Convenient indoor positioning has become an urgent need due to the improvement it offers to quality of life, which inspires researchers to focus on device-free indoor location. In areas covered with Wi-Fi, people in different locations will to varying degrees have an impact on the transmission of channel state information (CSI) of Wi-Fi signals. Because space is divided into several small regions, the idea of classification is used to locate. Therefore, a novel localization algorithm is put forward in this paper based on Deep Neural Networks (DNN) and a multi-model integration strategy. The approach consists of three stages. First, the local outlier factor (LOF), the anomaly detection algorithm, is used to correct the abnormal data. Second, in the training phase, 3 DNN models are trained to classify the region fingerprints by taking advantage of the processed CSI data from 3 antennas. Third, in the testing phase, a model fusion method named group method of data handling (GMDH) is adopted to integrate 3 predicted results of multiple models and give the final position result. The test-bed experiment was conducted in an empty corridor, and final positioning accuracy reached at least 97%.
RationaleFructose-1,6-bisphosphatase (FBP1) is a tumor suppressor and a key enzyme negatively regulating Warburg effect in cancer. However, regulation of FBP1 protein expression and its exact role in prostate cancer (PCa) is largely unclear. Phosphatase and tensin homolog (PTEN) is one of the most frequently deleted tumor suppressor genes in human PCa. However, the role of PTEN loss in aberrant Warburg effect in cancer remains poorly understood.MethodsExpression of PTEN and FBP1 was analyzed in several PCa cell lines and prostate tumor tissues in mice. Western blot (WB) and RT-PCR approaches were used to examine how PTEN regulates FBP1 expression. Co-immunoprecipitation (co-IP) and in vivo ubiquitination assays were used to define the regulatory mechanisms. A PCa xenograft model was employed to determine the impact of PTEN regulation of FBP1 on PCa growth in vivo.ResultWe demonstrated that in a manner dependent of PI3K/AKT signal pathway PTEN regulated FBP1 expression in various PCa cell lines and tumors in mice. We confirmed that this regulation took place at the protein level and was mediated by SKP2 E3 ubiquitin ligase. Mechanistically, we showed that serine 271 phosphorylation of FBP1 by cyclin-dependent kinases (CDKs) was essential for SKP2-mediated degradation of FBP1 protein induced by PTEN loss. Most importantly, we further showed that loss of PTEN expression enhanced Warburg effect and PCa growth in mice in a manner dependent, at least partially on FBP1 protein degradation.ConclusionsOur results reveal a novel tumor-suppressive feature of PTEN in restraining FBP1 degradation and the Warburg effect. These results also suggest that prohibiting FBP1 protein degradation could be a viable therapeutic strategy for PTEN-deficient PCa.
BackgroundYolk sac tumor is the most common malignant nonseminomatous germ-cell tumor in children characterized by elevated level of α-fetoprotein (AFP), accounting for 70%–80% of all cases. However, giant yolk sac tumors that involve the entire testicle may be misdiagnosed by color Doppler ultrasonography as orchitis. Therefore, we described a case of a 2-year-old pediatric patient with a giant testicular yolk sac tumor that was misdiagnosed by ultrasonography as orchitis, in order to evaluate the role of measuring AFP levels in the initial diagnosis to aid in the accuracy of the definitive diagnosis of testicular yolk sac tumor.Case presentationA 2-year-old boy received outpatient visits for unintentional swelling of the right scrotum for 7 days. Physical examination showed a rubbery swelling of the right scrotum with rejective touch. Then, the patient underwent perineal color Doppler ultrasonography in outpatient visits. The result showed a right testicle size of 29 mm × 22 mm × 20 mm with heterogeneous echogenicity and abundant blood flow, supporting the initial diagnosis of orchitis. However, the initial surgeon was skeptical of the ultrasonography diagnosis. Thus, the patient was admitted to the Department of Andrology on day 2 for further serological and imaging examination. The serum AFP level on day 3 was 323.77 ng/ml. The results of CT and MRI showed a giant tumor of the right testis (26 mm × 21 mm × 29.6 mm) with multiple lymphoid hyperplasia in the inguinal region bilaterally. The patient received radical orchidectomy without lymph node dissection on day 9. The results of postoperative pathological examination confirmed giant testicular yolk sac tumor (T1N0M0S1, Stage Is) and was positive for AFP and SALL4 in immunohistochemistry staining. The patient received three courses of bleomycin–etoposide–cisplatin chemotherapy in the Department of Pediatrics after multidisciplinary team meeting on postoperative days 14, 37, and 58, respectively. During chemotherapy and follow-up, the patient's AFP and lactate dehydrogenase levels continued to decline, and eventually remained within normal range on postoperative day 84.ConclusionMeasuring the AFP level was necessary for initial diagnosis and follow-up in pediatric cases of testicular enlargement. Radical orchidectomy combined with postoperative bleomycin–etoposide–cisplatin adjuvant chemotherapy was an effective treatment strategy for pediatric giant testicular yolk sac tumors.
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