SummaryLow-dose exposures to common environmental chemicals that are deemed safe individually may be combining to instigate carcinogenesis, thereby contributing to the incidence of cancer. This risk may be overlooked by current regulatory practices and needs to be vigorously investigated.

In contrast to TF vascular access, TR percutaneous coronary revascularization for UPLM disease is feasible and associated with similar procedural success, abbreviated hospitalization, reduced bleeding, and comparable late-term clinical safety and efficacy.

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OBJECTIVES Acute kidney injury (AKI) is a relatively common complication after an operation for type A acute aortic dissection and is indicative of a poor prognosis. We examined the risk factors for and the outcomes of developing AKI in patients being operated on for thoracic aortic diseases. METHODS We retrospectively analysed 712 patients with acute type A dissection who had deep hypothermic circulatory operations from January 2014 to December 2018, emphasizing those who developed AKI. Logistic regression models were used to identify predisposing factors for the postoperative development of AKI. RESULTS Among all enrolled patients, 359 (50.4%) had AKI; of these, 133 were diagnosed as stage 1 (18.7%), 126 were stage 2 (17.7%) and 100 were stage 3 (14.0%). Postoperative haemodialysis was required in 111 patients (15.9%). The development of AKI after aortic surgery contributed to the higher mortality rate within 30 days after surgery (P < 0.001), longer stay in the intensive care unit (P = 0.01) and longer hospital stay (P < 0.001). Binary logistic regression analysis showed that preoperative cystatin C levels [odds ratio (OR) 2.615, 95% confidence interval (CI) 1.139–6.002; P = 0.023] and postoperative ventilation time (OR 1.019, 95% CI 1.005–1.034; P = 0.009) were independent risk factors for developing AKI. Multiple ordinal logistic regression analyses showed that the preoperative cystatin C level (OR 2.921, 95% CI 1.542–5.540; P = 0.001) was an independent risk factor associated with the severity of AKI. CONCLUSIONS Our data suggested that the development of AKI after surgery for type A acute aortic dissection was common and associated with an increased short-term mortality rate. The preoperative cystatin C level was identified as an indicator for the occurrence and severity of AKI postoperatively. Furthermore, we discovered that longer postoperative ventilation time was also associated with the development of AKI.

Adjuvant chemotherapy may cause alterations in serum lipids in postoperative breast cancer (BC) patients, but the specific alterations caused by different chemotherapy regimens remain unclear. The aim of this study was to investigate the status of serum lipids pre- and post-chemotherapy and to compare the side effects of different chemotherapy regimens on serum lipid. We retrospectively analysed the lipid profiles of 1934 consecutive postoperative BC patients who received one of the following chemotherapy regimens: doxorubicin and cyclophosphamide followed by paclitaxel (AC-T); epirubicin and cyclophosphamide followed by paclitaxel (EC-T); cyclophosphamide and paclitaxel (TC); and fluorouracil, cyclophosphamide, and epirubicin (FEC). The levels of triglycerides (TG), total cholesterols (TC), and low-density lipoprotein (LDL-C) were significantly elevated in patients who received chemotherapy regimens above ( P < .001). With respect to different chemotherapy regimens, FEC had less side effects on lipid profiles (TG ( P = .006), high-density lipoprotein (HDL-C) ( P < .001), and LDL-C ( P < .001)) than TC regimen and AC-T and EC-T regimen. Also, the incidence of newly diagnosed dyslipidemia after chemotherapy was lower in FEC group than TC group and AC-T and EC-T group ( P < .001). Additionally, the magnitude of the alterations in lipid profiles (TG, TC, HDL-C, and LDL-C) was greater in premenopausal patients than that of the postmenopausal patients ( P = .004; P < .001; P = .002; P = .003, respectively). Moreover, after adjusting for multiple baseline covariates, anthracycline-plus-taxane-based regimens (AC-T and EC-T) were still statistically associated with a high level of TG ( P = .004) and a low level of HDL-C ( P = .033) after chemotherapy compared with FEC regimen. Also, body mass index (BMI) > 24 was associated with abnormal lipid profiles (TG, TC, HDL-C, LDL-C) post-chemotherapy compared with BMI ≤ 24 ( P < .001; P = .036; P = .012; P = .048, respectively). BC patients receiving chemotherapy may have elevated lipid profiles, and anthracycline-based regimen had less side effects on lipid profiles compared with regimens containing taxane. Therefore, it is necessary to take lipid metabolism into consideration when making chemotherapy decisions and dyslipidemia prevention and corresponding interventions are indispensable during the whole chemotherapy period.

Aim: To explore whether the synthetic cannabinoid receptor agonist WIN55,212-2 could protect oligodendrocyte precursor cells (OPCs) in stroke penumbra, thereby providing neuroprotection following permanent focal cerebral ischemia in rats. Methods: Adult male SD rats were subjected to permanent middle cerebral artery occlusion (p-MCAO). The animals were administered WIN55,212-2 at 2 h, and sacrificed at 24 h after the ischemic insult. The infarct volumes and brain swelling were assessed. The expression of cannabinoid receptor type 1 (CB1) in the stroke penumbra was examined using Western blot assay. The pathological changes and proliferation of neural glial antigen 2-positive OPCs (NG2 + cells) in the stroke penumbra were studied using immunohistochemistry staining. Results: p-MCAO significantly increased the expression of CB1 within the stroke penumbra with the highest level appearing at 2 h following the ischemic insult. Administration of WIN55,212-2 (9 mg/kg, iv) significantly attenuated the brain swelling, and reduced the infarct volume as well as the number of tau-immunoreactive NG2 + cells (tau-1 + /NG2 + cells) in the stroke penumbra. Moreover, WIN55,212-2 significantly promoted the proliferation of NG2 + cells in the stroke penumbra and in the ipsilateral subventricular zone at 24 h following the ischemic insult. Administration of the selective CB1 antagonist rimonabant (1 mg/kg, iv) partially blocked the effects caused by WIN55,212-2. Conclusion: Tau-1 is expressed in NG2 + cells following permanent focal cerebral ischemic injury. Treatment with WIN55,212-2 reduces the number of tau-1 + /NG2 + cells and promotes NG2 + cell proliferation in the stroke penumbra, which are mediated partially via CB1 and may contribute to its neuroprotective effects.

Background The Systolic Blood Pressure Intervention Trial (SPRINT) showed significant reductions in death and cardiovascular disease (CVD) risk with a systolic blood pressure (SBP) goal of <120 mm Hg compared with a SBP goal of <140 mm Hg. Our study aimed to assess the applicability of SPRINT to Chinese adults. Additionally, we sought to predict the medical and economic implications of this intensive SBP treatment among those meeting SPRINT eligibility. Methods and findings We used nationally representative baseline data from the China Health and Retirement Longitudinal Study (CHARLS) (2011–2012) to estimate the prevalence and number of Chinese adults aged 45 years and older who meet SPRINT criteria. A validated microsimulation model was employed to project costs, clinical outcomes, and quality-adjusted life-years (QALYs) among SPRINT-eligible adults, under 2 alternative treatment strategies (SBP goal of <120 mm Hg [intensive treatment] and SBP goal of <140 mm Hg [standard treatment]). Overall, 22.2% met the SPRINT criteria, representing 116.2 (95% CI 107.5 to 124.8) million people in China. Of these, 66.4%, representing 77.2 (95% CI 69.3 to 85.0) million, were not being treated for hypertension, and 22.9%, representing 26.6 (95% CI 22.4 to 30.7) million, had a SBP between 130 and 139 mm Hg, yet were not taking antihypertensive medication. We estimated that over 5 years, compared to standard treatment, intensive treatment would reduce heart failure incidence by 0.84 (95% CI 0.42 to 1.25) million cases, reduce CVD deaths by 2.03 (95% CI 1.44 to 2.63) million cases, and save 3.84 (95% CI 1.53 to 6.34) million life-years. Estimated reductions of 0.069 (95% CI −0.28, 0.42) million myocardial infarction cases and 0.36 (95% CI −0.10, 0.82) million stroke cases were not statistically significant. Furthermore, over a lifetime, moving from standard to intensive treatment increased the mean QALYs from 9.51 to 9.87 (an increment of 0.38 [95% CI 0.13 to 0.71]), at a cost of Int$10,997 per QALY gained. Of all 1-way sensitivity analyses, high antihypertensive drug cost and lower treatment efficacy for CVD death resulted in the 2 most unfavorable results (Int$25,291 and Int$18,995 per QALY were gained, respectively). Simulation results indicated that intensive treatment could be cost-effective (82.8% probability of being below the willingness-to-pay threshold of Int$16,782 [1× GDP per capita in China in 2017]), with a lower probability in people with SBP 130–139 mm Hg (72.9%) but a higher probability among females (91.2%). Main limitations include lack of specific SPRINT eligibility information in the CHARLS survey, uncertainty about the implications of different blood pressure measurement techniques, the use of several sources of data with large reliance on findings from SPPRINT, limited information about the serious adverse event rate, and lack of information and evidence for medication effectiveness on renal disease. Conclusions Although adoption of the SPRINT treatment strategy would increase the number of Chinese adults requiring SBP treatment intensification, this approach has the potential to prevent CVD events, to produce gains in life-years, and to be cost-effective under common thresholds.