Comprehensive analysis of metabolomics on flesh quality of yellow catfish (Pelteobagrus fulvidraco) fed plant-based protein diet.

Background: To investigate the mechanism of plant protein components on nutritional value, growth performance, flesh quality, flavor, and proliferation of myocytes of yellow catfish (Pelteobagrus fulvidraco). Methods: A total of 540 yellow catfish were randomly allotted into six experimental groups with three replicates and fed six different diets for 8 weeks. Results and Conclusions: The replacement of fish meal with cottonseed meal (CM), sesame meal (SEM), and corn gluten meal (CGM) in the diet significantly reduced growth performance, crude protein, and crude lipid, but the flesh texture (hardness and chewiness) was observably increased. Moreover, the flavor-related amino acid (glutamic acid, glycine, and proline) contents in the CM, SEM, and CGM groups of yellow catfish muscle were significantly increased compared with the fish meal group. The results of metabolomics showed that soybean meal (SBM), peanut meal (PM), CM, SEM, and CGM mainly regulated muscle protein biosynthesis by the variations in the content of vitamin B6, proline, glutamic acid, phenylalanine, and tyrosine in muscle, respectively. In addition, Pearson correlation analysis suggested that the increased glutamic acid content and the decreased tyrosine content were significantly correlated with the inhibition of myocyte proliferation genes. This study provides necessary insights into the mechanism of plant proteins on the dynamic changes of muscle protein, flesh quality, and myocyte proliferation in yellow catfish.

Effects of salinity stress on methylation of the liver genome and complement gene in large yellow croaker (Larimichthys crocea).

Salinity is an important environmental factor that affects the yield and quality of large yellow croaker (Larimichthys crocea) during aquaculture. Here, whole-genome bisulfite sequencing (WGBS), RNA-seq, bisulfite sequencing PCR (BSP), quantitative real-time PCR (qPCR), and dual luciferase reporter gene detection technologies were used to analyze the DNA methylation characteristics and patterns of the liver genome, the expression and methylation levels of important immune genes in large yellow croaker in response to salinity stress. The results of WGBS showed that the cytosine methylation of CG type was dominant, CpGIsland and repeat regions were important regions where DNA methylation occurred, and the DNA methylation in upstream 2k (2000bp upstream of the promoter) and repeat regions had different changes in the liver tissue of large yellow croaker in the response to the 12‰, 24‰, 36‰ salinity stress of 4 w (weeks). In the combined analysis of WGBS and transcriptome, the complement and coagulation cascade pathways were significantly enriched, in which the complement-related genes C7, C3, C5, C4, C1R, MASP1, and CD59 were mainly changed in response to salinity stress. In the studied area of MASP1 gene promoter, the methylation levels of many CpG sites as well as total cytosine were strongly negatively correlated with mRNA expression level. Methylation function analysis of MASP1 promoter further proved that DNA methylation could inhibit the activity of MASP1 promoter, indicating that salinity may affect the expressions of complement-related genes by DNA methylation of gene promoter region.

Ammonia stress disrupts intestinal microbial community and amino acid metabolism of juvenile yellow catfish (Pelteobagrus fulvidraco).

Ammonia has adverse effects on aquatic animals, which is also widely distributed in natural aquatic environments and intensive aquaculture systems. The intestine is a primary defensive line for aquatic animals, the accumulation of ammonia in the aquatic environment can cause irreversible damage to intestinal function. In this study, we investigated the effects of acute ammonia stress on the reaction characteristics of digestive function, amino acid metabolism, and the variation in the intestinal microbiota of juvenile yellow catfish (Pelteobagrus fulvidraco). Thus, the yellow catfish was placed in water with the addition of ammonia at 0 (control), 14.6, and 146 mg/L total ammonia nitrogen for 96-h. The present study observed that ammonia accumulated in the intestine and muscle (ammonia contents in the intestine and muscle increased) and induced the activities of protein digestive enzymes dysfunction (pepsin increased while trypsin decreased). Ammonia stress changed various amino acids composition (proline, arginine, lysine, histidine, phenylalanine, tyrosine, leucine, isoleucine, valine, alanine, glutamic acid, tyrosine, and aspartic acid contents were increased in muscle) and increased the activities of alanine aminotransferase and aspartate aminotransferase in muscle. Furthermore, through 16 S rRNA gene analysis, ammonia stress-induced reduction in diversity, richness, and evenness and structure of microbiota alteration in the intestine. At the phylum level, the abundance of Fusobacteria increased while Firmicutes and Actinobacteria decreased significantly. At the genus level, the abundance of beneficial microbiota Cetobacterium significantly increased after ammonia stress. In conclusion, activation of amino acid synthesis in muscle may be involved in ammonia detoxification after severe ammonia stress. The accumulation of ammonia can disrupt the intestinal digestive function and intestinal microbiota community. The Cetobacterium may be a new potential positive factor in the resistance of ammonia toxicity.

Arginase plays an important role in ammonia detoxification of yellow catfish Pelteobagrus fulvidraco.

A two-stage study was carried out to test the mechanism of arginase in ammonia detoxification of yellow catfish. At stage 1, fish was injected lethal half concentration ammonium acetate and 0.9% sodium chloride respectively every 12 h in six replicates for 72 h. The result found that no significant different in serum ammonia contents of fish in ammonium acetate group at hours 12, 24, 36, 48, 60 and 72. At stage 2, ammonium acetate group was split in two, one continued to injected with ammonium acetate (NH3 group) and the other with ammonium acetate and valine (an inhibitor of arginase; Val group); Sodium chloride group also was split in two, one continued to injected with sodium chloride (NaCl group) and the other with sodium chloride and valine (NaCl + Val group). The experiment continued for 12 h. Serum ammonia and liver arginine contents of fish in Val group were higher than those of fish in NH3 group; Compared with NaCl group, arginase activity and ARG 1 expression in liver of fish in Val group were lower; Fish in NaCl and NaCl + Val groups had the lowest serum superoxide dismutase activities, malondialdehyde, tumor necrosis factor-α, interleukin 1 and 8 contents, TNF-α, IL-1 and IL-8 expressions than fish in NH3 and Val groups, and had the higher lysozyme activities, complement 3 and 4 contents. This study indicates that ammonia poisoning would lead to oxidative damage, immunosuppression and inflammation in yellow catfish; Arginase may be an important target of ammonia toxicity in yellow catfish; Exogenous arginine supplementation might alleviate the symptoms of ammonia poisoning in yellow catfish.

The protective effects of selenium on chronic ammonia toxicity in yellow catfish (Pelteobagrus fulvidraco).

Ammonia is toxic to most fish, and its negative effects can be eliminated by nutritional manipulation. In this study, triplicate groups of yellow catfish (0.58 ± 0.03 g) were fed diets supplemented with 0, 0.30 and 0.60 mg selenium (Se) kg-1 diet for 56 days under three ammonia contents (0.00, 5.70 and 11.40 mg L-1 total ammonia nitrogen). The results showed that ammonia toxicity could affects growth (weight gain, feed efficiency ratio, Se contents in muscle and whole body declined) and survival, leads to oxidative stress (total antioxidant capacity, superoxide dismutase, catalase and glutathione peroxidase activities declined and malondialdehyde accumulation), immunosuppression (lysozyme activity, 50% hemolytic complement, immunoglobulin M, respiratory burst and phagocytic index declined) and cytokines release (TNF, IL 1 and IL 8 elevated), induces up-regulation of antioxidant enzymes (Cu/Zn-SOD, Mn-SOD, CAT and GPx), cytokines (TNFα, IL 1 and IL 8) and pro-apoptotic genes (p53, Bax, Cytochrome c, Caspase 3 and Caspase 9) transcription, and down-regulation of anti-apoptotic gene Bcl2 transcription. The dietary Se supplementation could mitigate the adverse effect of ammonia poisoning on fish growth, oxidative damage, immunosuppression and apoptotic.

Effect of nitrite exposure on haematological status, oxidative stress, immune response and apoptosis in yellow catfish (Pelteobagrus fulvidraco).

Nitrite can cause fishes poisoning. This study evaluated the effects of nitrite exposure on haematological status, ion concentration, antioxidant enzyme activity, immune response, cytokine release and apoptosis in yellow catfish. In this study, yellow catfish were exposed to three levels of nitrite (0, 3.00 and 30.00 mg L-1) for 96 h. The results showed that nitrite poisoning could lead to blood deterioration (red blood cell and hemoglobin reduced; white blood cell and methemoglobin elevated), ion imbalance (Na+ and Cl- declined; K+ elevated), oxidative stress (total antioxidant capacity, superoxide dismutase, catalase and glutathione peroxidase activities declined; malondialdehyde accumulation), immunosuppression (lysozyme activity, 50% hemolytic complement, immunoglobulin M, respiratory burst and phagocytic index declined) and cytokines release (TNF, IL 1 and IL 8 elevated). In addition, nitrite poisoning could induce up-regulation of antioxidant enzymes (Cu/Zn-SOD, Mn-SOD, CAT and GPx), cytokines (TNF, IL 1 and IL 8) and apoptosis (P53, Bax, Cytochrome c, Caspase 3, Caspase 9, ERK and JNK) genes transcription. This study suggesting that the nitrite exposure triggers blood deterioration, disrupts the ionic homeostasis, induces oxidative stress, immunosuppression, inflammation and apoptosis in yellow catfish.

Ammonia toxicity in the yellow catfish (Pelteobagrus fulvidraco): The mechanistic insight from physiological detoxification to poisoning.

Ammonia is toxic to fishes. Different fish have different defense strategies against ammonia, so the mechanism of ammonia poisoning is different. In this study, yellow catfish were exposed to three levels of ammonia (0, 5.70 and 57.00 mg L-1) for 96 h. The results showed that ammonia poisoning could lead to free amino acid imbalance (ornithine and citrulline contents declined; arginine content elevated), urea cycle enzymes deficiency (carbamyl phosphate synthetase and arginase contents declined), oxidative stress (superoxide dismutase, catalase and glutathione peroxidase activities declined), immunosuppression (lysozyme activity, 50% hemolytic complement and total immunoglobulin contents and phagocytic index declined) and cytokines release (TNF, IL 1 and IL 8 contents elevated). In addition, ammonia poisoning could induce up-regulation of antioxidant enzymes (Cu/Zn-SOD, Mn-SOD, CAT and GPx), cytokines (TNFα, IL 1 and IL 8) and apoptosis (p53, Bax, cytochrome c, Caspase 3 and Caspase 9) genes transcription. This study suggesting that the urea cycle and glutamine synthesis both were involved in the ammonia detoxification of yellow catfish, and the immunosuppression, inflammation and apoptotic induced by ammonia poisoning in yellow catfish are related to oxidative stress.

Effects of low salinity on gill and liver glycogen metabolism of great blue-spotted mudskippers (Boleophthalmus pectinirostris).

This study investigated the effects of low salinity exposure on glycogen and its metabolism biomarkers, glycogen synthase (GS) and glycogen phosphorylase (GP), representing glycogen synthesis and catabolism, respectively, in the gills and liver of great blue-spotted mudskippers (Boleophthalmus pectinirostris). The fish were accumulated at 10‰ salinity seawater for 1 week, then 270 healthy great blue-spotted mudskippers with similar size were randomly transferred to 10‰ (control group) or 3‰ (low salinity group) seawater for 72-hour stress experiment. Fish significantly elevated their blood glucose levels 12 h after low salinity challenge. At the end of experiments, a decrease in liver glycogen contents was observed in both the control and low salinity groups, the latter showing a pronounced decrease, while the gill glycogen contents were not changed for either group. The mRNA abundance and enzyme activity of GS and GP were both elevated in gill tissues, showing a rising glycogen synthesis and catabolism, probably resulting in the unchanging gill glycogen content. While in liver tissues, the mRNA abundance and enzyme activity were decreased for GS and increased for GP, showing a net increase for breaking down glycogen in liver, probably for supplying a sufficient glucose level for gills and other tissues/organs involved in the response to salinity changes.

Effects of α-ethinyl estradiol (EE2) and diethylhexyl phthalate (DEHP) on growth performance, antioxidant status and immune response of juvenile yellow catfish Pelteobagrus fulvidraco.

The four experimental groups were carried out to test the response of yellow catfish to EE2 and DEHP: control group was exposed to DMSO; EE2 group was exposed to 1.0 µg/L EE2; DEHP group was exposed to 1.0 mg/L DEHP; mix group was exposed to 1.0 µg/L EE2 and 1.0 mg/L DEHP. The experiment continued for 56 days. Fish survival rate was not different among experimental groups. Fish in DEHP and mix groups had the highest weight gain, and lowest value appeared in control group. The highest hepatosomatic index was found in DEHP and mix groups. Serum alanine transaminase of fish in control group was lower than other groups, but the alkaline phosphatase value was the highest. Serum total anti-oxidation capacity, superoxide dismutase and catalase activities of fish in control group were higher than other groups, but malondialdehyde content is opposite. Respiratory burst and phagocytic indices of fish in EE2 group were the lowest. After 96 h of ammonia stress, the survival rate of fish in mix group was significantly lower than control group. This study indicates that EE2 and DEHP exposure can lead to gain weight of yellow catfish, which is related to liver damage and fat accumulation; EE2 and DEHP exerts its toxic effects by inducing ROS generation, leading to lipid peroxidation and immunosuppression.

Modulation of lipid metabolism in juvenile yellow catfish (Pelteobagrus fulvidraco) as affected by feeding frequency and environmental ammonia.

In the intensive culture systems, excessive feeding leads to ammonia accumulation, which results in lipid metabolism disorder. However, little information is available on the modulation of lipid metabolism in fish as affected by feeding frequency and ammonia stress. In this study, weight gain increased as feeding frequency increased from one to four times daily, but feed conversion ratio is opposite. The highest survival was found in ammonia group when fish was fed two times daily. Liver ammonia content increased as feeding frequency increased from one to four times daily, and the highest brain ammonia content was found when fish was fed four times daily. The highest liver 6-phospho-gluconate dehydrogenase (6PGD), fatty acid synthase (FAS), carnitine palmitoyltransferase (CPT), and lipoprotein lipase (LPL) contents were found in control group when fish was fed four times daily; in comparison, the highest liver 6PGD, FAS, CPT, and LPL contents were found in ammonia group when fish was fed two times daily. Liver 6PGD, FAS, CPT 1, SREBP-1, and PPARα mRNA expression in control group increased significantly as feeding frequency increased from one to four times daily, and the highest expression of 6PGD, G6PD, and FAS was observed in ammonia group when fish was fed two times daily. This study indicated that the optimal feeding frequency is two times daily when yellow catfish exposed to ammonia.

Effects of remote ischemic post-conditioning on platelet activation of AMI patients.

The recovery of ischemic myocardium blood perfusion is the main treatment option for acute myocardial infarction (AMI). However, this treatment option has multiple side effects that directly affect the quality of life of the patients. The activation of platelet function plays an important role in the occurrence, development and treatment of AMI. The aim of the present study was to analyze the effects of remote ischemic post-conditioning on platelet activation of AMI patients with primary PCI treatment and clinical prognosis. A total of 71 patients with AMI were treated with primary percutaneous coronary intervention (PCI). They were randomly divided into control group (n=34) and observation group (n=37). The patients in the observation group were treated with remote ischemic post-conditioning. Further, flow cytometer was used to detect the platelet alpha granule membrane glycoprotein (CD62P) and the percentages of activated IIb/IIIa (PAC-1). The maximum platelet aggregation rate induced by adenosine diphosphate (ADP) and arachidonic acid (AA) was measured by light transmittance aggrometer. The incidence of major adverse cardiac events (MACE) was compared between the two groups during the follow-up period of 6 months. The percentage of CD62P (24 h after PCI) in the observation group was significantly lower than control group (P<0.05). Further, the incidence of MACE in the observation group was also lower than that of the control group (P<0.05). Remote ischemic post-conditioning could reduce the incidence of MACE in patients with AMI after primary PCI treatment. Moreover, the above observation may be related to the improvement of platelet CD62P activation.

Effect of dietary alanyl-glutamine dipeptide against chronic ammonia stress induced hyperammonemia in the juvenile yellow catfish (Pelteobagrus fulvidraco).

Triplicate groups of juvenile yellow catfish (1.98 ±â€¯0.01 g) were fed diets supplemented with 0% and 1% alanyl-glutamine dipeptide (AGD) for 56 days under three ammonia concentrations (0.01, 5.70 and 11.40 mg L-1 total ammonia nitrogen). The results showed that ammonia poisoning could induce growth (weight gain and specific growth rate) and survival reduction, live ammonia and serum malondialdehyde accumulation, and subsequently lead to blood deterioration (serum total protein, albumin, globulin, alkaline phosphatase and acid phosphatase reduced), oxidative stress (superoxide dismutase and glutathione peroxidase activities declined), and induce down-regulation of antioxidant enzymes (SOD, GPX and GRX) genes transcription. However, dietary supplemented with 1% AGD could mitigate the adverse effect of ammonia poisoning on fish growth performance.

Effects of acute ammonia toxicity on oxidative stress, immune response and apoptosis of juvenile yellow catfish Pelteobagrus fulvidraco and the mitigation of exogenous taurine.

Ammonia can easily form in intensive culture systems due to ammonification of uneaten food and animal excretion, which usually brings detrimental health effects to fish. However, little information is available on the mechanisms of the detrimental effects of ammonia stress and mitigate means in fish. In this study, the four experimental groups were carried out to test the response of yellow catfish to ammonia toxicity and their mitigation through taurine: group 1 was injected with NaCl, group 2 was injected with ammonium acetate, group 3 was injected with ammonium acetate and taurine, and group 4 was injected taurine. The results showed that ammonia poisoning could induce ammonia, glutamine, glutamate and malondialdehyde accumulation, and subsequently lead to blood deterioration (red blood cell, hemoglobin and serum biochemical index reduced), oxidative stress (superoxide dismutase and catalase activities declined) and immunosuppression (lysozyme, 50% hemolytic complement, total immunoglobulin, phagocytic index and respiratory burst reduced), but the exogenous taurine could mitigate the adverse effect of ammonia poisoning. In addition, ammonia poisoning could induce up-regulation of antioxidant enzymes (Cu/Zn-SOD, CAT, GPx and GR), inflammatory cytokines (TNF, IL-1 and IL-8) and apoptosis (p53, Bax, caspase 3 and caspase 9) genes transcription, suggesting that cell apoptotic and inflammation may relate to oxidative stress. This result will be helpful to understand the mechanism of aquatic toxicology induced by ammonia in fish.

Thiolated DNA-templated silver nanoclusters with strong fluorescence emission and a long shelf-life.

Thiolated DNA (DNA-SH) was employed as a template in the synthesis and stabilization of AgNCs (DNA-SH-AgNCs). Resulting from the synergistic protective effect of specific Ag+-DNA interactions and Ag-S bonding, DNA-SH-AgNCs exhibited high quantum yields and resistance to oxidation.

Growth, blood health, antioxidant status, immune response and resistance to Aeromonas hydrophila of juvenile yellow catfish exposed to di-2-ethylhexyl phthalate (DEHP).

Triplicate groups of juvenile yellow catfish Pelteobagrus fulvidraco were exposed to three levels of DEHP (0, 0.1 and 0.5mgL-1) for 56days. Fish survival (100%) was not affected by different levels of ambient DEHP. Final body weight, weight gain, specific growth rate and feed intake of fish exposed to 0.5mgL-1 DEHP were the highest. On the contrary, hepatosomatic index of fish exposed to 0.1 and 0.5mgL-1 DEHP were the lowest. Serum total protein, glutamic-pyruvic transaminase, glutamic-oxaloacetic transaminase, glucose and triglycerides increased with the increasing concentrations of DEHP exposure. Superoxide dismutase and glutathione peroxidase activities of fish exposed to 0.5mgL-1 DEHP were the lowest, but malondialdehyde contents of fish exposed to 0.1 and 0.5mgL-1 DEHP were higher than that of control fish. Phagocytic indices of the control group were the highest. After being intraperitoneally injected with Aeromonas hydrophila, fish in the control group had the highest expression of toll like receptor 5, and the expression of myeloid differentiation factor 88 of fish exposed to 0.5mgL-1 DEHP was the lowest. This study indicates that DEHP exerts its toxic effects by interfering with hepatic metabolism, inducing ROS generation and malondialdehyde accumulation, leading to blood deterioration and immunosuppression.

A Novel Water-Soluble Fluorescence Probe with Wash-Free Cellular Imaging Capacity Based on AIE Characteristics.

A potential real-time imaging water-soluble fluorescent polymer (P3) is facilely prepared via one-pot method. For P3, tetraphenylethene unit serves as the fluorescent unit, poly(acryloyl ethylene diamine) (a kind of polyelectrolyte) with specific degree of polymerization acts as water-soluble part. 1 H-NMR, gel permeation chromatography (GPC), UV-vis spectroscopy, photoluminescence (PL), and confocal laser scanning microscopy are undertaken to characterize the structure and property of P3. The results of wash-free cellular imaging show that the signal-to-noise ratio is high as the concentration of P3 is 50 µg mL-1 . In addition, the pH-responsive and Cd2+ -responsive are also investigated in this paper. The results coming from pH-responsive show that P3 solution displays significant fluorescence under near neutral. And the result from the cellular imaging shows that intracellular fluorescence intensity enhances with the augment of concentration of Cd2+ , which reveals that P3 can give a hint to resolve the dilemma of traditional fluorescent dyes used as living cellular fluorescent probe.

Melanoma cell adhesion molecule stimulates yes-associated protein transcription by enhancing CREB activity via c-Jun/c-Fos in hepatocellular carcinoma cells.

Dysfunction of the yes-associated protein (YAP) signaling pathway has previously been associated with liver tumorigenesis. Recently, the membrane protein melanoma cell adhesion molecule (MCAM) was identified as a novel, hepatocellular carcinoma (HCC)-specific YAP target protein that promotes carcinogenesis in HCC. However, whether MCAM conversely regulates YAP remains unknown. The aim of the current study was to demonstrate whether and how MCAM regulates YAP in HCC cells. The present study demonstrated that MCAM has a positive effect on the regulation of YAP activity and expression. Mechanistically, MCAM stimulated YAP transcription through its downstream effector c-Jun/c-Fos heterodimer. Gain and loss of function analysis by the present study indicated that c-Jun/c-Fos is capable of inducing cAMP response element-binding protein activation, which is a transcription factor that directly binds to the YAP promoter. Finally, it was identified that an impaired transformative phenotype in MCAM- or c-Jun/c-Fos-depleted HCC cells could be partially rescued by simultaneous overexpression of YAP, suggesting that YAP may function as a downstream effector of the MCAM-c-Jun/c-Fos signaling pathway. Collectively, a complete, positive, auto-regulatory loop was established by the present study, in which YAP is not only an upstream regulator, but also a downstream target of MCAM in HCC cells.

Serum albumin concentrations, effect modifiers and first incident acute myocardial infarction: A cross-sectional study of 1552 cases and 6680 controls.

BACKGROUND: The data regarding low serum albumin (LSA) concentrations as a risk factor of CAD have been inconsistent and previous studies also have not considered the potential presence of multicollinearity among covariates. Additionally, there has been to date no reports about the association of LSA with first incident acute myocardial infarction (AMI) in Chinese Han ethnic population. METHODS: Cross-sectional study of 1552 cases and 6680 controls was performed for identifying the association of LSA with first incident AMI and its possible interactions with risk factors on first incident AMI. RESULTS: On a continuous scale, 1SD (~5 g/l) decrease in serum albumin concentrations was significantly associated with a fully adjusted odds ratio of 1.79, 95% CI (1.54-2.04) for first incident AMI in women, 1.53, (1.41-1.69) in men, and 1.61, (1.49-1.72) in total. On a categorical scale, the association of LSA with risk of first incident AMI was stepwise significantly strengthened with the increased albumin quintiles in age categories in both sexes, without a threshold effect found. A significant interaction was found between LSA and primary hypertension, ischemic stroke and hematocrit on the risk of first incident AMI. CONCLUSIONS: LSA concentrations were significantly associated with first incident AMI in a dose-response manner in age categories in both sexes in Chinese Han ethnic population. Primary hypertension and hematocrit could modify this association. Whether the albumin transfusion for first incident AMI will improve patients' outcome deserves further studies.

A rare long-term survival of the life-threatening trio: silent myocardial infarction complicated by ventricular septal rupture, type 2 diabetes mellitus and chronic bronchitis.

Silent myocardial infarction followed by ventricular septal rupture (VSR) is a rare phenomenon. In the absence of a timely diagnosis and surgical correction, the short term mortality of such patients is greater than 90%. We present one such unique case of a patient with an asymptomatic myocardial infarction complicated by VSR, type 2 diabetes mellitus and chronic bronchitis. Unfortunately, this possibly life-threatening condition had been misdiagnosed for more than one month after initial medical contact. Lack of typical symptoms of chest pain and chronic bronchitis is primarily responsible for this long-time misdiagnosis. We want to emphasize the importance of systematic diagnostic work-up, high vigilance for possibility of VSR complicating myocardial infarction in aged patients with diabetes and chronic bronchitis, which may mislead doctors' judgments and put patients at high risk.

Percutaneous Pulmonary Balloon Valvuloplasty Provides Good Long-Term Outcomes in Adults With Pulmonary Valve Stenosis.

BACKGROUND: Percutaneous balloon pulmonary valvuloplasty (PBPV) is well described in children, but data on the efficacy and long-term outcomes in adult patients with pulmonary valve stenosis (PVS) are limited. OBJECTIVE: To estimate the long-term outcomes of PBPV in adult PVS patients. METHODS: We performed a retrospective analysis of 41 consecutive adult cases (18 females, 23 males) with moderate to severe PVS who underwent PBPV at the First Affiliated Hospital of Soochow University between January 1999 and December 2005. Follow-up was available for all patients (mean follow-up of 11.3 ± 2.1 years; range, 9-15 years). RESULTS: Before intervention, the peak systolic gradient (PSG) was 71.3 ± 27.8 mm Hg. Immediately after intervention, the PSG was reduced to 30.9 ± 10.9 mm Hg (P<.001). At short-term, mid-term, and long-term follow-up, the mean echocardiographic PSGs were 30.6 ± 11.9 mm Hg, 31.1 ± 16.8 mm Hg, and 27.9 ± 7.6 mm Hg, respectively (P<.001 compared with preintervention PSG). At the last follow-up, 37 of 41 patients (90.2%) had a PSG <36 mm Hg. Four patients (9.8%) underwent a second PBPV. Patients with immediate postintervention PSG ≥36 mm Hg were more likely to need a second PBPV. Two cases with immediate postintervention PSG ≥36 mm Hg experienced a spontaneous PSG reduction to <36 mm Hg. No serious adverse complications happened during or after the procedure. CONCLUSIONS: PBPV as a treatment for PVS was safe, and provided good long-term outcomes. Some patients with less-optimal immediate results may experience a spontaneous PSG reduction. A small proportion of patients required a second PBPV, especially those with poor immediate results. Close follow-up is necessary.