Effect of Face Blurring on Human Pose Estimation: Ensuring Subject Privacy for Medical and Occupational Health Applications.

The face blurring of images plays a key role in protecting privacy. However, in computer vision, especially for the human pose estimation task, machine-learning models are currently trained, validated, and tested on original datasets without face blurring. Additionally, the accuracy of human pose estimation is of great importance for kinematic analysis. This analysis is relevant in areas such as occupational safety and clinical gait analysis where privacy is crucial. Therefore, in this study, we explore the impact of face blurring on human pose estimation and the subsequent kinematic analysis. Firstly, we blurred the subjects' heads in the image dataset. Then we trained our neural networks using the face-blurred and the original unblurred dataset. Subsequently, the performances of the different models, in terms of landmark localization and joint angles, were estimated on blurred and unblurred testing data. Finally, we examined the statistical significance of the effect of face blurring on the kinematic analysis along with the strength of the effect. Our results reveal that the strength of the effect of face blurring was low and within acceptable limits (<1°). We have thus shown that for human pose estimation, face blurring guarantees subject privacy while not degrading the prediction performance of a deep learning model.

Association of Mortality-Related Risk Factors in Patients with COVID-19: A Retrospective Cohort Study.

COVID-19 is a rapidly disseminating infectious disease conferred by the World Health Organization (WHO) as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Epidemiological and clinical characteristics data have been identified for patients with COVID-19, but mortality-related risk factors and a comprehensive clinical course of disease in a developing country have not been specifically defined. This retrospective, single-center cohort study involved all successive inpatients having a positive COVID-19 polymerase chain reaction (PCR), with deceased or discharged clinical outcomes from 1 January to 10 May 2021. Data were extracted from electronic medical records on demographic, clinical, radiological, and laboratory findings as well as complications faced and treatment provided during follow-up, involving serial samples for viral RNA identification, and compared between the dead and survivors. To investigate the risk factors associated with in-hospital mortality, we employed the multivariate logistic regression model. In this study, 2048 patients were involved, 1458 of whom were discharged, and 590 died in hospital. More than half of patients were identified as male with old age being the potential risk factor of mortality. Exactly 94.8% of all patients presented with fever at the time of admission. Several comorbidities were present in the study population, with the most frequent comorbidity being cardiovascular diseases (1177 of 2048) and hypertension (975 of 2048) followed by cerebrovascular disease and diabetes mellitus. Mortality rates for infected patients were observed as higher in severe patients (46.3%) compared with non-severe cases (26.1%) during a follow-up. Multivariate regression analysis showed a significant association of in-hospital mortality of patients with older age, presence of hypertension and cardiovascular diseases as underlying comorbidities, increased level of cardiac troponin I and d-dimer concentration on admission, as well as septicemia and ARDS as a complication during illness. To minimize the risk of death in COVID19 patients, as well as the risk of severe complications, urgent public health measures should be properly planned and implemented on those vulnerable populations. To detect early manifestations of clinical problems, thorough and regular follow-up is warranted.

High CTSL2 expression predicts poor prognosis in patients with lung adenocarcinoma.

Cathepsin like 2 (CTSL2) is a lysosomal cysteine protease, and may be associated with tumor metastasis. However, CTSL2 has not been reported as a biomarker in lung adenocarcinoma (LUAD). In this study, bioinformatics analysis using data from The Cancer Genome Atlas was performed. Wilcoxon rank-sum test and chi-square test were carried out. Kaplan-Meier and Cox regression were performed to evaluate the effect of CTSL2 expression in the overall survival. Our results indicated that CTSL2 in tumor was significantly higher than that in normal tissue (P < 0.001). High CTSL2 expression was significantly associated with age (P = 0.02), vital status (P < 0.001), and T classification (P = 0.03), and correlated with poor overall survival (HR = 1.62, 95% CI = 1.21-2.18, P = 0.001). CTSL2 expression was an independent risk factor for overall survival in patients with LUAD (HR = 1.52, 95% CI = 1.12-2.05, P = 0.006). A nomogram was plotted for illustration of CTSL2 expression on the risk of LUAD. Furthermore, in vitro cell experiments showed the CTSL2 promoted the proliferation and migration of A549 cells. In summary, high CTSL2 expression predicts poor prognosis in patients with LUAD.

Successful surgical treatment of Cronkhite-Canada Syndrome with bilateral flail chest: a case report.

BACKGROUND: Development of multiple rib fractures leading to bilateral flail chest in Cronkhite-Canada Syndrome (CCS) has not been reported. CASE PRESENTATION: A 59-year-old man presented with complaints of fatigue, chest pain, respiratory distress and orthopnea requiring ventilatory support to maintain oxygenation. CCS with bilateral anterior and posterior flail chest due to multiple rib fractures (2nd-10th on the right side and 2nd-11th on the left side). He underwent open reduction and anterior and posterior internal fixation using a titanium alloy fixator and a nickel-titanium memory alloy embracing fixator for chest wall reconstruction. He recovered gradually from the ventilator and showed improvement in his symptoms. He gained about 20 kg of weight in the follow up period (6 months after discharge from the hospital). CONCLUSION: CCS is a rare, complex disease that increases the risk of developing multiple rib fractures, which can be successfully treated with open reduction and internal fixation.

MicroRNAs-491-5p suppresses cell proliferation and invasion by inhibiting IGF2BP1 in non-small cell lung cancer.

MicroRNAs-491-5p (miR-491-5p) has been found to involve in tumor initiation and development in several tumors. However, the biological function and underlying molecular mechanism of miR-491-5p in non-small lung cancer (NSCLC) remain unclear. This study was therefore to investigate biological role of and underlying molecular mechanisms of in NSCLC. It was found that miR-491-5p expression was significantly downregulated in NSCLC tissues when compared with corresponding adjacent normal tissues (P<0.01), and the value was negatively related to advanced and tumor-node-metastasis (TNM) stage and lymph node metastasis (both P<0.01). We also demonstrate that restoration of miR-491-5p suppressed NSCLC cell proliferation by arresting NSCLC cells in the G1/G0 phase and accelerating apoptosis. miR-491-5p also inhibited cell migration and invasion in NSCLC cells. Mechanically, IGF2BP1 was identified as direct targets of miR-491-5p. And IGF2BP1 expression was significantly upregulated, and correlated negative with miR-491-5p expression in NSCLC tissues. In vivo assay showed thatmiR-491-5p suppressed tumor growth in nude model by repressing IGF2BP1 expression. Collectively, miR-491-5p functioned as a tumor suppressor in NSCLC by targeting IGF2BP1. Restoration of miR-491-5p expression may represent a promising therapeutic approach for targeting malignant NSCLC.

MicroRNA-92a promotes growth, metastasis, and chemoresistance in non-small cell lung cancer cells by targeting PTEN.

MicroRNA-92a (miR-92a) has been reported to play important roles in tumorigenesis of human various cancers. However, the roles and underlying molecular mechanism of miR-92a in non-small cell lung cancer (NSCLC) have not been totally elucidated. Therefore, the aims of this study were to determine the role of miR-92a and to elucidate its regulatory mechanism in NSCLC. We found that miR-92a was significantly upregulated in NSCLC tissues compared to matched adjacent normal lung tissues, and its expression is significantly associated with clinical characteristics of patients, including tumor, node, and metastasis (TNM) stage; tumor size; and lymph node metastasis (all P < 0.01). Function assays demonstrated that upregulation of miR-92a in NSCLC cells promoted cell proliferation, migration, and invasion, decreased apoptosis and caspase-3 activity, and enhanced chemoresistance of NSCLC cells, whereas downregulation of miR-92a showed the opposite effects. Moreover, phosphatase and tensin homolog (PTEN), a unique tumor suppressor gene, was confirmed as a direct target of miR-92a, and PTEN messenger RNA (mRNA) expression was decreased in NSCLC tissues and was inversely correlated with miR-92a. Downregulation of PTEN could mimic the same effects of miR-92a mimic in NSCLC cells and rescue the effects on NSCLC cells induced by miR-92a inhibitor. Taken together, these findings suggested that miR-92a could promote growth, metastasis, and chemoresistance in NSCLC cells at least partially by targeting PTEN.