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Micro-LED has attracted tremendous attention as next-generation display, but InGaN red-green-blue (RGB) based high-efficiency micro-LEDs, especially red InGaN micro-LED, face significant challenges and the optoelectronic performance is inevitably affected by environmental factors such as varying temperature and operating current density. Here, we demonstrated the RGB InGaN micro-LEDs, and investigated the effects of temperature and current density for the InGaN RGB micro-LED display. We found that temperature increase can lead to the changes of electrical characteristics, the shifts in electroluminescence spectra, the increase of full width at half maximum and the decreases of light output power, external quantum efficiency, power efficiency, and ambient contrast ratios, while current density increase can also give rise to different changing trends of the varieties of parameters mentioned just above for the RGB micro-LED display, creating great challenges for its application in practical scenarios. Despite of the varying electrical and optical charateristics, relatively high and stable colour gamut of the RGB display can be maintained under changing temperature and current density. Based on the results above, mechanisms on the temperature and current density effects were analyzed in detail, which would be helpful to predict the parameters change of micro-LED display caused by temperature and current density, and provided guidance for improving the performance of InGaN micro-LED display in the future.
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This study aimed to investigate the function of Activatable Cell-Penetrating Peptides (ACPP) in detecting the changes of human intrahepatic bile duct epithelial cell(hIBDEC). ACPP, which target matrix metalloproteinases, were constructed. All were labeled with FITC and Gd-DTPA at the N-terminal. Fluorescence microscopy was used to observe the fluorescence intensity inside hIBDEC after stimulating with different concentrations of LPS and incubating with different concentrations of ACPP to determine the optimal concentration range for LPS stimulation and the optimal concentration for FITC-ACPP effect. Flow cytometry and magnetic resonance imaging were used to detect fluorescence signal intensity and nuclear magnetic resonance signal intensity, respectively, after stimulating with different concentrations of LPS. LPS stimulation time and ACPP incubation time were also evaluated, and variance analysis was conducted to analyze intracellular signal change characteristics for every group. Activatable Cell-Penetrating Peptides (ACPP), which were marked with FITC and Gd-DTPA had target-penetrating activity. The intracellular signal intensity gradually increased with the increase in LPS stimulation time and ACPP incubation time within a certain range; however, it did not increase with the increase of LPS concentration. ACPP can be used for imaging hIBDEC with epithelial-mesenchymal transition.
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Ductos Biliares Intra-Hepáticos/citologia , Ductos Biliares Intra-Hepáticos/diagnóstico por imagem , Peptídeos Penetradores de Células/análise , Células Epiteliais/citologia , Transição Epitelial-Mesenquimal , Citometria de Fluxo/métodos , Humanos , Lipopolissacarídeos/farmacologia , Imageamento por Ressonância Magnética/métodos , Coloração e RotulagemRESUMO
BACKGROUND: Nesidioblastosis usually refers to a series of clinical manifestations caused by the proliferation of ß-cells in pancreatic islets, and these clinical manifestations are hyperinsulinemia and persistent hypoglycemia. According to the size of the lesion, nesidioblastosis is divided into focal nesidioblastosis, diffuse nesidioblastosis and atypical nesidioblastosis, and its pathogenesis is still unclear. Nesidioblastosis is mainly seen in infants and rarely reported in adults, especially focal nesidioblastosis, which is difficult to distinguish from insulinoma. CASE SUMMARY: We report a case of adult focal ß-cell nesidioblastosis in which the preoperative diagnosis was insulinoma. The patient was a 48-year-old male who suffered from repeated morning and fasting palpitations, sweating, and severe disturbance of consciousness for 5 years. His blood glucose was found to be as low as 1.79 mmol/L during an attack. However, abdominal computed tomography showed no abnormalities. Magnetic resonance imaging and endoscopic ultrasonography demonstrated a nodular mass in the head of the pancreas, combined with hyperinsulinemia and high serum C-peptide. The patient was diagnosed with insulinoma and underwent Beger surgery; however, the postoperative pathological results showed nesidioblastosis. CONCLUSION: Although surgical resection is the preferred option for nesidioblastosis, some cases can be treated non-surgically. In order to increase clinicians' understanding of nesidioblastosis, it is necessary to review the pathogenesis, diagnosis and treatment of this disease.
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Objective: This study aimed to assess the efficacy of Endoscopic Retrograde Cholangiopancreatography (ERCP), common bile duct exploration, and percutaneous transhepatic cholangiography combined with common bile duct exploration for treating choledocholithiasis with acute cholangitis, to guide management strategies. Methods: A retrospective evaluation was conducted on a cohort of 283 inpatients diagnosed with choledocholithiasis and acute cholangitis at the affiliated hospital. Patients were categorized into three groups: Group A (ERCP group), Group B(common bile duct exploration group), and Group C(PTCD combine common bile duct exploration group.) Parameters such as hepatic function recovery, inflammation level control, blood loss, postoperative hospital duration, and postoperative complications were compared. Results: All groups exhibited notable reductions in postoperative biochemical parameters including alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT), total bilirubin (TBIL), and WBC (P < 0.05). Group A had the least blood loss(P < 0.05), and shortest hospital stay(P < 0.05), but a higher incidence of pancreatitis(P < 0.05), with a total of 8 cases occurred(7.3%). Group C had a shorter hospital stay compared to Group B(P < 0.05). Conclusion: For patients with fewer and smaller common bile duct stones and milder symptoms, it is recommended to primarily choose endoscopic retrograde cholangiopancreatography (ERCP), endoscopic sphincterotomy (EST), and endoscopic nasobiliary drainage (ENBD), it procedures offer quicker recovery and cause minimal trauma. For patients with numerous, larger common bile duct stones but stable conditions, bile duct exploration is recommended. For those with severe conditions and significant inflammation, PTCD and common bile duct exploration are advised.
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OBJECTIVES: This study aimed to investigate the effect and mechanism of hypoxia on pancreatic cancer (PC) cell dedifferentiation and tumorigenic potential. METHODS: Inhibition of hypoxia-inducible factor 1α (HIF-1α) and overexpression of Notch1 in PC HS766T cell lines were by lentiviral transfection. The expression of stem cell-specific markers C-X-C motif chemokine receptor 4, CD44, and Nestin was detected by immunofluorescence and Western blot assays. Cell invasion capacity was examined by Transwell assay. Tumorigenic potential was measured in an in situ tumor transplantation experiment. The expression of HIF-1α, Notch signals, and apoptosis signals was examined by Western blot assay. RESULTS: Hypoxia promoted PC cells to dedifferentiate into stem-like cells by upregulating HIF-1α and activating Notch signals. Silencing of HIF-1α significantly repressed cell dedifferentiation and invasion, whereas overexpression of Notch1 reversed the effect of HIF-1α repression. In situ tumor transplantation experiment further confirmed that hypoxia promoted tumorigenic ability through upregulating HIF-1α. Moreover, the expression of HIF-1α and Notch1 was significantly increased in human PC tissues, and high expression of HIF-1α was correlated with poor survival rate. CONCLUSIONS: Hypoxia promoted PC cell dedifferentiation to stem-like cell phenotypes with high tumorigenic potential by activating HIF-1α/Notch signaling pathway, indicating a novel role in regulating PC progression.
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Desdiferenciação Celular , Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo , Células-Tronco Neoplásicas/metabolismo , Neoplasias Pancreáticas/metabolismo , Receptor Notch1/metabolismo , Hipóxia Tumoral , Idoso , Animais , Linhagem Celular Tumoral , Movimento Celular , Feminino , Regulação Neoplásica da Expressão Gênica , Humanos , Subunidade alfa do Fator 1 Induzível por Hipóxia/genética , Masculino , Camundongos Nus , Invasividade Neoplásica , Células-Tronco Neoplásicas/patologia , Neoplasias Pancreáticas/genética , Neoplasias Pancreáticas/patologia , Fenótipo , Receptor Notch1/genética , Transdução de SinaisRESUMO
BACKGROUND AND AIM: Intrahepatic biliary epithelial cells (IBECs) of the bile duct in liver tissue of patients with hepatolithiasis promoted the development of diseases through epithelial-mesenchymal transition (EMT). This study investigated whether lipopolysaccharide (LPS), a cell-wall constituent of gram-negative bacteria, could induce EMT of IBECs and toll-like receptor 4 (TLR4) had a regulatory role via activating the nuclear factor-κB (NF-κB)/Snail signaling pathway during this process in vivo. METHODS: TLR4 short hairpin RNA (shRNA) adenovirus or negative control shRNA (NC shRNA) adenovirus (1 × 109 plaque-forming unit (PFU), respectively) was injected into the caudal vein of rats. After 96 h, 1 mg/kg LPS was infused retrogradely into the common bile duct for 48 h per rat. The effects of TLR4 shRNA on LPS-induced EMT were determined by evaluating the histopathological changes in IBECs using hematoxylin and eosin staining and the changes in the levels of EMT markers, TLR4, NF-κB p65, pNF-κB p65, and Snail using real-time polymerase chain reaction and Western blot analysis. RESULTS: Compared with normal saline treatment, a loss of epithelial cell markers (E-cadherin and cytokeratin 7) and a gain of mesenchymal cell markers (N-cadherin and matrix metalloproteinase 2) were revealed. The levels of TLR4, NF-κB phosphorylation, and Snail significantly increased after LPS treatment, whereas pretreatment with TLR4 shRNA inhibited the LPS-induced EMT by downregulating the NF-κB/Snail signaling pathway. CONCLUSIONS: LPS induced the EMT of IBECs by activating TLR4. The RNAi-mediated knockdown of TLR4 suppressed EMT occurrence via downregulating the NF-κB/Snail signaling pathway, implicating TLR4 as a new target for human hepatolithiasis.