Objective To explore the hemostatic effect of a novel mammalian-derived bioadhesive in partial liver resection in rats.Methods The model of the left lateral lobectomy in SD rats established earlier was used in this study.The rats were divided into model group,test group and positive control group,with 10 rats in each group.The novel mammalian-derived bioadhesive and porcine fibrin sealant were sprayed on the wound in the test group and positive control group,respectively.The hemostatic effect was evaluated by calculating the amount and time of bleeding.Results Compared with the model group[(504.6±190.0)s,(194.4±144.2)mg],the bleeding time[(96.1±26.4)s,(4.8±17.8)mg]and the amount of bleeding[(156.7±139.3)s,(47.8±121.3)mg]were significantly shortened in the test group and positive control group(P<0.01).There was no significant difference in the bleeding time and the amount of bleeding between the positive control group and test group(P>0.05).Conclusion The novel mammalian-derived bioadhesive can reduce bleeding and shorten bleeding time in rat models with partial liver resection.In clinical practice,it can reduce hemostatic procedures,thereby shortening the surgical time and achieving the goal of sealing and hemostasis

Immunotherapy combined with effective therapeutics such as chemotherapy and photodynamic therapy have been shown to be a successful strategy to activate anti-tumor immune responses for improved anticancer treatment. However, developing multifunctional biodegradable, biocompatible, low-toxic but highly efficient, and clinically available transformed nano-immunostimulants remains a challenge and is in great demand. Herein, we report and design of a novel carrier-free photo-chemotherapeutic nano-prodrug COS-BA/Ce6 NPs by combining three multifunctional components-a self-assembled natural small molecule betulinic acid (BA), a water-soluble chitosan oligosaccharide (COS), and a low toxic photosensitizer chlorin e6 (Ce6)-to augment the antitumor efficacy of the immune adjuvant anti-PD-L1-mediated cancer immunotherapy. We show that the designed nanodrugs harbored a smart and distinctive "dormancy" characteristic in chemotherapeutic effect with desired lower cytotoxicity, and multiple favorable therapeutic features including improved ¹O₂ generation induced by the reduced energy gap of Ce6, pH-responsiveness, good biodegradability, and biocompatibility, ensuring a highly efficient, synergistic photochemotherapy. Moreover, when combined with anti-PD-L1 therapy, both nano-coassembly based chemotherapy and chemotherapy/photodynamic therapy (PDT) could effectively activate antitumor immunity when treating primary or distant tumors, opening up potentially attractive possibilities for clinical immunotherapy.

Lung cancer is one of the most lethal malignancies in the world, with non-small cell lung cancer (NSCLC) accounting for approximately 80%-85% of all pathological types. Approximately 30%-55% of NSCLC patients develop brain metastases. It has been reported that 5%-6% of patients with brain metastases harbor anaplastic lymphoma kinase (ALK) fusion. ALK-positive NSCLC patients have shown significant therapeutic benefits after treatment with ALK inhibitors. Over the past decade, ALK inhibitors have rapidly evolved and now exist in three generations: first-generation drugs such as Crizotinib; second-generation drugs including Alectinib, Brigatinib, Ceritinib, and Ensartinib; and third-generation drugs like Lorlatinib. These drugs have exhibited varying efficacy in treating brain metastases in ALK-positive NSCLC patients. However, the numerous options available for ALK inhibition present a challenge for clinical decision-making. Therefore, this review aims to provide clinical guidance by summarizing the efficacy and safety of ALK inhibitors in treating NSCLC brain metastases.
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Humans ; Carcinoma, Non-Small-Cell Lung/drug therapy* ; Lung Neoplasms/drug therapy* ; Brain Neoplasms/drug therapy* ; Protein Kinase Inhibitors/adverse effects* ; Crizotinib

Objective To elucidate the effect of hydroxysafflor yellow A (HYSA) on the proliferation of vascular smooth muscle cells (VSMCs) and the related mechanism.Methods VSMCs derived from SD rats were treated with DMEC culture medium (Control),10 ng/ml PDGF (PDGF group),pretreatment with HYSA at different doses (1,5,10,20,40,60 μmol/L) for 24 h then cotreatment with PDGF.After 24 h,MTT assay,Western blot and immunohistochemical staining were performed to evaluate the inhibitory effects of HYSA on VSMCs proliferation.Results HYSA inhibited PDGF induced VSMCs proliferation in a dose-dependent manner,dowregulated proliferating cell nuclear antigen (PCNA) expression and blocked PDGF activated PDGFR-MEK-ERK1/2 signaling pathway.Conclusions HYSA inhibits VSMCs proliferation possibly via downregulating the expression of PCNA and blocking MEK-ERK1/2 signal transduction in VSMCs.