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Biomedical subjects

S S Kim

Publications and source records attributed to S S Kim.

At least 91 records · Page 5Linked to original sources

FcgammaRIIa/IIIa polymorphism and its association with clinical manifestations in Korean lupus patients.

The aim of this study was to determine the distribution of the FcgammaRlla and FcgammaRIIIa polymorphisms and their association with clinical manifestations in Korean lupus patients. Three hundred SLE (systemic lupus erythematosus) patients (48 male, 252 female) meeting 1982 ACR criteria and 197 Korean disease-free controls were enrolled. Genotyping for FcgammaRlla 131 R/H and FcgammaRIIIa 176 F/V was performed by PCR of genomic DNA using allele-specific primers and the FcgammaRIIIa genotype was confirmed by direct sequencing of PCR product in some cases. There was significant skewing in the distribution of the three FcgammaRIIa genotypes between the SLE and the controls (P=0.002 for R/R131 vs R/H131 and H/H131, OR 2.5 (95% Cl 1.4-4.5), but not in FcgammaRIIIa genotypes. FcgammaRIIa-R allele was a significant predictor of lupus nephritis, as compared with SLE patients without nephritis (P=0.034 for R131 vs H131, OR 1.4 (95% Cl 1.03-1.9)), but proliferative nephritis (WHO class III and IV) was less common in patients with FcgammaRlla-R/R131 and in FcgammaRIIa-R allele. In 300 SLE patients, high binding allele combination H131/V176 was less common in SLE with nephritis than in SLE without nephritis. Hemolytic anemia was less common in R131/F176 allele combination among four FcgammaRIIa/FcgammaRIIIa allelic combinations. Male SLE patients showed a higher frequency of renal involvement, serositis, thrombocytopenia, malar rash and discoid rash than female SLE, and male SLE had a higher frequency of FcgammaRIIa-R/R131 or R131-allele than male controls, but FcgammaRIIa or FcgammaRIIIa genotypes had no association with renal involvement in male SLE patients. FcgammaRIIa-H/H131 showed a higher frequency of hemolytic anemia and less pulmonary complications in male SLE. Female SLE patients showed higher frequency of any hematologic abnormality, lymphopenia, anticardiolipin antibody (+) and anti-Ro antibody (+) than male SLE, and had earlier onset of first symptoms. There was no skewing in FcgammaRIIa or FcgammaRIIIa genotypes between female SLE and female controls, but FcgammaRIIa-R131 allele showed skewing between female SLE with nephritis and female SLE without nephritis. The age at onset of thrombocytopenia was earlier in FcgammaRIIa R/R131 among three FcgammaRIIa genotypes, and serositis in FcgammaRIIIa-F/F176 among three FcgammaRIIIa genotypes. FcgammaRIIa-R131 homozygote was a major predisposing factor to the development of SLE and FcgammaRIIa-RI31 homozygote and R131 allele were a predisposing factor, and H131/V176 was a protective allele combination in lupus nephritis. In contrast to other ethnic patients, in our study cohort, clinical manifestation was different between male and female, and FcgammaRIIa and FcgammaRIIIa showed somewhat different clinical associations between the genders.

Adolescent↗

A case of glaucoma associated with Sturge-Weber syndrome and Nevus of Ota.

The Sturge-Weber syndrome consists of a unilateral port-wine hemangioma of the skin along the trigeminal distribution and is accompanied by an ipsilateral leptomeningeal angioma. Glaucoma is present in approximately half of the cases. The Nevus of Ota is a melanocytic pigmentary disorder, most commonly involving the area innervated by the trigeminal nerve. Elevated intraocular pressure, with or without glaucomatous damage, is observed in 10% of the cases. We report the first case of glaucoma associated with Sturge-Weber syndrome and Nevus of Ota in Korea.

Antihypertensive Agents↗

Short term surgical outcomes of modified deep sclerectomy with catgut implant.

We compared the effectiveness of and complications resulting from modified deep sclerectomy with catgut implant (modified-DSCI) with those of standard deep sclerectomy with collagen implant (DSCI) in the short term following surgery. In this retrospective study, standard-DSCI was performed on thirteen patients (17 eyes), and modified-DSCI was performed on seven patients (11 eyes). After dissection of a 5x5 mm sized superficial scleral flap, a 3x4 mm sized rectangular deep scleral flap was constructed in DSCI and a 2x3 mm sized triangular deep scleral flap in modified DSCI. A collagen implant was placed on the scleral bed in DSCI and # 0 CHROMIC Catgut Absorbable Suture was used in modified DSCI. The mean follow up was 11.0+/-6.1 months in DSCI and 9.3+/-4.7 months in modified DSCI. The mean preoperative intraocular pressure (IOP) was 38.6+/-10.9 mmHg in DSCI and 34.8+/-8.6 mmHg in modified DSCI. In the DSCI group, the IOP was 13.4+/-3.0 mmHg at final follow up, and was 11.4+/-3.2 mmHg in the modified DSCI group. The number of Nd:YAG goniopuncture was 3 cases (25%) in the modified DSCI group, and 3 cases (21.4%) in the DSCI group. The number of intraoperative microperforations was 3 in the DSCI group and 2 in the modified DSCI group. Temporary hypotony was encountered in 8 eyes (57.1%) of the DSCI group and 4 eyes (50%) of the modified DSCI group. There was no significant difference observed between the two groups in regards to the effectiveness or rate of complications seen during short term follow up.

Adult↗

Diverse profiles of specific IgE response to toluene diisocyanate (TDI)-human serum albumin conjugate in TDI-induced asthma patients.

The prevalence studies on specific IgE to toluene diisocyanate (TDI)-human serum albumin (HSA) conjugate in TDI-induced asthma have shown variable results. In this study, we attempted to compare specific IgE bindings to TDI-HSA conjugate and its specificity using 3 different conjugates. Sera were collected from 20 TDI-induced asthma and 10 controls. Specific IgE were measured by ELISA using three TDI-HSA conjugates; two from Carnegie Mellon (CM; 98 and 99 CM conjugates) and one from Ajou University. To evaluate specificity and cross-reactivity, ELISA inhibition tests were applied. Positive and negative predictive values between Ajou conjugate and 98 CM conjugate were 75% and 100%. Those between Ajou and 99 CM were 100% and 93.8%. One patient showed an isolated positive response to the Ajou with negative responses to the other two conjugates. ELISA inhibition test using this patient's serum revealed the significant inhibitions by the Ajou and minimal inhibitions by the others. On the other hand, another patient showed an isolated positive response to 99 CM with negative responses to the others, and ELISA inhibition test showed significant inhibition by 99 CM with minimal inhibitions by the others. These results suggest that specific IgE bindings to a new antigenic determinant of TDI-HSA conjugate can be heterogeneous and differ from one individual to another.

Asthma↗

Increased levels of circulating autoantibodies to cultured human bronchial epithelial cell in adult patients with nonatopic asthma.

The pathogenetic mechanism of nonatopic asthma has not yet been defined. The idea of a possible involvement of autoimmunity in the pathogenesis of nonatopic asthma has been proposed by earlier studies. To evaluate the possible involvement of autoimmune response against bronchial epithelial cell in the pathogenesis of nonatopic asthma, we measured circulating autoantibodies to cultured human bronchial epithelial cell (BEAS-2B cell line) using enzyme-linked immunosorbent assay. We used stored serum samples form 38 age-matched healthy controls, 26 adult patients with atopic asthma, 16 adult patients with nonatopic asthma, and 12 adult patients with systemic lupus erythematosus. Levels of IgG autoantibodies to bronchial epithelial cell were significantly higher in patients with nonatopic asthma (mean+/-SD of absorbance values; 0.135+/-0.030) and systemic lupus erythematosus (0.293+/-0.181) than in healthy controls (0.112+/-0.016) and patients with atopic asthma (0.116+/-0.031) (p<0.05). This study showed that levels of circulating IgG autoantibodies to bronchial epithelial cell were increased in adult patients with nonatopic asthma. Further studies are needed to evaluate the possible involvement of autoimmune mechanism in the pathogenesis of nonatopic asthma.

Adult↗

A case of hypothermia combined with systemic lupus erythematosus.

Systemic lupus erythematosus(SLE) is a prototypic autoimmune disease affecting various organ systems. Hypothermia is a rare manifestation of SLE. We experienced a case of SLE combined with hypothermia. A 36-year-old woman, who had been diagnosed as SLE 3 days before admission, admitted complaining of mental confusion. After admission, her body temperature, initially 36.1 degrees C, became 32.6 degrees C. Her core body temperature was less than 35.0 degrees C. Despite of warming with heating lamp and blankets, her core temperature did not reach 35.0 degrees C during 18 hours. Ten days later, her temperature exceeded 36.0 degrees C.

Adrenal Cortex Hormones↗

Cost-effectiveness and cost-benefit of sumatriptan in patients with migraine.

OBJECTIVE: To investigate the cost-effectiveness and cost-benefit of initiating sumatriptan therapy in patients with acute migraine who were previously taking nontriptan drugs. PATIENTS AND METHODS: This is an economic analysis of a prospective, pretest-posttest, observational 6-month outcomes study of 178 patients with a physician diagnosis of migraine who received their first prescription for sumatriptan between October 1994 and August 1996 and were members of a mixed-model managed care organization in western Pennsylvania. Migraine-related resource use data were obtained from the managed care organization's medical and pharmacy claims databases. The primary outcome measure for this economic analysis was the total disability time that patients experienced because of migraine. Patients reported time missed from work and usual nonwork activities because of migraine on self-administered questionnaires at baseline and at 3 and 6 months after initiation of sumatriptan. RESULTS: Initiation of sumatriptan resulted in a decrease of 662 migraine-disability-days for work and 1236 migraine-disability-days for nonwork activities during the 6 months of the study (decrease from 27.8 to 17.2 days per person), totaling 1898 migraine-disability-days averted with sumatriptan therapy. Migraine-related medical costs were lower after sumatriptan was initiated ($18,351 vs $26,192), whereas migraine-related pharmacy costs were lower with prior nontriptan drug therapy ($22,209 vs $74,861). The overall net cost savings after sumatriptan was initiated in these patients was $222,332 ($1249 per patient) with a benefit-to-cost ratio of $5.67 gained for each health care dollar spent from a societal perspective. The incremental cost-effectiveness ratio was $25 for each additional migraine-disability-day averted by using sumatriptan vs nontriptan drug therapy. Sensitivity analysis showed that changes in medical costs had little effect on the ratios and that sumatriptan remained cost-beneficial across a wide range of patient wages. CONCLUSION: This study showed that initiation of sumatriptan in patients previously receiving nontriptan therapy was cost-effective and had an economic benefit for patients, employers, and society. Sumatriptan also helped patients and physicians achieve goals recommended by the US Headache Consortium by reducing patients' disability and thus improving their ability to function at work and nonwork activities.

Absenteeism↗

Long-term results with St. Jude Medical and CarboMedics prosthetic heart valves.

BACKGROUND AND AIM OF THE STUDY: The clinical evaluation and comparison of St. Jude Medical (SJM) and CarboMedics (CM) prosthetic heart valves implanted between 1988 and 1997 is presented. METHODS: In total, 648 SJM valves were implanted in 641 patients, and 601 CM valves in 591 patients. There were 684 mitral valve replacements, 256 aortic valve replacements, 252 mitral and aortic (double) valve replacements, 16 triple valve replacements, and 41 other tricuspid-related valve replacements. Total follow up was 98%. The overall incidence of valve-related events was compared before and after establishment of a 'valve clinic' in 1993. RESULTS: The overall hospital mortality was 3.4%; late mortality was 8.2%. The five- and ten-year survival for all patients was 92.1% and 86.2%, respectively. There were 31 episodes of thromboembolism in 27 patients (including valve thrombosis in three), 21 episodes of bleeding events in 20 patients, and 18 re-replacements of implanted valves. No structural valve deterioration was observed. Freedom from thromboembolism was 97.8% at five years and 96.3% at ten years; freedom from bleeding episodes was 98.1% and 97.6%, respectively. In terms of hospital and late mortality, and incidence of thromboembolism, hemorrhagic episodes and structural valve failure, no statistically significant differences were found between the SJM and CarboMedics patient groups. Freedom from thromboembolism was 96.7% at five years before initiation of an intensive follow up program, and 99.0% thereafter (p = 0.031). In contrast, freedom from bleeding episodes fell from 99.3% to 96.1% during the same time period (p = 0.0004). CONCLUSION: Both the SJM and CM prosthetic heart valves performed well in our study, and no discernible differences in clinical performance of the two valves were detected. The intensive follow up program resulted in a reduced incidence of thromboembolism, but an increased number of bleeding complications. An optimum anticoagulation regimen to manage these two conflicting problems has yet to be elucidated.

Adolescent↗

The Na+ -Ca2+ exchanger is essential for embryonic heart development in mice.

The cardiac Na+ -Ca2+ exchanger 1 (NCX1) is thought to be the major calcium extrusion mechanism and to play an important role in the regulation of intracellular calcium in the heart. The Na+ -Ca2+ exchanger is particularly abundant in the heart, although it is found in a variety of other tissues. To investigate the role of NCX1, we have generated NCX1-deficient mice. Mice heterozygous for the NCX1 mutation showed no discernable phenotype, grew normally, and were fertile; however, no viable homozygote was observed among 175 offspring obtained from intercrosses of heterozygotes. All the homozygous mutant mice died in utero before E10.5. Morphological analysis indicated that homozygotes of NCX1 mutation at E9.5 died with an underdeveloped heart with a dilated pericardium. Microscopic analysis of these embryos showed myocardial cell loss due to apoptosis. The apoptosis was first observed in E8.5 mutant heart. Areas outside the heart appeared normal in the mutant embryos at E8.5. In contrast, at E9.0, various regions of mutant embryos showed extensive cell loss. These results suggest that mutant embryos die owing to cardiac abnormalities caused by apoptotic cell loss, indicating that NCX1 is essential for normal development of the heart.

Animals↗

The structural basis of DNA target discrimination by papillomavirus E2 proteins.

The papillomavirus E2 proteins regulate the transcription of all papillomavirus genes and are necessary for viral DNA replication. Disruption of the E2 gene is commonly associated with malignancy in cervical carcinoma, indicating that E2 has a role in regulating tumor progression. Although the E2 proteins from all characterized papillomaviruses bind specifically to the same 12-base pair DNA sequence, the cancer-associated human papillomavirus E2 proteins display a unique ability to detect DNA flexibility and intrinsic curvature. To understand the structural basis for this phenomenon, we have determined the crystal structures of the human papillomavirus-18 E2 DNA-binding domain and its complexes with high and low affinity binding sites. The E2 protein is a dimeric beta-barrel and the E2-DNA interaction is accompanied by a large deformation of the DNA as it conforms to the E2 surface. DNA conformation and E2-DNA contacts are similar in both high and low affinity complexes. The differences in affinity correlate with the flexibility of the DNA sequence. Preferences of E2 proteins from different papillomavirus strains for flexible or prevent DNA targets correlate with the distribution of positive charge on their DNA interaction surfaces, suggesting a role for electrostatic forces in the recognition of DNA deformability.

Amino Acid Sequence↗

Phosphatidylinositol 3-kinase stimulates muscle differentiation by activating p38 mitogen-activated protein kinase.

The activation of both phosphatidylinositol 3-kinase (PI3-kinase) and p38 mitogen-activated protein kinase (p38 MAPK) is required for muscle differentiation. However, it is not known whether the signals from these two kinases interact during this process. In this work, we have investigated this using H9c2 cardiac myoblasts. The p38 MAPK-specific inhibitor SB203580 blocked muscle differentiation and suppressed the expression of myogenin and myosin heavy chain in a concentration-dependent manner. Consistent with this, expression of a wild-type p38 MAPK (Ha-p38) or a constitutively active MAPK kinase 6 (MKK6(glu)) promoted the rate of differentiation into multinucleated myotubes. LY294002, a PI3-kinase inhibitor, suppressed in a dose-dependent manner not only muscle differentiation but also activation of p38 MAPK. In addition, expression of a constitutively active form of PI3-kinase (p110*) enhanced myotube formation and p38 MAPK activation, while expression of a dominant negative form of PI3-kinase (Deltap85) attenuated these responses. Furthermore, SB203580 suppressed differentiation of H9c2 cells expressing p110*. Interestingly, LY294002 also suppressed differentiation of H9c2 cells expressing Ha-p38 or MKK6(glu). However, SB203580 did not affect PI3-kinase activity, suggesting that PI3-kinase myogenic signaling to p38 MAPK is unidirectional. Taken together, we concluded that PI3-kinase activates p38 MAPK, which in turn stimulates muscle differentiation, but that p38 MAPK does not substitute for PI3-kinase in this process.

Animals↗

Recombinant bactericidal/permeability-increasing protein (rBPI21) as adjunctive treatment for children with severe meningococcal sepsis: a randomised trial. rBPI21 Meningococcal Sepsis Study Group.

BACKGROUND: Endotoxin is a primary trigger of the inflammatory processes that lead to shock, multiorgan failure, and purpura fulminans in meningococcal sepsis. Bactericidal/permeability-increasing protein (BPI) is a natural protein, stored within the neutrophil granules, that binds to and neutralises the effects of endotoxin in vitro, in laboratory animals, and in humans. To establish whether a recombinant 21-kDa modified fragment of human BPI (rBPI21), containing the active antimicrobial and endotoxin-neutralising moiety, would decrease death and long-term disability from meningococcal sepsis, we did a randomised, double-blind, placebo-controlled trial of rBPI21 in children with severe meningococcal sepsis. METHODS: We enrolled children (2 weeks to 18 years of age) presenting to 22 centres in the UK and the USA with a clinical picture suggestive of meningococcal sepsis, and with evidence of severe disease. Children were randomly assigned rBPI21 (2 mg/kg over 30 min followed by 2 mg/kg over 24 h) or placebo (0.2 mg/mL human albumin solution) in addition to conventional medical therapy. Primary outcome variables were mortality, amputations, and change in paediatric overall performance category (POPC) from before illness to day 60. Analysis was by intention to treat. FINDINGS: Of 1287 patients screened, 892 were excluded, including 57 patients who died or who met criteria for imminent death before receiving the study drug. 190 patients received rBPI21, and 203 placebo. 34 (8.7%) of 393 patients died during the study: 14 (7.4%) in the rBPI21 group and 20 (9.9%) in the placebo group (odds ratio 1.31 [95% CI 0.62-2.74], p=0.48). Compared with patients randomised to placebo, fewer patients treated with rBPI21 had multiple severe amputations (six of 190 [3.2%] vs 15 of 203 [7.4%], odds ratio 2.47 [0.94-6.51], p=0.067), and more had a functional outcome similar to that before illness (as measured by the POPC scale) at day 60 (136 of 176 [77.3%] vs 126 of 190 [66.3%], p=0.019). INTERPRETATION: Because most deaths occurred in the interval between identification of patients and study drug administration, the mortality rate in the placebo group was substantially lower than predicted. The trial was therefore underpowered to detect significant differences in mortality. However, patients receiving rBPI21 had a trend towards improved outcome in all primary outcome variables. Given the excellent severity match between placebo and rBPI21 groups at study entry, the results overall indicate that rBPI21 is beneficial in decreasing complications of meningococcal disease.

Adolescent↗

Evidence that the reactivity of the martian soil is due to superoxide ions.

The Viking Landers were unable to detect evidence of life on Mars but, instead, found a chemically reactive soil capable of decomposing organic molecules. This reactivity was attributed to the presence of one or more as-yet-unidentified inorganic superoxides or peroxides in the martian soil. Using electron paramagnetic resonance spectroscopy, we show that superoxide radical ions (O2-) form directly on Mars-analog mineral surfaces exposed to ultraviolet radiation under a simulated martian atmosphere. These oxygen radicals can explain the reactive nature of the soil and the apparent absence of organic material at the martian surface.

Aluminum Silicates↗

Progression of hepatic stellate cell activation is associated with the level of oxidative stress rather than cytokines during CCl4-induced fibrogenesis.

In order to identify a fibrogenic factor associated with the potential of hepatic stellate cells (HSC) activation that arises during the CCl4-induced fibrogenic process, the relationship between the activation of HSC and levels of several fibrogenic factors were investigated. After isolation of HSC from the liver at different stages of CCl4 intoxication, the activation of HSC was assessed by the expression of alpha-smooth muscle actin. Levels of cytokines and oxidative stress in liver homogenates and plasma were measured by enzyme linked immunosorbent assay and the colorimetric method. In primary culture, HSC isolated from a rat liver were gradually activated in a time-dependent manner according to CCl4 administration. The progression of HSC activation was closely correlated with parameters related to oxidative stress in liver homogenates rather than the tissue levels of several cytokines. Also, the levels of antioxidants and arginase activity were inversely correlated with HSC activation. In plasma, the levels of oxidative stress and cytokines in CCl4-treated rat livers were not associated with the activation of HSC found during the CCl4-induced fibrogenic process. The relationship between HSC activation and oxidative stress was also confirmed through several factor-treated HSC cultures. In conclusion, the activation of HSC was accelerated according to CCl4 administration, and the progression of HSC activation is absolutely related to the oxidative stress. These results show that enhanced oxidative stress is an important signal for activation of HSC in experimental liver fibrogenesis.

Actins↗

APP carboxyl-terminal fragment without or with abeta domain equally induces cytotoxicity in differentiated PC12 cells and cortical neurons.

Mutations in the beta-amyloid precursor protein (APP) gene cause familial Alzheimer's disease (AD). Although amyloid beta peptide (Abeta) is the principal constituent of senile plaques in AD, other cleavage products of APP are also implicated in playing a role in the pathogenesis of AD. C-terminal fragments of APP (APP-CTs), that contain complete Abeta sequence, are found in neuritic plaques, neurofibrillary tangles and the cytosol of lymphoblastoid cells obtained from AD patients. Our previous report demonstrated that APP-CT105 causes death of differentiated PC12 cells and cultured rat cortical neurons (Kim and Suh [1996] J. Neurochem. 67:1172-1182) and induces strong inward currents in Xenopus oocyte (Fraser et al., [1996] J. Neurochem. 66:2034-2040). In the present study, to investigate which domain of APP-CT105 is responsible for the neurotoxicity, we have made deletion mutants of APP-CT105 without Abeta and transmembrane domain (TM) or without NPTY domain, a putative endocytosis signaling sequence, using the PCR-amplified strategy and the recombinant GST-fusion protein strategy. The effect on cell survival of the deletion mutants of APP-CT105 (8 microM) was then determined by the LDH and MTT assay. We found that C-terminal fragment without NPTY significantly causes cell death in NGF-differentiated PC12 cells and cultured rat cortical neurons. This finding suggests that NPTY may not play an important role in APP-CT105 mediated neurotoxicity. We found, however, that C-terminal fragment without Abeta and TM significantly induces neuronal cell death. Our results suggest that in addition to Abeta, C-terminal fragment of APP without Abeta and TM domain itself may also participate in the neuronal degeneration in AD.

Amyloid beta-Protein Precursor↗

Long-term follow-up of tissue-engineered intestine after anastomosis to native small bowel.

BACKGROUND: Our laboratory has investigated the fabrication of a tissue-engineered intestine using biodegradable polymer scaffolds. Previously we reported that isolated intestinal epithelial organoid units on biodegradable polymer scaffolds formed cysts and the neointestine was successfully anastomosed to the native small bowel. The purpose of this study was to observe the development of tissue-engineered intestine after anastomosis and to demonstrate the effect of the anastomosis over a 9-month period. METHODS: Microporous biodegradable polymer tubes were created from polyglycolic acid. Intestinal epithelial organoid units were harvested from neonatal Lewis rats and seeded onto the polymers, which were implanted into the abdominal cavity of adult male Lewis rats followed by 75% small bowel resection (n=24). Three weeks after implantation, the unit/polymer constructs were anastomosed to the native jejunum in a side-to-side fashion. The anastomosed tissue-engineered intestine was measured by laparotomy 10, 24, and 36 weeks after the implantation (n= 14). During the laparotomy, all rats with an obstruction in their anastomosis were killed and excluded from the statistical analysis. Another five rats were also killed at 10 and 36 weeks for histological and morphometric studies. RESULTS: All analyzed rats survived this study and significantly increased their body weight by 36 weeks. Obstruction of the anastomosis was observed in one rat at 24 weeks and in two rats at 36 weeks; however, the anastomosis was patent in the other 11 rats by 36 weeks. The tissue-engineered intestine of these 11 rats increased in length and diameter at 10, 24, and 36 weeks after anastomosis; there were statistically significant differences between each time point except between the length of 10 and 24 weeks (P<0.016 by Wilcoxon signed rank test). Histologically the inner surface of the tissue-engineered intestine was lined with well-developed neomucosa at 10 and 36 weeks; however, there were small bare areas lacking neomucosa in the tissue-engineered intestine at 36 weeks. Morphometric analysis demonstrated no significant differences in villus number, villus height, and surface length of the neomucosa at 10 and 36 weeks. CONCLUSIONS: Anastomosis between tissue-engineered intestine and native small bowel resulted in no complications after operation and maintained a high patency rate for up to 36 weeks. The tissue-engineered intestine increased in size and was lined with well-developed neomucosa for the duration of the study.

Anastomosis, Surgical↗

Is the left atrial v. wave the determinant of peak pulmonary artery pressure in patients with pure mitral stenosis?

A large left atrial (LA) v. wave can be observed in patients with pure mitral stenosis (MS) because of decreased LA compliance. Few data are available regarding the relation between the magnitude of the LA v wave and pulmonary artery pressure in MS. We hypothesized that pulmonary artery pressure may be higher in patients with decreased LA compliance and thus a large v. wave. We analyzed the right-sided cardiac and transseptal catheterization data in 113 patients (16 men and 97 women, mean age 39 years) with pure rheumatic MS in sinus rhythm. Peak systolic, diastolic, and mean pulmonary artery pressures were measured with right-sided cardiac catheterization. The magnitude of LA a and v. waves were measured through transseptal catheterization. Two-dimensional and Doppler echocardiography were also performed to measure LA size, mitral valve area, mean mitral gradient, and valvular regurgitation. Multiple regression analysis was performed to identify the most important factor in the determination of pulmonary artery pressure. A large v wave, defined if peak v wave height exceeded the mean LA pressure by > or =10 mm Hg, was observed in 43 of 113 patients (38%). Increased pulmonary artery systolic pressure (> or =50 mm Hg) was observed in 38 patients (34%). Univariate analysis showed that the factors associated with increased pulmonary artery systolic pressure were smaller mitral valve area, higher mean mitral gradient, higher mean LA pressure, and higher LA v. wave; among them, LA v wave (p <0. 001) and mean mitral gradient (p<0.001) were significant independent factors for pulmonary artery systolic pressure in multivariate analysis. In conclusion, in patients with pure MS and sinus rhythm, the magnitude of the LA v. wave is strongly associated with pulmonary artery pressure. This finding may suggest that LA compliance is a major contributing factor determining pulmonary artery pressure in pure MS.

Adult↗