as bleeding diatheses or pulmonary dysfunction. The pathophysiology has been attributed to the activation of cellular and humoral components of blood after contact with an artificial surface. Development of a surface that would be nonthrombogenic and also would constitute a less potent inflammatory stimulus would therefore be beneficial. In the following experiments, we evaluated the heparin-bonded Carmeda Bioactive Surface (Medtronics Cardiopulmonary, Anaheim, Calif.) in an in vitro model of extracorporeal circulation at standard-dose heparin (5 U/ml), to examine the effects of the surface treatment on activation of blood elements, and at reduced-dose heparin (1 U/ml), to determine whether surface-bound heparin would serve as an effective anticoagulant. During the initial recirculation period, platelet counts in the Carmeda (n = 12) circuits were preserved at both doses of heparin and compared with control values (n = 12): At 5 U/ml, control 36% +/- 4% (mean +/- standard error of the mean) versus Carmeda 81% +/- 5%; at 1 U/ml, 43% +/- 3% versus 61% +/- 10%, expressed as a percent of baseline at 30 minutes, p < 0.05. Furthermore, plasma levels of platelet factor 4 and beta-thromboglobulin were significantly reduced in the Carmeda circuits throughout the experiment: At heparin 5 U/ml, 2500 +/- 340 ng/ml versus 604 +/- 191 ng/ml; at 1 U/ml, 2933 +/- 275 ng/ml versus 577 +/- 164 ng/ml of platelet factor 4 at 2 hours (p < 0.05). The pattern of beta-thromboglobulin release was similar, with effects more pronounced at the lower dose of heparin. Surface modification also reduced leukocyte depletion (p < 0.05) and release of elastase at both concentrations of heparin (5 U/ml, 0.72 +/- 0.29 ng/ml versus 0.33 +/- 0.23 ng/ml; 1 U/ml, 0.85 +/- 0.08 ng/ml versus 0.20 +/- 0.05 ng/ml, at 2 hours, p < 0.05). Moreover, as heparin concentration was reduced, Carmeda surface treatment significantly decreased generation of C3a des Arg (1 U/ml, 14,410 +/- 3558 ng/ml versus 3053 +/- 1039 ng/ml at 2 hours, p < 0.05). Although heparin bonding was originally intended to obviate the need for systemic heparinization, Carmeda treatment did not reduce fibrinopeptide A generation at the lower dose of heparin. In summary, Carmeda treatment failed to exhibit anticoagulant efficacy in this model; however, the data suggest that surface modification may have a role in ameliorating the typical inflammatory response initiated by blood contact with an artificial surface.

Anticoagulants↗
PubMed1995

Congenital fibrosarcoma masquerading as congenital hemangioma: report of two cases.

The authors report on two infants who had large congenital fibrosarcomas that initially were believed to be hemangiomas. Although hemangioma and congenital fibrosarcoma can have a similar presentation, their treatment is dissimilar. The authors review the anatomic findings, hematologic differences, and radiological clues that can help to differentiate congenital fibrosarcoma from congenital hemangioma.

Diagnosis, Differential↗
PubMed1994

Unilateral pseudo-Kaposi's sarcoma (Bluefarb-Stewart type).

Unilateral pseudo-Kaposi's sarcoma has been associated with Klippel-Trenaunay syndrome. A case is described here of a 17-year-old man in whom clinical and histopathologic findings suggested pseudo-Kaposi's sarcoma of this type. In addition to Kaposi's sarcoma, this entity should be differentiated from lymphangioendothelioma and lymphangioma. Positive factor VIII reactivity, which is evident in our case, may eliminate confusion.

Adolescent↗
PubMed1993

Hemangiomas and vascular malformations of infancy and childhood.

The vast majority of vascular anomalies of infancy and childhood can be biologically classified as hemangioma or vascular malformation. Hemangiomas are benign neoplasms that proliferate rapidly in infancy only to involute in early childhood. The majority of hemangiomas do not need treatment. Pharmacologic therapy, with corticosteroids or interferon-alpha-2a, is indicated for lesions that threaten vital function or are grossly deforming. Vascular malformations are not tumors, but rather vessel abnormalities due to errors of vascular morphogenesis. They derive from embryonal capillary, venous, arterial, or lymphatic channels, or combinations thereof. The appearance, clinical behavior, and therapy differ based on their channel types. All too often, unfortunately, children with vascular anomalies are shuffled from physician-to-physician because a single practitioner, even a specialist, does not have sufficient knowledge to properly treat the vascular lesion. The authors recommend that every major referral center have a multidisciplinary "Vascular Anomalies Team." We also endorse a biologic classification of vascular lesions to facilitate interspecialty communication regarding diagnosis, natural history, and therapy.

Blood Vessels↗
PubMed1993

Cellular angiolipoma of the breast.

Cellular angiolipomas are benign fatty tumors that occur as multiple subcutaneous nodules on the extremities and trunks of young adults. Although clinically benign, they may occasionally mimic Kaposi's sarcoma or angiosarcoma histologically. We report the first case of cellular angiolipoma occurring in the subcutaneous tissue of the breast, a rare but well-recognized site of benign and malignant vascular tumors.

Breast Neoplasms↗
PubMed1992

Case report: myiasis--the botfly boil.

Cutaneous furunculoid myiasis arises from the infestation of skin or mucous membranes with dipterous larvae. Myiasis from the botfly Dermatobia hominis is a common parasitic disease of the tropics of Central and South America, and may present in the United States. With increasing travel by U.S. citizens, there is potential for increased occurrence; it is important to be able to accurately diagnose myiasis and differentiate it from entities with similar presentations, such as leishmaniasis. The authors describe four cases of myiasis from D. hominis infestation and review clinical features, differential diagnosis, and treatment.

Adult↗
PubMed1991

Cyclosporin A augments human platelet sensitivity to aggregating agents by increasing fibrinogen receptor availability.

Clinical use of cyclosporin A (CsA) has been associated with platelet hypersensitivity and an increased incidence of thrombotic and vasoactive events. The purpose of this study was (1) to confirm that CsA enhances platelet sensitivity to the soluble agonists, adenosine diphosphate (ADP) and epinephrine (EPI), and (2) to determine if this enhancement is mediated by alteration in the availability of platelet surface fibrinogen receptors, a final mediator of platelet activation. Mean log dose of ADP required to achieve complete second-wave platelet aggregation in vitro decreased from 1.90 to 1.49 microM (n = 19, paired t test, P less than 0.05) and 2.86 to 2.11 microM (n = 16, P less than 0.05) following a 15-min and 3-hr incubation in the absence (saline) and presence of CsA (1000 ng/ml), respectively. At the threshold dose of ADP, concurrent thromboxane B2 levels at 15 min were 245 +/- 44 ng/ml (n = 12, saline) and 265 +/- 54 ng/ml (n = 9, CsA; P greater than 0.05). At 3 hr respective levels were 333 +/- 57 and 442 +/- 81 ng/ml (P greater than 0.05). Similar results were obtained with EPI. The number of fibrinogen binding sites in response to 50 microM ADP was determined in washed platelets in the absence and presence of CsA by radioligand binding. In 6 of 7 volunteers, CsA increased fibrinogen receptors from 26,635 +/- 4841 to 35,925 +/- 7290 sites/platelet (means +/- SEM; P less than 0.05). No change in receptor affinity was noted. In conclusion, cyclosporine does augment platelet reactivity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗