ObjectiveTo evaluate the clinical efficacy of intracoronary stenting for senile patients with acute myocardial infarction(AMI).Methods42 senile patients with AMI underwent intracoronary stenting were analysed. Before and after stenting, the changes of the patients' blood pressures, heart rates and cardiac functions tested by ultrasonography were observed.Results45 intracoronary stents were implanted in 42 patients, one patient falled during hospitalization. The blood pressure was increased significantly, the heart rate decreased and the candiac function improved after stenting.ConclusionIntracoronary stenting is a very effective and safe therapy for the senile patients with AMI.

Cardiovascular Diseases ; Growth Differentiation Factor 15 ; Humans

Abstract: Objective　To explore the antiviral effect of baricitinib in the SARS-CoV-2 infection and influence on cytokine levels. Methods　Calu-3 cells were infected with SARS-CoV-2 at MOI of 0.1, and the levels of inflammatory cytokines (IL-6, IL-8, TNF-α and IL-1β), interferon β (IFN-β) and interferon-stimulated gene, IFIT2 in the infected cells were analyzed by qRT-PCR methods. At the same time, Calu-3 cells were infected with SARS-CoV-2 (MOI=0.1) after being treated with baricitinib for 2 hours. Cells were collected at 0, 24, 36, and 48 hours, and analyzed for the mRNA of the above genes in the drug-treated and untreated groups. Results　The mRNA levels of IL-6, TNF-a, IL-1β, IFN-β and IFIT2 in Calu-3 infected by SARS-CoV-2 cells were increased significantly. These cytokines were increased by nearly 100-fold post-infection 48 h compared with the control (P<0.000 1), and continued to increase with the infection time (P<0.001 or P<0.000 1). The increase of IL-8 mRNA level was not as significant as IL-6, TNF-α, IL-8, IL-1β, but it also showed a 2-4 folds increase. Baricitinib does not affect the level of viral RNA in Calu-3 cells after SARS-CoV-2 infection (P>0.05). However, baricitinib can significantly inhibit the up-regulation of IL-6 and TNF-α levels induced by SARS-CoV-2 infection (5.25-fold and 3.90-fold down-regulation, respectively, P<0.01), and has little effect on the levels of IL-8 and IL-1β . In addition, the drug could also significantly down-regulate the increase in IFN-β and IFIT2 levels caused by viral infection (10.51-fold and 90.78-fold down-regulation, respectively, P<0.000 1). Conclusions　Baricitinib inhibits the release of inflammatory cytokines to some extent, but it drastically down-regulates the expression of interferons and interferon-stimulated genes (ISGs), and has limited antiviral effect on SARS-CoV-2. Considering that interferon signal pathways play important roles on viral infection, caution should be exercised when using baricitinib to treat COVID-19 patients.

This study was to investigate the protective effects of puerarin on myocardial ischemia/reperfusion (MI/R) injury and the underlying mechanism. The MI/R-model was established by ligating the left anterior descending artery (LAD) for 60 min followed by 24 h reperfusion, puerarin (10, 30, and 100 mg·kg^-1) was orally administered 20 min before reperfusion. Cardiac function, myocardial infarct index, cardiac damage markers, inflammatory cytokines, and apoptosis index were measured to evaluate the protective effects of puerarin on MI/R injury. The activation of Nod-like receptor protein 3 (NLRP3) inflammasome and Toll like receptor 4 (TLR4)/myeloid differentiation factor 88 (Myd88)/nuclear factor kappa B (NF-κB) pathway were determined by Western blot. All animal experimental procedures were approved by the ethics committee of the Institute of Materia Medica, Peking Union Medical College, Chinese Academy of Medical Sciences. The results showed that puerarin could significantly improve cardiac function, reduce myocardial infarct size, decease the levels of lactic dehydrogenase (LDH), aspartate transaminase (AST), creatine kinase-MB (CK-MB), and cardiac troponin T (cTnT) and suppress cardiomyocyte apoptosis. Meanwhile, puerarin could notably decrease the levels of inflammatory cytokines such as interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α). Western blot analysis revealed that puerarin could downregulate the expression of TLR4, Myd88, NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), cleaved-caspase 1, cleaved-gasdermin-D (GSDMD), IL-1β, and IL-18, as well as the phosphorylation levels of inhibitor of NF-κB α (IκBα), IκB kinase β (IKKβ), and NF-κB. These findings demonstrated that puerarin could alleviate MI/R injury by suppressing NLRP3 inflammasome activation, possibly via TLR4/Myd88/NF-κB pathway.

Objective To investigate the expression of caspase-10 in differentiated thyroid carcinoma and association with its development and metastasis. Methods Thyroid samples from 37 patients in a period from January 2006 to December 2007, with differentiated thyroid carcinoma were retrospectively analyzed for caspase-10 by immunohistocbemistry(streptavidin-perosidase, S-P), compared to control group of 46 cases with nodtdar goiter. The relationship between the expression of caspase-10 and the clinical pathologic characteristics of thyroid carcinoma were also explored simultaneously. Results caspase-10 were observed as brown or yellow particles located in the cytoplasm or cell membrane of nodular goiter but there were no significant evidence for its positive expression in thyroid carcinoma, caspase-10 expression was markedly down-regulated in differentiated thyroid carcinoma(29.73%,11/37) compared with benign nodules(71.74%,33/46, χ2=14.528, P<0.01). The positive expression in 18 cases with lymph node metastasis(11.11%,2/18) was significantly lower than those in 19 patients without lymph node metastasis(47.37%,9/19; χ2=4.210, P<0.01). There was no significant correlation(P> 0.05) between the expression of caspase-10 and the clinical pathologic characteristics including male, age, TNM stage and pathologic type. Conclusion Down-regulation of caspase-10 may play a critical role in carcinogenesis and development of differentiated thyroid carcinoma.

Objective To investigate the inhibition effect of Minocycline on hippocampal microglia in epileptic rats. Methods Forty male SD rats were equally randomized into normal saline control group (NS), penicillin inducement group, Minocycline post-treatment group and Minocycline pre-treatment group (n=10). Rat epilepsy models in the later 3 groups were induced by intraperitoneal injection of penicillin G at a dosage of 740 million to 7.6 million units/kg. The level of hippocampal microglia in rats of the 4 groups on the 1st and 3rd d of inducement was detected by immunofluorescence and the tumor growth factor-α (TNF-α) protein level was detected by Western blotting on the 1st and 3rd d of inducement. Results Seizure could activate microglia. As compared with those in rats of the penicillin inducement group, the activation and hyperplasia of microglia in the hippoeampus in rats of the minoeyeline post- and pre-treatment groups were obviously inhibited on the 1st and 3rd d of inducement (P≤0.05), and the effects were much obvious in the pretreatment group. The level of TNF-α protein in the penicillin inducement group, minoeycline post- and pre-treatment groups was significantly higher than that in the NS group on the 1st and 3rd d of inducement (P≤0.05); as compared with that in the penicillin inducement group, the level of TNF-α protein in the minocycline post- and pre-treatment groups decreased significantly on the 1st and 3rd of inducement (P≤0.05), especially that in the pretreatment group. Conclusion Minocycline can effectively inhibit the activation and hyperplasia of hippocampal microglia and the releasing of inflammatory factor TNF-αt in epileptic rats.

Objective To investigate the treatment effects of operation and nerve growth factor on adult multisegmental cervical spinal cord injury without fracture dislocation.Methods Sixty-eight patients with multiple segmental cervical spinal cord injury without fracture dislocation,admitted to our hospital from January 2004 to May 2011,were chosen in our study; according to the will of the patients,18 patients received conservative treatment (group A),25 patients were treated by posterior single open-door laminoplasty (group B) and the other 25 patients were treated with posterior single open-door laminoplasty combined with nerve growth factor (group C,once daily for 4 weeks); their clinical data were retrospectively analyzed.Follow up was performed at 3,6 and 12 months after the treatments;Japanese Orthopaedic Association (JOA) scale was employed to evaluate the clinical efficacy.Results Three,6,12 months after the treatments,the JOA scale scores were statistically different among the three groups (P＜0.05); the scores in group B and C were significantly higher than those in group A at all time points (P＜0.05); 6 and 12 months after the treatmemts,the JOA scale scores in group C were significantly higher than those in group B (P＜0.05).Conclusion To patients with multisegmental cervical spinal cord injury without fracture dislocation,conservative treatment can make the spinal cord function partially restored,but the effect is limited; exogenous nerve growth factor has good repairing effect on spinal cord injury.

Objective To investigate and compare the curative effect between delayed percutaneous coronary intervention (PCI) for patients with acute myocardial infarction presenting 12-24 hours from symptom onset and medical therapy on acute myocardial infarction patients presenting with ST-segment elevation (STEMI). Methods Using a prospective,open,parallel,controlled research approach,186 patients with STEMI were divided into delayed PCI group(n=89),which received PCI within 12-24 hours after STEMI and medical therapy group(n=97),which received medical therapy after STEMI. All patients were followed up 1-6 months with average follow-up (5.6 ± 1.4) months. Data of hospitalization period, the cardiac structures detected by echocardiography such as left atrial diameter (LAD), left ventricular diastolic diameter(LVDd),left ventricular ejection fraction LVEF,left ventricular fractional shortening(LVFS),composite end point events and major adverse cardiac events(MACE)were compared between the two groups.Results Compared with medical therapy group, the hospitalization cycle was significantly shorter in delayed PCI group. Data of the LAD and LVDd were significantly decreased,but LVEF and LVFS were increased in delayed PCI group compared with those of medical therapy group at 30 d and 6-month follow-up. The incidence of MACE and composite end point events were significantly less in delayed PCI group than those of medical therapy group (P<0.05). Conclusion Delayed PCI treatment can decrease the time of hospital stay and decrease the incidence rates of MACE and composite end point events,and improve left ventricular function and prognosis of patients.

Animals ; Extremities ; blood supply ; Heparin ; pharmacology ; Male ; Mesentery ; blood supply ; Microcirculation ; drug effects ; Rats ; Rats, Wistar ; Reperfusion Injury ; Splanchnic Circulation ; drug effects

AIMTo study the effects of PKC activation on apoptosis during ischemia/reperfusion in L-6TG rat skeletal myoblasts.

METHODSCultured L-6TG cells were divided into 3 groups: control group (C), ischemia/reperfusion group (I/R), PMA + ischemia/ reperfusion group (PMA), SOD, XOD and free calcium and mitochondrial respiration in L-6TG cell were evaluated in each group. Apoptosis was detected by flow cytometer with PI staining method and agarose gel electrophoresis, the immunohistochemical method was used to determine the expression of caspase-3.

RESULTSCompared with I/R group, in PMA group, XOD , free calcium in L-6TG cell and apoptotic percentage all decreased significantly, while SOD and mitochondrial respiration in L-6TG cell increased. DNA fragmentation analysis of L-6TG cell showed no laddering pattern. The expression of caspase-3 was down regulated significantly.

CONCLUSIONActivation of PKC can lessen ischemia/reperfusion injury and apoptosis through lessening oxidative injury and mitochondrial injury, adjusting calcium dyshomeostasis and down expression of caspase-3.

Animals ; Apoptosis ; Calcium ; metabolism ; Caspase 3 ; metabolism ; Cells, Cultured ; Mitochondria ; metabolism ; Myoblasts, Skeletal ; cytology ; metabolism ; Oxidative Stress ; Protein Kinase C ; metabolism ; Rats ; Reperfusion Injury ; metabolism ; pathology