Based on the theory of cancer-toxin pathogenesis， this article proposes that cancer toxin persists throughout the entire course of colorectal cancer （CRC）， with spleen qi depletion as the root of disease and damp-heat and stasis toxin as key factors in the evolution of pathogenesis. It further explores the intrinsic relationship between these pathogenetic features and the modern pathological process of "inflammasome pre-activation/repeated activation/gasdermin D-mediated pyroptotic microenvironmental imbalance". Spleen qi depletion is regarded as an upstream pathological basis for inflammasome pre-activation， while damp-heat and stasis toxin are considered key drivers of repeated inflammasome activation， the gasdermin D-mediated amplification of pyroptotic inflammation， and persistent microenvironmental imbalance. These two pathogenetic aspects interact sequentially and concurrently， jointly contributing to the early development and progression of CRC. Guided by the principle of anti-cancer and detoxification， and based on the traditional Chinese medicine （TCM） treatment strategy of simultaneously fortifying the spleen and replenishing qi， clearing and resolving damp-heat， and resolving stasis and toxins， this study further elucidates the modern mechanistic connotations of how these relevant therapies intervene in the gasdermin D-mediated pyroptotic microenvironment imbalance in CRC. The ultimate aim is to provide a theoretical basis for the modern scientific interpretation of cancer-toxin pathogenesis and the clinical syndrome differentiation and treatment of CRC.

Based on the theory of cancer-toxin pathogenesis， this article proposes that cancer toxin persists throughout the entire course of colorectal cancer （CRC）， with spleen qi depletion as the root of disease and damp-heat and stasis toxin as key factors in the evolution of pathogenesis. It further explores the intrinsic relationship between these pathogenetic features and the modern pathological process of "inflammasome pre-activation/repeated activation/gasdermin D-mediated pyroptotic microenvironmental imbalance". Spleen qi depletion is regarded as an upstream pathological basis for inflammasome pre-activation， while damp-heat and stasis toxin are considered key drivers of repeated inflammasome activation， the gasdermin D-mediated amplification of pyroptotic inflammation， and persistent microenvironmental imbalance. These two pathogenetic aspects interact sequentially and concurrently， jointly contributing to the early development and progression of CRC. Guided by the principle of anti-cancer and detoxification， and based on the traditional Chinese medicine （TCM） treatment strategy of simultaneously fortifying the spleen and replenishing qi， clearing and resolving damp-heat， and resolving stasis and toxins， this study further elucidates the modern mechanistic connotations of how these relevant therapies intervene in the gasdermin D-mediated pyroptotic microenvironment imbalance in CRC. The ultimate aim is to provide a theoretical basis for the modern scientific interpretation of cancer-toxin pathogenesis and the clinical syndrome differentiation and treatment of CRC.

Objective To investigate the effect of sufentanil postconditioning on acute lung in-jury induced by ischemia-reperfusion of uterine in rats.Methods Fourty-five adult female Sprague-Dawley rats were randomly divided into 3 groups(n = 1 5 each):control group (group C),ischemia-reperfusion group (group IR)and sufentanil postconditioning group(group SPC).Group SPC received sufentanil 10 μg/kg via intraperitoneal injection before inducing reperfusion of uterine.Ischemia-reper-fusion of uterine was produced by occlusion of bilateral uterine arteries for 45 min followed by reper-fusion for 2 h in group IR and group SPC.Then the content of tumor necrosis factor-α(TNF-α),mal-odiadehyde (MDA)and superoxide dismutase (SOD)activity were measured in uterus,serum and lung tissue,lung wet to dry weight ratio (W/D),lung permeability index (LPI)were compared. Results Compared with group C,TNF-α,MDA content,W/D and LPI in uterus,serum and lung tissue were significantly increased in group IR and group SPC(P <0.05).TNF-α,MDA content,W/D and LPI in uterus,serum and lung tissue were significantly attenuated in group SPC as compared with group IR (P <0.05 ).Compared with group C,SOD activity in uterus,serum and lung tissue was significantly attenuated in group IR and group SPC (P <0.05).SOD in uterus,serum and lung tissue were significantly increased in group SPC as compared with group IR (P < 0.05 ). Conclusion Sufentanil postconditioning attenuates pulmonary injury caused by ischemia-reperfusion of uterine in rats by inhibiting the inflammatory reaction and suppressing the activation of oxyradical.

Objective To investigate the role of Clara cells in lung ischemia-reperfusion (I/R) injury in rabbits.Methods Twenty-four healthy 10-12 month old rabbits of either sex weighing 1.5-2.0 kg were randomly divided into 3 groups ( n = 8 each) ; group A sham operation (group S) ; group B lung I/R and group C Clara cell elimination+ lung I/R. The animals were anesthetized with iv pentobarbital 30 mg/kg , tracheostomized and mechanically ventilated. In group B and C lung I/R was induced by clamping the left hilum of lung for 60 min followed by 120 min repeffusion. In group C Clara ceils were eliminated by ventilating the lungs with 89.28 mg/m2 naphthalin vapor for 12 h before lung I/R. The animals were killed by iv KCI at the end of 120 min reperfusion after lung isehemia. The left lung was immediately removed for microscopic examination, determination of W/D lung weight ratio and serum TNF-α level and MDA content. The percentage of neutrophi] in bronchoalveolar lavage fluid (BALF) was detected as index of lung injury. The expression of Clara cell secreting protein (CCSP) in the lung was detected by immuno-histoebemistry to indicate the number and distribution of Clara cells in the lung.Results Microscopic examination showed that there were severe leukocyte infiltration in alveolar spaces, alveolar edema and destroyed alveolar structure in group B and C. The serum TNF-u leve],W/D ratio and MDA content in the left lung and neutrophil percentage and WBC counts in BALF were significantly higher in group C than in group B. Conclusion Clara cells can protect the lungs against I/R injury through inhibiting inflammatory responses.

Objective: To optimize matrix composition and technology for Jiefushuang Emulsion. Methods: Orthogonal design was used, oil phase, agitation velocity, emulsifiers and emulsify temperature were selected as variable factors. Results: The optimum matrix composition and technology were: The ratio of oil to water was 2∶3, emulsifiers: 320g(oil 500mL), HLB: 15, emulsity temperature: 70?C , agitation velocity: 800 revolutions per minute, lasting for 20 minutes. Conclusion: The emulsion prepared accords with the stipulation of the appendix of Chinese pharmacopoeia (2000).