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In this paper, an antenna design with a multiband and a small size for connecting a sensor network and the Internet has been proposed. The antenna has an antenna portion of 20 × 12 mm2 and a ground plane of 40 × 12 mm2 which is printed on a flame retardant 4 (FR4) substrate 1.6 mm thick and with a relative dielectric constant of 4.4. A 50-ohm mini-coaxial cable is adopted to feed the RF input. The antenna portion consists of two meandered arms, and another small L-shaped arm with a chip inductor of 3.3 nH is connected to the feed point of the design. A monopole with two meandered arms connected by a via hole is extended from the ground plane, which produces the modes of a low-frequency band. In addtion, the modes of high-frequency bands are also produced by these two meandered arms and the ground plane. The simulated and measured results of the proposed antenna cover the bands of LTE700/LTE2300/LTE2500/GSM1800/GSM1900/ UMTS. This USB antenna design with multibands and a small size is suitable for connecting a sensor network and the Internet. [ABSTRACT FROM AUTHOR]

Background and Objective: miR-22-3p functions as a tumor suppressor by targeting a variety of downstream genes, while its role and downstream targets in gastric cancer (GC) remain to be determined. We aimed to explore the role of miR-22-3p in gastric cancer and the potential mechanism., Methods: miR-22-3p mimic and inhibitor were used to overexpress or knockdown the expression of miR-22-3p separately. Quantitative real-time PCR (RT-qPCR) and Western blot were used to analyse the abundance of mRNA or protein level respectively. CCK-8 assay, cell colony formation assay, and flow cytometry were implemented to investigate the effect of miR-22-3p on gastric cancer cell proliferation and apoptosis. Luciferase assay was used to evaluate the role of miR-22-3p on the expression of glycolytic enzyme enolase 1 (ENO1)., Results: In this study, we found that miR-22-3p was downregulated in GC cells. By transfecting the cells with miR-22-3p inhibitors or mimics, we showed that miR-22-3p suppressed GC cell proliferation and migration, as well as triggered cell death. In addition, we discovered that miR-22-3p was engaged in glycolysis by controlling the generation of lactate as well as the consumption of glucose. TargetScan database suggested that the ENO1 may be a target of the miR-22-3p, and the luciferase experiment verified this hypothesis. Recovery assays showed that the proliferation and migration of GC cells suppressed by miR-22-3p could be rescued by overexpression of ENO1., Conclusion: Collectively, we identified a new axis of miR-22-3p/ENO1 for GC development, which could be investigated as a therapeutic target for GC.

Objective: To detect the aberrant promoter CpG islands hypermethylation status of GSTP1 gene in hepatocellular carcinomas (HCC) and to assess its significant role in hepatocarcinogenesis., Methods: Surgically resected cancerous and non-cancerous liver tissues of 26 hepatocellular carcinoma patients were obtained from West China Hospital, and 11 peripheral blood samples from healthy donors as negative control were collected. Breast cancer cell line MCF-7 with CpG islands hypermethylation of GSTP1 as positive control was obtained from the Cell Bank of Chinese Academy of Sciences in Shanghai. All genomic DNA were extracted using common phenolchloroform approach, and the 5' CpG islands methylation status of GSTP1 gene was studied by methylation-specific polymerase chain reaction (MSP)., Results: GSTP1 gene promoter CpG island hyperthylation was detected in 88.5% (23/26) of cancerous tissues and in 69% (18/26) of corresponding non-cancerous tissues from the 26 HCC patients. None of the 11 control samples were methylation positive., Conclusion: The data indicates that the detection of GSTP1 gene methyl-lation may be a valuable biomarker by MSP for HCC early diagnosis and disease monitoring.

Objective: To investigate the diagnostic methods and reasonable treatment of Peutz-Jeghers syndrome (PJS)., Methods: Clinical data of six patients with PJS were reviewed., Results: Repeated abdominal pain, intussusception and intestinal polyp with bleeding were main manifestations. Four patients father,three patients grandfather and one patients mother were diagnosed with PJS. Three patients had family history of cancer. Case 4 and case 5 underwent laparotomy for many times because of intussusceptions caused by polyps or recurrent abdominal pain. Case 1 and case 4 had polyps synchronous with adenoma, and case 2 had polyp with gastric cancer. Main treatment included polyp resection and partial small intestinal and colon resection., Conclusions: Patients with PJS have family history of cancer and a high incidence of polyp recurrence of small intestine. Surgical intervention is the first choice regimen. Surveillance should be emphasized on gastrointestinal tract and other potential malignant organs in PJS patients.

Aim: To explore the etiology, pathogenesis, diagnosis, and treatment of postsurgical gastroparesis syndrome (PGS) after pancreatic cancer cryotherapy (PCC) or pancreatico-duodenectomy (PD), and to analyze the correlation between the multiple factors and PGS caused by the operations., Methods: Clinical data of 210 patients undergoing PD and 46 undergoing PCC were analyzed retrospectively., Results: There were 31 (67%, 31/46) patients suffering PGS in PCC group, including 29 with pancreatic head and uncinate tumors and 2 with pancreatic body and tail tumors. Ten patients (4.8%, 10/210) developed PGS in PD group, which had a significantly lower incidence of PGS than PCC group (chi= 145, P<0.001). In PCC group, 9 patients with PGS were managed with non-operative treatment (drugs, diet, nasogastric suction, etc.), and one received reoperation at the 16th day, but the symptoms were not relieved. In PD group, all the patients with PGS were managed with non-operative treatment. The PGS in patients undergoing PCC had close association with PCC, tumor location, but not with age, gender, obstructive jaundice, hypoproteinemia, preoperative gastric outlet obstruction and the type and number of gastric biliary tract operations. The mechanisms of PGS caused by PD were similar to those of PGS following gastrectomy. The damage to interstitial cells of Cajal might play a role in the pathogenesis of PGS after PCC, for which multiple factors were possibly responsible, including ischemic and neural injury to the antropyloric muscle and the duodenum after freezing of the pancreatico-duodenal regions or reduced circulating levels of motilin., Conclusion: PGS after PCC or PD is induced by multiple factors and the exact mechanisms, which might differ between these two operations, remain unknown. Radiography of the upper gastrointestinal tract and gastroscopy are main diagnostic modalities for PGS. Non-operative treatments are effective for PGS, and reoperation should be avoided in patients with PGS caused by PCC.