SUMMARYFollow-up data on 2700 subjects who had had maximum stress tests were assembled in life tables. A positive test, characterized by ST-segment depression of 1.5 mm, 0.08 sec from the J point, predicted an incidence of some new coronary event of 9.5% a year, as compared with 1.7% in those with a negative test.The incidence of infarction and death was also significantly higher than in the negative responders. Early onset of ischemia occurring at moderate exercise (4 metabolic equivalents-METS) resulted in an incidence of all coronary events of 15% a year, while ischemia first manifested at the seventh minute of exercise (approximately 8 METS) results in an incidence of only 4% per year. The magnitude of ST depression and the age of onset of ischemia failed to influence the incidence of coronary events. A myocardial infarction previous to the test increased the incidence of events in both positive and negative responders. The positives with a previous infarction had more than double the incidence of coronary events than the positive responders with no pre-existing infarction. Those with chronotropic incompetence had a high incidence of coronary events even though the ECG response to exercise was normal. Additional Indexing Words:ST-segment depression Exerc Chronotropic incompetence T HERE HAS BEEN considerable criticism of stress testing because of its failure to distinguish with certainty those with coronary heart disease from those without.' This study was designed to determine the incidence of coronary events in subjects who had been subjected to a maximum stress test by evaluating follow-up information. Robb and Marks2 published follow-up data on patients who had been tested with a Master's Test in 1957 and established for the first time the prognostic significance of findings obtained on stress testing. Since then stress testing has evolved into a more strenuous and complex procedure, but adequate follow-up data to correlate this with future events has not been assembled.

Colorectal cancer (CRC) is the third most common malignancy and one of the leading causes of cancer-related death among men worldwide. CRC is a multifactor digestive pathology, which is a huge problem faced not only by clinicians but also by researchers. Importantly, a unique feature of CRC is the dysregulation of molecular signaling pathways. To date, a series of reviews have indicated that different signaling pathways are disordered and have potential as therapeutic targets in CRC. Nevertheless, an overview of the function and interaction of multiple signaling pathways in CRC is needed. Therefore, we summarized the pathways, biological functions and important interactions involved in CRC. First, we investigated the involvement of signaling pathways, including Wnt, PI3K/Akt, Hedgehog, ErbB, RHOA, Notch, BMP, Hippo, AMPK, NF-κB, MAPK and JNK. Subsequently, we discussed the biological function of these pathways in pathophysiological aspects of CRC, such as proliferation, apoptosis and metastasis. Finally, we summarized important interactions among these pathways in CRC. We believe that the interaction of these pathways could provide new strategies for the treatment of CRC.

An increased incidence of training injuries was found in more recent years, underscoring the need for further research on the risk factors associated with their causation.

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Purpose: To investigate the effect of jatrorrhizine on hepatic cancer cell proliferation and its mechanism of action. Methods: Jatrorrhizine-mediated changes in cell viability were measured using (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, while apoptosis induction was evaluated by flow cytometry. Transwell assay was used for the measurement of cell invasion, whereas cell migration was assessed by wound healing assay. The protein expression of Axin2 was determined with western blotting assay. Results: Jatrorrhizine significantly (p < 0.049) suppressed the viability of HepG2 and HCCLM3 cells in the concentration range of 0.5 to 16.0 μM. Treatment of HepG2 and HCCLM3 cells with 4.0 μM jatrorrhizine markedly suppressed cell invasion, when compared to untreated cells (p < 0.0493). Jatrorrhizine significantly promoted the apoptosis of HepG2 and HCCLM3 cells at 48 h, relative to untreated cells, but 16.0 μM jatrorrhizine markedly suppressed the expressions of miR-221-3p and miR-15b-5p (p < 0.0493). Moreover, jatrorrhizine significantly up-regulated the protein expressions of Axin2 in HepG2 and HCCLM3 cells at 48 h (p < 0.0493). Conclusion: Jatrorrhizine inhibits the proliferation, and suppressed the invasiveness and migration of HepG2 and HCCLM3 liver cancer cells, but increases their apoptosis. Moreover, it down-regulates the expressions of miR-221-3p and miR15b-5p and promotes Axin2 protein expression in HepG2 and HCCLM3 cells. Therefore, jatrorrhizine is a potential drug candidate for the treatment of liver cancer.