Gp85 protein encapsulated by alginate-chitosan composite microspheres induced strong immunogenicity against avian leukosis virus in chicken.

Introduction: Avian leukosis, a viral disease affecting birds such as chickens, presents significant challenges in poultry farming due to tumor formation, decreased egg production, and increased mortality. Despite the absence of a commercial vaccine, avian leukosis virus (ALV) infections have been extensively documented, resulting in substantial economic losses in the poultry industry. This study aimed to develop alginate-chitosan composite microspheres loaded with ALV-J Gp85 protein (referred to as aCHP-gp85) as a potential vaccine candidate. Methods: Sodium alginate and chitosan were utilized as encapsulating materials, with the ALV-J Gp85 protein serving as the active ingredient. The study involved 45 specific pathogen-free (SPF) chickens to evaluate the immunological effectiveness of aCHP-gp85 compared to a traditional Freund adjuvant-gp85 vaccine (Freund-gp85). Two rounds of vaccination were administered, and antibody levels, mRNA expression of immune markers, splenic lymphocyte proliferation, and immune response were assessed. An animal challenge experiment was conducted to evaluate the vaccine's efficacy in reducing ALV-J virus presence and improving clinical conditions. Results: The results demonstrated that aCHP-gp85 induced a significant and sustained increase in antibody levels compared to Freund-gp85, with the elevated response lasting for 84 days. Furthermore, aCHP-gp85 significantly upregulated mRNA expression levels of key immune markers, notably TNF-α and IFN-γ. The application of ALV-J Gp85 protein within the aCHP-gp85 group led to a significant increase in splenic lymphocyte proliferation and immune response. In the animal challenge experiment, aCHP-gp85 effectively reduced ALV-J virus presence and improved clinical conditions compared to other groups, with no significant pathological changes observed. Discussion: The findings suggest that aCHP-gp85 elicits a strong and prolonged immune response compared to Freund-gp85, indicating its potential as an innovative ALV-J vaccine candidate. These results provide valuable insights for addressing avian leukosis in the poultry industry, both academically and practically.

MiR-199a-5p enhances neuronal differentiation of neural stem cells and promotes neurogenesis by targeting Cav-1 after cerebral ischemia.

AIMS: MicroRNAs (miRs) are involved in endogenous neurogenesis, enhancing of which has been regarded as a potential therapeutic strategy for ischemic stroke treatment; however, whether miR-199a-5p mediates postischemic neurogenesis remains unclear. This study aims to investigate the proneurogenesis effects of miR-199a-5p and its possible mechanism after ischemic stroke. METHODS: Neural stem cells (NSCs) were transfected using Lipofectamine 3000 reagent, and the differentiation of NSCs was evaluated by immunofluorescence and Western blotting. Dual-luciferase reporter assay was performed to verify the target gene of miR-199a-5p. MiR-199a-5p agomir/antagomir were injected intracerebroventricularly. The sensorimotor functions were evaluated by neurobehavioral tests, infarct volume was measured by toluidine blue staining, neurogenesis was detected by immunofluorescence assay, and the protein levels of neuronal nuclei (NeuN), glial fibrillary acidic protein (GFAP), caveolin-1 (Cav-1), vascular endothelial growth factor (VEGF), and brain-derived neurotrophic factor (BDNF) were measured by Western blotting. RESULTS: MiR-199a-5p mimic enhanced neuronal differentiation and inhibited astrocyte differentiation of NSCs, while a miR-199a-5p inhibitor induced the opposite effects, which can be reversed by Cav-1 siRNA. Cav-1 was through the dual-luciferase reporter assay confirmed as a target gene of miR-199a-5p. miR-199a-5p agomir in rat stroke models manifested multiple benefits, such as improving neurological deficits, reducing infarct volume, promoting neurogenesis, inhibiting Cav-1, and increasing VEGF and BDNF, which was reversed by the miR-199a-5p antagomir. CONCLUSION: MiR-199a-5p may target and inhibit Cav-1 to enhance neurogenesis and thus promote functional recovery after cerebral ischemia. These findings indicate that miR-199a-5p is a promising target for the treatment of ischemic stroke.

Taurine inhibits necroptosis helps to alleviate inflammatory and injury induced by Klebsiella infection.

Klebsiella infection is widely acknowledged to inflict severe inflammatory damage in bovines. Herein, we demonstrate significant death of EpH4-Ev cells incubated with Klebsiella. And compelling evidence shows that Klebsiella infection increases interactions between the Receptor-interacting serine/threonine-protein kinase 1 (RIPK1) and RIPK3, which promotes phosphorylation of RIPK3 and MLKL to induce necroptosis. However, these changes can be partially reversed by taurine and Nec-1s. Moreover, using taurine and Nec-1s to partially inhibit necroptosis significantly reduce TNF-α, IL-1ß and IL-6 levels and NAGase activity induced by Klebsiella infection. Taken together, taurine partially inhibits necroptosis induced by Klebsiella infection and hence alleviates inflammatory and injury in EpH4-Ev cells.

The decreased exclusion of nuclear eccDNA: From molecular and subcellular levels to human aging and age-related diseases.

Extrachromosomal circular DNA (eccDNA) accumulates within the nucleus of eukaryotic cells during physiological aging and in age-related diseases (ARDs) and the accumulation could be caused by the declined exclusion of nuclear eccDNA in these states. This review focuses on the formation of eccDNA and the roles of some main factors, such as nuclear pore complexes (NPCs), nucleoplasmic reticulum (NR), and nuclear actin, in eccDNA exclusion. eccDNAs are mostly formed from non-coding DNA during DNA damage repair. They move to NPCs along nuclear actin and are excluded out of the nucleus through functional NPCs in young and healthy cells. However, it has been demonstrated that defective NPCs, abnormal NPC components and nuclear actin rods are increased in aged cells, various cancers and certain other ARDs such as cardiovascular diseases, premature aging, neurodegenerative diseases and myopathies. Therefore, mainly resulting from the increase of dysfunctional NPCs, the exclusion of nuclear eccDNAs may be reduced and eccDNAs thus accumulate within the nucleus in aging and the aforementioned ARDs. In addition, the protective function of non-coding DNA in tumorigenesis is further discussed.

A Study on the Preparation of Microbial and Nonstarch Polysaccharide Enzyme Synergistic Fermented Maize Cob Feed and Its Feeding Efficiency in Finishing Pigs.

1000 g maize cob mixed material was synergistically fermented by adding 2.5% composite probiotics and 0.06-0.08% NSP (nonstarch polysaccharide) enzyme to prepare fermented feed, and its effectiveness as feed for fattening pigs was investigated. The results showed that the appearance, texture, and nutrient quality of maize cobs significantly improved after fermentation, the total number of bacteria was 4.5 × 1010 CFU/g, and the protein content was 7.1%. Compared to the control group, the pigs in the 6% fermented maize cob feed experimental group showed significantly increased daily feed intake, daily weight gain, and nutrient digestion rate (p < 0.05) and reduced feed conversion ratio (p < 0.05). Most indicators including slaughter performance and meat quality significantly improved. In addition, beneficial bacteria including Lactobacillus in the intestines of the finishing pigs significantly increased, and pathogenic bacteria including Escherichia coli in the intestines and feces were found to be significantly reduced (p < 0.05). The intestinal crypt depth, VH/CD ratio, and ileal mucosal immunity of the finishing pigs also significantly improved (p < 0.05). The cytokine content and gene expression of sIgA, IL-8, and TNF-α were found to be significantly increased (p < 0.05). It could be concluded that the addition of 6% fermented maize cob feed to the diets of finishing pigs could promote their growth, improve their production performance and slaughter performance meat quality, and enhance their intestinal microecological balance and immunity.

Gender-specific associations of CD36 polymorphisms with the lipid profile and susceptibility to premature multi-vessel coronary artery heart disease in the Northern Han Chinese.

BACKGROUND: The aim of the present study was to detect potential gender-specific associations between some common CD36 single nucleotide polymorphisms (SNPs) and the lipid profile, as well as the susceptibility to premature multi-vessel coronary artery heart disease (CHD) in the Han population of Northern China. METHODS: A systematic three-step study process was employed to detect associations between CD36 gene variants and blood lipid profiles, as well as premature multi-vessel CHD in a gender-specific manner. RESULTS: The current study documented the following novel findings: (I) the full population-based association study in 329 Northern Han Chinese showed that four common CD36 polymorphisms were significantly related to extreme lipid profiles, with statistically significant effects based on gender interactions (rs1049673: P = 0.001; rs7755: P = 0.008; rs3211956: P = 0.034; and rs3173798: P = 0.004); (ii) these statistically significant effects could be decomposed into statistically significant atherogenic effects in males, but non-significant non-atherogenic effects in females; (iii) the results of logistic regression analysis indicated that current smoking status, low density lipoprotein cholesterol (LDL-C) levels, and type-2 diabetes were independent risk factors for premature multi-vessel CHD phenotype (P < 0.0001). CONCLUSIONS: Four common CD36 polymorphisms (rs1049673, rs7755, rs3211956, and rs3173798) were identified to be significantly associated with extreme lipid profiles and had statistically opposite gender-specific clinical lipid profile effects. Thus, the 3'-untranslated regions (3'-UTR) CD36 SNPs could be a novel target for metabolic abnormalities in males of the Han nationality from Northern China.

[Astragaloside â £ inhibits inflammation after cerebral ischemia in rats through promoting microglia/macrophage M2 polarization].

OBJECTIVE: To investigate the effects of astragaloside Ⅳ (AS-Ⅳ) on microglia/macrophage M1/M2 polarization and inflammatory response after cerebral ischemia in rats. METHODS: Forty eight male SD rats were randomly divided into sham operation control group, model control group and AS-Ⅳ group with 16 rats in each. Focal cerebral ischemia model was induced by occlusion of the right middle cerebral artery (MCAO) using the intraluminal filament. After ischemia induced, the rats in AS-Ⅳ group were intraperitoneally injected with 40 mg/kg AS-Ⅳ once a day for 3 days. The neurological functions were evaluated by the modified neurological severity score (mNSS) and the corner test on d1 and d3 after modelling. The infarct volume was measured by 2, 3, 5-triphenyl tetrazolium chloride (TTC) staining on d3 after ischemia. The expression of M1 microglia/macrophage markers CD86, inducible nitric oxide synthase (iNOS) and pro-inflammatory factors TNF-α, IL-1ß, IL-6, M2 microglia/macrophages markers CD206, arginase-1 (Arg-1), chitinase-like protein (YM1/2) and anti-inflammatory factors interleukin-10 (IL-10) and transforming growth factor beta (TGF-ß) was detected by real-time RT-PCR. The expression of CD16/32/Iba1 and CD206/Iba1 was determined by double labeling immunefluorescence method in the peripheral area of cerebral ischemia. RESULTS: Compared with model control group, AS-Ⅳ treatment improved neurological function recovery and reduced infarct volume after ischemia (P<0.05 or P<0.01). The qRT-PCR results showed that AS-Ⅳ treatment down-regulated the expression of CD86, iNOS, TNF-α, IL-1ß, IL-6 mRNA (all P<0.01), and up-regulated the expression of CD206, Arg-1, YM1/2, IL-10 and TGF-ß mRNA (all P<0.01). Furthermore, the results of immunefluorescence labeling showed that AS-Ⅳ treatment reduced the number of CD16/32+/Iba1+ cells (P<0.05) and increased the number of CD206+/Iba1+ cells (P<0.01) after cerebral ischemia. CONCLUSIONS: The findings suggest that AS-Ⅳ ameliorates brain injury after cerebral ischemia in rats, which may be related to inhibiting inflammation through promoting the polarization of the microglia/macrophage from M1 to M2 phenotype in the ischemic brain.

The protective function of non-coding DNA in DNA damage accumulation with age and its roles in age-related diseases.

Aging is a progressive decline of physiological function in tissue and organ accompanying both accumulation of DNA damage and reduction of non-coding DNA. Peripheral non-coding DNA/heterochromatin has been proposed to protect the genome and centrally-located protein-coding sequences in soma and male germ cells against radiation and the invasion of exogenous nucleic acids. Therefore, this review summarizes the reduction of non-coding DNA/heterochromatin (including telomeric DNA and rDNA) and DNA damage accumulation during normal physiological aging and in various aging-related diseases. Based on analysis of data, it is found that DNA damage accumulation is roughly negatively correlated with the reduction of non-coding DNA and therefore speculated that DNA damage accumulation is likely due to the reduction of non-coding DNA protection in genome defense during aging. Therefore, it is proposed here that means to increase the total amount of non-coding DNA and/or heterochromatin prior to the onset of these diseases could potentially better protect the genome and protein-coding DNA, reduce the incidence of aging-related diseases, and thus lead to better health during aging.

The pro-survival function of DLEC1 and its protection of cancer cells against 5-FU-induced apoptosis through up-regulation of BCL-XL.

The tumor suppressor DLEC1 has been shown to promote cell proliferation when AP-2α2 is down-regulated in HCT116 stable clones, suggesting its pro-survival nature. However, the pro-survival function of DLEC1 has not been confirmed in other cells and its underlying mechanisms remain elusive. Therefore, we knocked down DLEC1 in a panel of cell lines and found that DLEC1 depletion caused various extents of cell death through intrinsic pathway. DLEC1 overexpression promoted cell survival and reduced cell death in cancer cells after 5-FU treatment, while DLEC1 down-regulation sensitized cancer cells to 5-FU. Further studies demonstrated that DLEC1 attenuated the increase in cleaved PARP, caspase-3 and caspase-7, the activity of caspase-9 and the diffusion of cytosolic cytochrome c from mitochondria. Our data also showed that BCL-XL was up-regulated by DLEC1 in stable clones after 5-FU treatment. Altogether, these results indicated that DLEC1 protects cells against cell death induced by 5-FU through the attenuation of active proteins in caspase cascade and the up-regulation of BCL-XL. Therefore, DLEC1 can be a pro-survival protein under certain circumstances and a potential therapeutic target for increasing sensitivity of cancer cells to 5-FU.

Nuciferine alleviates LPS-induced mastitis in mice via suppressing the TLR4-NF-κB signaling pathway.

BACKGROUND: Nuciferine, a major bioactive component from the lotus leaf, has been reported to have notable anti-inflammatory activities such as renal inflammation and acute lung injury in previous studies. Mastitis is one of the most prevalent diseases in the dairy cattle, which causes large economic losses for the dairy industry. However, the effects of nuciferine on lipopolysaccharide (LPS)-induced mastitis have not been reported. METHODS AND RESULTS: Here, we investigated the anti-inflammatory effects of nuciferine on LPS-induced mastitis in mice and illuminated its potential mechanism on the TLR4-mediated signaling pathway in mouse mammary epithelial cells (mMECs). Histopathological changes and myeloperoxidase (MPO) activity assay showed that nuciferine treatment significantly alleviated the LPS-induced injury of mammary gland flocculus, inflammatory cells infiltration. qPCR and ELISA assays indicated that nuciferine dose-dependently reduced the levels of TNF-α and IL-1ß, which indicated that nuciferine might have therapeutic effects on mastitis. Furthermore, nuciferine treatment significantly decreased the expression of TLR4 in a dose-dependent manner. Besides, nuciferine was also found to suppress LPS-induced NF-κB activation. CONCLUSION: These findings indicate that nuciferine potently ameliorates LPS-induced mastitis by inhibition of the TLR4-NF-κB signaling pathway.

The protective function of noncoding DNA in genome defense of eukaryotic male germ cells.

Peripheral and abundant noncoding DNA has been hypothesized to protect the genome and the central protein-coding sequences against DNA damage in somatic genome. In the cytosol, invading exogenous nucleic acids may first be deactivated by small RNAs encoded by noncoding DNA via mechanisms similar to the prokaryotic CRISPR-Cas system. In the nucleus, the radicals generated by radiation in the cytosol, radiation energy and invading exogenous nucleic acids are absorbed, blocked and/or reduced by peripheral heterochromatin, and damaged DNA in heterochromatin is removed and excluded from the nucleus to the cytoplasm through nuclear pore complexes. To further strengthen the hypothesis, this review summarizes the experimental evidence supporting the protective function of noncoding DNA in the genome of male germ cells. Based on these data, this review provides evidence supporting the protective role of noncoding DNA in the genome defense of sperm genome through similar mechanisms to those of the somatic genome.

The eukaryotic genome is structurally and functionally more like a social insect colony than a book.

Traditionally, the genome has been described as the 'book of life'. However, the metaphor of a book may not reflect the dynamic nature of the structure and function of the genome. In the eukaryotic genome, the number of centrally located protein-coding sequences is relatively constant across species, but the amount of noncoding DNA increases considerably with the increase of organismal evolutional complexity. Therefore, it has been hypothesized that the abundant peripheral noncoding DNA protects the genome and the central protein-coding sequences in the eukaryotic genome. Upon comparison with the habitation, sociality and defense mechanisms of a social insect colony, it is found that the genome is similar to a social insect colony in various aspects. A social insect colony may thus be a better metaphor than a book to describe the spatial organization and physical functions of the genome. The potential implications of the metaphor are also discussed.

Omp16-based vaccine encapsulated by alginate-chitosan microspheres provides significant protection against Haemophilus parasuis in mice.

Haemophilus parasuis (H. parasuis) is the etiological agent of swine Glässer's disease, which leads to significant economic loss in swine industry over the world. Subunit vaccine based on outer membrane protein is one of the promising choices to protect pigs against H. parasuis infection despite low immunity efficiency. In this paper, outer membrane protein 16 (Omp16) of H. parasuis encapsulated by alginate-chitosan microspheres as antigen carriers was explored for the first time in a mouse model. Our results showed that the microspheres with Omp16 induced significant higher H. parasuis-specific antibodies, and higher titers of IL-2, IL-4, and IFN-γ than those by Omp16-FIA in treated mice (p<0.05). Moreover, H. parasuis load in the tissues from liver, spleen, and lung of mice immunized with microspheres containing Omp16 was significantly decreased (p<0.05) than that in the same counterpart tissues of control groups. In addition, 80% mice treated with Omp16 and 70% mice with Omp16-FIA were survived after challenged with H. parasuis virulent strain LY02 (serovar 5). Therefore, Omp16-based microsphere vaccine induces both humoral and cellular immune responses and provides promising protection against H. parasuis infection in mice.

Adjunctive loading dose of cilostazol in preventing periprocedural myocardial infarction.

INTRODUCTION: Periprocedural myocardial infarction (PMI) is a common complication of percutaneous coronary intervention (PCI). This study evaluated the safety and efficacy of adjunctive loading dose of cilostazol in preventing PMI in patients with acute coronary syndrome (ACS). METHODS: A total of 113 patients with ACS undergoing PCI were randomized to receive loading doses of dual (aspirin plus clopidogrel; DAPT group; n=57) or triple antiplatelet therapy (aspirin plus clopidogrel plus cilostazol; TAPT group; n=56). The loading and maintenance doses were 100 and 50 mg bid for cilostazol. Patients in the TAPT group received adjunctive cilostazol for 1 week. Cardiac biomarkers were measured before PCI, 8 and 24 hours after PCI to determine the incidence of PMI. RESULTS: There was no significant difference in the incidence of PMI between the TAPT and DAPT groups (32.1% vs 47.4%, P=.098). However, in the antiplatelet-naïve subgroup, TAPT significantly lowered the incidence of PMI compared to DAPT (17.9% vs 42.9%, P=.042). In the antiplatelet-treated subgroup, the incidences of PMI were comparable (46.4% vs 51.7%, P=.698). Multivariable logistic analysis showed that antiplatelet-treated (vs antiplatelet-naïve) (hazard ratio [HR]: 2.45; 95% confidence interval [CI]: 1.09-5.52; P=.030) subgroup was independently associated with PMI. However, TAPT (vs DAPT) (HR: 0.51; 95% CI: 0.23-1.14; P=.102) was not an independent protective factor of PMI. CONCLUSIONS: The present single-center, randomized study indicates that TAPT with adjunctive cilostazol was not associated with lower incidence of PCI-related PMI in patients with ACS. Further study with large study population is needed to get definite conclusions.

Low-dose adjunctive cilostazol in patients with complex lesions undergoing percutaneous coronary intervention.

Patients with complex coronary lesions undergoing percutaneous coronary intervention (PCI) have more major adverse cardiac events (MACE) than do those with simpler cases. Therefore, intensive antiplatelet therapy might be needed in these patients. A total of 127 patients with complex lesions undergoing PCI in the Second Hospital of Tianjin Medical University from October 2012 to April 2014 were randomized to receive either dual (aspirin plus clopidogrel, DAPT, n = 66), or triple antiplatelet therapy (aspirin plus clopidogrel plus cilostazol; TAPT, n = 61). Patients in the TAPT group received low-dose cilostazol (100 mg loading, followed with 50 mg twice per day) for 3-6 months. The primary endpoint was composite MACE. The complex coronary target lesions were defined as at least one of the following: left main disease; severe 3-vessel disease; chronic total occlusion lesions; true bifurcation lesion; ostial lesions; severe calcified lesions; and highly thrombotic lesions. The two groups had similar baseline clinical and angiographic characteristics. One-year clinical outcomes showed that the TAPT group had significantly lower incidences of myocardial infarction (1.6% vs 13.6%, P = 0.018) and MACE (1.6% vs 16.7%, P = 0.004) than DAPT group. The DAPT group had two cases of stent thrombosis, while the TAPT group did not. Furthermore, adjunctive low-dose cilostazol didn't significantly increase the incidence of bleeding events (26.2% vs 19.7%, P = 0.381) regardless of major (4.9% vs 4.5%, P = 0.921) or minor (21.3% vs 15.2%, P = 0.368) bleeding events. In conclusion, low-dose adjunctive cilostazol seems superior to dual antiplatelet therapy in reducing recurrent ischemic events in patients with complex coronary lesions and the two test groups have a similar incidence of bleeding events.

Probucol for the prevention of cystatin C-based contrast-induced acute kidney injury following primary or urgent angioplasty: a randomized, controlled trial.

BACKGROUND: Probucol, a lipid-lowering drug with potent antioxidant properties, may reduce the risk of cystatin C (CyC)-based contrast-induced acute kidney injury (CIAKI). The aim of this study was to observe the incidence of CyC-based CIAKI and assess the efficacy of probucol on prevention of CIAKI following primary or urgent coronary angioplasty. METHODS: A total of 204 patients with acute coronary syndrome (ACS) were prospectively randomized to a control group (108 patients, 74 male, 65.4 ± 12.5 years) or probucol group (96 patients, 67 male, 65.1 ± 10.5 years) 1000 mg orally before primary or urgent angioplasty and 500 mg twice daily for 3 days following intervention. Serum CyC and serum creatinine (Scr) concentrations were measured before, and on day 1, day 2 and day 3 after coronary intervention. RESULTS: The clinical characteristics of the patients from the two groups were similar. Scr-based CIAKI was developed in 23 patients of the control group (21.3%) and in 4 patients of the probucol group (4.2%) (P<0.001). Furthermore, CyC-based CIAKI occurred in 56 patients of the control group (51.9%) and 28 patients of the probucol group (29.2%) (P<0.001). The CyC increase ≥ 10% after exposure to contrast medium was the best increment cutoff value for the early identification of patients at risk of CIAKI. CONCLUSIONS: Our study suggests that CyC is a reliable marker for early identification and ruling out the patients at the risk of CIAKI. Among the patients with ACS who are undergoing primary or urgent angioplasty, prophylactic treatment with probucol reduces the risk of both Scr and CyC-based CIAKI.

[Cloning and analysis of the complete genomes of pigeon circovirus from Zhejiang Province].

Pigeon circovrius (PiCV) is a member of circovirus, which is usually regarded as an immunosuppression agent. There were reports that pigeons infected by PiCV showed symptoms of lethargy, weight loss, vomiting, diarrhea, respiratory distress, etc. In this study, we established a PCR method for the detection of PiCV DNA. Samples from 5 different farms in Zhejiang Province were examined and samples from a farm in Hangzhou were positive. Furthermore, the genomic segments of 2 strains of PiCV were amplified, cloned and sequenced using designed primers and the complete genomes of the strains were then assembled and named as PiCV-zj1 and PiCV-zj2, respectively. The sequences were deposited in GenBank under the GenBank Accession number of DQ090945 and DQ090944, respectively. Sequence Analysis had shown that the complete genomes of 2 strains of PiCV from Zhejiang Province had 2 039 nucleotides totally in length and common characters of circovirus such as a stem-loop structure and conserved motifs for Rep protein, which were supposed to be related to the replication of the virus. Pairwise comparisons showed that the nucleotide sequence of the genome of PiCV strains from Zhejiang Province had 86%-89.1% identities to that of 11 published PiCV strains, and that the amino acid identities of the replication-associated protein (Rep) and capsid protein (Cap) displayed 92.1%-94.7% and 76.6%-81.4%, respectively. A phylogenic tree was built using PHYLIP with bootstrap support for 1 000 replicates. The result showed that 10 strains from Europe and America formed one big branch and the others from Zhejiang Province and Australia formed the other two, respectively. This was the first report on the detection and full genome sequencing of PiCV in China.

[Role of probucol in preventing contrast induced acute kidney injury after coronary interventional procedure: a randomized trial].

OBJECTIVE: Contrast induced acute kidney injury (CIAKI) is a significant clinical problem. We, therefore, performed a prospective, randomized trial to investigate the role of probucol in the prevention of CIAKI in patients with unstable angina pectoris (UAP) undergoing percutaneous coronary angiography (CAG) and interventions (PCI). METHODS: We studied 205 patients with UAP, who underwent CAG or PCI prospectively. Patients were randomly assigned to probucol group (n = 102) and control group (n = 103). In the probucol group, the patients received probucol tablets 500 mg b.i.d for 3 days before and after intervention. All the patients, after intervention, underwent hydration with intravenous saline at a rate of 1 ml per kilogram of body weight per hour for 12 hours. RESULTS: Patients were well-matched with no significant difference at baseline in majority measured parameters between two groups. CIAKI occurred in 23 of the 205 (11.22%) patients. Multivariate logistic regression was used to identify correlates of CIAKI and clinical data. CIAKI was most strongly associated with Scr > or = 132.6 micromol/L (OR = 21.11, 95%CI 1.95 - 56.06, P < 0.001), Ccr < 60 ml/min (OR = 4.19, 95%CI 1.94 - 9.05, P < 0.001), heart function > class II (OR = 6.23, 95%CI 2.73 - 14.21, P < 0.001), Diabetes (OR = 2.049, 95%CI 1.19 - 5.25, P < 0.001), age > or = 70 yrs (OR = 3.52, 95%CI 1.66 - 7.43, P < 0.001), coronary artery calcification shown by CAG (OR = 4.29, 95%CI 1.99 - 9.24, P < 0.001). The rate of CIAKI in probucol groups was slightly lower compared with control group (7.84% vs. 14.56%), without significant difference. The post-procedure mean peak of Scr [(101.62 +/- 42.98) micromol/L vs. (117.67 +/- 68.77) micromol/L, P = 0.047] and the post-procedure increasing Scr from baseline (DeltaScr) [(13.49 +/- 19.61) micromol/L vs. (22.50 +/- 18.31) micromol/L, P = 0.001] in the probucol group decreased significantly compared with that of control group. CONCLUSION: Prophylactic treatment with probucol 500 mg b.i.d during periprocedural stage in patients with UAP has preventing role against CIAKI after cardiac catheterization.

Role of probucol in preventing contrast-induced acute kidney injury after coronary interventional procedure.

Enhanced production and reduced removal of oxygen free radicals may play an important role in the pathogenesis of the contrast-induced acute kidney injury (CIAKI). Probucol, a lipid-lowering drug with potent antioxidant properties, has been widely used clinically for the prevention of the progression of atherosclerosis. We performed a prospective, randomized controlled trial to investigate the role of probucol in the prevention of CIAKI in patients undergoing planned coronary angiography (CAG) or intervention. The 205 patients who underwent planned CAG or intervention were randomly assigned to either the probucol group (n = 102; 500 mg orally twice daily) or the control group (n = 103). Renal function was assessed at the time of hospital admission and on days 1, 2, and 3 after the procedure. CIAKI occurred in 23 (11.22%) of the 205 patients. The incidence of CIAKI in the probucol group was slightly lower compared with the control group (7.84% vs 14.56%) but without significant difference (p = 0.13). The postprocedure mean peak of serum creatinine (1.15 +/- 0.49 vs 1.33 +/- 0.78 mg/dl, p = 0.04) and the postprocedure increasing Scr from baseline (0.15 +/- 0.22 vs 0.25 +/- 0.21 mg/dl, p = 0.001) in the probucol group were significantly lower than those in the control group. In conclusion, prophylactic treatment with probucol during the periprocedural stage in patients undergoing coronary angiography or intervention has a preventive role against CIAKI.

Plasma fatty acids metabolic profiling analysis of coronary heart disease based on GC-MS and pattern recognition.

A simple approach for comprehensive profiling of fatty acids in human plasma based on gas chromatography-mass spectrometry (GC-MS) was described and validated. With this method, plasma fatty acid metabolic profiles of 23 coronary heart disease (CHD) patients and 25 healthy subjects were determined. Pattern recognition technology was used to establishing differences in the metabolic profiles of these two groups. Furthermore, CHD patients with two different patterns in Traditional Chinese Medicine clinical practices could be classified by the corresponding metabolic profiles, and several potential biomarkers were discussed.