H1N1 influenza infection in children: Frequency, pattern, and outcome of chest radiographic abnormalities.

AIM: To describe the frequency, pattern, and outcome of chest radiographic abnormalities in children with H1N1 influenza infection. MATERIALS AND METHODS: Three hundred and fourteen paediatric patients with confirmed H1N1 influenza infection who underwent chest radiography at presentation at a single institution during the outbreak in 2009 were retrospectively reviewed. Abnormal chest radiographic findings related to acute infection were analysed in terms of frequency, pattern, and distribution. Medical records and follow-up radiographs were also reviewed to assess clinical features and outcomes. RESULTS: Chest lesions suggesting acute infection were identified in 49 (16%) patients (mean age 8.2 years, range approximately 1.8-18.5 years). The most common finding was prominent peribronchial marking (71%), followed by air-space opacity (51%) with or without volume decrease, generalized hyperinflation (24%), and pleural effusion (20%). Other minor findings included pneumomediastinum (n=2) and a nodule (n=1). Distributions were bilateral (55%) or unilateral (45%) with frequent involvement of lower (78%), and middle (59%) lung zones. Thirty-nine patients (80%) were hospitalized and six (12%) required mechanical ventilation, followed by recovery. Thirty-one out of the 33 patients that underwent follow-up radiography showed marked resolution of all radiographic abnormalities. CONCLUSION: The frequency of a chest radiographic abnormality was found to be low in children with H1N1 influenza infection. Although typical radiographic findings of a viral lower respiratory infection were more common, unilateral involvement and air-space opacity were common, often with pleural effusion. Furthermore, pulmonary lesions showed near complete resolution on follow-up radiographs in the majority of patients.

Infectious complications associated with alemtuzumab use for allogeneic hematopoietic stem cell transplantation: comparison with anti-thymocyte globulin.

OBJECTIVES: To evaluate the incidence of infectious complications after receiving alemtuzumab as part of a conditioning regimen for allogeneic hematopoietic stem cell transplantation (HSCT) in Korean patients. METHODS: From November 2004 to January 2006, 12 patients who received alemtuzumab-based conditioning regimens for allogeneic HSCT were evaluated retrospectively until death or until the end of the follow-up in July 2007; they were compared with 18 patients who received rabbit anti-thymocyte globulin (ATG)-containing conditioning regimens from January 2002 to January 2006. RESULTS: Post-engraftment infections occurred more frequently in the alemtuzumab recipients than in the ATG recipients; the mean number of infections, excluding cytomegalovirus (CMV) infections, per patient during the follow-up period was 2.6+/-1.4 vs. 1.0+/-0.8 (P=0.003), respectively. Although there was no statistical difference in the cumulative incidence of CMV infection between the 2 groups (91.7% vs. 55.6%, P=0.381), the alemtuzumab recipients had a higher incidence of CMV diseases (41.6% vs. 0%, P=0.0006) and a higher recurrence rate of CMV infection (90.0% vs. 27.3%, P=0.008) than did the ATG recipients, irrespective of the dose of alemtuzumab. Hemorrhagic cystitis (HC) (66.7% vs. 16.7%, P=0.009) and BK virus-associated HC (41.7% vs. 5.6%, P=0.026) developed more frequently in the alemtuzumab recipients. The all-cause mortality rate was not significantly different between the alemtuzumab and the ATG recipients (75% vs. 55.6%, P=0.28). CONCLUSION: Alemtuzumab recipients had a high incidence of CMV disease as well as BK virus-associated HC compared with the ATG recipients. The dose of alemtuzumab should be tailored to patients' risk; in addition, the implementation of the appropriate prophylaxis for CMV and early detection strategies for BK virus are recommended.

Population pharmacokinetics of intravenous itraconazole in patients with persistent neutropenic fever.

PURPOSE: Empirical use of intravenous (IV) itraconazole (ITZ) for febrile neutropenic patients has recently been introduced in Korea. This study was designed to investigate the population pharmacokinetics (PK) of IV-ITZ. METHODS: Sparse PK data were collected from febrile neutropenic patients undergoing empirical ITZ therapy at 200 mg/day after loading doses. NONMEM (Version. 5.1.1) was used to estimate population PK parameters. RESULTS: Forty-two patients were enrolled in the study. Mean population CL and V of IV-ITZ were 10 L/h and 1050 L, respectively. Body weight was the only contributing covariate of CL. The median simulated trough concentration of ITZ after 10 days was predicted to be about 700 ng/mL. CONCLUSIONS: In this study, we explored the population PK profile of ITZ given in IV formulation. We found that the current dosage regimen of IV-ITZ (200 mg/day) was appropriate to obtain therapeutic trough concentrations for neutropenic patients in Korea.

Nitric oxide decreases cytokine-induced endothelial activation. Nitric oxide selectively reduces endothelial expression of adhesion molecules and proinflammatory cytokines.

To test the hypothesis that nitric oxide (NO) limits endothelial activation, we treated cytokine-stimulated human saphenous vein endothelial cells with several NO donors and assessed their effects on the inducible expression of vascular cell adhesion molecule-1 (VCAM-1). In a concentration-dependent manner, NO inhibited interleukin (IL)-1 alpha-stimulated VCAM-1 expression by 35-55% as determined by cell surface enzyme immunoassays and flow cytometry. This inhibition was paralleled by reduced monocyte adhesion to endothelial monolayers in nonstatic assays, was unaffected by cGMP analogues, and was quantitatively similar after stimulation by either IL-1 alpha, IL-1 beta, IL-4, tumor necrosis factor (TNF alpha), or bacterial lipopolysaccharide. NO also decreased the endothelial expression of other leukocyte adhesion molecules (E-selectin and to a lesser extent, intercellular adhesion molecule-1) and secretable cytokines (IL-6 and IL-8). Inhibition of endogenous NO production by L-N-monomethyl-arginine also induced the expression of VCAM-1, but did not augment cytokine-induced VCAM-1 expression. Nuclear run-on assays, transfection studies using various VCAM-1 promoter reporter gene constructs, and electrophoretic mobility shift assays indicated that NO represses VCAM-1 gene transcription, in part, by inhibiting NF-kappa B. We propose that NO's ability to limit endothelial activation and inhibit monocyte adhesion may contribute to some of its antiatherogenic and antiinflammatory properties within the vessel wall.

Inhibition of UL54 and UL97 genes of human cytomegalovirus by RNA interference.

Short interfering RNAs (siRNAs), namely siUL54-1 and siU54-2 targeting UL54 (DNA polymerase) gene, and siUL97-1 and siUL97-2 targeting UL97 (phosphotransferase) gene, were used to inhibit respective genes of Human cytomegalovirus (HCMV) and consequently the virus infection process in human foreskin fibroblast (HFF) cultures. The virus infection was monitored by cell morphology (CPE), levels of UL83 and IE86 mRNAs, and virus antigen. The results showed that siUL97-2 remarkably inhibited viral CPE while other siRNAs were less inhibitory. The siRNAs reduced the levels of UL83 mRNA but not that of IE86 mRNA; again, siUL97-2 was most inhibitory. Particularly, siUL97-2 reduced the UL83 mRNA level 14, 19, 203, and 37 times at 24, 48, 72, and 96 hrs post infection (p.i.), respectively. When tested for the effect on viral antigen by immunofluorescent assay (IFA), UL97-2 exerted a marked inhibition. These results demonstrate the effectiveness of siRNAs against experimental HCMV infection and indicate their therapeutic potential.

Application of a combined process of moving-bed biofilm reactor (MBBR) and chemical coagulation for dyeing wastewater treatment.

A combined process consisted of a Moving-Bed Biofilm Reactor (MBBR) and chemical coagulation was investigated for textile wastewater treatment. The pilot scale MBBR system is composed of three MBBRs (anaerobic, aerobic-1 and aerobic-2 in series), each reactor was filled with 20% (v/v) of polyurethane-activated carbon (PU-AC) carrier for biological treatment followed by chemical coagulation with FeCl2. ln the MBBR process, 85% of COD and 70% of color (influent COD = 807.5 mg/L and color = 3,400 PtCo unit) were removed using relatively low MLSS concentration and short hydraulic retention time (HRT = 44 hr). The biologically treated dyeing wastewater was subjected to chemical coagulation. After coagulation with FeCl2, 95% of COD and 97% of color were removed overall. The combined process of MBBR and chemical coagulation has promising potential for dyeing wastewater treatment.

Morphological onset and early diagnosis in apical hypertrophic cardiomyopathy: a long term analysis with nuclear magnetic resonance imaging.

OBJECTIVES: A long-term follow-up study with nuclear magnetic resonance (NMR) imaging was undertaken to detect the morphological onset and to establish the early diagnosis in apical hypertrophic cardiomyopathy (HCM). BACKGROUND: A spadelike configuration on left ventriculogram (LVG) is regarded as a diagnostic criterion for the classical apical HCM. There also exists a segmented hypertrophy at the apical level without indicating the spadelike features (a nonspade configuration). To detect the hypertrophied myocardium of the nonspade configuration, circumferential scrutiny of the apex is required. Although both configurations can be underlying causes of giant negative T waves, etiological relationship between the two is not clarified. METHODS: The criteria for the spadelike configuration defined on left ventricular short-axis NMR images were as follows: (apical maximal thickness > or = 15 mm), (apical anterior thickness over basal anterior thickness > or = 1.3) and (apical posterior thickness over basal posterior thickness > or =1.3). Thirteen patients who had predominant hypertrophy (> or = 15 mm) at the apical level without the spadelike configuration underwent NMR imaging twice before and after 54+/-10 months' follow-up. RESULTS: Apical hypertrophy that had been confined to the lateral wall in four, the anterior-lateral wall in two, and the septal-anterior wall in one developed to become circumferential hypertrophy that fulfilled the criteria for the spadelike configuration after the follow-up period. CONCLUSIONS: The spadelike configuration can begin with the nonspade configuration and therefore, both can constitute a single disease entity of apical HCM. The early diagnosis of apical HCM can be achieved by identifying the hypertrophy frequently confined to the lateral wall at the apical level.

Direct action of nitric oxide on osteoblastic differentiation.

The effect of nitric oxide (NO) on osteoblastic differentiation was examined in cultured mouse osteoblasts. Interleukin-1beta and tumor necrosis factor-alpha expressed inducible NO synthase gene with little effect on constitutive NO synthase gene. These cytokines increased NO production, which was inhibited by L-NMMA pretreatment, and decreased alkaline phosphatase (AIPase) activity, which was not restored by L-NMMA. Furthermore, NO donors, sodium nitroprusside and NONOate dose-dependently elevated AIPase activity and expression of osteocalcin gene. These results suggest that NO directly facilitates osteoblastic differentiation and the cytokine-induced inhibition of AIPase activity is mediated via mechanism other than NO.

Strain- and age-dependent loss of sarcoglycan complex in cardiomyopathic hamster hearts and its re-expression by delta-sarcoglycan gene transfer in vivo.

The delta-sarcoglycan (SG) gene is deleted in hamsters with hereditary cardiomyopathies. Immunological analyses of heart before, but not after, the progression of cardiomyopathy (CM) revealed that the BIO 14.6 strain, a model of hypertrophic CM, heterogeneously preserved alpha- and gamma-SG with loss of beta- and delta-SG. In contrast, the TO-2 strain, a model of dilated CM, did not show either SG. Furthermore, in vivo transfer of the full length delta-SG gene to TO-2 hearts expressed all four SGs. Thus, this age- and strain-dependent features suggest a more feasible setting for TO-2 than BIO 14.6 to verify both CM progression and the efficacy of gene therapy.

Effects of atrial natriuretic peptide on endothelin-induced vasoconstriction and intracellular calcium mobilization.

Mechanisms for the antagonistic action of atrial natriuretic peptide (ANP) toward endothelin were studied. We examined the effects of ANP on endothelin-induced vasoconstriction in isolated perfused kidney and the elevation of intracellular free calcium concentration using Fura-2 in cultured rat vascular smooth muscle cells (VSMC). Endothelin produced an increase in renal vascular resistance in isolated perfused kidney (2 x 10(-10) mol/l, +109%; P less than 0.01). ANP completely abolished renal vasoconstriction induced by endothelin. Endothelin produced a biphasic elevation in intracellular calcium concentration in the VSMC. Ethyleneglycol-bis-(beta-amino-ethylether)-N,N,N',N'-tetr aac etic acid (EGTA; 3 mmol/l) or nicardipine (10(-8) mol/l) decreased the sustained elevation of intracellular calcium concentration by 10(-8) mol/l endothelin to the basal level (endothelin, +15% versus EGTA + endothelin, -1%; P less than 0.05; endothelin, +18% versus nicardipine + endothelin, +5%; P less than 0.01). Pretreatment with 10(-6) mol/l ANP suppressed neither the peak phase of intracellular calcium concentration elevation (endothelin, 10(-8) mol/l, +35% versus endothelin + ANP, +31%; not significant) nor the sustained phase of intracellular calcium concentration elevation (endothelin, 10(-8) mol/l, +21% versus endothelin + ANP, +16%; not significant). ANP markedly increased the production of cyclic 3',5'-guanosine monophosphate (cGMP) in the VSMC (ANP, 10(-6) mol/l, +1100%; P less than 0.01). However, endothelin did not influence cGMP production in the presence or absence of ANP. ANP may antagonize the vasoconstrictive action of endothelin through an effect on the steps subsequent to the mobilization of intracellular calcium in the pathway of vascular smooth muscle contraction.

Coronary microangiopathy in type 2 diabetic patients: relation to glycemic control, sex, and microvascular angina rather than to coronary artery disease.

UNLABELLED: Coronary microangiopathy is a major complication in diabetics. However, the presence of independent factors in association with coronary microangiopathy in patients with non-insulin-dependent diabetes mellitus (NIDDM) or the difference in coronary microangiopathy between diabetics with coronary artery disease (CAD) and those with microvascular angina is unclear. METHODS: Nineteen patients with NIDDM and microvascular angina, 18 patients with NIDDM and CAD, and 17 age-matched control subjects were studied. Myocardial segments that were perfused by angiographically normal coronary arteries were studied. The baseline myocardial blood flow (MBF) and the MBF during dipyridamole administration were measured using PET and 13N-ammonia, after which the myocardial flow reserve (MFR) was calculated to assess coronary microangiopathy. RESULTS: The baseline MBF was comparable among NIDDM patients with microvascular angina, NIDDM patients with CAD, and control subjects. However, the MBF during dipyridamole administration was significantly lower in NIDDM patients with microvascular angina (126 +/- 42.7 mL/min/100 g) than that in either NIDDM patients with CAD (210 +/- 70.1 mL/min/100 g; P < 0.01) or control subjects (293 +/- 159 mL/min/100 g; P < 0.01), as was the MFR (NIDDM with microvascular angina, 1.90 +/- 0.73; NIDDM with CAD, 2.59 +/- 0.81 [P < 0.01]; control subjects, 3.69 +/- 1.09 [P < 0.01]). Multivariate stepwise regression analysis showed that, among the factors considered, glycemic control was independently related to the MFR (r = 0.838; P < 0.05). CONCLUSION: Glycemic control appears to be essential for coronary microangiopathy in NIDDM.

Bile acids increase intracellular Ca(2+) concentration and nitric oxide production in vascular endothelial cells.

The effects of bile acids on intracellular Ca(2+) concentration [Ca(2+)](i) and nitric oxide production were investigated in vascular endothelial cells. Whole-cell patch clamp techniques and fluorescence measurements of [Ca(2+)](i) were applied in vascular endothelial cells obtained from human umbilical and calf aortic endothelial cells. Nitric oxide released was determined by measuring the concentration of NO(2)(-). Deoxycholic acid, chenodeoxycholic acid and the taurine conjugates increased [Ca(2+)](i) concentration-dependently, while cholic acid showed no significant effect. These effects resulted from the first mobilization of Ca(2+) from an inositol 1,4,5-triphosphate (IP(3))-sensitive store, which was released by ATP, then followed by Ca(2+) influx. Both bile acids and ATP induced the activation of Ca(2+)-dependent K(+) current. Oscillations of [Ca(2+)](i) were occasionally monitored with the Ca(2+)-dependent K(+) current in voltage-clamped cells and Ca(2+) measurements of single cells. The intracellular perfusion of heparin completely abolished the ATP effect, but failed to inhibit the bile acid effect. Deoxycholic acid and chenodeoxycholic acid enhanced NO(2)(-) production concentration-dependently, while cholic acid did not enhance it. The bile acids-induced nitric oxide production was suppressed by N(G)-nitro-L-arginine methyl ester, exclusion of extracellular Ca(2+) or N-(6-aminohexyl)-5-chloro-l-naphthalenesulphonamide hydrochloride (W-7) and calmidazolium, calmodulin inhibitors. These results provide novel evidence showing that bile acids increase [Ca(2+)](i) and subsequently nitric oxide production in vascular endothelial cells. The nitric oxide production induced by bile acids may be involved in the pathogenesis of circulatory abnormalities in liver diseases including cirrhosis.

High fidelity SNP genotyping using sequence-specific primer elongation and fluorescence correlation spectroscopy.

Reliable, efficient and cost-effective modalities are urgently needed for mass screening of gene mutations. Previous reports have shown that SSCP or genechip methods require substantial time and monetary costs, thus limiting their appeal. Sequence Specific Primer Polymerase Chain Reaction (SSP-PCR) is a reliable and cost-effective method that utilizes the 3'-end discrimination properties of polymerase. However, the applicability of conventional SSP-PCR is limited due to the difficulties associated with determining optimal conditions and because mis-matched primers are amplified, resulting in signal noise during end-point assay. To overcome this problem, we eliminated the reverse primers from SSP-PCR, thus preventing amplification of mis-matched primers. We designated this method Sequence-Specific Primer Cycle Elongation (SSPCE). However, the detection of elongated sequence specific primers was difficult using conventional electrophoresis due to the small amounts of amplification product present. We therefore combined SSPCE and Fluorescence Correlation Spectroscopy, which is a novel technique used to determine the number and size of fluorophores at nano-molar concentrations, and designated the method SSPCE-FCS. We compared conventional SSP-PCR and SSPCE-FCS with regard to determining optimal conditions using two Mitochondrial SNPs (G --> A at position 1598, G --> A at position 12192). We were able to determine the optimal conditions for the SNP at position 1598 using either method. However, optimal conditions could only be determined for SSPCE-FCS with the 12192 mutation because non-specific amplification was observed at a wide range of annealing temperatures in SSP-PCR. We then applied this method to three other SNPs and the results were consistent with the results of sequencing data.

Liver disease during the first post-transplant year in bone marrow transplantation recipients: retrospective study.

Liver dysfunction is a common problem in BMT recipients and it is important to determine the etiology in order to institute appropriate therapy. The purpose of this study was to evaluate the possible causes of liver dysfunction during the first post-transplant year in BMT recipients and to identify a possible relationship between pre-existing liver dysfunction and viral hepatitis with prognosis after BMT. We reviewed liver status before and after BMT in 130 consecutive patients at the Catholic Hematopoietic Stem Cell Transplantation Center. Liver dysfunction during the first post-transplant year occurred in 85 out of 101 (84. 2%) allogeneic BMT recipients and 13 out of 29 (44.8%) autologous BMT recipients. In allogeneic BMT, GVHD and drug hepatotoxicity were major causes. In autologous BMT, drug hepatotoxicity was the most common cause. Eighteen out of 130 patients (13.8%) had abnormal liver function tests before BMT. These patients did not have an increased risk of post-transplant liver dysfunction, GVHD, and death compared to patients who had normal liver function tests prior to BMT. Nine patients were hepatitis B antigen positive and three patients were anti-HCV positive prior to BMT. There was no significant increase in the incidence of post-transplant liver dysfunction, GVHD, and death in these patients.

Esophageal aspergillosis after bone marrow transplant.

The prolonged immune suppression associated with bone marrow transplants predisposes to fungal infections including Aspergillus. Disseminated aspergillosis occurs in up to 60% of patients with invasive pulmonary aspergillosis; sites of involvement include the brain, gastrointestinal tract, kidney, liver, thyroid, heart, and spleen. There is only one report of isolated esophageal aspergillosis. A recent acute myelogenous leukemia patient had isolated esophageal aspergillosis after bone marrow transplantation which was successfully treated with amphotericin B.

Pre-emptive ganciclovir treatment can play a role in restoration of hematopoiesis after allogeneic bone marrow transplantation.

We performed pre-emptive ganciclovir therapy on two allogeneic bone marrow transplant (BMT) recipients with myelosuppression associated with cytomegalovirus (CMV) antigenemia after successful engraftment. During the hypoplastic phase, the nucleated cells in the bone marrow and peripheral blood were revealed to be of donor origin by DNA fingerprinting. These two patients had CMV antigen in their peripheral leukocytes. Following the pre-emptive ganciclovir treatment, both of them showed gradual recovery of granulocytes and platelets. They are still alive with stable bone marrow function. From these results, we suppose that infection or reactivation of CMV can suppress bone marrow function after bone marrow transplantation, and the pre-emptive ganciclovir therapy based on the CMV antigenemia may be beneficial if bone marrow function deteriorates after engraftment.

Infectious complications and outcomes after allogeneic hematopoietic stem cell transplantation in Korea.

We reviewed 242 allogeneic hematopoietic stem cell transplantation (HSCT) recipients retrospectively over a 2-year period (January 1998-December 1999) in order to analyze the characteristics and assess the outcomes of infectious complications in patients after HSCT in Korea. Bacteria were the major pathogens before engraftment, and viral and fungal infections predominated during the post-engraftment period. Varicella zoster virus was the most common viral pathogen after engraftment. Cytomegalovirus disease occurred mainly in the late-recovery phase. The frequency of mold infection was higher than that of yeast. There was a relatively high incidence of tuberculosis (3.0%) and Pneumocystis carinii pneumonia (6.5%). One case of death by measles confirmed by autopsy was also noted. Overall, cumulative mortality was 43% (104/242), and 59.6% of these deaths (62/104) were infection-related. Allogeneic HSCT recipients from unrelated donors were prone to infectious complication and higher mortality than those from matched sibling (17/39 (43.6%) vs 45/203 (22.2%), respectively; P<0.01; odd ratio 2.5; 95% confidence interval 1.2-5.1). As infection was the main post-HSCT complication in our data, more attention should be given to the management of infections in HSCT recipients.

Epstein-Barr virus-associated gastric adenocarcinomas among Koreans.

Epstein-Barr virus (EBV)-associated gastric carcinomas have been reported from various regions of the world. Epstein-Barr virus appears to be pathogenetically related to some gastric carcinomas. To determine the incidence of EBV association with gastric carcinomas among Koreans, the authors have studied EBV genome expression in 89 consecutive patients with gastric carcinomas diagnosed at the Catholic University Hospitals in Seoul, Korea, using in situ hybridization (ISH) for EBV-encoded small RNAs (EBERs), and immunohistochemistry for EBV latent membrane proteins (LMP) and CD21 antigen on paraffin sections. Thirty-seven gastric specimens with benign ulcer disease were used controls. EBV-encoded small RNAs were expressed in tumor cell nuclei in 12 patients (13.5%). None of the controls or benign portions of the cases were positive. In the positive cases, all tumor cell nuclei were uniformly stained and the staining intensity was strong. Immunohistochemistry for LMP was positive in 3 of 12 EBERs positive patients and none of EBERs negative patients. EBV latent membrane proteins was localized only in the lymphoid cells infiltrating the tumor in two patients, and tumor cells as well as infiltrating lymphoid cells in one patient. These results indicate that the rate of EBV association with gastric carcinomas in Koreans is relatively high and comparable to other Far Eastern Asian regions. The expression pattern in EBV-associated gastric carcinomas is similar to those of nasopharyngeal carcinomas in which clonality analysis using specific probes to the tandem repeat region of EBV yielded single episomal bands suggesting that EBV infection in EBV-associated gastric carcinomas are also clonal and pathogenetically related to the neoplasm. However, the mechanism of tumorigenesis remains to be elucidated.

The role of nitric oxide in the cardiovascular system.

Nitric oxide (NO) exerts various pathophysiological effects on the cardiovascular system; inhibition of platelet aggregation or leukocyte adhesion on endothelium and vasorelaxation including lethal hypotension in endotoxic shock. In spite of these significant roles of NO, its direct action on individual cardiovascular cells remains unclarified. Therefore, we have investigated the function of NO on cells which constitute vascular wall and heart, and have found this new evidence. 1) ATP increased intracellular ([Ca2+]i) in vascular endothelial cells (ECs) and decreased [Ca2+]i of adjacently cocultured vascular smooth muscle cells (VSMCs), as detected by 2-D fura-2 image analysis. 2) The [Ca2+]i reduction in cocultured VSMCs with ECs by ATP was attenuated by pretreatment of several types of NO inhibitor, whereas the NO inhibitor potentiated the [Ca2+]i elevation in ECs, suggesting that NO affects VSMCs in a paracrine manner while ECs in an autocrine fashion. 3) Physiological concentration of lysophosphatidylcholine, which is an atherogenic constituent of oxidized LDL, but not native phosphatidylcholine, acted on ECs and VSMCs like a NO inhibitor, indicating that this material attenuates NO effect and disturbs vessel relaxation in the short term. 4) Highly efficient transfection of the ecNOS gene in rat heart showed a toxic effect on individual cardiomyocytes in vivo. In conclusion, NO may exert both beneficial and harmful effects on the cardiovascular system.

Necrotizing enterocolitis: experience of 27 cases from a single Korean institution.

Necrotizing enterocolitis (NEC) can involve any site in the gastrointestinal tract and is a fatal complication of immunosuppression. To characterize NEC, clinical and radiological characteristics were analyzed. A total of 27 cases of NEC were identified from January 1993 to August 1998, and medical records were reviewed. NEC was diagnosed by clinical and radiological criteria, and other mimicking conditions were excluded. Of the NEC cases, 22 (81.5%) occurred in patients with underlying hematologic malignancy. All patients complained of abdominal pain and fever at the time of inclusion. Escherichia coli was the most common pathogen identified. The most common finding by computed tomography was single-layered diffuse bowel wall thickening with variable density. Other findings were ascites, fascial thickening, pneumatosis, and mesenteric lymphadenopathy. Of the patients, 25 were treated with antimicrobials with or without recombinant hematopoietic growth factors, and 2 were treated with surgery because of perforation and profound bleeding. Among the 12 patients who died, NEC was the direct cause of death in 7 patients. In conclusion, computed tomography is an effective tool for early diagnosis of NEC. Bowel rest, broad-spectrum antimicrobials, and recombinant hematopoietic growth factors are important aspects of treatment. Surgery should be reserved for complicated cases.