Optimal Control of Investment-Reinsurance Problem for an Insurer with Jump-Diffusion Risk Process: Independence of Brownian Motions

This paper investigates the excess-of-loss reinsurance and investment problem for a compound Poisson jump-diffusion risk process, with the risk asset price modeled by a constant elasticity of variance (CEV) model. It aims at obtaining the explicit optimal control strategy and the optimal value function. Applying stochastic control technique of jump diffusion, a Hamilton-Jacobi-Bellman (HJB) equation is established. Moreover, we show that a closed-form solution for the HJB equation can be found by maximizing the insurer’s exponential utility of terminal wealth with the independence of two Brownian motions W(t) and W1(t). A verification theorem is also proved to verify that the solution of HJB equation is indeed a solution of this optimal control problem. Then, we quantitatively analyze the effect of different parameter impacts on optimal control strategy and the optimal value function, which show that optimal control strategy is decreasing with the initial wealth x and decreasing with the volatility rate of risk asset price. However, the optimal value function V(t;x;s) is increasing with the appreciation rate μ of risk asset

Elliptical Galaxies with Emission Lines from the Sloan Digital Sky Survey

We present the results of 11 elliptical galaxies with strong nebular emission lines during our study of star formation history along the Hubble sequence. After removing the dilution from the underlying old stellar populations by use of stellar population synthesis model, we derive the accurate fluxes of all emission lines for these objects, which are later classified with emission line ratios into one Seyfert 2, six LINERs and four HII galaxies. We also identify one HII galaxy (A1216+04) as a hitherto unknown Wolf-Rayet galaxy from the presence of the Wolf-Rayet broad bump at 4650 \AA. We propose that the star-forming activities in elliptical galaxies are triggered by either galaxy-galaxy interaction or the merging of a small satellite/a massive star cluster, as already suggested by recent numerical simulations

miR-124 Suppresses Pancreatic Ductal Adenocarcinoma Growth by Regulating Monocarboxylate Transporter 1-Mediated Cancer Lactate Metabolism

Background/Aims: Increasing evidence shows that reprogramming of energy metabolism is a hallmark of cancer. Considering the emergence of microRNAs as crucial modulators of cancer, this study aimed to better understand the molecular mechanisms of miR-124 in regulating glycolysis in human pancreatic cancer. Methods: RT-PCR was used to investigate the expression of monocarboxylate transporters (MCTs) in pancreatic ductal adenocarcinoma (PDAC) patient samples and the PANC-1 cell line. A public database and immunochemistry were used for comprehensive analysis of MCT1 expression. The targeting of MCT1 by miR-124 was predicted by software and validated for the MCT1 3’-UTR by dual-luciferase reporter analysis. Cell proliferation, apoptosis, migration, xenografting, and the intracellular pH and L-lactate levels were assessed. Hypoxia-inducible factor-α (HIF-1α) and lactate dehydrogenase A (LDH-A) expression levels were determined by RT-PCR and western blotting. Results: MCT1 expression was higher in PDAC tissue than in normal tissue. Inhibition of MCT1 affected lactate metabolism, resulting in a higher intracellular pH and less proliferation of PANC-1 cells. MCT1 was the target gene of miR-124. In in vitro experiments, miR-124 inhibited the glycolytic activity of PANC-1 cells by targeting MCT1, further decreasing the tumor phenotype by increasing the intracellular pH through LDH-A and HIF-1α. In in vivo experiments, overexpression of miR-124 and silencing of MCT1 significantly inhibited tumor growth. Conclusion: miR-124 inhibits the progression of PANC-1 by targeting MCT1 in the lactate metabolic pathway. Our findings provide novel evidence for further functional studies of miR-124, which might be useful for future therapeutic approaches to PDAC

Complex in vitro 3D models of digestive system tumors to advance precision medicine and drug testing: Progress, challenges, and trends

Digestive system cancers account for nearly half of all cancers around the world and have a high mortality rate. Cell culture and animal models represent cornerstones of digestive cancer research. However, their ability to en- able cancer precision medicine is limited. Cell culture models cannot retain the genetic and phenotypic heteroge- neity of tumors and lack tumor microenvironment (TME). Patient-derived xenograft mouse models are not suitable for immune-oncology research. While humanized mouse models are time- and cost-consuming. Suitable preclinical models, which can facilitate the understanding of mechanisms of tumor progression and develop new therapeutic strategies, are in high demand. This review article summarizes the recent progress on the establish- ment of TME by using tumor organoid models and microfluidic systems. The main challenges regarding the translation of organoid models from bench to bedside are discussed. The integration of organoids and a microflu- idic platform is the emerging trend in drug screening and precision medicine. A future prospective on this field is also provided.This study was supported by the National Natural Science Foundation of China (Grant No.82073148), the Guangdong Provincial Key Laboratory of Digestive Cancer Research (No. 2021B1212040006), the Sanming Project of Medicine in Shenzhen (SZSM201911010), the Shenzhen Key Medical Discipline Construction Fund (SZXK016), the Shenzhen Sustainable Project (KCXFZ202002011010593), and the Shenzhen-Hong Kong-Macau Technology Research Programme (Type C) (Grant No. SGDX2020110309260100)

An ALMA Study of the FU Ori─type Object V900 Mon: Implications for the Progenitor

We present ALMA observations of 12CO, 13CO, and C18O J = 2─1 lines and the 230 GHz continuum for the F Ori─type object (FUor) V900 Mon (d ∼ 1.5 kpc), for which the accretio burst was triggered between 1953 and 2009. We identified CO emissio associated with a molecular bipolar outflow extending up to a ∼104 au scale and a rotating molecular envelope extendin over >104 au. The interaction with the hot energetic FUo wind, which was observed using optical spectroscopy, appears limited t a region within ∼400 au of the star. The envelope mass and collimatio of the extended CO outflow suggest that the progenitor of this FUor is low-mass Class I young stellar object (YSO). These parameters for V90 Mon, another FUor, and a few FUor-like stars are consistent with th idea that FUor outbursts are associated with normal YSOs. The continuu emission is marginally resolved in our observations with a 0.″2 × 0.″1 (∼300 × 225 au) beam, and a Gaussian model provides a deconvolved FWH of ∼90 au. The emission is presumably associated with a dust circumstellar disk, plus a possible contribution from a wind or win cavity close to the star. The warm compact nature of the disk continuu emission could be explained with viscous heating of the disk, whil gravitational fragmentation in the outer disk and/or a combination o grain growth and their inward drift may also contribute to its compac nature

Life-threatening hemobilia caused by hepatic pseudoaneurysm after T-tube choledochostomy: report of a case

<p>Abstract</p> <p>Background</p> <p>Hemobilia is a rare but lethal biliary tract complication. There are several causes of hemobilia which might be classified as traumatic or nontraumatic. Hemobilia caused by pseudoaneurysm might result from hepatobiliary surgery or percutaneous interventional hepatobiliary procedures. However, to our knowledge, there are no previous reports pertaining to hemobilia caused by hepatic pseudoaneurysm after T-tube choledochostomy.</p> <p>Case presentation</p> <p>A 65-year-old male was admitted to our hospital because of acute calculous cholecystitis and cholangitis. He underwent cholecystectomy, choledocholithotomy via a right upper quadrant laparotomy and a temporary T-tube choledochostomy was created. However, on the 19th day after operation, he suffered from sudden onset of hematemesis and massive fresh blood drainage from the T-tube choledochostomy. Imaging studies confirmed the diagnosis of pseudoaneurysm associated hemobilia. The probable association of T-tube choledochostomy with pseudoaneurysm and hemobilia is also demonstrated. He underwent emergent selective microcoils emobolization to occlude the feeding artery of the pseudoaneurysm.</p> <p>Conclusions</p> <p>Pseudoaneurysm associated hemobilia may occur after T-tube choledochostomy. This case also highlights the importance that hemobilia should be highly suspected in a patient presenting with jaundice, right upper quadrant abdominal pain and upper gastrointestinal bleeding after liver or biliary surgery.</p

Association of Interleukin-10 A-592C Polymorphism in Taiwanese Children with Kawasaki Disease

Elevated serum levels of interleukin-10 (IL-10) have been reported in patients with Kawasaki disease (KD). IL-10 reduces the inflammatory actions of macrophages and T cells and it may play a significant role in the regulation of inflammatory vascular damage associated with systemic vasculitis. The aim of this study was to examine whether -592 IL-10 promoter polymorphism is a susceptibility or severity marker of KD in Chinese patients in Taiwan. The study included 105 KD patients and 100 normal controls. Genotype and allelic frequencies for the IL-10 gene polymorphism in both groups were compared. There were no significant between-group differences in the genotype distribution of IL-10 A-592C gene polymorphism (P=0.08). However, the frequency of the -592*A allele was significantly increased in the patients with KD compared with controls (71.9% vs. 61.0%, P=0.019). The odds ratio for developing KD in individuals with IL-10-592*A allele was 1.64 (95% confidence interval, 1.06-2.52) compared to individuals with the IL-10-592*C allele. No significant difference was observed in the genotype and allelic frequencies for the IL-10 A-592C polymorphism between patients with and without coronary artery lesions. The IL-10-592*A allele may be involved in the development of KD in Taiwanese children