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Background/aim: Laparoscopic hepatectomy has become a common management strategy for liver tumors owing to its less invasive nature and enhanced visual perspective. Yet, its use in the caudate lobe poses challenges. This study evaluates the experiences of patients who underwent laparoscopic hepatectomy for hepatic tumors in the caudate lobe and aims to propose strategies for performing such procedures. Methods: We retrospectively analyzed the clinical data of twelve patients who underwent laparoscopic hepatic caudate lobe resection at the Department of Hepatopancreatobiliary Surgery, Second Affiliated Hospital of Kunming Medical University. Results: All twelve laparoscopic procedures were successful, with none requiring conversion to open surgery. The surgical methods varied: five cases involved simple resection of the Spiegel lobe, one case involved total caudate lobe resection, three cases involved paravena cava lobe resection, and three cases involved resection of the caudate process. The operation time ranged from 49 to 319 min (mean, 219 min). Intraoperative blood loss ranged from 20 to 500 ml, averaging 194 ml. No patients needed blood transfusions during or after the operation, and there were no instances of postoperative bleeding, bile leakage, or abdominal infection. Conclusion: Given adequate control of hepatic inflow, sufficient exposure to the surgical field, and an appropriate approach, laparoscopic hepatectomy in the caudate lobe could potentially become a standard surgical technique. [ABSTRACT FROM AUTHOR]

Background: Acute kidney injury (AKI) is a frequent syndrome in the intensive care unit (ICU). AKI patients with kidney function recovery have better short-term and long-term prognoses compared with those with non-recovery. Numerous studies focus on biomarkers to distinguish them. To better understand the predictive performance of urinary biomarkers of renal recovery in patients with AKI, we evaluated C–C motif chemokine ligand 14 (CCL14) and two first-generation biomarkers (cell cycle arrest biomarkers and neutrophil gelatinase-associated lipocalin) in two ICU settings. Methods: We performed a prospective study to analyze urinary biomarkers for predicting renal recovery from AKI. Patients who developed AKI after ICU admission were enrolled and urinary biomarkers including tissue inhibitor of metalloproteinase-2 (TIMP-2), insulin-like growth factor-binding protein 7 (IGFBP7), CCL14, and neutrophil gelatinase-associated lipocalin (NGAL) were detected on the day of AKI diagnosis. The primary endpoint was non-recovery from AKI within 7 days. The individual discriminative ability of CCL14, [TIMP-2] × [IGFBP7] and NGAL to predict renal non-recovery were evaluated by the area under receiver operating characteristics curve (AUC). Results: Of 164 AKI patients, 64 (39.0%) failed to recover from AKI onset. CCL14 showed a fair prediction ability for renal non-recovery with an AUC of 0.71 (95% CI 0.63–0.77, p < 0.001). [TIMP-2] × [IGFBP7] showed the best prediction for renal non-recovery with an AUC of 0.78 (95% CI 0.71–0.84, p < 0.001). However, NGAL had no use in predicting non-recovery with an AUC of 0.53 (95% CI 0.45–0.60, p = 0.562). A two-parameter model (non-renal SOFA score and AKI stage) predicted renal non-recovery with an AUC of 0.77 (95% CI 0.77–0.83, p = 0.004). When [TIMP-2] × [IGFBP7] was combined with the clinical factors, the AUC was significantly improved to 0.82 (95% CI 0.74–0.87, p = 0.049). Conclusions: Urinary CCL14 and [TIMP-2] × [IGFBP7] were fair predictors of renal non-recovery from AKI. Combing urinary [TIMP-2] × [IGFBP7] with a clinical model consisting of non-renal SOFA score and AKI stage enhanced the predictive power for renal non-recovery. Urinary CCL14 showed no significant advantage in predicting renal non-recovery compared to [TIMP-2] × [IGFBP7]. [ABSTRACT FROM AUTHOR]

Aim: To evaluate the antimicrobial and antibiofilm effects of chelerythrine (CHE) against carbapenem-resistant Serratia marcescens (CRSM). Materials and Methods: The minimum inhibitory concentration (MIC) of CHE against CRSM was determined using the agar dilution method. Changes in intracellular adenosine triphosphate (ATP) concentration, intracellular pH, cell membrane potential, and cell membrane integrity were investigated to assess the influence of CHE on the cell membrane. The effects of CHE on cell morphology were observed by field emission scanning electron microscopy (FESEM) and transmission electron microscopy. The antibiofilm formation of CHE was measured by crystal violet staining and visualized with confocal laser scanning microscopy (CLSM) and FESEM. The influence of CHE on biofilm components was further investigated using CLSM specific combined with double-dyeing methods. Results: Our results showed that CHE had an MIC at 125 μg/mL against CRSM was capable of inhibiting the growth of CRSM and destroying its cell membrane integrity, as well as obviously changing the cell morphology. Sub-MIC CHE displayed robust inhibitory effects against CRSM biofilm formation by mediating the production of biofilm components. In addition, CLSM- and FESEM-mediated evaluation of the damage of biofilm cells and biofilm persistence revealed that at high concentrations, CHE could compromise the cells within biofilms and remove preformed biofilms. Conclusion: CHE shows promise as a natural antimicrobial substance against biofilm-positive CRSM, with the potential to serve as an alternative therapeutic agent. [ABSTRACT FROM AUTHOR]

6‐Cyano‐7‐aminoquinoline (6CN−7AQ) and 3‐cyano‐7‐aminoquinoline (3CN−7AQ) were synthesized and found to exhibit intense emission with quantum yield as high as 63 % and 85 %, respectively, in water. Conversely, their derivatives 6‐cyano‐7‐azidoquinoline (6CN−7N3Q) and 3‐cyano‐7‐azidoquinoline (3CN−7N3Q) show virtually no emission, which makes them suitable to be used as recognition agents in azide reactions based on fluorescence recovery. Moreover, conjugation of 6CN−7AQ with a hydrophobic biomembrane‐penetration peptide PFVYLI renders a nearly non‐emissive 6CN−7AQ‐PFVYLI composite, which can be digested by proteinase K, recovering the highly emissive 6CN−7AQ with ∼200‐fold enhancement. The result provides an effective early confirmation for RT‐qPCR in viral detection. [ABSTRACT FROM AUTHOR]