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Biomedical subjects

A C Chang

Publications and source records attributed to A C Chang.

At least 91 records · Page 5Linked to original sources
PubMed1996

One-stage repair of interrupted aortic arch, ventricular septal defect, and subaortic obstruction in the neonate: a novel approach.

BACKGROUND: One-stage repair of interrupted aortic arch, ventricular septal defect, and severe subaortic stenosis represents a surgical challenge. Techniques that use extracardiac conduits to bypass the subaortic area or involve transaortic or transatrial resection of the conal septum have shown limitations and have failed to reduce the high mortality rate associated with subaortic obstruction. METHODS AND RESULTS: A new operative approach was used in nine neonates (2.1 to 3.9 kg) who underwent one-stage repair of interrupted aortic arch (type B, eight patients; type C, one patient), ventricular septal defect, and severe subaortic stenosis. All patients had severe subaortic stenosis according to preoperative echocardiography (mean ratio of subaortic to descending aortic diameter, 0.63 +/- 0.08). With a transpulmonary (seven patients) or transatrial (two patients) approach and without resection of the conal septum, the ventricular septal patch was placed on the left side of the septum to deflect the conal septum anteriorly and away from the subaortic area. There were no early or late deaths. Median intensive care unit and hospital stays were 17 days (6 to 47 days) and 21 days (10 to 55 days), respectively. On follow-up echocardiography (1 to 29 months, median 12 months), no patients had significant residual subaortic obstruction and one patient had mild residual arch obstruction (20 mm Hg). Growth of the subaortic region was demonstrated in all patients (mean ratio of subaortic to descending aortic diameter, 1.20 +/- 0.10; < 0.001). CONCLUSIONS: Relief of severe subaortic stenosis during one-stage neonatal repair of aortic arch interruption and ventricular septal defect can be accomplished successfully without resection of the conal septum.

Aorta↗
PubMed1996

In vivo distribution of radioactivity in mice after injection of biodegradable polymer microspheres containing 14C-labeled tetanus toxoid.

Radiolabeled tetanus toxoid (TT) was prepared by detoxifying chromatographically purified tetanus toxin with 14C-labeled formaldehyde. 14C-TT was encapsulated inside poly (D,L-lactide-co-glycolide, 50/50) microspheres (MS) of varying average size (approximately 10 microns and approximately 50 microns). Balb/c mice were injected subcutaneously with 5 Lf (approximately 15 micrograms) of 14C-TT, encapsulated in MS, mixed with blank MS without encapsulated antigen, as soluble antigen or adsorbed onto aluminum phosphate (AlPO4) and radioactivity was monitored at the site of injection, draining lymph nodes, blood, liver, spleen, and kidneys at various intervals. At one day, approximately 95% and 90% radioactivity disappeared from site of injection for soluble TT or blank MS mixed TT and AlPO4 adsorbed TT, respectively, whereas approximately 55% and 70% radioactivity disappeared from site of injection for MS of average size approximately 50 microns and approximately 10 microns, respectively. By 7 days, 99% of radioactivity disappeared from site of injection for soluble TT or blank MS mixed TT, whereas 2-3% radioactivity persisted at the site of injection for AlPO4 adsorbed TT for 4 weeks. In contrast, approximately 20% radioactivity stayed at the site of injection for MS injected mice up to 4 weeks. At all time points, large MS (approximately 50 microns) showed more radioactivity at the site of injection than small MS (approximately 10 microns). Other organs showing radioactivity were draining lymph nodes and kidneys. Small MS with encapsulated TT showed highest level of radioactivity in lymph nodes at 4 h. In kidneys, soluble and AlPO4 adsorbed TT showed a peak of radioactivity at 4 h whereas TT encapsulated in MS showed a peak of radioactivity at 7 days. These results indicate that AlPO4 did not act as a depot for TT at the site of injection, but TT encapsulated in MS did form a depot for approximately 1 month.

Animals↗
PubMed1996

Stabilization of tetanus toxoid in poly(DL-lactic-co-glycolic acid) microspheres for the controlled release of antigen.

Sustained release of antigenically active tetanus toxoid (TT) for several weeks from biodegradable poly (DL-lactic-co-glycolic acid) (PLGA) microspheres is very important for the development of a single dose vaccine. With a view to developing such a formulation, we evaluated in the vitro release of antigenic TT from TT-containing PLGA films and microspheres stabilized with gelatin or human serum albumin. Without stabilizer, TT-containing PLGA films released low levels of antigenic TT whereas TT-containing PLGA microspheres (average size 50 microMs) released 18% of antigenic TT in 4 weeks. Inclusion of gelatin and human serum albumin increased the amount of antigenic TT released from PLGA films and microspheres. As the concentration of gelatin increased from 0.08% to 2.2% in PLGA films, release of antigenic TT also increased. Similar results were found with gelatin-stabilized TT-containing microspheres. But the significant increase by higher concentration of gelatin was on the initial burst during the first week. A concentration of 0.2% gelatin was found suitable for getting approximately 40% of antigenic TT in 4 weeks. The proportion of antigenic TT to total protein was higher during the first 2 weeks of the release studies (50% during the first week and 23% during the second week). After 2 weeks, the proportion of antigenic TT was approximately 10% for the next 2 weeks. TT-containing microspheres stabilized with gelatin and human serum albumin showed stability of antigenic TT release when these microspheres were stored at 37 degrees C for 4 weeks. Gelatin appears to be a good stabilizer for TT-containing microspheres, but further studies are required to increase the proportion of antigenic TT beyond 2 weeks.

Antigens↗
PubMed1996

Comparison of the capacity of rhTNF-alpha and Escherichia coli to induce procoagulant activity by baboon mononuclear cells in vivo and in vitro.

The procoagulant activity of mononuclear cells (MNCs) may play an important role in the disseminated intravascular coagulation seen in septic shock. This study compares the capacity of Escherichia coli (E. coli) and recombinant human TNF-alpha (rhTNF-alpha) to induce procoagulant activity by baboon MNCs. In vivo studies showed that MNC procoagulant activity was significantly increased at T + 120 min after LD100 E. coli infusion into baboons. Most of this procoagulant activity was attributable to tissue factor. In contrast, a bolus infusion of rhTNF-alpha (150 micrograms/kg) and a monoclonal antibody to activated protein C (2 mg/kg) did not induce any increase of MNC procoagulant activity at T + 120 min even though the plasma TNF-alpha level was 10 times higher than that seen following infusion of E. coli. In vitro studies showed that E. coli at concentrations comparable to that observed in the vivo study and LPS at a concentration of 2.5 ng/mL induced more intense tissue factor expression by both human and baboon monocytes than rhTNF-alpha in the concentrations ranging from 10 to 1,000 ng/mL. These results suggest that TNF-alpha alone is not sufficient to induced noticeable MNC procoagulant activity, at least, in the early stage of this septic shock model.

Animals↗
PubMed1996

Genetic organization and functional analysis of the otn DNA essential for cell-wall polysaccharide synthesis in Vibrio cholerae O139.

In 1992 a new Vibrio cholerae strain, designated V. cholerae O139 Bengal, emerged which has been responsible for large outbreaks of cholera in India and Bangladesh. Previously, we have shown that this strain arose from a V. cholerae O1 strain by the acquisition of novel DNA. Sequence analysis revealed that the novel DNA is flanked by two genes, rfaD and rfbQRS, which are also found in O1 strains. The mosaic structure of rfaDVCO139 indicated that it was one of the regions involved in recombination between donor and acceptor DNA. However, sequence divergence between the O1 and O139 rfbQRS genes indicated that the second recombination site between donor and O1-acceptor DNA is probably located downstream of rfbDVCO139. The DNA region between rfaDVCO139 and rfbQRSVCO139, designated otn, contained seven open reading frames (ORFs). Two ORFs, otnA and otnB, showed homology with genes involved in cell-wall polysaccharide synthesis. Mutations in otnA and otnB indicated that they are required for capsule synthesis but not lipopolysaccharide synthesis. The otn DNA is also found in V. cholerae O69 and O141 strains, and the organization of this DNA was essentially identical to that in the O139 strain. However, sequence divergence of the otnAB genes indicated that the O139 otn DNA region was not derived from the O69 or O141 strains. No antigenic relationship was found between the different V. cholerae serotypes carrying otn DNA, so the genes determining the antigenic specificity of the O antigen or capsule must be located outside the otn DNA. The O139 otn DNA contained a JUMPstart sequence, which is associated with polysaccharide-synthetic genes in several bacterial species. Furthermore, a repeat motif was observed in extragenic regions. A number of observations suggest that these sequences may facilitate gene flow between V. cholerae strains and the assembly of clusters of functionally related genes.

Antigens, Bacterial↗
PubMed1996

Canine infectious cyclic thrombocytopenia found in Taiwan.

Here were report the first canine infectious cyclic thrombocytopenia (CICT) found in Taiwan. Platelet-specific inclusions were detected in the blood smear of a military working dog. To identify the etiologic agent, the patient's blood was transmitted to three six-month-old German Shepherd dogs. The Ehrlichia platys-like inclusions were observed six to eight days after inoculation. Indirect fluorescent antibody test showed that the serum from the patient reacted specifically with the microorganisms within the platelets. Typical hematologic manifestations of E. platys infection, cyclic parasitemia and concomitant thrombocytopenia, were observed in these dogs. The prevalence of CICT in north Taiwan was also studied, and the incidence was 8.9% (4 out of 45) in civilian dogs and 97.1% (34 out of 35) in dogs from a heavily tick infested kennel.

Animals↗
PubMed1996

Endoscopic cecal perforation: mechanisms of injury.

OBJECTIVE: Most endoscopic perforations of the colon occur in the rectosigmoid area and are thought to be secondary to direct injury from the endoscopic instrument. The aim of this study was to describe the mechanisms of injury and clinical outcome of endoscopic perforation involving the cecum. METHODS: Retrospective review of 6684 consecutive colonoscopic procedures performed at a university hospital over a 7-yr period. RESULTS: Colonoscopy was complicated by perforation in 0.22%. Five of the 15 perforations occurred in the cecum. The mean age of these five patients was 79.6 +/- 17.7 yr (mean +/- SD). Indications for the procedure were bleeding (n = 4) and suspected obstructing cecal mass (n = 1). Abnormal endoscopic findings included diverticulosis, vascular malformations, cecal ulcer/inflammation, mass, and polyps. Perforation was directly attributable to an ancillary procedure (three routine biopsies, one electrocautery) in the cecal area in four patients, and cecal pathology (inflammation, ulceration) was a contributing risk factor in three patients. Mortality was 80%. In contrast, a noncecal perforation usually occurred at the sigmoid region and was associated with technical difficulties, e.g., inability to traverse a stricture or reach the cecum. CONCLUSIONS: Routine forceps biopsy (without electrocautery) is an under-recognized cause of cecal perforation. Ancillary endoscopic interventions in the cecal region should be minimized in elderly patients with evidence of cecal inflammation. Pneumatic injury may be an additional risk factor for cecal perforation in patients with a colonic stricture or a tortuous colon.

Aged↗
PubMed1996

Infusion of phospholipid vesicles amplifies the local thrombotic response to TNF and anti-protein C into a consumptive response.

Inflammation often is considered a contributing factor to both thrombosis and disseminated intravascular coagulation. The molecular mechanisms that dictate which of these clinical manifestations will result from the inflammatory stimulus remain obscure. Bacterial infection and certain tumors are common initiators of the disseminated intravascular coagulant response. Complement activation resulting from bacterial infection shares with selected tumors the capacity to generate or release membrane particles that lack functional adhesion receptors and hence could circulate to amplify a disseminated intravascular coagulant response. We developed a model of venous thrombosis that resulted in localized thrombus formation without disseminated intravascular coagulation. The model involves infusion of tumor necrosis factor, blockade of protein C and a partial decrease in venous flow caused by ligation of the superficial femoral vein without obstruction of the deep formal vein. Infusion of phospholipid vesicles into this model resulted in amplification of a localized thrombotic response into a consumptive response. Seven different groups of animals were studied. The first three groups established the conditions necessary to produce deep vein thrombosis. The second four groups established the conditions necessary to produce disseminated intravascular coagulation. The infusion of phospholipid vesicles plus tumor necrosis factor and anti-protein C antibody resulted in consumption of fibrinogen, the production of thrombin/antithrombin complexes, a fall in platelet count, and venous thrombosis. Without ligation and catheterization phospholipid vesicles failed to produce the consumptive response. We conclude, therefore, that phospholipid vesicles can amplify a local thrombotic response into a consumptive response, and that vesiculation accompanying inflammation is one means by which localized coagulant activity may be amplified to produce disseminated intravascular coagulation.

Animals↗
PubMed1996

Strategies for stabilising tetanus toxoid towards the development of a single-dose tetanus vaccine.

The stability of tetanus toxoid (TT) has been investigated for the purpose of enhancing its immunogenicity when encapsulated in TT-polylactide-co-glycolide (PLGA) microspheres. In this paper we describe our simulations of various potential inactivating events during microsphere processing and release of the antigen. These include: i) processing aqueous TT solutions in the presence of organic solvents, ii) exposing lyophilized TT to moisture, and iii) incubating vaccine with the degrading PLGA. At 37 degrees C, TT began to aggregate in solution a few hours after the addition of either methylene chloride or ethyl acetate to form a single oil-water interface. Similarly, exposure of the lyophilized vaccine to elevated humidity caused the antigen to lose solubility. Previous analysis of moisture-induced aggregates has revealed that formaldehyde, which is stored in labile linkages in the vaccine following its detoxification, is the precursor to the reactive species in the principal aggregation pathway [1]. Methods to inhibit this mechanism, such as blocking nucleophilic amino groups of TT with succinic anhydride, were verified. Succinylation of TT resulted in the incorporation of 10-fold greater antigenically active vaccine in PLGA microspheres relative to the unmodified TT following processing by double-emulsion/solvent evaporation with ethyl acetate, strongly suggesting the formaldehyde-mediated aggregation pathway also occurs during the deleterious conditions of microsphere processing. Incubation of solutions of TT in the presence of excess blank (unloaded) poly (D,L) lactide (mol. wt. 2000) microspheres led to a dramatic reduction in pH (approximately 3.2 units after one day at 45 degrees C) and simultaneous precipitation of TT. Stabilisation in the presence of the degrading polymer is likely to be the final obstacle before controlled-release preparations can be formulated to release antigenically active TT over extended time periods. Hence, mechanistic analyses as described here may be crucial for the development of effective single-dose vaccines.

Delayed-Action Preparations↗
PubMed1995

Differential expression of integrins on human thymocyte subpopulations.

Integrins represent a candidate group of cell surface receptors that may control the homing and population of the thymus by T-cell precursors and the subsequent migration of developing thymocytes through the thymic architecture. We have used multiparameter flow cytometric methods to characterize the expression of several members of the integrin family (alpha 3 beta 1, alpha 4 beta 1, alpha 5 beta 1, alpha 6 beta 1, and alpha L beta 2) on thymocyte subpopulations and have correlated integrin expression with other well-defined thymocyte differentiation markers. alpha 4 beta 1 was expressed by all thymocytes, but expression was highest on CD4-CD8- double-negative (DN) cells, high on CD+CD8+ double-positive (DP) cells, and lowest on mature single-positive (SP) cells, alpha 3 beta 1, alpha 5 beta 1, and alpha 6 beta 1 were present on 13%, 63%, and 26% of thymocytes, respectively, with maximal levels of expression on DN and SP cells, and low levels of expression on DP cells. Simultaneous analysis of alpha 4 beta 1, alpha 5 beta 1, and CD3 expression suggested a pathway of T-cell differentiation in the thymus in which the majority of the DN cells were alpha 4 beta 1hi alpha 5 beta 1hi, the DP cells alpha 4 beta 1hi alpha 5 beta 1lo/-, and the most mature SP cells were alpha 4 beta 1int. The stage-specific expression of integrins strongly implies their functional involvement during T-cell maturation in the thymus.

Cell Differentiation↗
PubMed1995

Postoperative course and hemodynamic profile after the arterial switch operation in neonates and infants. A comparison of low-flow cardiopulmonary bypass and circulatory arrest.

BACKGROUND: The neurological morbidity associated with prolonged periods of circulatory arrest has led some cardiac surgical teams to promote continuous low-flow cardiopulmonary bypass as an alternative strategy. The nonneurological postoperative effects of both techniques have been previously studied only in a limited fashion. METHODS AND RESULTS: We compared the hemodynamic profile (cardiac index and systemic and pulmonary vascular resistances), intraoperative and postoperative fluid balance, and perioperative course after deep hypothermia and support consisting predominantly of total circulatory arrest or low-flow cardiopulmonary bypass in a randomized, single-center trial. Eligibility criteria included a diagnosis of transposition of the great arteries and a planned arterial switch operation before the age of 3 months. Of the 171 patients, 129 (66 assigned to circulatory arrest and 63 to low-flow bypass) had an intact ventricular septum and 42 (21 assigned to circulatory arrest and 21 to low-flow bypass) had an associated ventricular septal defect. There were 3 (1.8%) hospital deaths. Patients assigned to low-flow bypass had significantly greater weight gain and positive fluid balance compared with patients assigned to circulatory arrest. Despite the increased weight gain in the infants assigned to low-flow bypass, the duration of mechanical ventilation, stay in the intensive care unit, and hospital stay were similar in both groups. Hemodynamic measurements were made in 122 patients. During the first postoperative night, the cardiac index decreased (32.1 +/- 15.4%, mean +/- SD), while pulmonary and systemic vascular resistance increased. The measured cardiac index was < 2.0 L.min-1.m-2 in 23.8% of the patients, with the lowest measurement typically occurring 9 to 12 hours after surgery. Perfusion strategy assignment was not associated with postoperative hemodynamics or other nonneurological postoperative events. CONCLUSIONS: After heart surgery in neonates and infants, both low-flow bypass and circulatory arrest perfusion strategies have comparable effects on the nonneurological postoperative course and hemodynamic profile.

Cardiopulmonary Bypass↗
PubMed1995

Role of free protein S and C4b binding protein in regulating the coagulant response to Escherichia coli.

Previous studies showed that infusion of C4b-binding protein with sublethal Escherichia coli (E. coli) in the primate produced a consumptive coagulopathy followed by microvascular thrombosis and renal failure. The first objective of this study was to characterize the pathophysiology and mechanism of this phenomena following infusion of both these agents with emphasis on defining the role of free protein S. The second objective was to examine the relevance of this model to the hemolytic uremic syndrome. Infusion of C4b-binding protein alone reduced free protein S and decreased platelet concentration to 20% of baseline, whereas infusion of the C4b-binding protein/protein S complex did not. There was no activation of other inflammatory or coagulant factors. Infusion of sublethal E coli alone produced a transient inflammatory response with no reduction of free protein S. However, coinfusion of C4b-binding protein with sublethal E coli reduced free protein S and produced a thrombocytopenia, anemia, and a microvascular thrombotic response, whereas infusion of the C4b-binding protein/protein S complex with sublethal E coli did not. Studies comparing the effects of neutralizing (S-163) and nonneutralizing (S-145) antibodies with protein S coinfused with sublethal E coli produced similar contrasting results. Therefore, we concluded that neutralization of free protein S, and not some other property of C4b-binding protein influenced by protein S, accounted for this microvascular thrombotic response. This response is similar to the hemolytic uremic syndrome characterized by thrombocytopenia, anemia, shistocytosis, and renal glomerular thrombosis with uremia. Comparison of the respective renal histopathologic appearance supports this conclusion. This raises the possibility that inhibition of protein S activity (possibly by one of the forms of C4b-binding proteins) might be one of the factors contributing to microvascular thrombotic disorder, such as the hemolytic uremic syndrome.

Animals↗
PubMed1995

Involvement of RB-1, p53, p16INK4 and telomerase in immortalisation of human cells.

Involvement of the retinoblastoma susceptibility (RB-1), p16INK4, p53 and telomerase genes in immortalisation was examined by determining their status in 15 human cell lines representing four immortalisation complementation groups. No abnormalities of RB-1, p53 and p16INK4 were detected in cell lines containing DNA tumour virus proteins known to bind to the protein products of the RB-1 and p53 genes. In contrast, in all other cell lines from each of the four groups either RB-1 was mutant or p16INK4 protein was undetectable and there were cell lines containing p53 mutations in three of the groups. Telomerase activity was detected in 12/15 lines, including some of the virally immortalised lines and in some lines from each group. Since none of these changes correlated with complementation group, other genetic changes must be required for immortalisation.

Base Sequence↗
PubMed1995

A novel human cDNA highly homologous to the fish hormone stanniocalcin.

Stanniocalcin is a glycoprotein hormone previously considered present only in bony fish where it is secreted by the corpuscles of Stannius, endocrine organs involved in Ca2+ homeostasis. In fish, stanniocalcin was thought to be an adaptation for Ca2+ regulation in aquatic environments, and its effects include inhibition of gill Ca2+ transport. We have obtained a human cDNA clone coding for a protein highly homologous to fish stanniocalcin. The mRNA is expressed in many human tissues, with the highest levels in ovary, prostate and thyroid. In vitro human cell culture studies show that the mRNA is positively regulated by extracellular Ca2+ in the medium. We conclude that a human protein similar to the fish hormone is expressed in multiple tissues rather than by a specialized endocrine organ.

Amino Acid Sequence↗
PubMed1995

Expression of a novel integrin beta 1 chain epitope and anti-beta 1 antibody-mediated enhancement of fibronectin binding are dependent on the stage of T cell differentiation.

Beta 1 integrins are a family of alpha beta heterodimers that serve as cell surface receptors for extracellular matrix proteins. We demonstrate that the anti-mouse integrin beta 1 chain mAb KMI6 selectively recognizes a beta 1 epitope that is constitutively expressed by certain immature thymocytes and is induced only slightly on mature thymocytes and peripheral T cells by activation with Con A. Because virtually all cells examined expressed beta 1 integrins on their surface, expression of the KMI6 epitope is T cell differentiation stage specific. Most CD3-4-8- thymocytes were KMI6+, with the lowest level of staining observed on the earliest CD44+IL-2R- cells within this subset. Expression was down-regulated during the CD3-4-8- to CD3-4-8+ transition, and lost by the CD4+8+ stage. Mature single positive thymocytes and resting peripheral T cells were also KMI6-. In contrast with the loss of the epitope before TCR expression by other thymocytes, most CD3+4-8- and certain CD8+ gamma delta TCR+ thymocytes were KMI6+ Addition of KMI6 to cell adhesion assays enhanced CD4-8- thymocyte, but not activated mature thymocyte or peripheral T cell, binding to fibronectin (via alpha 4 beta 1 and alpha 5 beta 1), whereas laminin binding (via alpha 6 beta 1) was unaffected. These properties distinguish the KMI6 epitope from other epitopes involved in beta 1 integrin activation in mice and other species. The unique selectivity of KMI6 recognition of beta 1 integrins, and its selective enhancement of ligand binding suggest that beta 1 integrin structure and factors that regulate beta 1 integrin binding are correlated with the stage of T cell differentiation.

Animals↗
PubMed1995

Alpha 3 beta 1 and alpha 6 beta 1 integrins mediate laminin/merosin binding and function as costimulatory molecules for human thymocyte proliferation.

Integrins comprise a superfamily of alpha beta heterodimers that serve as cell signaling as well as adhesion molecules. We demonstrate that the alpha 3 beta 1 and alpha 6 beta 1 integrins are laminin/merosin receptors expressed in human thymocytes. By reverse transcriptase-PCR analysis, we determined that the alpha 3A beta 1, but not the alpha 3B beta 1, cytoplasmic structural variant of alpha 3 beta 1 is expressed in thymocytes. In contrast, both alpha 6A beta 1 and alpha 6B beta 1 cytoplasmic structural variants of alpha 6 beta 1 are expressed. A small percentage (10 to 15%) of human thymocytes bind to immobilized laminin, and even fewer (3 to 5%) bind to merosin, the laminin isoform normally present in the thymus. This binding, however, can be increased to 39 to 41% after activation of thymocytes with Mn2+ (or PMA). Binding to either laminin or merosin is completely inhibited by anti-beta 1 mAb or by a mixture of anti-alpha 3 and anti-alpha 6 mAbs, indicating that both alpha 3 beta 1 and alpha 6 beta 1 participate in thymocyte adhesion to the laminin family of extracellular matrix proteins. The protein kinase C inhibitors, calphostin C and staurosporine, inhibit Mn(2+)-enhanced thymocyte binding, suggesting that protein kinase C activity is crucial for the binding. Furthermore, the data indicate that at least two divalent cation binding sites serve to regulate integrin binding activity. Finally, we show that both immobilized laminin and merosin have costimulatory function for anti-CD3-induced thymocyte proliferation, and both anti-alpha 3 and anti-alpha 6 mAbs can block this proliferative response. The cooperative function of alpha 3 beta 1 and alpha 6 beta 1 evidenced in the laminin/merosin binding and proliferation assays suggests that thymocyte-merosin interactions may play an important role in thymic T cell development.

Base Sequence↗
PubMed1995

Cerebrovascular accidents following the Fontan operation.

The Fontan operation is one of the most common cardiac operations for children with congenital heart disease beyond the first year of age. Although the surgical mortality of this procedure has improved over the past 2 decades, the neurologic outcome in this population is not well described. We performed a retrospective review of 645 patients who underwent the Fontan procedure at Children's Hospital in Boston over the 15-year period between August, 1978 and July, 1993, to describe the incidence of postoperative cerebrovascular accidents or strokes among survivors. We identified 17 patients (2.6%) who suffered a stroke following the Fontan operation. The risk period for stroke in our population extended from the first postoperative day to 32 months after the Fontan procedure. The pre-, intra-, and postoperative clinical features of these patients are described.

Adolescent↗