Cerulein pancreatitis was shown to be one of the best characterized models for acute pancreatitis. High doses of cerulein induce a dysregulation of the digestive enzyme production and cytoplasmic vacuolization and the death of acinar cells, edema formation, and an infiltration of inflammatory cells into the pancreas, which are similar symptoms shown in human acute pancreatitis. The present study aims to determine the differentially expressed proteins in cerulein-treated pancreatic acinar cells as an in vitro model for acute pancreatitis. Pancreatic acinar AR42J cells were treated with 10(-8) M cerulein for 24 h. The changed protein patterns separated by two-dimensional electrophoresis using pH gradients of 5-8 were conclusively identified by matrix-assisted laser desorption/ionization-time of flight mass spectrometry analysis of the peptide digests. Five differentially expressed proteins (heat shock protein 90, mitochondrial ATP synthase beta chain precursor, tubulin beta chain, 3-mercaptopyruvate sulfurtransferase, mitochondrial ATP synthase subunit D) were identified in cerulein-treated AR42J cells. These proteins are related to cellular stress such as reactive oxygen species, cytoskeletal function, and cell signaling. In conclusion, the differentially expressed proteins will provide valuable information to understand the pathophysiologic mechanism of acute pancreatitis and may be useful for prognostic indices of acute pancreatitis.

Background: Despite the superiority of non-HDL cholesterol (non-HDL-C) and apolipoprotein B (ApoB) as lipid markers for atherosclerotic cardiovascular disease (ASCVD), these are only suitable as secondary markers. We compared LDL cholesterol (LDL-C), non-HDL-C, and ApoB concentrations with respect to the occurrence of cardiovascular disease in adults enrolled in the Korean Genome and Epidemiology Study (KoGES).Methods: We used information on age; sex; medical history; family history of ASCVD; current lipid-lowering therapy; current smoking status; and creatinine, total cholesterol, HDL-C, LDL-C, triglyceride, and ApoB concentrations from 5,872 KoGES participants without ASCVD. New ASCVD development was monitored during the 8-year follow-up period. Adjusted hazard ratios (aHRs) for ASCVD of LDL-C, non-HDL-C, and ApoB concentrations were calculated based on the multivariate Cox regression analyses. The participants were also grouped as low and high according to the median values for each lipid marker, and calculated aHRs of each group combined by two lipid makers.Results: ApoB showed the highest aHR per 1-SD for ASCVD (1.26; 95% confidence interval [CI], 1.11-1.43), followed by non-HDL-C (1.25; 95% CI, 1.11-1.41) and LDL-C (1.20; 95% CI, 1.06-1.37). The group with low LDL-C and high ApoB concentrations had a significantly higher aHR for ASCVD (1.61; 95% CI, 1.05-2.48) compared to the reference group values (low LDL-C and low ApoB concentrations). The aHR for the group with high LDL-C and low ApoB concentrations was not significant (1.30; 95% CI, 0.79-2.16).Conclusions: ApoB, non-HDL-C, and LDL-C are independent risk factors for ASCVD. Increases in the aHR per 1-SD for ASCVD were more strongly affected by ApoB, followed by non-HDL-C and LDL-C. Participants with low LDL-C and high ApoB concentrations showed increased ASCVD risk. For individuals with ASCVD risk factors, even those presenting normal LDL-C concentrations, measuring ApoB concentrations can provide useful information for better evaluation of ASCVD risk.

Mitochondrion is a vulnerable intracellular target to reactive oxygen species (ROS). ROS have been considered to be important regulators of the pathogenesis of pancreatitis. This study aims to determine whether ROS induces mitochondrial damage by monitoring the expression level of mitochondrial ATP synthase as the key molecular component in mitochondria associated with cellular damage. Pancreatic acinar AR42J cells were treated with cerulein which induces symptoms similar to that associated with human acute pancreatitis. Proteins were separated by two-dimensional electrophoresis using pH gradients of 5-8 and identified using matrix-assisted laser desorption/ionization time-of-flight mass spectrometer (MS), quadrupole time-of-flight MS and MS/MS with nano-electrospray. Following cerulein treatment, mitochondrial ATP synthase beta chain was highly expressed compared to nontreated cell. The protein was identified by its pI of 5.2 and molecular weight (56 354 Da) with 27 matched peptides. Among the MS spectrum, precursor ions m/z 488.28, 544.81, 631.82, 693.34, 718.38, 729.41, 801.40, 809.39, 825.94, and 994.52 were further identified using MS/MS and confirmed the isolated protein to be mitochondrial ATP synthase beta chain. In conclusion, cerulein-induced oxidative injury may result in the induction of mitochondrial ATP synthase, which may act as an adaptive pathophysiological process in the pancreas.

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Background: Fusobacterium species are obligately anaerobic, gram-negative bacilli. Especially, F. nucleatum and F. necrophorum are highly relevant human pathogens. We investigated clinical differences in patients infected with Fusobacterium spp. and determined the antimicrobial susceptibility of Fusobacterium isolates.Methods: We collected clinical data of 86 patients from whom Fusobacterium spp. were isolated from clinical specimens at a tertiary-care hospital in Korea between 2003 and 2020. In total, 76 non-duplicated Fusobacterium isolates were selected for antimicrobial susceptibility testing by the agar dilution method, according to the Clinical and Laboratory Standards Institute guidelines (M11-A9).Results: F. nucleatum was most frequently isolated from blood cultures and was associated with hematologic malignancy, whereas F. necrophorum was mostly prevalent in head and neck infections. Anti-anaerobic agents were more commonly used to treat F. nucleatum and F. varium infections than to treat F. necrophorum infections. We observed no significant difference in mortality between patients infected with these species. All F. nucleatum and F. necrophorum isolates were susceptible to the antimicrobial agents tested. F. varium was resistant to clindamycin (48%) and moxifloxacin (24%), and F. mortiferum was resistant to penicillin G (22%) and ceftriaxone (67%). β-Lactamase activity was not detected.Conclusions: Despite the clinical differences among patients with clinically important Fusobacterium infections, there was no significant difference in the mortality rates. Some Fusobacterium spp. were resistant to penicillin G, ceftriaxone, clindamycin, or moxifloxacin. This study may provide clinically relevant data for implementing empirical treatment against Fusobacterium infections.