ABSTRACT
Stroke-associated pneumonia (SAP) is a spectrum of pulmonary infections in non-mechanical ventilation patients within 7 days of stroke. SAP is one of the most common complications after stroke, with an incidence of 7%-38%, which is significantly associated with poor prognosis of stroke. Stroke-induced immune-depression syndrome (SIDS) is one of the main pathogenesis of SAP, which is closely related to autoimmune, sympathetic nervous system (SNS), hypothalamic-pituitary-adrenalin axis (HPA axis), parasympathetic nervous system (PNS), and damage-related molecular patterns (DAMPs). It is unclear how the lungs and brain interact during the development of SAP. Some clinical studies have found that some clinical indicators such as monocyte human leukocyte antigen-DR (mHLA-DR), neutrophil to lymphocyte ratio (NLR) and heart rate variability (HRV) can be used to predict SAP occurrence. Old age, male, and diabetes are currently considered risk factors for SAP. Furthermore, a variety of SAP risk scales such as A2DS2 scale (age, atrial fibrillation, dysphagia, gender and stroke severity), preventive antibacterial therapy in acute ischemic stroke (PANTHERIS) scale, acute ischemic stroke-associated pneumonia scale (AIS-APS), and ISAN scale (pre-stroke independence, gender, age, and stroke severity) have been developed. According to the opinion of Pneumonia in Stroke Consensus in 2015, it is recommended to use the modified Centers for Disease Control and Prevention (CDC) pneumonia clinical diagnostic criteria for the diagnosis of SAP. Prevention of SAP is the most important part of clinical practice. Preventive antibiotics are not recommended, and once SAP is diagnosed, the antibiotic strategies should be followed. Neuroprotective and anti-inflammatory treatments are still being studied.
ABSTRACT
Stroke-associated pneumonia (SAP) is a spectrum of pulmonary infections in non-mechanical ventilation patients within 7 days of stroke. SAP is one of the most common complications after stroke, with an incidence of 7%-38%, which is significantly associated with poor prognosis of stroke. Stroke-induced immune-depression syndrome (SIDS) is one of the main pathogenesis of SAP, which is closely related to autoimmune, sympathetic nervous system (SNS), hypothalamic-pituitary-adrenalin axis (HPA axis), parasympathetic nervous system (PNS), and damage-related molecular patterns (DAMPs). It is unclear how the lungs and brain interact during the development of SAP. Some clinical studies have found that some clinical indicators such as monocyte human leukocyte antigen-DR (mHLA-DR), neutrophil to lymphocyte ratio (NLR) and heart rate variability (HRV) can be used to predict SAP occurrence. Old age, male, and diabetes are currently considered risk factors for SAP. Furthermore, a variety of SAP risk scales such as A2DS2 scale (age, atrial fibrillation, dysphagia, gender and stroke severity), preventive antibacterial therapy in acute ischemic stroke (PANTHERIS) scale, acute ischemic stroke-associated pneumonia scale (AIS-APS), and ISAN scale (pre-stroke independence, gender, age, and stroke severity) have been developed. According to the opinion of Pneumonia in Stroke Consensus in 2015, it is recommended to use the modified Centers for Disease Control and Prevention (CDC) pneumonia clinical diagnostic criteria for the diagnosis of SAP. Prevention of SAP is the most important part of clinical practice. Preventive antibiotics are not recommended, and once SAP is diagnosed, the antibiotic strategies should be followed. Neuroprotective and anti-inflammatory treatments are still being studied.
ABSTRACT
Arsenic trioxide (ATO) is used as a chemotherapeutic agent for the treatment of acute promyelocytic leukemia. However, increasing drug resistance is reducing its efficacy. Therefore, a better understanding of ATO resistance mechanism is required. In this study, we established an ATO-resistant human epidermoid carcinoma cell line, KB/ATO, from its parental KB-3-1 cells. In addition to ATO, KB/ATO cells also exhibited cross-resistance to other anticancer drugs such as cisplatin, antimony potassium tartrate, and 6-mercaptopurine. The arsenic accumulation in KB/ATO cells was significantly lower than that in KB-3-1 cells. Further analysis indicated that neither application of P-glycoprotein inhibitor, breast cancer resistant protein (BCRP) inhibitor, or multidrug resistance protein 1 (MRP1) inhibitor could eliminate ATO resistance. We found that the expression level of ABCB6 was increased in KB/ATO cells. In conclusion, ABCB6 could be an important factor for ATO resistance in KB/ATO cells. The ABCB6 level may serve as a predictive biomarker for the effectiveness of ATO therapy.
ABSTRACT
Vascular endothelial growth factor is a vascular endothelial cell-specific mitogen.It is the most important angiogenic factor.VEGF expresses highly after cerebral infarction.It plays importmt roles in angiogenesis and neuroprotection.At the same time,its overexpression will also increase vascular permeability;thereby it may aggravate brain edema.This article reviews the advances in research on VEGF and its receptors and cerebral infarction.
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C-reactive protein(CRP)is the most sensitive indicator of acute phase proteins.A growing body of evidence suggests that atherosclerosis,as a main cause of cerebral infarction,is a chronic inflammtory process.The present studies have found that the CRP levels and genetic polymorphisms are associated with atherosclerosis and cerebral infarction.As compared with coronary artery disease,the association between high-sensitive CRP and ischemic stroke is more closely.This article reviews the advaces in research on the biological characteristics of CRP,the factors influencing CRP levels,the CRP levels and the correlation between genetic polymorphisms and cerebral infarction.
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0.05). No significant association between Q/R 192 genotype and blood lipids was found.Conclusion The polymorphism of PON-1 Q/R 192 gene is not associated with CI.
ABSTRACT
Objective To explore the relationship between the level of high-sensitivity C-reactive protein (hs-CRP),CRP 1059G/C gene polymorphism and cerebral infarction(CI).Methods The CRP 1059G/C genotype and allele frequencies were assayed by polymerase chain reaction-restricted fragments length polymorphism (PCR-RFLP) in 105 patients with CI and 121 controls.The level of serum hs-CRP was detected by immune-turbidimetry.The relationship between the condition of CI patients,the level of serum hs-CRP and CRP 1059G/C genotype and allele frequencies were anaysed.Results Compared to the control group,the CRP 1059G/G genotype and G allele frequencies in CI group were statistically higher,G/C+C/C genotypes and C allele frequencies were statistically lower(all P
ABSTRACT
AIM To study the antiperoxide damage of injectio tanshin during dissolving thrombus to cure the acute myocardial infarction(AMI). METHODS AMI model formatted by electricity to irritate the left ventricular branch of coronary artery of open-chest rabbit,and observation aspects including electrocardiogram(ECG),cardiac output and contractility,serumal enzymatic activities and biochemistry and pathology of lipid peroxide extent of myocardial infarction zone. RESULTS By urinate kinase(UK) combining with injection tanshin,abnormal changes of ECG, descending of cardiac contractiles and cardiac output,going up of serum cardiac damage enzyme(CPK-MB and LDH),and the malondialdehyde(MDA)of serum and myocardial infarction zone could be remarkably reduced or avoided during UK dissolving the thrombus to cure AMI rabbits. CONCLUSION Injection tanshin can clearly reduce or avoid lipid peroxidation damage during UK dissolving the thrombus to cure the acute myocardial infarction.