| 16 | Prevention and treatment of hypoxia-induced colorectal cancer damage in albino Wister rats显示文摘Background:In the early metastasis of colon cancer,cancer cells detach,migrate,and infiltrate surrounding tissues,including lymph vessels and blood vessels.Tumor heterogeneity arises from both tumor cells and distinct microenvironments.Maldistribution of blood vessels,creates hypoxic regions within the tumors,fostering cancer stem cell-like properties due to reduced oxygen and nutrient supply.Under hypoxia,tumor cells shift to a glycolytic pathway,producing more lactic acid that acidifies the microenvironment and leads to unstable heart rate variability(HRV)factors,weight disparity,and a higher incidence of aberrant crypt foci(ACF).These hypoxic-induced parameters promote cancer cell invasion,increase radiation resistance,and facilitate cancer cell migration.Methods:In this study,we induced hypoxia-preneoplastic colon damage in albino Wister rats by administrating 1,2-dimethyl hydrazine(DMH).After successfully creating a hypoxic environment in albino Wister rats,resulting in preneoplastic colon damage,we randomly allocated Wistar albino rats into seven groups,each containing 8 animals,and conducted a 6-week study.Group 1-Normal control(administered 1 mM EDTA+saline,2 ml/kg/day,p.o.);group 2-Toxic control(administered DMH,30 mg/kg/week,s.c.);group 3-Standard treatment(DMH,30 mg/kg/week,s.c.for 6 weeks),followed by 5-fluorouracil and Leucovorin(25 mg/kg each on 1^(st),3^(rd),7^(th),and 10^(th) days,i.p.after 6 weeks administration of DMH);group 4-Low dose of P1(DMH,30 mg/kg/week,s.c.+P1,2 mg/kg,i.v.,weekly for 3 weeks);group 5-High dose P1(DMH,30 mg/kg/week,s.c.+P1,4 mg/kg,i.v.,weekly for 3 weeks),group 6-Low dose of P2(DMH,30 mg/kg/week,s.c.,+P2,2 mg/kg,i.v.,weekly for 3 weeks),group 7-High dose of P2(DMH,30 mg/kg/week,s.c.,+P2,4 mg/kg,i.v.weekly for 3 weeks).Results:DMH-treated rats exhibited alterations in HRV factors,weight disparity,elevated gastric pH,increased total acidity,a higher incidence of ACF,and changes in antioxidant markers(TBARs,SOD,catalase,GSH).Brightfield microscopy at 40x magnification revealed the presence of large crypts within aberrant crypt foci in the toxic control group.Conclusion:Treatment groups P1 and P2 containing triazine derivatives initiated proteasomal degradation of Hypoxia Inducible Factor-1α(HIF-1α)by activating Prolyl Hydroxylase(PHDs)pathways.HIF-1αunder a hypoxic environment is responsible for activating a multitude of genes involved in angiogenesis,metastasis,invasiveness,pH changes,metabolic reprogramming,stem cell maintenance,resistance to radiation,and downstream regulation of the immune system.Treatment with P1 and P2 groups helped minimize the ACF count and restored HRV factors,weight disparity,pH levels,total acidity,and oxidative balance.Our findings emphasize the potential role of 1,2,4-triazine derivatives in suppressing hypoxia-induced colon carcinogenesis. | Ishrat Jahan Manju Pandey Shalini Pal Bushra Jabi Mohd Yaqub Khan Gaurav Kaithwas | 2024 | Life Research2024，7，1： | 0 |
| 17 | Caseous mitral annular calcifications: Multimodality imaging characteristics显示文摘The authors report herein a series of 3 patients with caseous mitral annular calcifications (MAC). One of the patients presented with mass-like, caseous MAC as an incidental finding on a staging computed tomography (CT) for metastatic colorectal carcinoma. Another patient presented with a nodule on a chest radiograph, which was later found on CT to be due to caseous MAC. In the third patient, caseous MAC was initially detected on echocardiography, and was further evaluated with CT and cardiac magnetic resonance imag-ing. In all three patients, the appearances posed a diagnostic dilemma. The appearance of caseous MAC is dissimilar to non-caseous MAC and is usually seen as an ovoid, mass-like structure, with homogeneous hyperattenuation, representing a liquefied form of calcium and proteinaceous fluid. This homogeneous center is surrounded by peripheral, shell-like calcifications. Caseous MAC is likely an under-recognized entity and may present a diagnostic dilemma at CT, magnetic resonance imaging, or echocardiography. | Jabi Shriki Christine Rongey Bobby Ghosh Samuel Daneshvar Partick M Colletti Ali Farvid Alison Wilcox | 2010 | World Journal of Radiology2010，2，4： | 0 |
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