Objective To evaluate the methods and the efficacy of interventional therapy for huge aneurysm.Methods Seven patients with huge aneurysm including 2 with pulmonary aneurysm, 2 with renal aneurysm, 1 with humeral artery aneurysm, 1 with right common iliac artery aneurysm, 1 with right internal iliac artery aneurysm. Among these, 5 were true aneurysm, and 2 were pseudoaneurysms caused by congenital, trauma, arteriosclerosis. Three patients were treated with endovascular covered stent graft and 2 patients with embolization containing metallic coils. Two patients were treated with partial aneurysm and feeding artery trunk embolization with metallic coils. Results All 7 patients were successful carried out the interventional therapy with successful rate of 100%. Six aneurysms were completely obstructed with disappearance of symptoms and signs. One died of aneurysm rupture. No other complication occurred.Conclusion Interventional therapy for huge aneurysm is an effective method.

Objective To evaluate the improvement of lower urinary tract symptoms in benign prostatic hyperplasia (BPH) patients with bladder calculi by lithotripsy and adjuvant traditional Chinese decoction. Methods A total of 72 BPH patients with bladder calculi were recruited and randomly divided into the non-adjuvant treatment group (37 patients) and the adjuvant treatment group (35 patients). The adjuvant treatment group received adjuvant traditional Chinese decoction from 2 days before lithotripsy for 2 weeks. The maximum urinary flow rate (Qmax) , residual urine volume (RU), International Prostate Symptom Score (IPSS) and Quality of Life (QOL) were assessed before and after the treatment. The time of urine routine returned to normal and the indwelling time of catheter were compared between two groups. Urinary incontinence and recurrent bladder calculi were followed up for 6 months. Results After the treatment, the score of the IPSS (12.9 ± 4.5 vs. 15.7 ± 3.9;t=2.826, P=0.006) and the RU (47.3 ± 9.2 ml vs. 58.4 ± 11.3 ml;t=4.556, P<0.001) in the adjuvant treatment group were significantly lower than those in the non-adjuvant treatment group, and the Qmax (30.4 ± 4.7 ml/s vs. 21.4 ± 3.9 ml/s;t=8.862, P<0.001 ) was significantly higher. The indwelling time of catheter (5.7 ± 2.1 d vs. 8.1 ± 2.2d;t=4.730, P<0.001) and the time of urine routine returned to normal (6.9 ± 2.3 d vs. 10.2 ± 3.1 d;t=5.106, P<0.001) in the adjuvant treatment group were significantly shorter than those in the non-adjuvant treatment group. The 6-month follow-up showed that the incidence of urinary incontinence (2.9% vs. 18.9%;χ2=4.698, P=0.030) and recurrent bladder calculi (5.7% vs. 24.3%;χ2=4.813, P=0.028) in the adjuvant treatment group were significantly shorter than those in the non-adjuvant treatment group, and the total effective rate was significantly higher (62.9%vs. 29.7%; χ2=6.672, P=0.011). Conclusions Lithotripsy and adjuvant traditional Chinese decoction can reduce the IPSS score and RU, increase Qmax, decrease urinary incontinence and recurrent bladder calculi, and improve lower urinary tract symptoms in BPH patients with bladder calculi.

Objective To explore the influence of long-term low-dose ionizing radiation on 8-hydroxy-2-deoxyguanosine(8-OHdG) level in the serum of radiation workers in hospitals.Methods 307 age-and sex-matched hospital radiation workers were recruited by stratified random sampling method.After deleting the subjects without dosage information,230 individuals were divided into four groups according to their job title [including diagnostic radiology (n =75),radiotherapy (n =60),nuclear medicine (n =41) and interventional radiology (n =54)].Serum 8-OHdG level was measured by ELISA assay.Results According to the statistical analysis,there was significant difference in the serum 8-OHdG level among four groups (F =9.071,P ＜ 0.05),and the content of serum 8-OHdG was significantly higher in the interventional radiology group than that in the groups of diagnostic radiology,radiotherapy and nuclear medicine (t =-4.473,-3.011,-2.189,P ＜ 0.05).There were significant differences in serum 8-OHdG level among different dose groups and working period groups(F =7.659,3.058,P ＜ 0.05).The serum 8-OHdG levels significantly increased along with exposure dose and working period (r =0.300,0.142,P ＜ 0.05).Conclusions Serum 8-OHdG may be a potential biomarker of oxidative DNA damage in radiation workers exposed to low-dose ionizing radiation.

Objective:To explore the influence factors of chromosomal aberration levels in radiation workers in hospitals.Methods:Two hundred and fourteen age- and sex- matched hospital radiation workers were recruited by stratified random sampling method. According to the job title, the individuals were divided into four groups including diagnostic radiology group ( n=57), radiotherapy group ( n=49), nuclear medicine group ( n=52) and interventional radiology group ( n=56). Chromosomal aberrations in peripheral blood lymphocytes from the subjects were measured using conventional cytogenetic analysis method, and the influence factors of chromosomal aberrations were analyzed. Results:There was significant difference in the frequencies of acentric fragment, translocation and total chromosome-type aberrations among the four groups ( χ2=9.906, 19.965, 32.824, P<0.05), and the rates of aberrations were significantly higher in the interventional radiology group and the nuclear medicine groups than those in the diagnostic radiology (interventional group: χ2=4.711, 10.798, 10.845, P<0.05; nuclear medicine group: χ2=3.853, 7.674, 7.708, P<0.05) and the radiotherapy groups (interventional group: χ2=9.209, 9.772, 21.330, P<0.05; nuclear medicine group: χ2=8.010, 6.969, 10.812, P<0.05). The rates of translocation and total aberrations ( χ2=7.706, 6.667, P<0.05) and the frequencies of acentric fragment, translocation and total aberrations ( χ2=12.263, 15.360, 21.478, P<0.01) were dependent on the length of service and the dose among different groups. The rates of translocation and total aberrations significantly increased along with exposure doses ( r=0.347, 0.263, P<0.01). Poisson regression analysis indicated that the job titles and annual effective dose partly affected the levels of chromosomal aberrations[ IRR=1.797 (nuclear medicine group), 2.136 (interventional group) and 1.422 (0.5-1 mSv group); P<0.05]. Conclusions:The frequencies of chromosomal aberrations in the radiation workers of interventional and nuclear medicine groups remain higher levels in hospital, thus it is necessary to strengthen the radiation protection on these radiation workers.

Long-chain acyl-coenzyme A (CoA) synthase 4 (ACSL4) is an enzyme that esterifies CoA into specific polyunsaturated fatty acids, such as arachidonic acid and adrenic acid. Based on accumulated evidence, the ACSL4-catalyzed biosynthesis of arachidonoyl-CoA contributes to the execution of ferroptosis by triggering phospholipid peroxidation. Ferroptosis is a type of programmed cell death caused by iron-dependent peroxidation of lipids; ACSL4 and glutathione peroxidase 4 positively and negatively regulate ferroptosis, respectively. In addition, ACSL4 is an essential regulator of fatty acid (FA) metabolism. ACSL4 remodels the phospholipid composition of cell membranes, regulates steroidogenesis, and balances eicosanoid biosynthesis. In addition, ACSL4-mediated metabolic reprogramming and antitumor immunity have attracted much attention in cancer biology. Because it facilitates the cross-talk between ferroptosis and FA metabolism, ACSL4 is also a research hotspot in metabolic diseases and ischemia/reperfusion injuries. In this review, we focus on the structure, biological function, and unique role of ASCL4 in various human diseases. Finally, we propose that ACSL4 might be a potential therapeutic target.
Humans ; Ferroptosis ; Apoptosis ; Phospholipids/metabolism* ; Nitric Oxide Synthase

OBJECTIVE: To investigate the effect of blocking pannexin-1 against acute kidney injury induced by cisplatin. METHODS: Twenty-six male C57BL/6 mice aged 6-8 weeks were randomly divided into control group, cisplatin model (Cis) group and cisplatin + carbenoxolone treatment group (Cis + CBX). In Cis group and Cis + CBX group, the mice were injected intraperitoneally with 20 mg/kg of cisplatin and with CBX (20 mg/kg) at 30 min before and 24 and 48 h after cisplatin inhjection, respectively. All the mice were sacrificed at 72 h after cisplatin injection, and plasma and kidney samples were collected for testing mRNA and protein expression levels of pannexin-1 in the renal tissue using RT-qPCR and Western blotting and for detecting plasma creatinine and BUN levels; the pathological changes in the renal tissues were observed using Periodic Acid-Schiff staining. The expression of kidney injury molecule 1 (KIM-1) was examined using immunohistochemistry and the mRNA expressions of KIM-1 and neutrophil gelatinase- related lipid transport protein (NGAL) were detected by RT-qPCR to evaluate the injuries of the renal tubules. The infiltration of F4/80-positive macrophages and CD4-positive T cells were observed by immunofluorescence. In the experiment, human proximal tubule epithelial cell line HK-2 was stimulated with 50 μmol/L cisplatin to establish a cell model of acute kidney injury, and the mRNA and protein expressions of pannexin-1 were detected by RT-qPCR and Western blotting at 4, 6, 12, 18 and 24 h after the stimulation. RESULTS: Compared with the control mice, the cisplatin-treated mice showed significantly up-regulated protein levels ( < 0.05) and mRNA levels ( < 0.005) of pannexin-1 in the kidney tissue. Cisplatin stimulation also caused significant increases in the protein levels ( < 0.005) and mRNA levels ( < 0.005) of pannexin-1 in cultured HK-2 cells. Compared with cisplatin-treated mice, the mice treated with both cisplatin and the pannexin-1 inhibitor CBX showed obviously lessened kidney pathologies and milder renal tubular injuries with significantly reduced plasma BUN and Scr levels ( < 0.01), expressions of KIM-1 and NGAL in the kidney ( < 0.05), and infiltration of F4/80-positive macrophages ( < 0.01) and CD4- positive T cells ( < 0.05) in the kidney tissues. CONCLUSIONS In cisplatin induced acute kidney injury mice model, Pannexin-1 expression is up-regulated in the kidneys tissue, and blocking pannexin-1 alleviates the acute kidney injury reducing renal inflammatory cell infiltration.
Acute Kidney Injury ; drug therapy ; metabolism ; Animals ; Cisplatin ; pharmacology ; Connexins ; drug effects ; metabolism ; Cross-Linking Reagents ; pharmacology ; Humans ; Kidney ; Kidney Tubules ; Male ; Mice ; Mice, Inbred C57BL ; Nerve Tissue Proteins ; drug effects ; metabolism ; Random Allocation

OBJECTIVE: To investigate the effect of palbociclib on cell cycle progression and proliferation of human renal tubular epithelial cells. METHODS: Human renal tubular epithelial cell line HK-2 was treated with 1, 5, 10, and 20 μmol/L of palbociclib, and the changes in cell proliferation and viability were examined by cell counting and CCK8 assay. EDU staining was used to assess the proliferation of HK-2 cells following palbiciclib treatment at different concentrations for 5 days. The effect of palbociclib on cell cycle distribution of HK-2 cells was evaluated using flow cytometry. SA-β-Gal staining and C12FDG senescence staining were used to detect senescence phenotypes of HK-2 cells after palbociclib treatment at different concentrations for 5 days. The relative mRNA expression levels of P16, P21, and P53 and the genes associated with senescence-related secretion phenotypes were detected by RT-PCR, and the protein expressions of P16, P21 and P53 were detected by Western blotting. RESULTS: Palbociclib inhibited HK-2 cell proliferation and induced cell cycle arrest in G1 phase. Compared with the control cells, HK-2 cells treated with high-dose (10 μmol/L) palbociclib exhibited significantly suppressed cell proliferation activity, and the inhibitory effect was the most obvious on day 5 ( CONCLUSIONS Palbociclib induces HK-2 cell senescence by causing cell growth arrest and delaying cell cycle progression.
Cell Cycle ; Cell Cycle Checkpoints ; Cellular Senescence ; Epithelial Cells ; Humans ; Piperazines/pharmacology* ; Pyridines/pharmacology* ; Tumor Suppressor Protein p53/genetics*