IMPORTANCE Severe acute respiratory syndrome coronavirus 2 has caused a global outbreak of coronavirus disease 2019 (COVID-19). Severe acute respiratory syndrome coronavirus 2 binds angiotensin-converting enzyme 2 of the rennin-angiotensin system, resulting in hypokalemia. OBJECTIVE To investigate the prevalence, causes, and clinical implications of hypokalemia, including its possible association with treatment outcomes, among patients with COVID-19.
The present study aimed to evaluate the predictive value of pelvic anatomical and clinicopathological parameters for use in the estimation of the likely technical difficulties that may be encountered when performing open rectal surgery for mid-low rectal cancer. Sixty consecutive patients, undergoing open rectal surgery for mid-low rectal cancer were recruited between June 2009 and April 2014. All of the surgical procedures conducted, were low anterior resection (LAR) or abdominoperineal resection (APR). The operations were performed by the same surgeon and surgical team. Pelvic dimensions and angles were measured using three-dimensional reconstruction of spiral computerized tomography (CT) images. Operative time and intraoperative blood loss were used as indicators of operative difficulty. The independent variables were pelvic anatomical and clinicopathological parameters, and the dependent variables were operative time and intraoperative blood loss. Univariate and multivariate analyses were performed in order to determine the predictive significance of these variables. The pelvis width was significantly wider in females than in males (P<0.05), while the sacrococcygeal bending degree was significantly greater in males than in females (P<0.05). No significant difference were detected between the pelvis depth of females and males (P>0.05). Multivariate analyses showed that body mass index (BMI), tumor height, lymph node metastasis, anteroposterior diameter of the pelvic inlet, anteroposterior diameter of the pelvic outlet, height of the pubic symphysis, the sacrococcygeal distance, sacrococcygeal-pubic angle and diameter of the upper pubis to the coccyx were the main factors affecting the operative time (all P<0.05), while the maximum diameter of the tumor was the primary factor affecting intraoperative blood loss (P<0.05). Between the two procedures, the clinicopathological parameters appeared to be more valuable for predicting difficulty in LAR, in which operative time was associated with tumor height and tumor staging (RC2=0.312; P<0.001). By contrast, the pelvic anatomical parameters appeared to be more valuable predictors of variation in APR, in which intraoperative blood loss was associated with the anteroposterior diameter of the mid-pelvis, the anteroposterior diameter of the pelvic outlet, the interspinous diameter, the depth of the sacral curvature and the sacropubic distance (RC2=0.608; P=0.002). BMI, tumor height and the maximum diameter of the tumor may be used to predict the operative difficulty in performing open rectal surgery for mid-low rectal cancer. In addition to the associated clinicopathological parameters, wider, shallower and less curved pelvises may make the greatest contribution to reducing operative time and intraoperative blood loss. Operative difficulty is likely to be increased in deeper and narrower pelvises, or in those with greater sacrococcygeal curvature.
The molecular pathway regulating gastric carcinoma (GC) invasiveness and metastasis remains elusive. Here, we detected significant increase in the phosphorylated epidermal growth factor receptor (pEGFR), MMP7, and MMP13 in the resected GC, compared with the adjacent normal tissue, in patients. Moreover, strong positive correlation was detected between pEGFR and MMP7, and between pEGFR and MMP13 in GC. To examine whether a causal link exists, we used two human GC lines, SNU-5 and AGS, to study the cross talk between EGFR signaling activation, and expression of MMP7 and MMP13. We found that EGF-induced EGFR phosphorylation activated both MMP7 and MMP13, and consequently cancer invasiveness. EGF-induced activation of MMP7 and MMP13 can be both inhibited by use of an inhibitor for EGFR. EGF-induced activation of MMP7 can be also significantly inhibited by use of an inhibitor for Akt, but not an inhibitor for ERK1/2, while EGF-induced activation of MMP13 can be significantly inhibited by use of an inhibitor for ERK1/2, but not by an inhibitor for Akt. These data suggest that EGF-induced activation of MMP7 and MMP13 in GC is through phosphatidylinositol 3-kinase (PI3K) and extracellular-related kinase/mitogen-activated protein kinase (ERK/MAPK) signaling pathway, respectively. Our study thus highlights EGFR signaling regulated MMP7 and MMP13 activation as molecular basis for metastasis of GC, and further demonstrate that different signaling pathway cascades are involved in the downstream signaling transduction.
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