Z. Zhang

Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease caused by non-excessive alcohol consumption and is the most common cause of elevated levels of serum liver enzymes. We examined changes in adiponectin (APN) and tumor necrosis factor-α (TNF-α) in type 2 diabetes mellitus (T2DM) complicated by NAFLD and their relationships with insulin resistance (IR). Forty-two T2DM, 39 NAFLD, and 45 T2DM complicated with NAFLD (complicated group) patients were enrolled in this study. Body mass index, fasting blood plasma glucose (FPG), fasting insulin, triglyceride (TG), alanine aminotransferase, gamma-glutamyl transpeptidase, APN, TNF-α, and homeostasis model of assessment (HOMA)-IR were determined. The degree of fatty liver was graded according to liver/spleen computed tomography ratio and intrahepatic vessel manifestations. Compared with the T2DM and NAFLD groups, fasting blood plasma glucose, alanine aminotransferase, gamma-glutamyl transpeptidase, TG, TNF-α, and HOMA-IR in the complicated group were significantly increased, while APN was significantly reduced. Body mass index in the complicated group was significantly higher than in the T2DM group. The complicated group was prone to severe fatty liver compared with the NAFLD group. APN was negatively correlated with body mass index, fasting blood plasma glucose, TG, TNF-α, and HOMA-IR. TNF-α was negatively correlated with APN, but positively correlated with FPG, fasting insulin, TG, and HOMA-IR. The complicated group had clear IR. A more severe degree of fatty liver was associated with higher HOMA-IR and TNF-α and lower APN. APN was an important factor for antagonizing inflammation and mitigating IR.

"Simultaneous HPLC-DAD analysis of five flavonoids in diabetic rat plasma and its application in the study of pharmacokinetics" published on 01 Sep 2009 by Akadémiai Kiadó, co-published with Springer Science+Business Media B.V., Formerly Kluwer Academic Publishers B.V..

Redirecting endogenous antibodies toward tumor cells through rationally designed antibody-recruiting molecules (ARMs) has emerged as a promising strategy in cancer immunotherapy. However, current ARMs face inherent limitations, as they primarily depend on hapten-specific antibodies, which exhibit heterogeneity across populations and exist at suboptimal physiological concentrations. In this study, we explored the feasibility of leveraging Hepatitis B virus (HBV) vaccine-induced anti-HBV surface antigen (HBsAg) antibodies for cancer therapy. We developed a series of nanobody-peptide conjugates comprising an EGFR-targeting nanobody covalently linked to the LOOP2 peptide─an immunodominant epitope of HBsAg, through varying-length PEG spacers. The results demonstrated that these conjugates were capable of recruiting vaccine-induced anti-HBsAg antibodies onto the cancer cell surface and evoking potent antibody-dependent cell-mediated phagocytosis (ADCP) and complement-dependent cytotoxicity (CDC) for cell elimination. Interestingly, structure-activity relationship studies revealed that the PEG spacer had a minimal impact on ADCP efficacy, while it significantly affected CDC function. This proof-of-concept study establishes a novel paradigm for ARM-based therapeutics that leverages population-wide immunity from routine vaccination programs, thereby circumventing key limitations associated with the hapten-dependent system.