Objective To compare and analyze the supply of blood collection and clinical blood demand in Hangzhou during 2011-2016,and to put forward some countermeasures and suggestions.Methods The related data of blood collection in blood center and the indexs of clinical blood demand in all hospitals in Hangzhou were collected during 2011-2016,and the growth rates of both of them were compared and analyzed.Results 1) The data of blood collection and supply was the lowest in 2012,and then increased year by year.The average annual growth of platelet collection and supply was 8.09％ and 8.47％,respectively,and the other indicators grew relatively gently.In 2016,the rate of blood donation reached 18.28 per thousand people.At the same period,the number of staff in institutions was basically stable.2) During 2011-2016,the blood demand of all hospitals in Hangzhoa maintained rapid growth.In Hangzhou,the number of hospitals increased by 10.65％ annually,and until 2016,there was an increase of 65.87％ over 2011.The average annual growth of the number of beds,the number of emergency patients and the number of inpatients increased by 10.21％,6.09％ and 11.40％ respectively.The growth rate of number of inpatients was higher than that of outpatient and emergency departments.Hospital employees remained at an average annual growth rate of nearly 10％.3) The clinical demand for blood increased significantly more higher than the growth of blood collection and supply.Conclusion Speed up the pace of the construction of blood supply,and keep pace with the construction of hospitals.Strengthening the publicity,health education and promotion models,in order to encourage more people,who are eligible for blood donation,to join the blood donation.And also strengthening personnel team building,improving overall work efficiency and level.

Objective To explore the value of gemstone spectral imaging (GSI)in quantitative evaluation of Lauren classification of gastric cancer.Methods Fifty-two patients with gastric cancer confirmed by gastroscopy underwent contrast-enhanced spectral CT imaging preoperatively.The monoergic and iodine-based images were obtained by GSI Viewer software,CT value and iodine concentration (IC)of the lesions were measured,and normalized iodine concentration (NIC)was calculated.With the reference of postoperative pathology,data were analyzed by LSD method of one-way analysis of variance.Results The IC,NIC,spectrum curve slope of 40-70 keV,40-140 keV and 70-140 keV energy range of intestinal type,mixed type and diffuse type carcinoma in the arterial phase were 12.86±6.80 (100 μg/mL),0.13±0.06 ,2.50±1.26 ,0.99±0.51 ,0.34±0.20 ,18.54±6.49 (100 μg/mL),0.19±0.07, 3.56±1.24,1.42±0.50,0.50±0.18 and 24.52±9.68 (100 μg/mL),0.24±0.09,4.73±1.76,1.90±0.73,0.68±0.29,respectively. The values of intestinal type were all significantly lower than those of diffuse type (P <0.05).Comparison between intestinal-mixed type and mixed-diffuse type,the other parameters were no significant differences except IC between intestinal-mixed type (P=0.037).Conclusion The slope of spectrum curve,iodine concentration,and normalized iodine concentration could be helpful for preoperative evaluation of Lauren classification of gastric cancer.

Purpose: Gastric cancer (GC) is among the deadliest malignancies and the third leading cause of cancer-related deaths worldwide. Galectin-1 (Gal-1) is a primary protein secreted by cancer-associated fibroblasts (CAFs); however, its role and mechanisms of action of Gal-1 in GC remain unclear. In this study, we stimulated GC cells with exogenous human recombinant galectin-1 protein (rhGal-1) to investigate its effects on the proliferation, migration, and resistance to cisplatin. Materials and Methods: We used simulated rhGal-1 protein as a paracrine factor produced by CAFs to induce GC cells and investigated its promotional effects and mechanisms in GC progression and cisplatin resistance. Immunohistochemical (IHC) assay confirmed that Gal-1 expression was associated with clinicopathological parameters and correlated with the expression of neuropilin-1 (NRP-1), c-JUN, and Wee1. Results: Our study reveals Gal-1 expression was significantly associated with poor outcomes.Gal-1 boosts the proliferation and metastasis of GC cells by activating the NRP-1/C-JUN/ Wee1 pathway. Gal-1 notably increases GC cell resistance to cisplatin The NRP-1 inhibitor, EG00229, effectively counteracts these effects. Conclusions These findings revealed a potential mechanism by which Gal-1 promotes GC growth and contributes to chemoresistance, offering new therapeutic targets for the treatment of GC.

Purpose: Gastric cancer (GC) is among the deadliest malignancies and the third leading cause of cancer-related deaths worldwide. Galectin-1 (Gal-1) is a primary protein secreted by cancer-associated fibroblasts (CAFs); however, its role and mechanisms of action of Gal-1 in GC remain unclear. In this study, we stimulated GC cells with exogenous human recombinant galectin-1 protein (rhGal-1) to investigate its effects on the proliferation, migration, and resistance to cisplatin. Materials and Methods: We used simulated rhGal-1 protein as a paracrine factor produced by CAFs to induce GC cells and investigated its promotional effects and mechanisms in GC progression and cisplatin resistance. Immunohistochemical (IHC) assay confirmed that Gal-1 expression was associated with clinicopathological parameters and correlated with the expression of neuropilin-1 (NRP-1), c-JUN, and Wee1. Results: Our study reveals Gal-1 expression was significantly associated with poor outcomes.Gal-1 boosts the proliferation and metastasis of GC cells by activating the NRP-1/C-JUN/ Wee1 pathway. Gal-1 notably increases GC cell resistance to cisplatin The NRP-1 inhibitor, EG00229, effectively counteracts these effects. Conclusions These findings revealed a potential mechanism by which Gal-1 promotes GC growth and contributes to chemoresistance, offering new therapeutic targets for the treatment of GC.

Purpose: Gastric cancer (GC) is among the deadliest malignancies and the third leading cause of cancer-related deaths worldwide. Galectin-1 (Gal-1) is a primary protein secreted by cancer-associated fibroblasts (CAFs); however, its role and mechanisms of action of Gal-1 in GC remain unclear. In this study, we stimulated GC cells with exogenous human recombinant galectin-1 protein (rhGal-1) to investigate its effects on the proliferation, migration, and resistance to cisplatin. Materials and Methods: We used simulated rhGal-1 protein as a paracrine factor produced by CAFs to induce GC cells and investigated its promotional effects and mechanisms in GC progression and cisplatin resistance. Immunohistochemical (IHC) assay confirmed that Gal-1 expression was associated with clinicopathological parameters and correlated with the expression of neuropilin-1 (NRP-1), c-JUN, and Wee1. Results: Our study reveals Gal-1 expression was significantly associated with poor outcomes.Gal-1 boosts the proliferation and metastasis of GC cells by activating the NRP-1/C-JUN/ Wee1 pathway. Gal-1 notably increases GC cell resistance to cisplatin The NRP-1 inhibitor, EG00229, effectively counteracts these effects. Conclusions These findings revealed a potential mechanism by which Gal-1 promotes GC growth and contributes to chemoresistance, offering new therapeutic targets for the treatment of GC.

Purpose: Gastric cancer (GC) is among the deadliest malignancies and the third leading cause of cancer-related deaths worldwide. Galectin-1 (Gal-1) is a primary protein secreted by cancer-associated fibroblasts (CAFs); however, its role and mechanisms of action of Gal-1 in GC remain unclear. In this study, we stimulated GC cells with exogenous human recombinant galectin-1 protein (rhGal-1) to investigate its effects on the proliferation, migration, and resistance to cisplatin. Materials and Methods: We used simulated rhGal-1 protein as a paracrine factor produced by CAFs to induce GC cells and investigated its promotional effects and mechanisms in GC progression and cisplatin resistance. Immunohistochemical (IHC) assay confirmed that Gal-1 expression was associated with clinicopathological parameters and correlated with the expression of neuropilin-1 (NRP-1), c-JUN, and Wee1. Results: Our study reveals Gal-1 expression was significantly associated with poor outcomes.Gal-1 boosts the proliferation and metastasis of GC cells by activating the NRP-1/C-JUN/ Wee1 pathway. Gal-1 notably increases GC cell resistance to cisplatin The NRP-1 inhibitor, EG00229, effectively counteracts these effects. Conclusions These findings revealed a potential mechanism by which Gal-1 promotes GC growth and contributes to chemoresistance, offering new therapeutic targets for the treatment of GC.