Objective To evaluate the clinical value of serum procalcitonin (PCT) in the diagnosis of bacte-rial infections in the critically ill patients. Methods A loud d 100 cases of critical patients were divided into bacteri-al infection group(56 cases) and non-bacterial infection group(44 cases). Serum PCT was measured by immunolu-minometric assay. Results The concentration of PCT in bacterial infection group(21.54 ±5.72) μg/L, was signifi-cantly higher than non-bacterial infection group (11. 95±4. 58)μg/L (t =2.291,P<0.05);The APACHE Ⅲ score of bacterial infection group(62. 44 ± 19. 55) cent was significantly higher than non-bacterial infection group(44. 56 ± 25. 88) cent(t = 2. 195 ,P < 0. 05). The concentration of PCT of 1.0μg/L and 2. 0 p.g/L compared to the former sensitivity (96. 5) % higher than the latter (55.2) % (X2 = 3. 94, P < 0. 05), the former specificity (41.7) % lower than the latter (95.8)% (X2 = 4. 02 ,P < 0. 05);1.5μg/L as a positive standard Youden index and the Agreement (83.0 % ,0. 65), were significantly higher than 1 μg/L and 2 μg/L(71.7%, 0. 38 ;73.6% ,0. 51) (X2 = 3.84, X2=3. 90,X2 = 3.992 = 3.91 ,P < 0. 05);The concentration of PCT in death group (38. 9 ±12. 6)μg/L was signifi-canfly higher than the survival group(11.8± 8. 3) μg/L(t =2. 398 ,P <0. 05). Conclusion Serum PCT has clinical values in the diagnosis and therapy of bacterial infections in the critical patients.

OBJECTIVETo compare the effects of different approaches to establishing rat models of acute liver failure (ALF).

METHODSSixty-eight Sprague-Dawley rats were randomly divided into 3 groups for establishing ALF models using 3 different approaches, namely conventional hepatectomy for resecting 90% liver tissue as described by Higgins and Anderson, modified bloodless hepatectomy for resecting 90% liver tissue, and intraperitoneal injections of 700 mg/kg D-galactosamine (D-gal) and 5 µg/kg lipopolysaccharide (LPS). The mortality of the rats due to postoperative bleeding and survival rate at 7 days after the surgery were recorded. The levels of alanine aminotransferase (ALT), total bilimbin (Tbil), albumin (ALB), NH3, glucose (Glu) and prothrombin time (PT) were monitored, and histopathologies of the liver were examined at 24 and 72 h after the surgery.

RESULTSThe mortality rate due to postoperative bleeding was higher in conventional hepatectomy group than in the modified surgical group (15% vs 0). The survival rate at 7 days was 25%, 0%, 15% in conventional surgical group, modified surgical group and drug injection group, respectively. In the latter two groups, significant changes of ALT, Tbil, ALB, NH3, Glu, and PT were recorded at 24 and 72 h after the modeling (P<0.05), and these changes were the most obvious at 24 h in modified surgical group and at 72 h in the drug injection group; ALB in both groups declined to the lowest at 7 days and then increased gradually. Liver cell degeneration and necrosis were found in modified surgical group and drug injection group at 24 h and 72 h after the modeling.

CONCLUSIONBoth the modified 90% bloodless hepatectomy and injections of D-gal and LPS can be used to establish ideal rat models of ALF to suit different ALF-related researches.

Animals ; Disease Models, Animal ; Galactosamine ; adverse effects ; Hepatectomy ; Injections, Intraperitoneal ; Lipopolysaccharides ; adverse effects ; Liver Failure, Acute ; chemically induced ; pathology ; Rats ; Rats, Sprague-Dawley

Duchenne muscular dystrophy (DMD) is a severe X-linked recessive genetic disorder caused by mutations in the DMD gene, making it one of the most common forms of hereditary muscular dystrophy. The DMD gene, which encodes dystrophin, is the largest known gene in the human genome. Mutations in the DMD gene are highly diverse, including exon deletions, duplications, point mutations, and small insertions or deletions, posing significant challenges for treatment. Currently, there is no cure for DMD, and existing treatment strategies focus primarily on symptom management, which cannot reverse or halt disease progression. Advances in biotechnology position nucleic acid drugs and gene therapies at the forefront of DMD treatment research. These treatments aim to restore dystrophin expression by repairing or replacing mutated genes, thereby improving muscle function or slowing muscle degeneration. Preclinical studies in animal models and early-phase clinical trials demonstrate promising efficacy and offer new hope for DMD patients. This review briefly outlines the pathological mechanisms and genetic characteristics of DMD before delving into recent progress in therapeutic strategies, with a particular focus on nucleic acid drugs (including antisense oligonucleotides for exon skipping therapy and translation readthrough inducers) and gene therapy approaches (including gene replacement therapy and gene editing). The development and application of these therapies not only provide new treatment options for DMD patients, but also offer valuable insights for addressing other genetic disorders. However, numerous challenges impede the clinical translation of DMD treatments. Future studies must optimize existing therapeutic strategies, improve their efficacy and applicability, and explore innovative approaches to deliver more effective and sustainable treatments for DMD patients.