Objective To evaluate the application of intra-aortic balloon counterpulsation(IABP) in acute myocardial infarction(AMI) with cardiogenic shock.Methods The study enrolled 65 AMI patients with cardiogenic shock and all the patients underwent primary PCI treatment.Among them,30 patients had IABP suppont during operations.Results In all the 30 cases with IABP support,the hemodynamic parameters improved in 30 minutes and stabilized in 2-8 hours.There was no reocclusion and death during querations.The death rate of the IABP group during hospitalization was 40%.Among the other 35 patients without IABP support,6 patients died during PCI and the in hospital death rate was 74.3%.Conclusion IABP can improve hemodynamic parameters and the perfusion of coronary artery in patients with cardiogenic shock.It can increase the success rate of primaty PCI,reduce the risk of low cardiac output and reocclusion during operation.IABP support during PCI can also improve the prognosis and reduce the motality rate of AMI patients with cardiogenic shock.

OBJECTIVE: To study the relationship between fibrinogen level and pathogenesis of sudden sensorineural hearing loss(SSHI.). METHOD: Fifty patients (55 ears) with SSHL within 7 days of the onset were studied: a control group was consist of 50 normal-hearing people who were individually matched on a pairwise basis according to the same gender and age. Both the patients and the normal people were tested for the parameters of hemorheology, blood biochemistry, whole blood cell count and clotting function. RESULT: Fibrinogen level and plasma viscosity in patients with SSHL were significantly higher than that in control subjects. Prothrombin time and activated partial thromboplastic time were significantly less in the patients group than that in the control group (P < 0.05). There were statistical difference. The parameters of blood biochemistry, whole blood cell count and platelet adhesion test of two groups had no significant difference (P > 0.05). CONCLUSION Elevated plasma fibrinogen may be a major pathogenesis of SSHL. An increase in plasma fibrinogen level may lead to elevated plasma viscosity. All these may promote a prothrombin or hypercoagulable state and impair blood perfusion of cochlea.
Adolescent ; Adult ; Aged ; Case-Control Studies ; Female ; Fibrinogen ; metabolism ; Hearing Loss, Sensorineural ; blood ; etiology ; Hearing Loss, Sudden ; blood ; etiology ; Hemorheology ; Humans ; Male ; Middle Aged ; Young Adult

Irritable bowel syndrome is a gastrointestinal disorder of unknown etiology characterized by widespread, chronic abdominal pain associated with altered bowel movements. Increasing amounts of evidence indicate that injury and inflammation during the neonatal period have long-term effects on tissue structure and function in the adult that may predispose to gastrointestinal diseases. In this study we aimed to investigate how the epigenetic regulation of DNA demethylation of the p2x7r locus guided by the transcription factor GATA binding protein 1 (GATA1) in spinal astrocytes affects chronic visceral pain in adult rats with neonatal colonic inflammation (NCI). The spinal GATA1 targeting to DNA demethylation of p2x7r locus in these rats was assessed by assessing GATA1 function with luciferase assay, chromatin immunoprecipitation, patch clamp, and interference in vitro and in vivo. In addition, a decoy oligodeoxynucleotide was designed and applied to determine the influence of GATA1 on the DNA methylation of a p2x7r CpG island. We showed that NCI caused the induction of GATA1, Ten-eleven translocation 3 (TET3), and purinergic receptors (P2X7Rs) in astrocytes of the spinal dorsal horn, and demonstrated that inhibiting these molecules markedly increased the pain threshold, inhibited the activation of astrocytes, and decreased the spinal sEPSC frequency. NCI also markedly demethylated the p2x7r locus in a manner dependent on the enhancement of both a GATA1-TET3 physical interaction and GATA1 binding at the p2x7r promoter. Importantly, we showed that demethylation of the p2x7r locus (and the attendant increase in P2X7R expression) was reversed upon knockdown of GATA1 or TET3 expression, and demonstrated that a decoy oligodeoxynucleotide that selectively blocked the GATA1 binding site increased the methylation of a CpG island in the p2x7r promoter. These results demonstrate that chronic visceral pain is mediated synergistically by GATA1 and TET3 via a DNA-demethylation mechanism that controls p2x7r transcription in spinal dorsal horn astrocytes, and provide a potential therapeutic strategy by targeting GATA1 and p2x7r locus binding.
Animals ; Astrocytes/metabolism* ; DNA Demethylation ; Epigenesis, Genetic ; GATA1 Transcription Factor/metabolism* ; Inflammation/metabolism* ; Oligodeoxyribonucleotides/metabolism* ; Rats ; Rats, Sprague-Dawley ; Receptors, Purinergic P2X7/metabolism* ; Visceral Pain/metabolism*