BACKGROUND:Open reduction and Kirschner wire tension band technique has been a traditional surgical method for the treatment of patela fracture. However, there stil exist some complications such as Kirschner wire slippage and breakage. Cable-Pin system is a new fixation device. A series of good clinical results has been achieved in patients with patela fracture using this fixation device through a minimaly invasive way. OBJECTIVE:To compare and investigate the clinical results of minimaly invasive fixation with Cable-Pin system and Kirschner wire tension band technique for patela fracture and the complications. METHODS:Eighty patients with radiology-confirmed transverse displacement of patela participated in this trial, and were randomly divided into two groups. Forty patients underwent a minimaly invasive technique and the others had conventional open surgery using Kirschner wire. At postoperative intervals of 1, 3, 6, 12, and 24 months, pain was measured by Visual Analogue Scale scores, range of motion was measured by goniometry, and knee function was evaluated using the Bostman clinical grading scale. RESULTS AND CONCLUSION: Easement of pain was better in the minimaly invasive surgery group than in the control group at 1 and 3 months after treatment (P < 0.05). Above dominance disappeared at 6 months after treatment. At 3-24 months, the knee flexion training was faster and flexion angle was greater in the minimaly invasive surgery group, and results were significantly better than in the control group (P < 0.05). The incidence of discomfort fixation-induced complications was lower in the minimaly invasive surgery group than in the conventional open surgery group (P < 0.05). These data confirm that after minimaly invasive fixation with Cable-Pin system, pain was noticeably lessened, range of motion of affected knee was great, the recovery of knee function was better, the incidence of complications was reduced, and the repair effect was better than the conventional Kirschner wire fixation.

As the most important visceral organ in human body for metabolism, the liver is an important place for the synthesis and storage of nutrients. Patients with acute-on-chronic liver failure suffer from varying degrees of malnutrition due to abnormal metabolism of various nutrients, and malnutrition might accelerate the development and progression of liver diseases and lead to poor prognosis. Therefore, it is of great importance to perform early nutritional assessment and nutritional intervention. Although there are a variety of nutritional assessment methods, there are still defects in the nutritional assessment methods for patients with chronic liver diseases and liver cirrhosis, especially those with acute-on-chronic liver failure. This article elaborates on the nutritional assessment and clinical management of such patients, so as to provide a reference for related issues in clinical practice.

BACKGROUND: Acute-on-chronic liver failure (ACLF) is a severe liver disease with complex pathogenesis. Clinical hypoglycemia is common in patients with ACLF and often predicts a worse prognosis. Accumulating evidence suggests that glucose metabolic disturbance, especially gluconeogenesis dysfunction, plays a critical role in the disease progression of ACLF. Lon protease-1 (LONP1) is a novel mediator of energy and glucose metabolism. However, whether gluconeogenesis is a potential mechanism through which LONP1 modulates ACLF remains unknown. METHODS: In this study, we collected liver tissues from ACLF patients, established an ACLF mouse model with carbon tetrachloride (CCl 4 ), lipopolysaccharide (LPS), and D-galactose (D-gal), and constructed an in vitro hypoxia and hyperammonemia-triggered hepatocyte injury model. LONP1 overexpression and knockdown adenovirus were used to assess the protective effect of LONP1 on liver injury and gluconeogenesis regulation. Liver histopathology, biochemical index, mitochondrial morphology, cell viability and apoptosis, and the expression and activity of key gluconeogenic enzymes were detected to explore the underlying protective mechanisms of LONP1 in ACLF. RESULTS: We found that LONP1 and the expressions of gluconeogenic enzymes were downregulated in clinical ACLF liver tissues. Furthermore, LONP1 overexpression remarkably attenuated liver injury, which was characterized by improved liver histopathological lesions and decreased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in ACLF mice. Moreover, mitochondrial morphology was improved upon overexpression of LONP1. Meanwhile, the expression and activity of the key gluconeogenic enzymes were restored by LONP1 overexpression. Similarly, the hepatoprotective effect was also observed in the hepatocyte injury model, as evidenced by improved cell viability, reduced cell apoptosis, and improved gluconeogenesis level and activity, while LONP1 knockdown worsened liver injury and gluconeogenesis disorders. CONCLUSION We demonstrated that gluconeogenesis dysfunction exists in ACLF, and LONP1 could ameliorate liver injury and improve gluconeogenic dysfunction, which would provide a promising therapeutic target for patients with ACLF.
Animals ; Humans ; Mice ; Acute-On-Chronic Liver Failure/pathology* ; ATP-Dependent Proteases/metabolism* ; Gluconeogenesis ; Hepatocytes/pathology* ; Liver/metabolism* ; Mitochondrial Proteins/metabolism* ; Protease La/metabolism*

BACKGROUND: The Global Leadership Initiative on Malnutrition (GLIM) criteria were published to build a global consensus on nutritional diagnosis. Reduced muscle mass is a phenotypic criterion with strong evidence to support its inclusion in the GLIM consensus criteria. However, there is no consensus regarding how to accurately measure and define reduced muscle mass in clinical settings. This study aimed to investigate the optimal reference values of skeletal muscle mass index for diagnosing sarcopenia and GLIM-defined malnutrition, as well as the prevalence of GLIM-defined malnutrition in hospitalized cirrhotic patients. METHODS: This retrospective study was conducted on 1002 adult patients with liver cirrhosis between January 1, 2018, and February 28, 2022, at Beijing You-An Hospital, Capital Medical University. Adult patients with a clinical diagnosis of liver cirrhosis and who underwent an abdominal computed tomography (CT) examination during hospitalization were included in the study. These patients were randomly divided into a modeling group (cohort 1, 667 patients) and a validation group (cohort 2, 335 patients). In cohort 1, optimal cut-off values of skeletal muscle index at the third lumbar skeletal muscle index (L3-SMI) were determined using receiver operating characteristic analyses against in-hospital mortality in different gender groups. Next, patients in cohort 2 were screened for nutritional risk using the Nutritional Risk Screening 2002 (NRS-2002), and malnutrition was diagnosed by GLIM criteria. Additionally, the reference values of reduced muscle mass in GLIM criteria were derived from the L3-SMI values from cohort 1. Multivariate logistic regression analysis was used to analyze the association between GLIM-defined malnutrition and clinical outcomes. RESULTS: The optimal cut-off values of L3-SMI were 39.50 cm 2 /m 2 for male patients and 33.06 cm 2 /m 2 for female patients. Based on the cut-off values, 31.63% (68/215) of the male patients and 23.3% (28/120) of the female patients had CT-determined sarcopenia in cohort 2. The prevalence of GLIM-defined malnutrition in cirrhotic patients was 34.3% (115/335) and GLIM-defined malnutrition was an independent risk factor for in-hospital mortality in patients with liver cirrhosis ( Wald = 6.347, P  = 0.012). CONCLUSIONS This study provided reference values for skeletal muscle mass index and the prevalence of GLIM-defined malnutrition in hospitalized patients with liver cirrhosis. These reference values will contribute to applying the GLIM criteria in cirrhotic patients.
Adult ; Female ; Humans ; Male ; Leadership ; Liver Cirrhosis ; Malnutrition/diagnosis* ; Nutritional Status ; Retrospective Studies ; Sarcopenia/diagnosis*

The widespread of tigecycline resistance gene tet(X4) has a serious impact on the clinical efficacy of tigecycline. The development of effective antibiotic adjuvants to combat the looming tigecycline resistance is needed. The synergistic activity between the natural compound β-thujaplicin and tigecycline in vitro was determined by the checkerboard broth microdilution assay and time-dependent killing curve. The mechanism underlining the synergistic effect between β-thujaplicin and tigecycline against tet(X4)-positive Escherichia coli was investigated by determining cell membrane permeability, bacterial intracellular reactive oxygen species (ROS) content, iron content, and tigecycline content. β-thujaplicin exhibited potentiation effect on tigecycline against tet(X4)-positive E. coli in vitro, and presented no significant hemolysis and cytotoxicity within the range of antibacterial concentrations. Mechanistic studies demonstrated that β-thujaplicin significantly increased the permeability of bacterial cell membranes, chelated bacterial intracellular iron, disrupted the iron homeostasis and significantly increased intracellular ROS level. The synergistic effect of β-thujaplicin and tigecycline was identified to be related to interfere with bacterial iron metabolism and facilitate bacterial cell membrane permeability. Our studies provided theoretical and practical data for the application of combined β-thujaplicin with tigecycline in the treatment of tet(X4)-positive E. coli infection.
Humans ; Tigecycline/pharmacology* ; Escherichia coli/metabolism* ; Reactive Oxygen Species/therapeutic use* ; Plasmids ; Anti-Bacterial Agents/metabolism* ; Escherichia coli Infections/microbiology* ; Bacteria/genetics* ; Microbial Sensitivity Tests