Sepsis remains a significant challenge for healthcare systems worldwide,despite advancements in diagnostic and therapeutic approaches that have mitigated its impact.The underlying pathophysiological mechanisms of sepsis are not yet fully understood.Autophagy,a cellular stress response,has been shown to play a critical role in the de-velopment of sepsis.Golgiphagy,a specific autophagic process targeting the Golgi apparatus,has been identified as a key factor influencing sepsis pathophysiology.This process operates through autophagy-related receptors and contributes to or-gan damage during sepsis.This review will explore the receptors associated with Golgiphagy,its role in sepsis progres-sion,and its effects on various organs,with the goal of informing treatment strategies for sepsis.

Sepsis remains a significant challenge for healthcare systems worldwide,despite advancements in diagnostic and therapeutic approaches that have mitigated its impact.The underlying pathophysiological mechanisms of sepsis are not yet fully understood.Autophagy,a cellular stress response,has been shown to play a critical role in the de-velopment of sepsis.Golgiphagy,a specific autophagic process targeting the Golgi apparatus,has been identified as a key factor influencing sepsis pathophysiology.This process operates through autophagy-related receptors and contributes to or-gan damage during sepsis.This review will explore the receptors associated with Golgiphagy,its role in sepsis progres-sion,and its effects on various organs,with the goal of informing treatment strategies for sepsis.

This study explored the variation of bursting force of multi-chamber infusion bag with different geometry size, providing guidance for its optimal design. Models of single-chamber infusion bag with different size were established. The finite element based on fluid cavity method was adopted to calculate the fluid-solid coupling deformation process of infusion bag to obtain corresponding critical bursting force. As a result, we proposed an empirical formula predicting the critical bursting force of one chamber infusion bag with specified geometry size. Besides, a theoretical analysis, which determines the force condition of three chamber infusion bag when falling from high altitude, was conducted. The proportion of force loaded on different chamber was gained. The results indicated that critical bursting force is positively related to the length and width of the chamber, and negatively related to the height of the chamber. While the infusion bag falling, the impact force loaded on each chamber is proportional to the total liquid within it. To raise the critical bursting force of in fusion bag, a greater length and width corresponding to reduced height are recommended considering the volume of liquid needed to be filled in.

OBJECTIVETo study the effect of platelet derived growth factor-B and its receptor expression on the proliferation of renal cell carcinoma ACHN cells in vitro and in vivo.

METHODSPDGF-B gene was transfected into human renal carcinoma cell line ACHN cells, and the proliferation capability of ACHN cells transfected with or without PDGF-B was assessed by MTT assay. The effect of PDGF-B on the expression of p-PDGFR-β in endothelial cells and vascular smooth muscle cells (VSMC) was detected by Western blot. ACHN cells transfected with PDGF-B were injected into mice (untransfected ACHN as control) to induce tumor formation. Immunohistochemical staining was used to detect the expression of Ki-67 in tumor cells and the tumor volume was measured to compare the tumor growth in the two groups.

RESULTSThe PDGF-B expression of ACHN cells in transfected group was significantly increased than that in the untransfected group. MTT assay showed that the proliferation capability of ACHN cells in the transfected and untransfected groups had no significant differences at different time points (P>0.05). The expression of p-PDGFR-β in VSMC was significantly increased when cultured with PDGF-B overexpression culture medium. The mean tumor size of the PDGF-B group and control group was (0.305±0.108) cm(3) and (0.577±0.218) cm(3), respectively (P=0.007). Ki-67-positive tumor cells were (41.00±5.34)/HPF in the PDGF-B-transfected group and (55.80±2.95)/HPF in the untransfected group (P=0.001).

CONCLUSIONPDGF-B overexpression may up-regulate p-PDGFR-β expression of VSMC in renal cell carcinoma, and inhibit the tumor cell proliferation and tumor growth through paracrine signaling.

Animals ; Carcinoma, Renal Cell ; metabolism ; pathology ; Cell Line, Tumor ; Cell Proliferation ; Humans ; Kidney Neoplasms ; metabolism ; pathology ; Mice ; Proto-Oncogene Proteins c-sis ; Receptor, Platelet-Derived Growth Factor beta ; genetics ; metabolism

Objective To study the effect of platelet derived growth factor-B and its receptor expression on the proliferation of renal cell carcinoma ACHN cells in vitro and in vivo.Methods PDGF-B gene was transfected into human renal carcinoma cell line ACHN cells, and the proliferation capability of ACHN cells transfected with or without PDGF-B was assessed by MTT assay.The effect of PDGF-B on the expression of p-PDGFR-βin endothelial cells and vascular smooth muscle cells ( VSMC ) was detected by Western blot.ACHN cells transfected with PDGF-B were injected into mice ( untransfected ACHN as control) to induce tumor formation.Immunohistochemical staining was used to detect the expression of Ki-67 in tumor cells and the tumor volume was measured to compare the tumor growth in the two groups.Results The PDGF-B expression of ACHN cells in transfected group was significantly increased than that in the untransfected group.MTT assay showed that the proliferation capability of ACHN cells in the transfected and untransfected groups had no significant differences at different time points (P>0.05).The expression of p-PDGFR-βin VSMC was significantly increased when cultured with PDGF-B overexpression culture medium. The mean tumor size of the PDGF-B group and control group was (0.305 ±0.108) cm3 and (0.577 ± 0.218) cm3, respectively (P =0.007).Ki-67-positive tumor cells were (41.00 ±5.34)/HPF in the PDGF-B-transfected group and ( 5 5 .8 0 ±2 .9 5 )/HPF in the untransfected group ( P=0 .0 0 1 ) .Conclusion PDGF-B overexpression may up-regulate p-PDGFR-βexpression of VSMC in renal cell carcinoma, and inhibit the tumor cell proliferation and tumor growth through paracrine signaling.

Objective To study the effect of platelet derived growth factor-B and its receptor expression on the proliferation of renal cell carcinoma ACHN cells in vitro and in vivo.Methods PDGF-B gene was transfected into human renal carcinoma cell line ACHN cells, and the proliferation capability of ACHN cells transfected with or without PDGF-B was assessed by MTT assay.The effect of PDGF-B on the expression of p-PDGFR-βin endothelial cells and vascular smooth muscle cells ( VSMC ) was detected by Western blot.ACHN cells transfected with PDGF-B were injected into mice ( untransfected ACHN as control) to induce tumor formation.Immunohistochemical staining was used to detect the expression of Ki-67 in tumor cells and the tumor volume was measured to compare the tumor growth in the two groups.Results The PDGF-B expression of ACHN cells in transfected group was significantly increased than that in the untransfected group.MTT assay showed that the proliferation capability of ACHN cells in the transfected and untransfected groups had no significant differences at different time points (P>0.05).The expression of p-PDGFR-βin VSMC was significantly increased when cultured with PDGF-B overexpression culture medium. The mean tumor size of the PDGF-B group and control group was (0.305 ±0.108) cm3 and (0.577 ± 0.218) cm3, respectively (P =0.007).Ki-67-positive tumor cells were (41.00 ±5.34)/HPF in the PDGF-B-transfected group and ( 5 5 .8 0 ±2 .9 5 )/HPF in the untransfected group ( P=0 .0 0 1 ) .Conclusion PDGF-B overexpression may up-regulate p-PDGFR-βexpression of VSMC in renal cell carcinoma, and inhibit the tumor cell proliferation and tumor growth through paracrine signaling.