A bibliometric and visualized analysis of liver fibrosis from 2002 to 2022.

Fibrosis of the liver is a degenerative alteration that occurs in the majority of chronic liver disorders. Further progression can lead to cirrhosis, liver failure, and hepatocellular carcinoma, which can seriously affect the health and lives of patients. The field of liver fibrosis research has flourished in the last 20 years, with approximately 9000 articles retrieved from the Web of Science Core Collection database alone. In order to identify future research hotspots and potential paths in a thorough and scientifically reliable manner, it is important to organize and visualize the research on this topic from a holistic and very general perspective. This study used bibliometric analysis with CiteSpace and VOSviewer software to provide a quantitative analysis, hotspot mining, and commentary of articles published in the field of liver fibrosis over the last 20 years. This bibliometric analysis contains a total of 8994 articles with 45667 authors from 6872 institutions in 97 countries, published in 1371 journals and citing 156 309 references. The literature volume has steadily increased over the last 20 years. Research has focused on gastroenterology and hepatology, pharmacology and pharmacy, and medicine, research, and experimental areas. We found that the pathological mechanisms, diagnostic and quantitative methods, etiology, and antifibrotic strategies constitute the knowledge structure of liver fibrosis. Finding mechanisms for liver fibrosis regression, identifying precise noninvasive diagnostic and prognostic biomarkers, and creating efficient liver fibrosis patient treatments are the main goals of current research.

Develop adult extrapolation to pediatrics and pediatric dose optimization based on the physiological pharmacokinetic model of azithromycin.

Physiologically-based pharmacokinetic (PBPK) models are more frequently used for supporting pediatric dose selection in small-molecule drugs. Through literature research, drug parameters of azithromycin and clinical data from different studies were obtained. Through parameter optimization of the absorption and dissolution process, the adult intravenous model was extended to the adult oral model. The adult intravenous and oral PBPK models are precise to meet the AAFE<2 standard, and the pharmacokinetic parameters of the predicted values of the model are all within the mean standard deviation of the clinical observations. The values of plasma protein unbound fraction, renal clearance, and gastric juice pH between adults and pediatrics were changed by using the age-dependent pediatric organ maturity formula, and the adult model was extrapolated to the pediatric model. The final developed pediatric PBPK model was used to evaluate optimal dosing for children of different developmental ages. The relationship between the frist dose and age was as follows: 8.8 mg/kg/day from 0.5 to 2 years old, 9.2 mg/kg/day from 3 to 6 years old, 9.4 mg/kg/day from 7 to 12 years old, and 8.2 mg/kg/day from 13 to 18 years old, taken in half for 2-5 days. Simultaneously, the simulated exposures achieved with the dosing regimen proposed were comparable to adult plasma exposures for treatment of community-acquired pneumonia. A reasonable azithromycin pharmacokinetic-pharmacodynamic model for adults and pediatrics has been established, which can be demonstrated by the use of literature pediatric data to develop pediatric PBPK models, expanding the scope of this powerful modeling tool.

Genomic characterization of IncpA1763-KPC: IncFIIK7 type plasmids p13294-KPC and pA1966-NR from Klebsiella pneumoniae.

Aim: To characterize two plasmids p13294-KPC and pA1966-NR from clinical Klebsiella pneumoniae strains. Materials & methods: Plasmids p13294-KPC and pA1966-NR were fully sequenced and then detailed genomic analysis was performed in this work. The antimicrobial resistance phenotypes were determined. Results: p13294-KPC and pA1966-NR displayed IncpA1763-KPC:IncFIIK7 dual-replicon structures. The backbone of these two plasmids were closely related to each other. p13294-KPC contained two accessory modules, namely ΔISKpn25 and blaKPC-2 region, and the blaKPC-2 region carried a range of mobile elements and resistance gene blaKPC-2. while pA1966-NR contained four individual IS elements in its backbone and carried no resistance genes. Conclusion: This study provided a deeper insight into the genomic characterization of IncpA1763-KPC: IncFIIK7 type plasmids p13294-KPC and pA1966-NR.

[An observation of repair of burn wound with consanguineous skin pretreated with Tripterygium wilfordii].

OBJECTIVE: To explore new source of skin for burn wound coverage. METHODS: Split-thickness consanguineous skin was harvested from New Zealand white rabbit and was soaked in 200 g/L of multi-peptides of Tripterygium wilfordii, 50 g/L of dexamethasonel, on 9 g/L of normal saline solution for 15 - 30 mins, respectively. The consanguineous skin was thereafter grafted onto the whole layer skin defects in filial generation of rabbits with non-consanguineous skin as the control. The survival time and rejection of the grafted skin was observed. RESULTS: The rejection appeared evidently less intense and survived significantly longer (43 +/- 3.5 days) when the consanguineous skin was pretreated by Tripterygium wilfordii. However the grafted consanguineous skin survived for 30 +/- 2.5 days when it was pretreated by dexamethasone. The grafted skin was quickly rejected and survived only for 11 +/- 1.6 days when the skin was pretreated by normal saline or the skin was non-consanguineous. CONCLUSION: Consanguineous skin possessed partial compatibility with the recipient due to similar antigen, which was beneficial to the its survival, especially after the skin was pretreated.