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BackgroundSerum albumin and prealbumin are both negative acute-phase reactants, and usually at low levels in stress. We aim to determine their predictive values for poor outcome of traumatic brain injury (TBI).MethodsA total of 326 patients of TBI were enrolled and followed-up by telephone 6 months after discharge. They were divided into a favorable group (GOS: 3 to 5) and an unfavorable group (GOS: 1 to 2). Serum albumin and prealbumin were measured from vein blood within 24 h after admission.ResultsNinety one (27.9%) patients were with poor outcome (GOS: 1 to 2). The unfavorable group had lower albumin and prealbumin (P<0.001). Albumin and prealbumin were both positively correlated with GCS (r = 0.489, P<0.001; r = 0.222, P<0.001, respectively) and GOS (r = 0.518, P<0.001; r = 0.314, P<0.001, respectively). After adjustment for confounding factors, the odds ratios of albumin and prealbumin were 0.866, 95% CI: 0.829 to 0.904 and 0.990, 95% CI: 0.985 to 0.995, respectively. In subgroup of GCS≤8 (n = 101), the crude and adjusted odds ratios of serum albumin were both statistically significant (P = 0.027, P = 0.033, respectively), while prealbumin were not (P = 0.553, P = 0.576, respectively). The AUC of albumin for predicting poor outcome was 0.762, 95% CI: 0.712 to 0.807, which was significantly higher than that of prealbumin (0.664, 95% CI: 0.610 to 0.715). In analyses of all patients and subgroup of GCS≤8, the AUCs of serum albumin were both significantly higher than those of prealbumin (P = 0.001, P = 0.045, respectively).ConclusionsBoth serum albumin and prealbumin could predict the poor outcome of TBI, but the former is much better, especially, in patients with severe TBI.

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Cantharidin (C(10)H(12)O(4)) is a monoterpene defensive toxin in insects involved in chemical defence as well as in courtship and mating behaviours. It is relatively well known in the medical literature because of its high anticancer activity and as an effective therapy for molluscum contagiosum. However, little is known about its biosynthesis pathway in vivo, and no enzyme involved in cantharidin biosynthesis has been identified. The purpose of this study was to identify the crucial enzyme that is involved in the biosynthesis of cantharidin. Using the homology cloning method, a 3-hydroxy-3-methyl glutaryl coenzyme A reductase (HMGR) gene, the rate-limiting enzyme in the mevalonate pathway, was cloned from the blister beetle Epicauta chinensis. Quantitative reverse transcription PCR and gas chromatography methods revealed that the HMGR transcripts had a positive correlation with cantharidin production in the beetles (R = 0.891). RNA interference (RNAi) knockdown of HMGR mRNA expression was achieved by microinjection of a specific double-stranded RNA with more than 90% RNAi efficiency, and an apparent decrease of cantharidin production was observed. Furthermore, the HMGR mRNA was greatly upregulated by exogenous juvenile hormone III (JH III), and cantharidin production was also raised in males; however, when injecting the JH III with RNAi of HMGR mRNA at the same time, cantharidin production did not rise. These results demonstrate that HMGR is an essential enzyme in cantharidin biosynthesis in the blister beetle E. chinensis, which further verifies previous research results demonstrating that cantharidin is synthesized de novo by the mevalonate pathway in blister beetles.

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Well-preserved molecular cargo in circulating extracellular vesicles (EVs) offers an ideal material for detecting oncogenic gene alterations in cancer patients, providing a noninvasive diagnostic solution for detection of disease status and monitoring treatment response. Therefore, technologies that conveniently isolate EVs with sufficient efficiency are desperately needed. Here, a lipid labeling and click chemistry-based EV capture platform ("Click Beads"), which is ideal for EV message ribonucleic acid (mRNA) assays due to its efficient, convenient, and rapid purification of EVs, enabling downstream molecular quantification using reverse transcription digital polymerase chain reaction (RT-dPCR) is described and demonstrated. Ewing sarcoma protein (EWS) gene rearrangements and kirsten rat sarcoma viral oncogene homolog (KRAS) gene mutation status are detected and quantified using EVs isolated by Click Beads and matched with those identified in biopsy specimens from Ewing sarcoma or pancreatic cancer patients. Moreover, the quantification of gene alterations can be used for monitoring treatment responses and disease progression.

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Background/Aims: Acute pancreatitis (AP) is an inflammatory disease characterized by acinar cell damage and inflammation of the pancreas with infiltration of leukocytes, predominantly neutrophils. We investigated whether neutrophil depletion protects against experimental AP induced by L-arginine. Methods: AP was induced in C57BL/6 mice via two intraperitoneal L-arginine (4 g/kg) injections. Mice were pretreated with 250 and 100 µg anti-Gr-1 antibody via intraperitoneal injection at 24 and 4 h, respectively, before L-arginine challenge for neutrophil depletion. At 48 and 72 h after injection, the severity of AP was determined with the aid of biochemical and histological analyses. Amylase and MPO activity was detected using specific assay kits. The plasma cytokines levels were detected using ELISA. Results: Neutrophil depletion resulted in significantly reduced plasma amylase levels in pancreas, myeloperoxidase (MPO) activity in pancreas and lung, reactive oxygen species (ROS) generation and cell apoptosis, and decreased circulating neutrophil, tissue damage as well as expression levels of nuclear factor NF-κB. Conclusion: Neutrophil depletion is capable of reducing tissue damage of pancreas and lung in mice with acute pancreatitis.