Drug-coated balloons: A better revascularization strategy in patients with multivessel coronary artery disease undergoing one-stop hybrid coronary revascularization surgery.

BACKGROUND: The optimal revascularization strategy for non-left anterior descending coronary artery (LAD) lesions during one-stop hybrid coronary revascularization (HCR) surgery lacks current evidence. AIMS: This study aimed to compare the outcomes of the drug-coated balloon (DCB) and drug-eluting stent (DES) strategies in patients with non-small non-LAD lesions undergoing one-stop HCR. METHODS: A total of 141 consecutive patients with multivessel coronary artery disease (MVCAD) undergoing one-stop HCR between June 1, 2018 and March 1, 2022 were retrospectively included in this study. In-hospital outcomes and mid-term major adverse cardiovascular and cerebrovascular events (MACCE) were observed. Kaplan-Meier curve analysis was used to evaluate the MACCE-free survival rate. The Cox proportional hazard model was used to identify risk factors of mid-term MACCE. RESULTS: Thirty-eight and 103 patients received only DCB or DES therapy, respectively, in this study. There were no significant differences in demographic characteristics and laboratory parameters between the two groups. The in-hospital MACCE rate in the DES group was numerically higher than that in the DCB group (9.7% vs. 5.3%, respectively), but the difference was not statistically significant (P = 0.4). The incidence of MACCE after patients' discharge was significantly higher in the DES group (22% vs. 5.3%, respectively, P = 0.02) during a median follow-up of 20 months. After multivariable Cox proportional hazard analysis, DCB therapy was independently associated with reduced risk of mid-term MACCE (hazard ratio, 0.21; 95% confidence interval, 0.06-0.91; P = 0.04). CONCLUSION: For patients with MVCAD undergoing one-stop HCR, DCB therapy may be the optimal revascularization strategy for non-small non-LAD coronary artery lesions with a significantly lower rate of mid-term MACCE.

The long-term impact of a chronic total occlusion in a non-infarct-related artery on acute ST-segment elevation myocardial infarction after primary coronary intervention.

OBJECTIVES: To investigate the long-term outcome of patients with acute ST-segment elevation myocardial infarction (STEMI) and a chronic total occlusion (CTO) in a non-infarct-related artery (IRA) and the risk factors for mortality. METHODS: The enrolled cohort comprised 323 patients with STEMI and multivessel diseases (MVD) that received a primary percutaneous coronary intervention between January 2008 and November 2013. The patients were divided into two groups: the CTO group (n = 97) and the non-CTO group (n = 236). The long-term major adverse cardiovascular and cerebrovascular events (MACCE) experienced by each group were compared. RESULTS: The rates of all-cause mortality and MACCE were significantly higher in the CTO group than they were in the non-CTO group. Cox regression analysis showed that an age ≥ 65 years (OR = 3.94, 95% CI: 1.47-10.56, P = 0.01), a CTO in a non-IRA(OR = 5.09, 95% CI: 1.79 ~ 14.54, P < 0.01), an in-hospital Killip class ≥ 3 (OR = 4.32, 95% CI: 1.71 ~ 10.95, P < 0.01), and the presence of renal insufficiency (OR = 5.32, 95% CI: 1.49 ~ 19.01, P = 0.01), stress ulcer with gastraintestinal bleeding (SUB) (OR = 6.36, 95% CI: (1.45 ~ 28.01, P = 0.01) were significantly related the 10-year mortality of patients with STEMI and MVD; an in-hospital Killip class ≥ 3 (OR = 2.97,95% CI:1.46 ~ 6.03, P < 0.01) and the presence of renal insufficiency (OR = 5.61, 95% CI: 1.19 ~ 26.39, P = 0.03) were significantly related to the 10-year mortality of patients with STEMI and a CTO. CONCLUSIONS: The presence of a CTO in a non-IRA, an age ≥ 65 years, an in-hospital Killip class ≥ 3, and the presence of renal insufficiency, and SUB were independent risk predictors for the long-term mortality of patients with STEMI and MVD; an in-hospital Killip class ≥ 3 and renal insufficiency were independent risk predictors for the long-term mortality of patients with STEMI and a CTO.

Effects of Nano-Protein Complexes on Apoptosis of Myocardial Infarction Cells Based on Complex Curve Analysis.

Myocardial infarction is one of the common types of coronary heart disease in the clinic. Its morbidity, lethality and disability are high, and it has become a serious threat to human health. At present, it is shown that in the early stage of acute myocardial infarction, myocardial cells are mainly apoptotic, suggesting that effectively blocking myocardial apoptosis in the early stage of myocardial infarction is of great significance for reducing tissue necrosis in the infarcted area. Recent studies have shown that NG nano-protein complexes have a better therapeutic effect on acute myocardial infarction and can inhibit left ventricular remodeling in patients with acute myocardial infarction. However, there are few studies on the effect of NG nano-protein complexes on myocardial cell apoptosis after ischemia. This study used a rat model of acute myocardial infarction to analyze its effect on apoptotic proteins of myocardial cells in rats with acute myocardial infarction in order to provide a certain theoretical basis for its clinical application. In this study, 45 SD rats were randomly divided into a sham operation group, a myocardial infarction group, and a NG nano-protein complex group, with 15 in each group. The sham operation group only underwent thoracotomy, and received normal saline gavage postoperatively; the myocardial infarction group and the NG nano-protein complex group were ligated to the left anterior descending coronary artery of the rat to establish an acute myocardial infarction model, and were performed separately treatment with saline and NG nanoprotein complexes. Finally, we conclude that this nano-protein complex can significantly reduce the expression level of myocardial apoptosis-related proteins in rats with acute myocardial infarction, and is of great significance in inhibiting the apoptosis of acute myocardial infarction cells.

Genome-wide genotyping uncovers genetic diversity, phylogeny, signatures of selection, and population structure of Chinese Jiangquhai pigs in a global perspective1.

Jiangquhai pigs are one of the 42 representative local breeds listed in the national livestock genetic resources conservation project of China. This breed is known for its prolificacy, desirable meat quality, and excellent adaptability to crude feed and local environments. In this study, we genotyped 105 Jiangquhai pigs from the state conservation farm using GeneSeek GGP Porcine 80K SNP chip, and explored the SNP data to unravel genetic diversity, evolutionary phylogeny, signatures of selection, and population structure of Jiangquhai pigs in a context of 33 global breeds. Five indices of observed heterozygosity, expected heterozygosity, effective population size, runs of homozygosity, and linkage disequilibrium extent indicate that the Jiangquhai breed are still rich in genetic diversity in comparison with other breeds also from East China despite the recent decline of its population size. Phylogenetic, principal component, TreeMix, and admixture analyses show that Jiangquhai pigs represent an authentic genetic resource and have close genetic relationships with East Chinese breeds, their geographical neighbors. A genome scan unravels a list of reproduction-related genes potentially under selection in Jiangquhai pigs. Using the neighbor-joining clustering approach, we reconstructed the family structure of the conservation population of Jiangquhai pigs. This finding allowed us to suggest a rotational mating scheme across the reconstructed families to reduce the risk of inbreeding depression in the population.

Circulating microRNAs as potential biomarkers for coronary plaque rupture.

Coronary plaque rupture is the most common cause of acute coronary syndrome. However, the timely biomarker-based diagnosis of plaque rupture remains a major unmet clinical challenge. Balloon dilatation and stent implantation during percutaneous coronary intervention (PCI) could cause plaque injury and rupture. Here we aimed to assess the possibility of circulating microRNAs (miRNAs) as biomarkers of acute coronary plaque rupture by virtue of the natural model of PCI-induced plaque rupture. Stable coronary artery disease patients underwent PCI with single stent implantation were recruited and a three-phase approach was conducted in the present study: (i) profiling of plasma miRNAs in a group of patients before (0 h) and after balloon dilatation for 1 h (1 h vs. 0 h), (ii) replication of significant miRNAs in the second group of patients (1 h vs. 0 h), (iii) validation of a multi-miRNAs panel in the third group of patients (0.5 h, 1 h vs. 0 h). Out of 24 miRNAs selected for replication, 6 miRNAs remained significantly associated with plaque rupture. In the validation phase, combinations of miR-483-5p and miR-451a showed the highest area under the receiver-operating-characteristic curve (AUC) (0.982; CI: 0.907-0.999) in patients with plaque rupture for 0.5 h; combinations of miR-483-5p and miR-155-5p showed the highest AUC (0.898; CI: 0.790-0.962) after plaque rupture for 1 h. In conclusion, using a profiling-replication-validation model, we identified 3 miRNAs including miR-155-5p, miR-483-5p and miR-451a, which may be biomarkers for the early identification of plaque rupture.

Parathyroid hormone, cardiovascular and all-cause mortality: A meta-analysis.

BACKGROUND: Inconsistent findings have reported on parathyroid hormone (PTH) concentration and cardiovascular or all-cause mortality. OBJECTIVE: To investigate whether elevated PTH concentration was an independent predictor for cardiovascular or all-cause mortality in the general population by conducting a meta-analysis based on prospective studies. METHOD: We searched Cochrane Library, Pubmed, and Embase databases up to June 2015. Only prospective studies evaluating serum PTH concentration and cardiovascular or all-cause mortality were included. Pooled adjust risk ratio (RR) and corresponding 95% confidence intervals (CI) were calculated for the highest vs. lowest PTH concentration. RESULTS: Ten studies with 31,616 subjects were identified and analyzed. Compared the highest to the lowest PTH concentration, elevated serum PTH concentration increased the risk of all-cause mortality (RR 1.19; 95% CI 1.08-1.30) but not for cardiovascular mortality (RR 1.26; 95% CI 0.96-1.66). Subgroup analyses indicated that cardiovascular mortality risk appeared to be more pronounced among men (RR 1.68; 95% CI 1.05-2.67). CONCLUSIONS: Elevated PTH concentration is an independent predictor of all-cause mortality. Elevated serum PTH concentration appears to increase risk of cardiovascular mortality among men.

Positive effects of bFGF modified rat amniotic epithelial cells transplantation on transected rat optic nerve.

PURPOSE: Effective therapy for visual loss caused by optic nerve injury or diseases has not been achieved even though the optic nerve has the regeneration potential after injury. This study was designed to modify amniotic epithelial cells (AECs) with basic fibroblast growth factor (bFGF) gene, preliminarily investigating its effect on transected optic nerve. METHODS: A human bFGF gene segment was delivered into rat AECs (AECs/hbFGF) by lentiviral vector, and the gene expression was examined by RT-PCR and ELISA. The AECs/hbFGF and untransfected rat AECs were transplanted into the transected site of the rat optic nerve. At 28 days post transplantation, the survival and migration of the transplanted cells was observed by tracking labeled cells; meanwhile retinal ganglion cells (RGCs) were observed and counted by employing biotin dextran amine (BDA) and Nissl staining. Furthermore, the expression of growth associated protein 43 (GAP-43) within the injury site was examined with immunohistochemical staining. RESULTS: The AECs/hbFGF was proven to express bFGF gene and secrete bFGF peptide. Both AECs/hbFGF and AECs could survive and migrate after transplantation. RGCs counting implicated that RGCs numbers of the cell transplantation groups were significantly higher than that of the control group, and the AECs/hbFGF group was significantly higher than that of the AECs group. Moreover GAP-43 integral optical density value in the control group was significantly lower than that of the cell transplantation groups, and the value in the AECs/hbFGF group was significantly higher than that of the AECs group. CONCLUSIONS: AECs modified with bFGF could reduce RGCs loss and promote expression of GAP-43 in the rat optic nerve transected model, facilitating the process of neural restoration following injury.

FJU-C4, a new 2-pyridone compound, attenuates lipopolysaccharide-induced systemic inflammation via p38MAPK and NF-κB in mice.

Despite advances in antibiotic therapy and intensive care, the mortality caused by systemic inflammatory response syndrome and severe sepsis remains high. The use of anti-inflammatory agents to attenuate inflammatory response during acute systemic inflammatory reactions may improve survival rates. Here we show that a newly synthesized 2-pyridone compound (FJU-C4) can suppress the expression of late inflammatory mediators such as iNOS and COX-2 in murine macrophages. The pro-inflammatory cytokines, including TNFα, IL-1ß, and IL-6, were dose-dependently suppressed by FJU-C4 both in mRNA and protein levels. In addition, the expression of TNFα was inhibited from as early as 2 hours after exposure to LPS stimulation. The production of mature pro-inflammatory cytokines was also suppressed by pretreatment with FJU-C4 in either cell culture medium or mice serum when stimulated by LPS. FJU-C4 prolongs mouse survival and prevents mouse death from LPS-induced systemic inflammation when the dose of FJU-C4 is over 5 mg/kg. The activities of ERK, JNK, and p38MAPK were induced by LPS stimulation on murine macrophage cell line, but only p38MAPK signaling was dramatically suppressed by pretreatment with the FJU-C4 compound in a dose-dependent manner. NF-κB activation also was suppressed by FJU-C4 compound. These findings suggest that the FJU-C4 compound may act as a promising therapeutic agent against inflammatory diseases by inhibiting the p38MAPK and NF-κB signaling pathway.

The association between atherosclerotic renal artery stenosis and acute kidney injury in patients undergoing cardiac surgery.

BACKGROUND: Atherosclerotic renal artery stenosis (ARAS) and coronary artery disease (CAD) commonly co-exist. Some patients with unidentified ARAS may undergo cardiac surgery. While acute kidney injury (AKI) is a frequent and serious complication of cardiac surgery, we aim to evaluate the influence of ARAS on the occurrence of postoperative AKI in patients with normal or near-normal baseline renal function following cardiac surgery. METHODS: A total of 212 consecutive patients undergoing aortography after coronary angiography and cardiac surgery were retrospectively studied for their preoperative and intraoperative conditions. AKI was defined as an absolute increase in serum creatinine of more than or equal to 0.3 mg/dl (≥26.4 µmol/l) or a percentage increase in creatinine of more than or equal to 50% (1.5-fold from baseline) after cardiac surgery. A propensity score-adjusted logistic regression models was used in estimating the effect of ARAS on the risk of postoperative AKI. RESULTS: ARAS (≥50%) was observed in 50 (23.6%) patients, and 83 (39.2%) developed AKI after cardiac surgery. A correlation existed between renal artery patency and preoperative-to-postoperative %ΔCr in patients with ARAS (r = 0.297, P<0.0001). The propensity score-adjusted regression model showed the occurrence of postoperative AKI in patients with ARAS was significantly higher than those without ARAS (OR 2.858, 95% CI 1.260-6.480, P = 0.011). CONCLUSION: ARAS is associated with postoperative AKI in patients with normal or near-normal baseline renal function after cardiac surgery.

PPAR-α Agonist Fenofibrate Upregulates Tetrahydrobiopterin Level through Increasing the Expression of Guanosine 5'-Triphosphate Cyclohydrolase-I in Human Umbilical Vein Endothelial Cells.

Tetrahydrobiopterin (BH4) is an essential cofactor for endothelial nitric oxide (NO) synthase. Guanosine 5'-triphosphate cyclohydrolase-I (GTPCH-I) is a key limiting enzyme for BH4 synthesis. In the present in vitro study, we investigated whether peroxisome proliferator-activated receptor α (PPAR-α) agonist fenofibrate could recouple eNOS by reversing low-expression of intracellular BH4 in endothelial cells and discussed the potential mechanisms. After human umbilical vein endothelial cells (HUVECs) were treated with lipopolysaccharide (LPS) for 24 hours, the levels of cellular eNOS, BH4 and cell supernatant NO were significantly reduced compared to control group. And the fluorescence intensity of intracellular ROS was significantly increased. But pretreated with fenofibrate (10 umol/L) for 2 hours before cells were induced by LPS, the levels of eNOS, NO, and BH4 were significantly raised compared to LPS treatment alone. ROS production was markedly reduced in fenofibrate group than LPS group. In addition, our results showed that the level of intracellular GTPCH-I detected by western blot was increased in a concentration-dependent manner after being treated with fenofibrate. These results suggested that fenofibrate might help protect endothelial function and against atherosclerosis by increasing level of BH4 and decreasing production of ROS through upregulating the level of intracellular GTPCH-I.

Single-chain variable fragments antibody of CART inhibits the expression of cocaine-induced behavioral sensitization.

Cocaine and amphetamine-regulated transcript (CART) peptides are neurotransmitters with important roles in drug abuse. The increase of CART expression in the brain induced by psychostimulants is associated with changes of behavior in addicted animals. We expressed and purified the single-chain variable fragments antibody (scFv) against CART55-102, and observed the effect of CART scFv on the expression of cocaine-induced behavior sensitization in mice. Results showed that the titer of CART scFv was 1.6 µg/ml. Single administration of CART scFv (intraperitoneal 0.04, 0.2, and 1 mg/kg) reduced the increasing locomotor activity induced by chronic cocaine intake in mice (P<0.05-0.01), but failed to affect the locomotor activity of naive mice. These results suggested that CART scFv may be a potential therapeutic tool to treat drug abuse.

In-hospital delay to primary angioplasty for patients with ST-elevated myocardial infarction between cardiac specialized hospitals and non-specialized hospitals in Beijing, China.

BACKGROUND: Evidence indicates that early reperfusion therapy in patients with ST-elevation myocardial infarction (STEMI) reduces complications. This study was undertaken to compare the in-hospital delay to primary percutaneous coronary intervention (PPCI) for patients with STEMI between specialized hospitals and non-specialized hospitals in Beijing, China. METHODS: Two specialized hospitals and fifteen non-specialized hospitals capable of performing PPCI were selected to participate in this study. A total of 308 patients, within 12 hours of the onset of symptoms and undergoing PPCI between November 1, 2005 and December 31, 2006 were enrolled. Data were collected by structured interview and review of medical records. RESULTS: The median in-hospital delay was 98 (interquartile range 105 to 180) minutes, and 16.9% of the patients were treated within 90 minutes. Total in-hospital delay and ECG-to-treatment decision-making time were longer in the non-specialized hospitals than in the cardiac specialized hospitals (147 minutes vs. 120 minutes, P < 0.001; 55 minutes vs. 45 minutes, P = 0.035). After controlling the confounding factors, the non-specialized hospitals were independently associated with an increased risk of being in the upper median of in-hospital delays. CONCLUSIONS: There were substantial in-hospital delays between arrival at the hospital and the administration of PPCI for patients with STEMI in Beijing. Patients admitted to the cardiac specialized hospitals had a shorter in-hospital delay than those to the non-specialized hospitals because of a shorter time of ECG-to-treatment decision-making.

Chronic kidney disease, all-cause mortality and cardiovascular mortality among Chinese patients with established cardiovascular disease.

AIM: This study was conducted to investigate the role of chronic kidney disease (CKD) in 1-year all cause mortality and cardiovascular mortality among Chinese patients who were at least 50 years old and had a history of coronary artery disease (CAD), stroke, or peripheral vascular disease (PAD), or with two or more cardiovascular risks. METHODS: Of 3,732 hospitalized patients enrolled, 3,423 patients (91.7%) with complete data were eligible for 1-year follow-up. CKD was defined as an estimated glomerular filtration rate (eGFR) of <60 mL/min/1.73 m(2). RESULTS: 1,166 (34.1%) were diagnosed with CKD. Most cases were unrecognized. Patients having an eGFR of <30 mL/min/1.73 m(2) were less likely to be prescribed beta-blockers, statins, or aspirin (all p<0.001). A powerful relationship was observed between the severity of renal dysfunction and all causes of death or cardiovascular death. Adjusted for other covariates, the hazard ratio (HR) for all causes of death and for cardiovascular death among patients with an eGFR of 30-45 mL/min/1.73 m(2) was 1.70 (95% CI, 1.18-2.45) and 1.85 (95% CI, 1.12-3.01) as compared with 2.93 (95% CI, 1.96-4.38) and 3.47 (95% CI, 1.91-6.31) for patients with an eGFR of <30 mL/min/1.73 m(2). CONCLUSIONS: One third of Chinese patients at high risk for atherosclerotic events were diagnosed with CKD. Most of these cases were unrecognized and undertreated. An eGFR of <45 mL/min/1.73 m(2) was an independent predictor of all causes of death and of cardiovascular death.

Nogo-A inhibits necdin-accelerated neurite outgrowth by retaining necdin in the cytoplasm.

Nogo-A has been identified in the central nervous system as an inhibitor for axonal regeneration. Previous works have mainly focused on Nogo-A in oligodendrocytes and the roles of neuronal intracellular Nogo-A remain elusive. To gain deep insight into the physiological functions of Nogo-A, a yeast two-hybrid screening was performed with Nogo-66 as bait. We identified a new interaction between Nogo-66 and necdin. Mutagenesis analysis revealed that the central region of necdin was indispensable for the interaction of necdin with Nogo-66. The interaction was further confirmed by co-immunoprecipitation in neural tissues and cultured cortical neurons. Morphological evidence showed that Nogo-A and necdin highly colocalized in rat cortical and dorsal root ganglia neurons. Ectopic expression of Nogo-A in HEK293 cells led to retention of necdin from the nucleus to the cytoplasm. Furthermore, overexpression of Nogo-A in PC12 cells and cultured cortical neurons inhibited necdin-accelerated neurite outgrowth. Meanwhile, necdin was found to be significantly sequestered in the cytoplasm of PC12 cells stably overexpressing Nogo-A. Together, these data suggest that Nogo-A is a novel necdin binding protein and inhibits necdin-accelerated neuronal neurite outgrowth by sequestering necdin in the cytoplasm.

Recombinant ciliary neurotrophic factor promotes nerve regeneration and induces gene expression in silicon tube-bridged transected sciatic nerves in adult rats.

Sciatic nerves in adult male rats were transected and reunited via a silicone chamber. This was followed by a focal injection of recombinant ciliary neurotrophic factor (CNTF). To evaluate the effect of this therapeutic approach and to explore its possible mechanisms, nerve regeneration was traced by horseradish peroxidase retrograde labeling. Functional recovery was evaluated by functional assessment of the hind feet and the expression of a number of proteins was detected using immunohistochemistry. The results showed that a single administration of CNTF could promote regeneration of motor axons, with improved functional recovery in adult rats. Growth associated protein (GAP)-43, S100, CD68 and major histocompatibility complex class II immunoreactivity in the regenerative and distal nerves suggested that CNTF could promote axon regeneration, Schwann cell migration, monocyte infiltration and activation. CNTF might also indirectly promote axonal regeneration by further activating the JAK-STAT3 pathway and subsequently upregulating phosphotyrosine, GAP-43 and S100 expression to enhance proliferation, growth and migration of Schwann cells. CNTF has suggested important targets for pharmacological intervention in peripheral nerve disease and injury.

[Effects of socioeconomic status on the distribution of cardiovascular risk factors and clinical treatments of patients with acute myocardial infarction in Beijing].

OBJECTIVE: To evaluate the effects of socioeconomic status on the distribution of cardiovascular risk factors and clinical treatments of patients with acute myocardial infarction in Beijing. METHODS: In Beijing, a prospective, multi-center, registration study was carried out which including 800 patients who were consecutively hospitalized for ST-segment elevation acute myocardial infarction within 24 hours after event attack in 19 different hospitals in Beijing between November, 2005 and December, 2006. Indicators of socioeconomic status included self-reported personal income (< 500, 500-2000, > 2000 RMB/ month), educational attainment (< or = 12 and > 12 years) and status of medical insurance (yes/no). According to categories of education, patients were categorized into two groups of lower socioeconomic status and higher socioeconomic status. Differences of cardiovascular risk factors and clinical treatments were compared across the two groups respectively. RESULTS: Proportion of diabetes and hyperlipidemia in patients with higher socioeconomic status was much higher than that of patients with lower socioeconomic status (P < 0.05, P < 0.01 respectively). Patients with lower socioeconomic status were more likely to be smokers (P < 0.05). The rates of receiving coronary angiography and PTCA were much lower in patients with lower socioeconomic status. Medical insurance and income were the most important two socioeconomic factors determining the use of PTCA. CONCLUSION: Compared to patients with lower socioeconomic status, patients with higher socioeconomic status had higher rates of hyperlipidemia and diabetes but lower smoking rate among cardiovascular risk factors. The rates of receiving interventional therapies were much lower in patients with lower socioeconomic status.

Corticotropin-releasing hormone stimulates SGK-1 kinase expression in cultured hippocampal neurons via CRH-R1.

Corticotropin-releasing hormone (CRH) has been shown to exhibit various functions in hippocampus. In the present study, we examined the effect of CRH on the expression of serum/glucocorticoid-inducible protein kinase-1 (SGK-1), a novel protein kinase, in primary cultured hippocampal neurons. A dose-dependent increase in mRNA and protein levels of SGK-1 as well as frequency of SGK-1-positive neurons occurred upon exposure to CRH (1 pmol/l to 10 nmol/l). These effects can be reversed by the specific CRH-R1 antagonist antalarmin but not by the CRH-R2 antagonist astressin 2B. Blocking adenylate cyclase (AC) activity with SQ22536 and PKA with H89 completely prevented CRH-induced mRNA and protein expression of SGK-1. Blockage of PLC or PKC did not block CRH-induced SGK-1 expression. Our results suggest that CRH act on CRH-R1 to stimulate SGK-1 mRNA and protein expression in cultured hippocampal neurons via a mechanism that is involved in AC/PKA signaling pathways.

[Effect of low-dose folate treatment on plasma homocystyeine and chemokine levels in patients with hyperhomocysteinemia].

OBJECTIVE: To explore the effect of low-dose folate on plasma homocysteinemia (Hcy) and chemokine levels in patients with hyperhomocysteinemia (HHcy). METHODS: Forty HHcy patients were treated with 0.8 mg/d folate for 6 months. Plasma levels of Hcy, monocyte chemoattractant protein-1 (MCP-1), interleukin-8 (IL-8), malondialdehyde (MDA), and superoxide dismutase (SOD) were measured before and after folate treatment. RESULTS: Plasma level of Hcy significantly decreased after folate treatment [(57.1 +/- 18.0) micromol/L vs (25.8 +/- 12.0) micromol/L, P <0.05]. However, the plasma levels of MCP-1, IL-8, SOD, and MDA were not changed after folate treatment. CONCLUSION: Folate treatment can decrease the plasma Hcy level in HHcy patients; however, it has no obvious effects on the chemokine levels.

G protein-coupled inwardly rectifying potassium channels in dorsal root ganglion neurons.

AIM: G protein-coupled inwardly rectifying potassium channels (GIRK) are important for neuronal signaling and membrane excitability. In the present study, we intend to find whether GIRK channels express functionally in adult rat dorsal root ganglion (DRG) neurons. METHODS: We used RT-PCR to detect mRNA for 4 subunits of GIRK in the adult DRG. The whole-cell patch clamp recording was used to confirm GIRK channels functionally expressed. RESULTS: The mRNA for the 4 subunits of GIRK were detected in the adult DRG. GTPgammaS enhanced inwardly rectifying potassium (K+) currents of the DRG neurons, while Ba2+ inhibited such currents. Furthermore, the GIRK channels were shown to be coupled to the GABA(B) receptor, a member of the G protein-coupled receptor family, as baclofen increased the inwardly rectifying K+ currents. CONCLUSION: GIRK channels are expressed and functionally coupled with GABA(B) receptors in adult rat DRG neurons.

[Effectiveness and safety of nadroparin in acute coronary syndrome].

OBJECTIVE: To evaluate the effectiveness and safety of subcutaneous low molecular weight heparin (LMWH) used in acute management of patients with non-ST segment elevation acute coronary syndrome (ACS). METHODS: A total of 102 patients with non-ST segment elevation ACS were treated for at least 48 hours ( > or =5 times) with subcutaneous nadroparin (1 mg/kg each 12 hours). All 102 patients underwent coronary angiographies (CAG) within 8 hours after LMWH injection, followed by immediate percutaneous coronary intervention (PCI). RESULTS: Anti-Xa activity at the time of catheterization was (0.62 +/- 0.18) IU/ml, and 90% of the patients had anti-Xa activity > 0.5 IU/ml. No death, myocardial infarction relapse or emergent revascularization occurred after PCI. Thrombosis and/or embolism occurred in 2 patients (3.5%) during PCI. Mild hemorrhage was observed in 4 patients (3.9%) of PCI group and in 2 patients (4.4%) in CAG group. No major hemorrhage occurred. CONCLUSION: PCI within 8-12 hours of the last dose after > or =48 hours nadroparin subcutaneous injection seems to be effective and safe.