Days Of Repair Research Articles

Factors associated with moderate or severe left atrioventricular valve regurgitation within 30 days of repair of complete atrioventricular septal defect.

IntroductionLeft atrioventricular valve regurgitation is the most concerning residual lesion after surgical correction of atrioventricular septal defects.ObjectiveTo determine factors associated with moderate or severe left atrioventricular valve regurgitation within 30 days of surgical repair of complete atrioventricular septal defect.MethodsWe assessed the results of 53 consecutive patients 3 years-old and younger presenting with complete atrioventricular septal defect that were operated on at our practice between 2002 and 2010. The following variables were considered: age, weight, absence of Down syndrome, grade of preoperative atrioventricular valve regurgitation, abnormalities on the left atrioventricular valve and the use of annuloplasty. Median age was 6.7 months; median weight was 5.3 Kg; 86.8% had Down syndrome. At the time of preoperative evaluation, there were 26 cases with moderate or severe left atrioventricular valve regurgitation (49.1%). Abnormalities on the left atrioventricular valve were found in 11.3%; annuloplasty was performed in 34% of the patients.ResultsAt the time of postoperative evaluation, there were 21 cases with moderate or severe left atrioventricular valve regurgitation (39.6%). After performing a multivariate analysis, the only significant factor associated with moderate or severe left atrioventricular valve regurgitation was the absence of Down syndrome (P=0.03).ConclusionAbsence of Down syndrome was associated with moderate or severe postoperative left atrioventricular valve regurgitation after surgical repair of complete atrioventricular septal defect at our practice.

Frailty increases the risk of 30-day mortality, morbidity, and failure to rescue after elective abdominal aortic aneurysm repair independent of age and comorbidities

Frailty, defined as a biologic syndrome of decreased reserve and resistance to stressors, has been linked to adverse outcomes after surgery. We evaluated the effect of frailty on 30-day mortality, morbidity, and failure to rescue (FTR) in patients undergoing elective abdominal aortic aneurysm (AAA) repair. Patients undergoing elective endovascular AAA repair (EVAR) or open AAA repair (OAR) were identified in the National Surgical Quality Improvement Program database for the years 2005 to 2012. Frailty was assessed using the modified frailty index (mFI) derived from the Canadian Study of Health and Aging (CSHA). The primary outcome was 30-day mortality, and secondary outcomes included 30-day morbidity and FTR. The effect of frailty on outcomes was assessed by multivariate regression analysis, adjusted for age, American Society of Anesthesiology (ASA) class, and significant comorbidities. Of 23,207 patients, 339 (1.5% overall; 1.0% EVAR and 3.0% OAR) died ≤30 days of repair. One or more complications occurred in 2567 patients (11.2% overall; 7.8% EVAR and 22.1% OAR). Odds ratios (ORs) for mortality adjusted for age, ASA class, and other comorbidities in the group with the highest frailty score were 1.9 (95% confidence interval [CI], 1.2-3.0) after EVAR and 2.3 (95% CI, 1.4-3.7) after OAR. Similarly, compared with the least frail, the most frail patients were significantly more likely to experience severe (Clavien-Dindo class IV) complications after EVAR (OR, 1.7; 95% CI, 1.3-2.1) and OAR (OR, 1.8; 95%, CI, 1.5-2.1). There was also a higher FTR rate among frail patients, with 1.7-fold higher risk odds of mortality (95% CI, 1.2-2.5) in the highest tertile of frailty compared with the lowest when postoperative complications occurred. Higher mFI, independent of other risk factors, is associated with higher mortality and morbidity in patients undergoing elective EVAR and OAR. The mortality in frail patients is further driven by FTR from postoperative complications. Preoperative recognition of frailty may serve as a useful adjunct for risk assessment.

Experience of Managing Urogenital Fistula

Aim: The study was done to review the demography of urogenital fistulae including obstetric fistula (OF) and its surgical outcome in the early phase of fistula surgery and to create awareness about OF. Methods: This was a retrospective study of 47 patients who underwent fistula surgery during the period of January 2012 to May 2014 in Kathmandu Model Hospital, Helping Hand Community Hospital, Camp in Mid-wetern Regional Hospital Surkhet and Hamlin Hospital, Ethiopia. The primary outcome was in terms of urinary continence after 14 days of repair. Results: In the study 70% (n=33) of fistula were due to obstructed labour and 30% (n=14) were due to hysterectomy for gynecological indications. Ninety six percent (n=45) had successful closure of fistula. Seventy seven percent (n=36) were continent after surgery, and 17% (n=8) had some stress incontinence. Conclusions: The study showed obstructed labour was the major cause of OF, however iatrogenic fistula was also becoming common. The success of repair depended on the type, site, size of fistula and urethral length. Majority of our cases had successful closure of fistula with some degree of stress in some patients. DOI: http://dx.doi.org/10.3126/njog.v9i1.11181 NJOG 2014 Jan-Jun; 2(1):17-20

Effect of Recombinant Human Growth Hormone on Osseointegration of Titanium Implants: A Histologic and Biomechanical Study in Rabbits.

To evaluate the action of recombinant human growth hormone (rhGH) on osseointegration of titanium implants in rabbits. Fourteen adult New Zealand rabbits, aged 30 weeks, were used in the study, and randomly divided into 2 groups. In each animal, 2 (2.2 mm × 6 mm) pure titanium implants were placed in the left tibia. In one group (test group), 1 IU (0.3 mg) of rhGH as a lyophilized powder was applied to each osteotomy site prior to implant placement. Only titanium implants were placed in osteotomy sites of the other group (control). Animals were humanely killed at 14 and 42 days after surgery, and samples were then prepared for histologic analysis and biomechanical test. The biomechanical test showed tensile pull-out stress values of 33.88 N/cm(2) for controls and 59.26 N/cm(2) for the rhGH group at 14 days and 25.99 N/cm(2) and 29.69 N/cm(2) for the control and the test group, respectively, at 42 days. Scanning electron microscope analysis showed more uniform and abundant bone tissue in contact with the implants for the test group at 14 days, and no differences between groups at 42 days. Furthermore, histologic analysis also showed accelerated bone repair in 14 days and a more advanced stage of bone remodeling for the rhGH-treated group when compared to controls after 42 days of repair. Such results show that the topical use of rhGH induces new bone formation in the early stages of bone repair and hence accelerates osseointegration of titanium dental implants.

Defective Wound-healing in Aging Gingival Tissue

Aging may negatively affect gingival wound-healing. However, little is known about the mechanisms underlying this phenomenon. The present study examined the cellular responses associated with gingival wound-healing in aging. Primary cultures of human gingival fibroblasts were obtained from healthy young and aged donors for the analysis of cell proliferation, cell invasion, myofibroblastic differentiation, and collagen gel remodeling. Serum from young and old rats was used to stimulate cell migration. Gingival repair was evaluated in Sprague-Dawley rats of different ages. Data were analyzed by the Mann-Whitney and Kruskal-Wallis tests, with a p value of .05. Fibroblasts from aged donors showed a significant decrease in cell proliferation, migration, Rac activation, and collagen remodeling when compared with young fibroblasts. Serum from young rats induced higher cell migration when compared with serum from old rats. After TGF-beta1 stimulation, both young and old fibroblasts demonstrated increased levels of alpha-SMA. However, alpha-SMA was incorporated into actin stress fibers in young but not in old fibroblasts. After 7 days of repair, a significant delay in gingival wound-healing was observed in old rats. The present study suggests that cell migration, myofibroblastic differentiation, collagen gel remodeling, and proliferation are decreased in aged fibroblasts. In addition, altered cell migration in wound-healing may be attributable not only to cellular defects but also to changes in serum factors associated with the senescence process.

Results of elective repair at 6 months or younger in 277 patients with tetralogy of Fallot: A 14-year experience at a single center

To report practice and outcomes in infants undergoing elective repair of tetralogy of Fallot. A review of a retrospective cohort of elective complete repair of infants age 6 months or younger from 1995 to 2009 was performed. Patients were excluded because of previous interventions, hypercyanotic episodes, intensive care admissions, additional major cardiac defects, or if they were not discharged after birth. Length of stay, mortality, and complications were recorded. Association was determined using logistic or linear regression models and univariate testing determined the multivariate model. There were 277 patients included. The hospital mortality rate was zero. A total of 87.4% of patients were discharged home within 7 days of repair, and 21.6% of patients were discharged on or before the third postoperative day. The postoperative course was uncomplicated in 245 patients (88.4%). Longer support time was associated independently with increased odds of complications (P < .001). Longer support time, younger age, chromosomal abnormality, and presence of a complication were associated independently with a longer hospital stay (all P < .001). Patients younger than 3 months (n = 110) had a longer median hospital stay (4 vs 3 days; P < .001) and longer support times (77.3 ± 35.1 min vs 66.4 ± 34 min; P < .01). Elective tetralogy of Fallot repair was performed at 6 months or younger with low morbidity, no hospital mortality, and an 11.6% complication rate. Longer support times, lower weight, chromosomal abnormalities, and complications were associated with a significantly increased duration of hospital stay.

Central Venous Catheter Repair Is Associated With an Increased Risk of Bacteremia and Central Line-associated Bloodstream Infection in Pediatric Patients

Repair of broken central venous catheters (CVCs) is common in pediatric patients. We hypothesized that this practice predisposes to bacteremia and central line-associated bloodstream infections (CLABSI). We conducted a retrospective case-crossover study of pediatric patients 1 month to 21 years of age with CVC breakages who underwent a first-time repair at our institution, using repair kits provided by CVC manufacturers. We compared rates of bacteremia and CLABSI (defined by Centers for Disease Control and Prevention criteria) in the 30 days prerepair (control period) and the 30 days postrepair (exposure period), with adjustment for within-patient correlation using conditional Poisson regression. The mean prerepair rate of bacteremia was 9.9 per 1000 catheter-days, which increased to 24.5 postrepair, resulting in an adjusted incidence rate ratio (IRR) of 1.87 (95% CI: 1.05-3.33, P = 0.034). Risk of CLABSI demonstrated a greater than 2-fold increase (IRR: 2.15, 95% CI: 1.02-4.53, P = 0.045) when all catheter-days were included, and a 4-fold increase when days on antibiotics were excluded (IRR: 4.07, 95% CI: 1.43-11.57, P = 0.008). We found that repair of a broken CVC was associated with a 2- to 4-fold higher risk of developing CLABSI within 30 days of repair in pediatric patients. Further studies are needed to determine interventions to reduce this risk and to better define the relative merits of CVC repair compared with replacement in selected patient populations.

Once-Yearly Zoledronic Acid in Older Men Compared with Women with Recent Hip Fracture

To assess the efficacy of once-yearly zoledronic acid (ZOL) 5 mg in increasing bone mineral density (BMD) in men with a recent hip fracture participating in the Health Outcomes and Reduced Incidence with Zoledronic Acid Once- Yearly Recurrent Fracture Trial and to compare the efficacy with that in women from the same study. Randomized, placebo-controlled, double-blind trial. International multicenter. Five hundred and eight men and 1,619 women within 90 days of surgical repair of low-trauma hip fracture in the same study (for comparison). Once-yearly intravenous (IV) ZOL 5 mg (n = 248) or placebo (n = 260), loading dose of vitamin D, daily calcium, and vitamin D supplements. Changes in BMD. Percentage change from baseline in total hip BMD at Months 12 and 24 was significantly higher with ZOL than with placebo (between-group difference, 2.0%, P = .003, and 3.8%, P = .002, respectively). Percentage change from baseline in femoral neck BMD at Month 24 was significantly higher with ZOL than with placebo (3.8%, P = .003). The BMD benefit was comparable with that observed in women in this study. New clinical fractures occurred in 36 (7.1%) participants (ZOL, n = 16; placebo, n = 20; P = .64). The ZOL safety profile was comparable with that of placebo, with no significant differences in cardiovascular or long-term renal function and a trend toward lower mortality in ZOL-treated men. Once-yearly IV ZOL 5 mg increases bone mass at the hip and femoral neck in men within 90 days of repair of a low-trauma hip fracture. Increases were of a similar magnitude to those observed in women in the same study.

&lt;strong&gt;Case-repair in three genera of caddisflies (Trichoptera)&lt;/strong&gt;

Case-building is energetically expensive and case-repair may be a viable alternative to rebuilding for caddisflies when the case is damaged. In this study, we damaged the larval cases of 3 Trichoptera genera: Lepidostoma spp.; Neophylax rickeri Milne, 1935; and Onocosmoecus unicolor (Banks, 1897). We manually damaged the anterior, middle, or posterior portions of the larval case. We measured case lengths before damage, immediately after damage, and after allowing 2 days for repair. Overall, 74.2% of Lepidostoma spp. (n=31), 23.5% of N. rickeri (n=34), and 50.0% of O. unicolor (n=44) repaired their cases. Lepidostoma spp. had the highest odds of repair (2.88:1), followed by O. unicolor (1:1). Neophylax rickeri (0.308:1) was unlikely to repair its case after damage. For all genera, the percentage of the damaged portion repaired by location was not statistically significant. In Lepidostoma spp., at all locations, the average percentage of the damaged portion repaired was greater than 100% (larvae repaired the damage fully and continued to add material to the anterior end of the case). The occurrence of repair across the 3 genera at all damage locations suggests that the behavior may be beneficial for protection and more energetically favorable than entirely rebuilding the case, however life history may influence the likelihood of repair.

Temporal and spatial modulation of chondrogenic foci in subchondral microdrill holes by chitosan-glycerol phosphate/blood implants

Subchondral drilling initiates a cartilage repair response involving formation of chondrogenic foci in the subchondral compartment. The purpose of this study was to structurally characterize these sites of chondrogenesis and to investigate the effects of chitosan-glycerol phosphate (GP)/blood implants on their formation. Thirty-two New Zealand White rabbits received bilateral cartilage defects bearing four subchondral drill holes. One knee per rabbit was treated by solidifying a chitosan-GP/blood implant over the defect. After 1-56 days of repair, chondrogenic foci were characterized by histostaining and immunostaining. Collagen fiber orientation was characterized by polarized light microscopy. Glycosaminoglycan and collagen type II were present throughout the foci while the upper zone expressed collagen type I and the lower zone collagen type X. Large chondrogenic foci had a stratified structure with flatter cells closer to the articular surface, and round or hypertrophic chondrocytes deeper in the drill holes that showed signs of calcification after 3 weeks of repair in control defects. Markers for pre-hypertrophic chondrocytes (Patched) and for proliferation (Ki-67) were detected within foci. Some cells displayed a columnar arrangement where collagen was vertically oriented. For treated defects, chondrogenic foci appeared 1-3 weeks later, foci were nascent and mature rather than resorbing, and foci developed closer to the articular surface. Chondrogenic foci bear some similarities to growth cartilage and can give rise to a repair tissue that has similar zonal stratification as articular cartilage. The temporal and spatial formation of chondrogenic foci can be modulated by cartilage repair therapies.

Wound Healing in Mice with High-Fat Diet- orobGene-Induced Diabetes-Obesity Syndromes: A Comparative Study

In the past, the genetically diabetic-obese diabetes/diabetes (db/db) and obese/obese (ob/ob) mouse strains were used to investigate mechanisms of diabetes-impaired wound healing. Here we determined patterns of skin repair in genetically normal C57Bl/6J mice that were fed using a high fat diet (HFD) to induce a diabetes-obesity syndrome. Wound closure was markedly delayed in HFD-fed mice compared to mice which had received a standard chow diet (CD). Impaired wound tissue of HFD mice showed a marked prolongation of wound inflammation. Expression of vascular endothelial growth factor (VEGF) was delayed and associated with the disturbed formation of wound margin epithelia and an impaired angiogenesis in the reduced granulation tissue. Normal wound contraction was retarded and disordered. Wound disorders in obese C57Bl/6J mice were paralleled by a prominent degradation of the inhibitor of NFκB (IκB-α) in the absence of an Akt activation. By contrast to impaired wound conditions in ob/ob mice, late wounds of HFD mice did not develop a chronic inflammatory state and were epithelialized after 11 days of repair. Thus, only genetically obese and diabetic ob/ob mice finally developed chronic wounds and therefore represent a better suited experimental model to investigate diabetes-induced wound healing disorders.

Hepatic macrophages promote the neutrophil-dependent resolution of fibrosis in repairing cholestatic rat livers

Cholestatic liver injury from extrahepatic biliary obstruction is well characterized by inflammatory and fibrogenic mechanisms. Little is known, however, about mechanisms required to reverse injury and effect liver repair. We sought to determine the cellular and molecular requirements for repair after biliary decompression, focusing on the role of hepatic macrophages in regulating inflammation and matrix resolution. Male Sprague-Dawley rats underwent bile duct obstruction for 7 days followed by ductular decompression. Rats were treated with gadolinium chloride (GdCl(3)) to deplete the macrophage populations 24 or 48 hours before decompression. Liver tissue obtained at the time of decompression or after 2 days of repair was processed for morphometric analysis, immunohistochemistry, quantitative RT-PCR and in situ hybridization. GdCl(3) treatment for either 24 or 48 hours before decompression reduced the numbers of ED2(+) Kupffer cells and ED1(+) inflammatory macrophages in obstructed livers; only 48 hours of pretreatment, however, reduced the neutrophil counts. Furthermore, 48-hour GdCl(3) pretreatment blocked matrix degradation. Quantitative polymerase chain reaction demonstrated decreased cytokine-induced neutrophil chemoattractant-1 (CINC-1; CXCL1) and intercellular adhesion molecule-1 mRNA expression after GdCl(3) treatment and the elimination of hepatic macrophages. Immunohistochemistry and in situ hybridization revealed that neutrophils and CINC-1 mRNA localize within regions of fibrotic activity during both injury and repair. We conclude that the macrophage population is not directly involved in fibrotic liver repair. Rather, hepatic macrophages regulate the influx of neutrophils, which may play a direct role in matrix degradation.

Facial Fracture Repair in the Traumatic Brain Injury Patient

To review the surgical complications of patients who had facial fractures repairs in the setting of a traumatic brain injury (TBI). A review of all individuals admitted with the diagnosis of TBI based on an evaluation by the neurotrauma service who also underwent facial fracture repair was performed. More than 600 charts were reviewed and 99 patients met study criteria. Univariate and mulitvariate logistic regression model analysis were performed comparing the complication rate in the immediate postoperative period to the patients' age, gender, mechanism of injury, zone of facial injury, preoperative Glasgow Coma score, presence of multisystem injury, mechanism of TBI and treatment, length of time from injury to surgical repair and length of surgical procedure. Of the 99 individuals studied, there was an 11% complication rate (8 minor, 3 major) in the immediate postoperative period. After univariate analysis, the length of time from injury to surgical repair, zone 1 facial injury and low Glasgow Coma score were all factors associated with increased complications. Multivariate logistic regression model analysis revealed that the odds of a patient sustaining a postoperative complication was 1.298 as the hour of procedure increased by 1 hour (95% CI, 1.065-1.582) and was 1.152 as the days of repair increased by 1 day (95% CI, 1.030-1.288). The overall complication rate of facial fracture repair in the TBI patient was 11%. A prolonged surgical procedure and delay in surgical repair were associated with higher complication rates as identified by multivariate logistical regression analysis.

Repair after cholestatic liver injury correlates with neutrophil infiltration and matrix metalloproteinase 8 activity

Although timely surgical treatment of liver disease can interrupt inflammation and reduce fibrosis, the mechanisms of repair are unknown. We questioned whether these mechanisms of repair include changes in the inflammatory infiltrate and associated biological activity of matrix metalloproteinases (MMPs) 8 and 2. Rats (n >or= 3) underwent biliary ductal suspension for 7 days followed by decompression. Livers were collected after 7 days of obstruction (d0) and after 2, 5, and 7 days of repair (d2, d5, d7, respectively), and assessed morphometrically for collagen, polymorphonuclear cells (PMNs), Kupffer cells (KCs), and inflammatory mononuclear phagocytes (MNPs). In situ zymography was performed by using fluorogenic substrates for MMP-8 and MMP-2 to spatially localize enzymatic activity. Cholestatic injury resulted in significantly elevated (P <or= .001) collagen deposition (3-fold), and elevated numbers of MNPs (10-fold), KCs (5-fold), and PMNs (4-fold), compared with shams. PMNs remained elevated through d7, while collagen deposition, KCs, and MNPs returned to sham levels by d2. In situ zymography showed no significant changes in MMP-2 activity after cholestatic injury and repair. MMP-8 activity was significantly (P <or= .05) elevated only during repair. Activity was localized to fibrotic portal triads containing PMNs. Cholestatic injury results in increased fibrosis, MNPs, KCs, and PMNs but no MMP-2 or MMP-8 activity. Biliary decompression results in increased MMP-8 activity co-localized to areas of portal fibrosis and PMN accumulation. We conclude that secretion of MMP-8 by neutrophils may play a critical role in resolving the fibrotic scar generated during cholestasis.

Substantiation of a lower estimate for the bunker inventory: Comment on “Updated emissions from ocean shipping” by James J. Corbett and Horst W. Koehler

Substantiation of a lower estimate for the bunker inventory: Comment on “Updated emissions from ocean shipping” by James J. Corbett and Horst W. Koehler

Macrophage phenotype during cholestatic injury and repair: The persistent inflammatory response

Biliary decompression for congenital or acquired obstruction (eg, biliary atresia) does not uniformly lead to liver repair, restore function, or prevent cholangitis. The authors hypothesize that failed repair is caused by altered macrophage (Mo) phenotypes central to an ongoing inflammatory and fibrogenic response. In adult rats, biliary obstruction was performed by suspension of the common bile duct for 5 or 7 days. Decompression followed release of the loop until death during the course of liver repair. To determine Mo phenotype in the presence or absence of resident macrophages, animals were either administered gadolinium chloride or saline before injury and repair. At death, hepatic Mo were isolated, stained with MAC-1 (CD11b/CD 18) and OX-3 (MHC class II), and quantified with flow cytometry. Liver sections were immunostained for ED-1 and ED2; positive Mo were counted per square millimeter of tissue. Obstruction led to bile duct proliferation, fibrosis, and inflammation. Decompression relieved jaundice and ductal hyperplasia. After injury, hepatic Mo showed an 80% phenotypic conversion to MAC-1 and OX-3-positive cells. Cells isolated from livers at 9 days of repair persisted with 60% MAC-1 and 77% OX-3 expression. Gadolinium reduced Kupffer cells at all stages of repair. Recruited Mo in treated animals increased 4-fold greater than controls. Kupffer cells appear to limit the recruitment and persistence of a systemic macrophage phenotype in liver injury and repair. Cell surface markers for systemic macrophages appear after injury and persist during repair, despite adequate biliary decompression. After biliary decompression, this macrophage phenotype accounts for inflammatory complications such as cholangitis and ongoing fibrosis.

The Utility of Lymphocyte Premature Chromosome Condensation Analysis for Biological Dosimetry Following Accidental Overexposure to Ionising Radiation

Premature chromosome condensation (PCC) appears to have a possible utility for biological dosimetry purposes. The PCC technique may be adapted for cases of suspicion of overexposure where sampling is performed at least one day after an accident. For this purpose, human blood samples were exposed in vitro to 60Co (0.5 Gy.min-1) up to 4 Gy and the PCC technique was performed after 24 h, 48 h, and 72 h of DNA repair at 37(C. Analysis of excess PCC fragments distribution showed an overdispersion and the dose-effect relationship was best characterised by linear regression. Radiation-induced damage was reduced to 32% between the first and the second day of repair and to 42% the following day. Statistical precision of the dose was found to be dependent on the irradiation dose and on the number of cells examined. The necessity to establish dose-response relationships after different periods of DNA repair is demonstrated, and the use of PCC excess fragments yield as a bioindicator should take this fact into account.

Cardiac malposition, redistribution of fetal cardiac output, and left heart hypoplasia reduce survival in neonates with congenital diaphragmatic hernia requiring extracorporeal membrane oxygenation.

To evaluate cardiac position, left ventricular (LV) mass, and distribution of fetal cardiac output in infants with congenital diaphragmatic hernia (CDH) who required extracorporeal membrane oxygenation (ECMO), and in control subjects. Echocardiograms were performed on 23 neonates with CDH shortly after birth, and repeated within 5 days of repair on ECMO in 21 infants,aand on 12 infants receiving ECMO for other diagnoses, and on 10 healthy, term neonates. Cardiac angle between the midline saggital plane and the interventriculak septum was measured, and deviation from normal (45 degrees) was determined. The ratio of cross-sectional areas (proportional to flows) across the pulmonary (PV) and aortic (AV) valves was determined (PV2/AV2) in 19 infants with CDH and in the healthy control subjects. Thirteen (57%) infants with CDH survived and 10 (43%) died, with no difference in cardiac deviation before surgical repair (35 +/- 13 degrees vs Cardiac deviation persisted after repair in nonsurvivors (27 +/- 14 degrees vs 800.01 and LV mass was significantly less (1.68 +/- 0.39 vs 3.05 +/- 1.20 gm/kg, p00.0005). Neonates requiring ECMO for other diagnoses and well term babies did not have cardiac angle deviations; both these groups had a greater LV mass than did the infants with CDH. The PV2/AV2 flow ratios were higher in infants with CDH (median, 1.73; range, 1.25 to 16.50) compared with those of the healthy infants (0.96, 0.79 to 1.69, p < 0.0002). Cardiac malposition persisted despite CDH repair in nonsurvivors with low LV mass, and fetal cardiac output was redistributed away from the left ventricle. Lung hypoplasia with reduced pulmonary flow returning to the left atrium and altered left atrial hemodynamics may result in LV hypoplasia

Expression of transforming growth factor-beta receptors during hyperoxia-induced lung injury and repair.

Lung injury and repair processes involve many cellular activities, including cell growth, differentiation, and remodeling of extracellular matrix components. Transforming growth factor-beta (TGF-beta) is a major class of signaling peptide growth factors regulating these cellular activities. Type I (T beta RI) and type II (T beta RII) receptors for TGF-beta are transmembrane serine/threonine kinases that are essential for TGF-beta signaling. To gain insight into the possible molecular mechanisms of lung injury and repair, we investigated the expression of T beta RI and T beta RII in an acute hyperoxia-induced model of lung injury and repair. Localization of message expression of T beta RI and T beta RII in oxygen-exposed rat lung tissue was analyzed by using in situ hybridization. T beta RI mRNA expression was found in the interstitium, capillaries, and the alveolar septa of rat lungs exposed for 60 h to 100% oxygen. The distribution of T beta RII mRNA in oxygen-exposed rat lung tissue overlapped the localization of T beta RI mRNA. Temporal changes of T beta RI and T beta RII mRNA expressions in rat lung during hyperoxic exposure and repair were examined by Northern analysis. We found that expression of T beta RI was upregulated in adult rats undergoing prolonged exposure to 100% oxygen, and the increase of T beta RI expression persisted during 2 wk of repair of lung injury. The pattern of T beta RII expression during hyperoxic exposure and repair was distinct from that of T beta RI. The expression of T beta RII increased with a peak at 3 days postexposure and then declined after 7 days of repair. Changes of T beta RI and T beta RII protein expressions in rat lung during hyperoxic exposure and repair were examined further by Western blot analysis, which correlated with the mRNA expression. The results suggest that T beta RI and T beta RII may play important roles during the lung injury and repair by mediating signaling activity of TGF-beta and may regulate interactions between the mesenchyme and the epithelium.

Technique of Thoracoabdominal Aneurysm Repair

Surgical repair of thoracoabdominal aneurysms (TAA) is a formidable task because of the scope of the procedure and the physiologic consequences of interrupting the blood supply to major organs and segmental spinal arteries. In the early days of repair of these aneurysms, mortality rates as high as 30% were reported. The addition of renal failure and paraplegia associated with repair pushed combined morbidity and mortality rates still higher.’ Dr. Stanley Crawford2 of Baylor University in Houston, Texas, reported his first personal series in 1974. He demonstrated that simplifying the surgical technique by use of graft inclusion and simple aortic cross-clamping without assisted circulation could lower the elective mortality rate to the 10% range and reduce overall significant morbidity rates to 25% with a 15% incidence of paraplegia or paraparesis. His vast experience and results set the standard for r e ~ a i r . ~ Dr. Crawford categorized patients by length of aortic replacement (Crawford types I to IV) and demonstrated that the risks of paraplegia and death were related to the amount of aorta being replaced and the clinical presentation (elective, ruptured, acute, or chronic dissection). He reimplanted intercostal arteries but was unable to demonstrate that reimplantation reduced the incidence of paraplegia, and the paraplegia rate remained constant during his career. He also demonstrated that assisted circulation during repair did not alter the paraplegia risk.4 The risk factors for paraplegia as defined by Dr. Crawford remain constant, and we were able to quantitatively model paraplegia risk.’ These efforts show that 95% or more of the