BACKGROUND: The available evidence regarding the benefits of percutaneous coronary intervention (PCI) on patients receiving dialysis with coronary artery disease (CAD) is limited and inconsistent. This study aimed to evaluate the association between PCI and clinical outcomes as compared with medical therapy alone in patients undergoing dialysis with CAD in China. METHODS: This multicenter, retrospective study was conducted in 30 tertiary medical centers across 12 provinces in China from January 2015 to June 2021 to include patients on dialysis with CAD. The primary outcome was major adverse cardiovascular events (MACE), defined as a composite of cardiovascular death, non-fatal myocardial infarction, and non-fatal stroke. Secondary outcomes included all-cause death, the individual components of MACE, and Bleeding Academic Research Consortium criteria types 2, 3, or 5 bleeding. Multivariable Cox proportional hazard models were used to assess the association between PCI and outcomes. Inverse probability of treatment weighting (IPTW) and propensity score matching (PSM) were performed to account for potential between-group differences. RESULTS: Of the 1146 patients on dialysis with significant CAD, 821 (71.6%) underwent PCI. After a median follow-up of 23.0 months, PCI was associated with a 43.0% significantly lower risk for MACE (33.9% [ n  = 278] vs . 43.7% [ n  = 142]; adjusted hazards ratio 0.57, 95% confidence interval 0.45-0.71), along with a slightly increased risk for bleeding outcomes that did not reach statistical significance (11.1% vs . 8.3%; adjusted hazards ratio 1.31, 95% confidence interval, 0.82-2.11). Furthermore, PCI was associated with a significant reduction in all-cause and cardiovascular mortalities. Subgroup analysis did not modify the association of PCI with patient outcomes. These primary findings were consistent across IPTW, PSM, and competing risk analyses. CONCLUSION This study indicated that PCI in patients on dialysis with CAD was significantly associated with lower MACE and mortality when comparing with those with medical therapy alone, albeit with a slightly increased risk for bleeding events that did not reach statistical significance.
Humans ; Percutaneous Coronary Intervention/methods* ; Male ; Female ; Coronary Artery Disease/drug therapy* ; Retrospective Studies ; Renal Dialysis/methods* ; Middle Aged ; Aged ; China ; Proportional Hazards Models ; Treatment Outcome

ObjectiveTo explore the effect and regulatory mechanism of notoginseng total saponins on apoptosis of mammary gland cells in rats with mammary gland hyperplasia. MethodSixty female non-pregnant SD rats were randomly divided into control group， model group， Notoginseng total saponins low-， medium- and high-dose （10， 20， 40 mg·kg^-1， respectively） groups and tamoxifen group （1.8 mg·kg^-1）， 10 rats per group. Rat model of mammary gland hyperplasia was established by intramuscular injection of estradiol benzoate and progesterone. Oral administration was performed according to the experimental dose of each group， once a day for 30 consecutive days. The rats in the control group and the model group were given equal volume of normal saline by gavage every day. After administration， the diameter of the second pair of nipples of the rats was measured with vernier calipers， and breast tissue samples were collected and stained with hematoxylin and eosin （HE） to observe the pathological changes. Immunohistochemistry was used to determine the expression of apoptosis regulators B-cell lymphoma-2 （Bcl-2）-associated X （Bax） and Bcl-2， and Western blot was conducted to detect the expression of phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin （PI3K/Akt/mTOR） signaling pathway-related proteins. ResultCompared with the control group， the model group had increased diameter of the second pair of nipples （P<0.05）， elevated volume of mammary lobules and number of acinus， diffuse mammary gland hyperplasia， and up-regulated expression of Bcl-2 protein， increased ratio of p-PI3K/PI3K， p-Akt/Akt， p-mTOR/mTOR （P<0.05） and decreased expression of Bax in the mammary gland （P<0.05）. Compared with the conditions in the model group， the diameter of the second pair of nipples of the rats in the notoginseng total saponins low-， medium- and high-dose groups and tamoxifen group was decreased （P<0.05）， and the number of mammary lobules and acinus and the amount of secretions were reduced. In addition， the mammary gland hyperplasia was alleviated， and a decrease was observed in the expression of Bcl-2 protein and the ratio of p-PI3K/PI3K， p-Akt/Akt， p-mTOR/mTOR （P<0.05）， and an increase in the expression of Bax （P<0.05）. ConclusionNotoginseng total saponins could improve mammary gland hyperplasia in rats， and its mechanism was related to regulating PI3K/Akt/mTOR pathway and promoting apoptosis of mammary gland cells.

Systematic light chain (AL) amyloidosis is the most common forms of amyloidosis, which manifests as multiple organ system involvement, rapid progress, dire prognosis, difficult therapy and high mortality. Many patients may miss the optimal treatment as a result of not being diagnosed timely. Therefore, early diagnosis and assessment of involved extent of AL are clinical focuses. Related clinical studies have demonstrated that nuclear medicine imaging can be non-invasive in detecting amyloid deposits. It can not only early assess the extent and distribution of amyloid deposits in systemic AL amyloidosis, but also offer the indications for risk stratification, treatment response monitoring and prognosis assessment of the patients, especially for positron amyloidosis-specific tracers, which may have great prospects in the future. This review summarizes the application of nuclear medicine imaging in the systematic AL amyloidosis.

OBJECTIVE To in vestigate inhibitory effect s of gallic acid （GA）on human esophageal cancer TE- 1 cells in vitro and its potential mechanism. METHODS The effects of GA on the proliferation of TE- 1 cells were determined by MTT assay after treated with GA for 24 h and 48 h. Cell fluorescence counting （CCK-F）method and inverted fluorescence microscope were used to observe the changes in the number and morphology of TE- 1 cells after treated with GA. The change of cell migration ability was detected by scratch test. The effects of GA on the colony-forming ability of TE- 1 cells were tested by plate colony formation experiment. Cell apoptosis was detected by flow cytometry. Fluorescence probe （DCFH-DA）method was used to observe reactive oxygen species （ROS）production. Western blot assay was used to detect the expression of caspase- 3，caspase-9，Bcl-2，Bcl-2 associated X protein （Bax），cyclin D 1 and cyclin D 3. RESULTS GA significantly reduced the proliferation ability of TE- 1 cells in time and concentration dependent manner. the IC 50 of GA to TE- 1 cells were （281.22±26.81）μmol/L（24 h）and（220.90±31.15） μ mol/L（48 h），respectively. Compared with control group ，the cells in the administration group showed shrinkage ，sparse arrangement and nuclear pyknosis ，and the number of cells decreased significantly. Compared with control group ，the cell migration ability and colony formation ability were decreased significantly in administration groups （P＜0.01 or P＜0.05）. The apoptosis rates of TE- 1 cells were （6.21±0.32）％，（12.59±0.58）％ and（15.41±0.41）％ after treated with 100，300 and 500 μmol/L GA for 24 h，all of which were significantly higher than （5.29±0.28）％ of control group （P＜0.01 or P＜0.05）. Except for GA 100 μmol/L group，the level of ROS in other administration groups were significantly increased （P＜0.01 or P＜0.05）. Compared with control group，the expressions of Bcl- 2（only GA 200 μmol/L group），Bax（except for GA 100 μmol/L），caspase-3 and caspase- 9（except for GA 100 μmol/L）were increased significantly （P＜0.01 or P＜0.05），while the protein expressions of Bcl- 2（except GA 100， 200 μmol/L group），cyclin D 1 and cyclin D 3 were significantly decreased （P＜0.01 or P＜0.05）. CONCLUSIONS GA can inhibit the proliferation of esophageal cancer TE- 1 cells， E-mail：1209364115@qq.com restrict their migration ability and colony-forming ability ，and promote apoptosis. The mechanism may be related to the increase of ROS level ，up-regulation of the expressions of pro-apoptotic proteins caspase- 3，caspase-9 and Bax ，and down-regulation of the expressions of anti-apoptotic protein Bcl- 2，cyclin D1 and cyclin D 3.

OBJECTIVE To study the protective effect of phenolic acid components from Salvia deserta Schang on the oxidative stress injury of human renal tubular epithelial cells HK -2 induced by high glucose and high fat . METHODS HK-2 cells were divided into control group ，model group ，canagliflozin group （positive control group ，15 μmol/L），purified product of phenolic acids from S. deserta Schang group （10.8 μg/mL），4 monomers group （salvianic acid ，protocatechuic aldehyde ，caffeic acid，rosmarinic acid ，50 μmol/L）. In addition to the control group ，cell injury model of high glucose and high fat was established in other groups （500 μmol/L palmitic acid+ 30 mmol/L glucose for 48 h）and cultured for 48 h. The cell apoptotic rate ，the contents of malondialdehyde （MDA）and glutathione （GSH），and the activity of superoxide dismutase （SOD）were detected in each group ； the expression levels of nuclear erythroid 2-related factor 2（Nrf2），Kelch-like ECH -associated protein 1（Keap1）protein，heme oxygenase-1（HO-1）and NADH ：quinone acceptor oxidoreductase 1（NQO1）were determined in above 5 groups（except for salvianic acid ，protocatechuic aldehyde ，caffeic acid ）. RESULTS Compared with control group ，the apoptotic rate of HK -2 cells in model group was increased significantly （P＜0.01）；the content of MDA was increased significantly （P＜0.01），while the content of GSH and the activity of SOD were decreased significantly ；protein expressions of Nrf 2，NQO1 and HO -1 2018D01C169） were significantly down -regulated（P＜0.01），while the protein expression of Keap 1 was up -regulated significantly （P＜0.01）. Compared with model group ， the apoptotic rate and the content of MDA were decreased significantly in administration groups（P＜0.01）；the content of GSH in administration groups and the activity of SOD in purified product of phenolic acids group，protocatechuic aldehyde group and rosmarinic acid group were increased significantly （P＜0.01）. The protein expressions of Nrf2，HO-1 and NQO 1 in purified product of phenolic acids group as well as the protein expression of Nrf 2 in rosmarinic acid group were up -regulated significantly （P＜0.01），while the protein expression of Keap 1 was down -regulated significantly in purified product of phenolic acids group and rosmarinic acid group （P＜0.01）. CONCLUSIONS The phenolic acids components from S. deserta Schang can relieve oxidative stress injury of renal tubular epithelial cells induced by high glucose and high fat ，the mechanism of which may be associated with activating Keap 1/Nrf2 signaling pathway and inhibiting oxidative stress response .