Acute coronary syndromes occurring while driving: frequency and patient characteristics

Background

Acute coronary syndrome (ACS) may occur during any human activity, including driving. The objectives of this study were to report the frequency of ACS occurring while driving, clarify patient characteristics, and analyze the behavioral patterns of drivers who sustained ACS.

Methods

A single-center, retrospective observational study was conducted using prospectively acquired data. Among 1605 ACS patients admitted between January 2011 and December 2016, 65 (60 men/5 women) patients who sustained ACS while driving were identified. Clinical variables were compared between these 65 patients and 1540 patients who sustained ACS while performing other activities. Furthermore, multivariable regression analysis was performed to identify variables associated with ACS.

Results

The frequency of ACS occurring while driving was 4.0% (65/1605). Compared with patients who sustained ACS while performing other activities, those who sustained ACS while driving were significantly younger (66.2?±?13.0 vs. 57.5?±?12.2 years, p?<?0.001) and more likely to smoke (34.2 vs. 60.0%, p?<?0.001). Multivariable regression analysis showed that age (OR 0.961; 95% CI 0.940–0.982) and current smoking (OR 1.978; 95% CI 1.145–3.417) were associated with ACS. While 55 drivers (85%) who remained conscious after ACS could seek medical attention without causing accidents, the other 10 (15%) who sustained cardiac arrest caused accidents.

Conclusions

The association between current smoking and ACS occurring while driving suggests that smoking cessation is advised for smokers who drive from the standpoint of driving safety. We expect that prospective studies be conducted to verify our findings and identify individuals at risk for ACS while driving.

     

Intrascleral fixation of intraocular lens haptics: histological advantages in a comparison with scleral suture fixation in rabbits

Graefe's Archive for Clinical and Experimental Ophthalmology - To disclose histological advantages of intrascleral fixation of intraocular lens haptics, in comparison with scleral suture...     

Presence of Modic type 1 change increases risk of postoperative pyogenic discitis following decompression surgery for lumbar canal stenosis

Study Design

Multicenter retrospective study.

FBXW7 is involved in the acquisition of the malignant phenotype in epithelial ovarian tumors

FBXW7 is a ubiquitin ligase that mediates ubiquitylation of oncoproteins, such as c‐Myc, cyclin E, Notch and c‐Jun. FBXW7 is a known tumor‐suppressor gene, and mutations in FBXW7 have been reported in various human malignancies. In this study, we examined the sequences of the FBXW7 and p53 genes in 57 ovarian cancer clinical samples. Interestingly, we found no FBXW7 mutations associated with amino acid changes. We also investigated FBXW7 expression levels in 126 epithelial ovarian tumors. FBXW7 expression was negatively correlated with the malignant potential of ovarian tumors. That is to say, FBXW7 expression levels in ovarian cancer samples were significantly lower than those in borderline and benign tumors (P < 0.01). FBXW7 expression levels in serous carcinoma samples were the lowest among four major histological subtypes. In addition, p53‐mutated ovarian cancer samples showed significantly lower levels of FBXW7 expression compared with p53 wild‐type cancer samples (P < 0.001). DNA methylation arrays and bisulfite PCR sequencing experiments revealed that 5′‐upstream regions of FBXW7 gene in p53‐mutated samples were significantly higher methylated compared with those in p53 wild‐type samples (P < 0.01). This data indicates that p53 mutations might suppress FBXW7 expression through DNA hypermethylation of FBXW7 5′‐upstream regions. Thus, FBXW7 expression was downregulated in ovarian cancers, and was associated with p53 mutations and the DNA methylation status of the 5′‐upstream regions of FBXW7.     

Live imaging of transforming growth factor‐β activated kinase 1 activation in Lewis lung carcinoma 3LL cells implanted into syngeneic mice and treated with polyinosinic:polycytidylic acid

Transforming growth factor‐β activated kinase 1 (TAK1) has been shown to play a crucial role in cell death, differentiation, and inflammation. Here, we live‐imaged robust TAK1 activation in Lewis lung carcinoma 3LL cells implanted into the s.c. tissue of syngeneic C57BL/6 mice and treated with polyinosinic:polycytidylic acid (PolyI:C). First, we developed and characterized a Förster resonance energy transfer‐based biosensor for TAK1 activity. The TAK1 biosensor, named Eevee‐TAK1, responded to stress‐inducing reagents such as anisomycin, tumor necrosis factor‐α, and interleukin1‐β. The anisomycin‐induced increase in Förster resonance energy transfer was abolished by the TAK1 inhibitor (5z)‐7‐oxozeaenol. Activity of TAK1 in 3LL cells was markedly increased by PolyI:C in the presence of macrophages. 3LL cells expressing Eevee‐TAK1 were implanted into mice and observed through imaging window by two‐photon excitation microscopy. During the growth of tumor, the 3LL cells at the periphery of the tumor showed higher TAK1 activity than the 3LL cells located at the center of the tumor, suggesting that cells at the periphery of the tumor mass were under stronger stress. Injection of PolyI:C, which is known to induce regression of the implanted tumors, induced marked and homogenous TAK1 activation within the tumor tissues. The effect of PolyI:C faded within 4 days. These observations suggest that Eevee‐TAK1 is a versatile tool to monitor cellular stress in cancer tissues.