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1
Kawcak, C. E., G. M. Baxter, D. M. Getzy, T. S. Stashak, and P. L. Chapman. "Abnormalities in oxygenation, coagulation, and fibrinolysis in colonic blood of horses with experimentally induced strangulation obstruction." American Journal of Veterinary Research 56, no. 12 (1995): 1642–50. http://dx.doi.org/10.2460/ajvr.1995.56.12.1642.
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Abstract Objective To measure arterial and venous blood gas, coagulation, and fibrinolysis variables in blood from isolated segments of control and ischemic large colons for the purpose of identifying variables for rapid, indirect assessment of colonic mucosal injury. Design Variables were determined at specific intervals during the 4-hour study (3 hours of ischemia and 1 hour of reperfusion). Animals Seven clinically normal horses between 2 and 15 years old. Procedure Horses underwent laparotomy and occlusion of the lumen and vasculature of the mid-portion of the pelvic flexure of the large colon. During ischemia of 1 randomly-chosen colonic segment, variables were measured to determine colonic mucosal damage and were compared with histologic scores of colonic biopsy specimens. Results Significant (P < 0.05) differences from control values were observed over time for venous pH, Pco2, Po2, oxygen saturation, oxygen content, arteriovenous oxygen difference, and lactate and glucose concentrations. Mean histologic scores of biopsy specimens obtained from ischemic colons were significantly (P < 0.05) greater (indicating greater damage) than those from control colons, and increased significantly (P < 0.05) with duration of ischemia. Conclusions Venous lactate, oxygen saturation, and Po2 values were the most significant predictors of the severity of histologic damage within the ischemic colons (R2 = 0.661). Clinical Relevance Venous blood gas and lactate values in the large colon are good predictors of the amount of intestinal damage incurred during 3 hours of ischemia, and may be clinically useful for the rapid determination of colonic viability.
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Walrath, Travis, Robert A. Malizia, Xinjun Zhu та ін. "IFN-γ and IL-17A regulate intestinal crypt production of CXCL10 in the healthy and inflamed colon". American Journal of Physiology-Gastrointestinal and Liver Physiology 318, № 3 (2020): G479—G489. http://dx.doi.org/10.1152/ajpgi.00208.2019.
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During intestinal inflammation, immature cells within the intestinal crypt are called upon to replenish lost epithelial cell populations, promote tissue regeneration, and restore barrier integrity. Inflammatory mediators including TH1/TH17-associated cytokines influence tissue health and regenerative processes, yet how these cytokines directly influence the colon crypt epithelium and whether the crypt remains responsive to these cytokines during active damage and repair, remain unclear. Here, using laser-capture microdissection and primary colon organoid culture, we show that the cytokine milieu regulates the ability of the colonic crypt epithelium to participate in proinflammatory signaling. IFN-γ induces the TH1-recruiting, proinflammatory chemokine CXCL10/IP10 in primary murine intestinal crypt epithelium. CXCL10 was also induced in colonic organoids derived from mice with active, experimentally induced colitis, suggesting that the crypt can actively secrete CXCL10 in select cytokine environments during colitis. Colon expression of cxcl10 further increased during infectious and noninfectious colitis in Il17a−/− mice, demonstrating that IL-17A exerts a negative effect on CXCL10 in vivo. Furthermore, IL-17A directly antagonized CXCL10 production in ex vivo organoid cultures derived from healthy murine colons. Interestingly, direct antagonism of CXCL10 was not observed in organoids derived from colitic mouse colons bearing active lesions. These data, highlighting the complex interplay between the cytokine milieu and crypt epithelia, demonstrate proinflammatory chemokines can be induced within the colonic crypt and suggest the crypt remains responsive to cytokine modulation during inflammation. NEW & NOTEWORTHY Upon damage, the intestinal epithelium regenerates to restore barrier function. Here we observe that the local colonic cytokine milieu controls the production of procolitic chemokines within the crypt base and colon crypts remain responsive to cytokines during inflammation. IFN-γ promotes, while IL-17 antagonizes, CXCL10 production in healthy colonic crypts, while responses to cytokines differ in inflamed colon epithelium. These data reveal novel insight into colon crypt responses and inflammation-relevant alterations in signaling.
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Staiano, Annamaria, and Ennio Del Giudice. "Colonic Transit and Anorectal Manometry in Children With Severe Brain Damage." Pediatrics 94, no. 2 (1994): 169–73. http://dx.doi.org/10.1542/peds.94.2.169.
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Objective. This study was conceived to determine the physiologic abnormalities in distal gastrointestinal motility that are responsible for constipation in brain-damaged children. Design. Colonic transit and anorectal manometry were evaluated in 16 children with severe brain damage and constipation (mean age ± SD; 5.1 ± 3.5 years) and the results were compared with findings in 15 age- and sex-atched children with functional fecal retention and normal mental development. Anorectal motility findings also were compared with those from 11 asymptomatic children. The progress of radiopaque markers, as determined by sequential plain abdominal radiographs, was used to evaluate segmental colonic transit times. Results. In children with brain damage, colonic transit was prolonged at the level of left colon in 18.8% of the patients, at both left colon and rectum in 56.2%, and at rectum only in 25% These findings differed (P &lt; .05) from those in children with functional fecal retention wherein transit was prolonged in the left colon and rectum in 20% of the patients and the rectum only in 80%. By anorectal manometry, no significant intergroup differences were detected in anal pressures and in the anorectal motor responses to rectal distention. The rectal compliance in children with severe brain damage was similar to the asymptomatic controls, whereas children with functional fecal retention had increased rectal compliance. Conclusions. This study shows that colonic transit abnormalities in both the left colon and rectum may be responsible for constipation in children with severe brain damage.
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Schader, Tim, Christina Reschke, Manuela Spaeth, Susanne Wienstroer, Szeka Wong, and Katrin Schröder. "NoxO1 Knockout Promotes Longevity in Mice." Antioxidants 9, no. 3 (2020): 226. http://dx.doi.org/10.3390/antiox9030226.
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According to the free radical theory of aging, reactive oxygen species (ROS) have been proposed to be a major cause of aging for a long time. Meanwhile, it became clear that ROS have diverse functions in a healthy organism. They act as second messengers, and as transient inhibitors of phosphatases and others. In fact, their detrimental role is highly dependent on the context of their production. NADPH oxidases (Nox) have been discovered as a controllable source of ROS. NoxO1 enables constitutive ROS formation by Nox1 by acting as a constitutively active cytosolic subunit of the complex. We previously found that both Nox1 and NoxO1 were highly expressed in the colon, and that NoxO1-/- deficiency reduces colon health. We hypothesized that a healthy colon potentially contributes to longevity and NoxO1 deficiency would reduce lifetime, at least in mouse. In contrast, here we provide evidence that the knockout of NoxO1 results in an elongated life expectancy of mice. No better endothelial function, nor an improved expression of genes related to longevity, such as Sirt1, were found, and therefore may not serve as an explanation for a longer life in NoxO1 deficiency. Rather minor systemic differences, such as lower body weight occur. As a potential reason for longer life, we suggest better DNA repair capacity in NoxO1 deficient mice. Although final fatal DNA damage appears similar between wildtype and NoxO1 knockout animals, we identified less intermediate DNA damage in colon cells of NoxO1-/- mice, while the number of cells with intact DNA is elevated in NoxO1-/- colons. We conclude that NoxO1 deficiency prolongs lifetime of mice, which correlates with less intermediate and potentially fixable DNA damage at least in colon cells.
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Wang, Yan-Hong, Xiao-Lai Yang, Li Wang, et al. "Effects of proanthocyanidins from grape seed on treatment of recurrent ulcerative colitis in rats." Canadian Journal of Physiology and Pharmacology 88, no. 9 (2010): 888–98. http://dx.doi.org/10.1139/y10-071.
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The aim of the present study was to investigate the therapeutic effect and mechanism of proanthocyanidins from grape seed (GSPE) in the treatment of recurrent ulcerative colitis (UC) in rats. To induce recurrent colitis, rats were instilled with 2,4,6-trinitrobenzenesulfonic acid (TNBS) (80 mg/kg) into the colon through the cannula in the first induced phase, and then the rats were instilled a second time with TNBS (30 mg/kg) into the colon on the sixteenth day after the first induction UC. Rats were intragastrically administered GSPE (200 mg/kg) per day for 7 days after twice-induced colitis by TNBS. Sulfasalazine at 500 mg/kg was used as a positive control drug. Rats were killed 7 days after GSPE treatment. The colonic injury and inflammation were assessed by macroscopic and macroscopic damage scores, colon weight/length ratio (mg/cm), and myeloperoxidase activity. Then, superoxide dismutase, glutathione peroxidase, inducible nitric oxide synthase (iNOS) activities, and the levels of malonyldialdehyde, glutathione, and nitric oxide in serum and colonic tissues were measured. Compared with the recurrent UC group, GSPE treatment facilitated recovery of pathologic changes in the colon after induction of recurrent colitis, as demonstrated by reduced colonic weight/length ratio and macroscopic and microscopic damage scores. The myeloperoxidase and iNOS activities with malonyldialdehyde and nitric oxide levels in serum and colon tissues of colitis rats were significantly decreased in the GSPE group compared with those in the recurrent UC group. In addition, GSPE treatment was associated with notably increased superoxide dismutase, glutathione peroxidase activities, and glutathione levels of colon tissues and serum of rats. GSPE exerted a protective effect on recurrent colitis in rats by modifying the inflammatory response, inhibiting inflammatory cell infiltration and antioxidation damage, promoting damaged tissue repair to improve colonic oxidative stress, and inhibiting colonic iNOS activity to reduce the production of nitric oxide.
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Chesnokova, Vera, Svetlana M. Zonis, Robert Barrett, and Shlomo Melmed. "Abstract 5683: Growth hormone as a SASP component." Cancer Research 82, no. 12_Supplement (2022): 5683. http://dx.doi.org/10.1158/1538-7445.am2022-5683.
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Abstract Senescence, largely initiated by unrepaired DNA damage, is initially sustained by upregulated p53. Although senescent cells enter proliferative arrest, early p53 supression may result in senescent cells re-entering the cell cycle. Senescent cells exhibit a senescence-associated secretory phenotype (SASP) that impacts the cell microenvironment, often promoting cell transformation. SASP molecular composition may be cell-specific and dependant on the type of SASP-producing cell. As growth hormone (GH) is induced by DNA damage, we elucidated whether GH is induced in senescent cells. Non-pituitary GH (npGH) synthesized locally in peripheral tissues is identical to endocrine GH1 produced by the pituitary and acts through autocrine/paracrine mechanisms via the widely expressed GH receptor that recognizes both pituitary GH and npGH ligands. We show that npGH is induced in aging human colon tissue, and in human non-tumorous colon cells and in human 3-dimensional intestinal organoids in response to oncogene-, therapy-, and/or replicative-induced senescence. Furthermore,DNA-damage-induced npGH is secreted from senescent cells, constituting a SASP component. In senescent cells, DNA damage is not repaired with fidelity, and we show that induced npGH suppresses DNA damage responses by attenuating phosphorylation of ATM, DNA-PKc, p53 and Chk2, resulting in p53 suppression and accumulation of damged DNA. Autocrine npGH also triggers senescent cell proliferation with increased Ki67 and BrdU incorporation. As proliferating cells with accumulated unrepaired DNA damage may acquire oncogenic mutations,we assessed npGH actions on cell transformation. We show that senescent colon cells expressing npGH form colonies in soft agar,while GH depletion by shRNA downregulates Ki67 and decreases colony formation and size, suggesting that npGH enables senescent cell transformation. Consistent with a SASP function, induced paracrine npGH also suppresses the p53/p21 pathway, triggering proliferation and exacerbates DNA damage in neighboring non-senescent cells. To further explore mechanisms underlying npGH induction we tested the role of the SASP chemokine CXCL1 which attracts immune effectors to eliminate senescent cells. CXCl1 is shown to induce npGH in senescent hNCC and in intestinal organoids, while GH, in turn, suppresses CXCL1, likely by inhibiting NFκB, a CXCL1 transcription factor. Both colon CXCL1 and NFκB are more abundant in GH-receptor knockout mice devoid of GH signalling, while mice bearing GH-secreting xenografts exhibit decreased colon CXCL1 abundance. Conclusions: The results elucidate a heretofore unappreciated GH action, whereby npGH, as a SASP component, attenuates senescent cell elimination by inhibiting CXCL1, and contributes to a tissue microenvironment favoring age-associated DNA damage accumulation and epithelial cell transformation. Citation Format: Vera Chesnokova, Svetlana M. Zonis, Robert Barrett, Shlomo Melmed. Growth hormone as a SASP component [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5683.
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Chesnokova, Vera M., Svetlana M. Zonis, Hannah Estrada, Robert Barrett, and Shlomo Melmed. "GH Is a Component of SASP in Aging Tissue." Journal of the Endocrine Society 5, Supplement_1 (2021): A539—A540. http://dx.doi.org/10.1210/jendso/bvab048.1099.
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Abstract Deficient GH signaling results in lifespan extension in murine and human models, while patients with uncontrolled acromegaly and transgenic mice overexpressing GH have a shorter lifespan. Colon polyp development increases with age, and also with GH excess in acromegaly. Aging is characterized by senescent cell accumulation with p53/p21 or p16 upregulation as well as cell cycle arrest and expression of a senescence-associated secretory phenotype (SASP). Senescence is reinforced by the SASP, which comprises pro-inflammatory cytokines, chemokines, growth modulators, angiogenic factors, and matrix metalloproteinases. SASP contributes to pro-aging phenotypes, and depletion or removal of senescent cells increases lifespan by partially protecting from age-related pathologies. Senescence, triggered by genotoxic insult with DNA damage, can be reversed by p53 inactivation; senescent cells with low p53 and unrepaired DNA damage can then re-enter the cell cycle (Beausejour et al, EMBO 2003), potentially resulting in chromosomal instability. We showed GH induction in non-pituitary senescent cells leading to suppressed p53/p21 (Chesnokova PNAS 2013). We now show that, in senescent human colon cells (hNCC) and in 3-dimensional human intestinal organoids, non-pituitary GH (npGH) is a component of SASP. In response to DNA damage, npGH is expressed and secreted locally as measured by RT-PCR, WB, and ELISA. High autocrine/paracrine GH further exacerbate DNA damage and reverses senescent in colon cells, enabling them to re-enter the cell cycle, as evidenced by p53 downregulation and increased Ki67 expression. Senescent colon cells expressing high intracellular GH form colonies in soft agar, indicative of cell transformation and proliferation, while GH deletion by shRNA results in Ki67 downregulation and decreased colony formation and size. The SASP protein CXCL1, a chemo-attractant that also functions to eliminate senescent cells, dose-dependently activates GH in hNCC and in intestinal organoids. GH, in turn, suppresses CXCL1 expression. Consistent with these findings, colon CXCL1 was induced in GHRKO mice, and also in hNCC with abrogated GH signaling by shRNA. Taken together with our finding that GH accumulates in aging normal human colon tissue and co-localizes in cells expressing senescence-associated β-galactosidase, these results suggest that GH, as a SASP component, initiates senescent cell proliferation and transformation. By inhibiting CXCL1, GH also functions to attenuate immune-mediated senescent cell elimination that protects aging tissue from deleterious effects of SASP. These mechanisms may underly an initial step in age-associated epithelial polyp development.
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Gumeniuk, K. V., and O. A. Lavrenchuk. "SIZE AND STRUCTURE OF SANITARY LOSSES IN WARS OF MODERN LOCAL ARMED CONFLICTS IN GUNSHOT INJURIES OF THE ABDOMEN WITH DAMAGE TO THE COLON." Kharkiv Surgical School, no. 5-6 (December 8, 2021): 47–51. http://dx.doi.org/10.37699/2308-7005.5-6.2021.10.
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The purpose of the study is to analyze the sources of domestic and world literature with the study of the magnitude and structure of sanitary losses in wars and modern local armed conflicts with gunshot wounds to the abdomen with damage to the colon. To investigate sanitary losses at gunshot wounds of a colon.
 Conclusions. Sanitary losses in wars of local armed conflicts with gunshot wounds to the abdomen with damage to the colon remain high worldwide, despite individual means of protecting the torso. In this regard, it is notable to further study the anatomical and clinical features of gunshot wounds of the colon in the experience of the antiterrorist operation in eastern Ukraine.
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Zhang, Ji, Xue-jun Wang, Li-jie Wu, et al. "Herb-partitioned moxibustion alleviates colonic inflammation in Crohn’s disease rats by inhibiting hyperactivation of the NLRP3 inflammasome via regulation of the P2X7R-Pannexin-1 signaling pathway." PLOS ONE 16, no. 5 (2021): e0252334. http://dx.doi.org/10.1371/journal.pone.0252334.
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Crohn’s disease is a chronic inflammatory bowel disease and the NLRP3 inflammasome plays an important role in Crohn’s disease. Previous studies have shown that Herb-partitioned moxibustion treating (at Qihai (CV 6) and Tianshu (ST 25)) prevented the excessive activation of the NLRP3 inflammasome and repaired damaged colonic mucosa in Crohn’s disease. However, the mechanism by which Herb-partitioned moxibustion (at CV 6 and ST 25) regulates NLRP3 remains unclear. In this study, we treated Crohn’s disease rats with herb-partitioned moxibustion (at CV 6 and ST 25) to investigate the mechanism by which Herb-partitioned moxibustion regulates the colonic NLRP3 inflammasome by observing colon length, the colon macroscopic damage indexes, and the expression of ATP, P2X7R, Pannexin-1, NF-κBp65, NLRP3, ASC, caspase-1, IL-1β and IL-18 in the colon in Crohn’s disease. Here, this study shows that herb-partitioned moxibustion (at CV 6 and ST 25) can reduce colon macroscopic damage indexes and colon histopathological scores, alleviate colon shortening and block the abnormal activation of the NLRP3 inflammasome by inhibiting the ATP content and the expression of P2X7R, Pannexin-1 and NF-κBp65, thereby reducing the release of the downstream inflammatory cytokine IL-1β and ultimately suppressing colonic inflammation in Crohn’s disease rats. This study for the first time identifies the mechanism by which herb-partitioned moxibustion (at CV 6 and ST 25) may inhibit the abnormal activation of the NLRP3 inflammasome by inhibiting the P2X7R-Pannexin-1 signaling pathway in Crohn’s disease rats.
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Li, Xiao-Li, Yong-Qing Cai, Hong Qin, and Yong-Jie Wu. "Therapeutic effect and mechanism of proanthocyanidins from grape seeds in rats with TNBS-induced ulcerative colitis." Canadian Journal of Physiology and Pharmacology 86, no. 12 (2008): 841–49. http://dx.doi.org/10.1139/y08-089.
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The aim of the study was to investigate the therapeutic effect and mechanism of proanthocyanidins from grape seeds (GSPE) in the treatment of ulcerative colitis (UC). Rats were intragastrically administered different doses of GSPE (100, 200, and 400 mg/kg) per day for 7 days after UC was twice-induced by intracolonic injection of 2,4,6-trinitrobenzene sulfonic acid (TNBS)dissolved in 50% ethanol. Sulfasalazine (SASP) at 200 mg/kg was used as a positive control drug. Macroscopic and microscopic damage scores and changes in weight/length ratio (mg/mm) of colon segments were analyzed. The levels of malonyldialdehyde (MDA), interleukin (IL)-1β, IL-2, IL-4, and myeloperoxidase (MPO) activity in the colon tissues and MPO activity in the serum were all measured by biochemical methods or double antibody sandwich ELISA methods. Compared with the TNBS control group, GSPE treatment facilitated recovery of pathologic changes in the colon after insult with TNBS, as demonstrated by increased body weight (p < 0.01) and decreased colonic weight/length ratio (p < 0.01); GSPE also notably reduced the colonic macroscopic and microscopic damage scores (p < 0.01). The MPO activity in colon tissues and serum of rats treated with GSPE was significantly lower than that in the TNBS control group. The MDA and IL-1β levels of colon tissues were also decreased in GSPE groups. The intestinal antiinflammatory effect of GSPE was accompanied by a significant improvement of IL-2 and IL-4 levels in the colon tissues of rats in the high-dose GSPE group (p < 0.05). Compared with the SASP group, GSPE groups had no significant difference in the therapeutic effect (p > 0.05). GSPE exerts a beneficial antiinflammatory effect in the acute phase of TNBS-induced colitis in rats by downregulating some of the mediators involved in the intestinal inflammatory response, inhibiting inflammatory cell infiltration and antioxidation damage, promoting damaged tissue repair to improve colonic oxidative stress, decreasing production of proinflammatory cytokines IL-1β, and increasing production of antiinflammatory cytokines IL-2 and IL-4.
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Martinez, Carlos Augusto Real, Marcelo Lima Ribeiro, Alessandra Gambero, Daniel Duarte da Conceição Miranda, José Aires Pereira, and Sidney Roberto Nadal. "The importance of oxygen free radicals in the etiopathogenesis of diversion colitis in rats." Acta Cirurgica Brasileira 25, no. 5 (2010): 387–95. http://dx.doi.org/10.1590/s0102-86502010000500002.
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PURPOSE: Quantify the levels of oxidative DNA damage of epithelial colon cells comparing segments with and without fecal stream. METHODS: Sixty Wistar rats were subjected to deviation of fecal stream by proximal colostomy and a distal mucosal fistula. Animals were divided into three experimental groups that were sacrificed 6, 12 and 24 weeks after surgery. In each experimental group, five animals underwent laparotomy without intestinal deviation (sham subgroup). The diagnosis of colitis was made by histopathological analysis and the inflammatory activity index by graduated scale. The neutrophil infiltration was determined by myeloperoxidase tissue levels and the intensity of oxidative DNA damage by comet assay. The Mann-Withney and Student t test were used to compare the results among experimental subgroups and the Kruskal-Wallis test for variance analysis, adopting a significance level of 5% (p<0.05). RESULTS: Colon segments without fecal stream was shown higher histological inflammatory score of the colon wall after 12 and 24 weeks (p=0.001) that increased with the time of diversion (p=0.01). The activity of myeloperoxidase in segments without fecal stream decreased with the time (p=0.001). Oxidative DNA damage levels were significantly higher in the segments without fecal stream, (p=0.0001), independent of time of colon diversion, and increase with the time (p=0.0007). CONCLUSIONS: Colon segments without fecal stream showed high levels of oxidative DNA damage related to histological alterations observed in diversion colitis. The levels of oxidative DNA damage in segments devoid of the fecal stream increase with the time of intestinal exclusion.
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Gumeniuk, K. V., I. P. Marcinkovsky, G. L. Bogush, and V. G. Verdesh. "RESULTS OF SURGICAL TREATMENT OF FIRE WOUNDS OF COLON." Kharkiv Surgical School, no. 5-6 (December 8, 2021): 52–56. http://dx.doi.org/10.37699/2308-7005.5-6.2021.11.
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The aim of the study. Evaluate the results of surgical treatment of wounded with gunshot wounds of the colon.
 Materials and methods of research. A retrospective analysis of the results of surgical treatment of 32 wounded with gunshot wounds of the colon, who were treated in the Central Medical Center and area of responsibility (II–IV level of medical care) from 2014 to 2017. Damage to the right half of the colon was observed in 12 wounded (37.4 %), the left half — in 17 (53.2 %), the rectum — in 3 (9.4 %). A differentiated approach to surgical treatment of colon injuries of different localization is applied.
 Results and discussion. The method of multi-stage surgical treatment “Damage Control Surgery” was used in 12.5 % of patients. The most common complications of the injury were adhesive intestinal obstruction in 6.3 % of cases, the formation of intestinal abscesses — in 6.3 %, the development of post-traumatic pneumonia in 25 % of patients.
 Conclusions. If the tactics of “Damage Control Surgery” are followed, it is possible to improve the results of surgical treatment of colon injuries in severe and extremely severe patients.
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Shan, Baocong, Ran Zhao, Jian Zhou, et al. "AURKA Increase the Chemosensitivity of Colon Cancer Cells to Oxaliplatin by Inhibiting the TP53-Mediated DNA Damage Response Genes." BioMed Research International 2020 (August 11, 2020): 1–11. http://dx.doi.org/10.1155/2020/8916729.
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AURKA, a cell cycle-regulated kinase, is associated with malignant transformation and progression in many cancer types. We analyzed the expression change of AURKA in pan-cancer and its effect on the prognosis of cancer patients using the TCGA dataset. We revealed that AURKA was extensively elevated and predicted a poor prognosis in most of the detected cancer types, with an exception in colon cancer. AURKA was elevated in colon cancer, but the upregulation of AURKA indicated better outcomes of colon cancer patients. Then we revealed that undermethylation of the AURKA gene and several transcription factors contributed to the upregulation of AURKA in colon cancer. Moreover, we demonstrated that AURKA overexpression promoted the death of colon cancer cells induced by Oxaliplatin, whereas knockdown of AURKA significantly weakened the chemosensitivity of colon cancer cells to Oxaliplatin. Mechanistically, AURKA inhibited DNA damage response by suppressing the expression of various DNA damage repair genes in a TP53-dependent manner, which can partly explain that ARUKA is associated with a beneficial outcome of colon cancer. This study provided a possibility to use AURKA as a biomarker to predict the chemosensitivity of colon cancer to platinum in the clinic.
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Gumenyuk, K. V., T. P. Yakymova, G. I. Gubina-Vakulyk, V. V. Nehoduiko, V. V. Makarov, and R. M. Mykhaylusov. "Histochemical assessment of colon damage degree in fire bullet injuries." Experimental and Clinical Medicine 91, no. 1 (2022): 71–79. http://dx.doi.org/10.35339/ekm.2022.91.1.gyg.
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The article analyzes and evaluates the protein damage in the wall of the large intestine during its gunshot bullet injury at different times after the injury with the help of histochemical studies. The extent and depth of local proteolysis in the tissues of the colon wall near the site of resection after a gunshot wound was determined, and an assessment of the adequacy of retreat from the damaged tissues of the colon wall and the prognosis of successful healing of the suture on the colon wall was provided. It is shown that the Red/Blue indicator is integral for assessing the condition of the connective tissue of the injured large intestine. Comparative indicators of the volumes of carboxyl (RED) R/B groups and amino groups (BLUE) in the peripheral areas of the removed fragment of the large intestine depending on the result of intestinal suture are presented. It has been proven that in injured young people, violations of the structure, function and vital activity of the large intestine are less pronounced. The presence of an increase in the number of carboxyl groups in tissue proteins was determined, which is evidenced by the increase in red staining and the morphometrically determined increase in the value of the M. Calvo coefficient. When the state of proteins is normalized and the amino groups are activated, the blue color becomes dominant, and the R/B ratio decreases to 1.0 and below. That is, the Red/Blue indicator is integral to assessing the condition of the connective tissue of the injured intestine. Most likely, the initial state of metabolic disturbance plays an important role in healing, inflammation or suppuration. Conclusions were made about the expediency of conducting a histochemical analysis of the damaged colon for adequate therapy. Keywords: histochemical examination, gunshot wound, colon injury.
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Lin, Hsi-Chiang, and Willard J. Visek. "Colon Mucosal Cell Damage by Ammonia in Rats." Journal of Nutrition 121, no. 6 (1991): 887–93. http://dx.doi.org/10.1093/jn/121.6.887.
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Prakash, Priya, William Symons, and Jad Chamieh. "Management of Destructive Colon Injuries after Damage Control Surgery." Clinics in Colon and Rectal Surgery 31, no. 01 (2017): 036–40. http://dx.doi.org/10.1055/s-0037-1602178.
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AbstractAfter the World War II, fecal diversion became the standard of care for colon injuries, although medical, logistic, and technical advancements have challenged this approach. Damage control surgery serves to temporize immediately life-threatening conditions, and definitive management of destructive colon injuries is delayed until after appropriate resuscitation. The bowel can be left in discontinuity for up to 3 days before edema ensues, but the optimal repair window remains within 12 to 48 hours. Delayed anastomosis performed at the take-back operation or stoma formation has been reported with variable results. Studies have revealed good outcomes in those undergoing anastomosis after damage control surgery; however, they point to a subgroup of trauma patients considered to be “high risk” that may benefit from fecal diversion. Risk factors influencing morbidity and mortality rates include hypotension, massive transfusion, the degree of intra-abdominal contamination, associated organ injuries, shock, left-sided colon injury, and multiple comorbid conditions. Patients who are not suitable for anastomosis by 36 hours after damage control may be best managed with a diverting stoma. Failures are more likely related to ongoing instability, and the management strategy of colorectal injury should be based mainly on the patient's overall condition.
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Saeedan, AS, S. Rastogi, and MN Ansari. "Roflumilast counteracts DMH-induced preneoplastic colon damage in albino Wistar rats." Human & Experimental Toxicology 39, no. 11 (2020): 1545–55. http://dx.doi.org/10.1177/0960327120931165.
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Objective: The study explored the chemoprophylactic potential of roflumilast against 1,2-dimethylhydrazine (DMH) actuated preneoplastic colon damage in albino Wistar rats. Methods: Animals were arbitrarily divided into five groups of six animals each. DMH was used to induce preneoplastic colon damage (20 mg/kg/7 days, subcutaneously, for 42 days). Roflumilast was administered subcutaneously at two doses (1 and 5 mg/kg/day, from day 28 to 42). At the end of the study, the animals were recorded for the electrocardiographic changes and heart rate variability (HRV) paradigms on 42nd day, using PowerLab system. Blood samples were collected from all the animals to measure hydrogen sulfide (H2S) and nitric acid. The colon tissue was dissected out and analyzed for inflammatory markers, biochemical parameters including, superoxide dismutase, thiobarbituric acid reactive substances, catalase, and glutathione reductase and histopathology. Results: DMH caused derangement of HRV factors, abnormal antioxidant markers, and elevated levels of inflammatory markers. H2S and nitric oxide levels upsurge in DMH-treated rats and promoted preneoplastic damage. Histopathologically, loss of crypts, goblet cells, and distorted lamina propria were observed in toxic group. Treatment with roflumilast was able to curtail down oxidative stress and inflammatory markers and stabilitate the hemodynamic derangements as well as was able to restore the normal architecture of colonic mucosa. Conclusion: The findings from the present study conclude that treatment with roflumilast positively modulates the preneoplastic colon damage.
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Miller, Preston R., Michael C. Chang, J. Jason Hoth, James H. Holmes, and J. Wayne Meredith. "Colonic Resection in the Setting of Damage Control Laparotomy: Is Delayed Anastomosis Safe?" American Surgeon 73, no. 6 (2007): 606–9. http://dx.doi.org/10.1177/000313480707300613.
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Based on a large body of literature concerning the subject, trauma surgeons are becoming more comfortable with anastomosis rather than stoma creation in patients with destructive colon injuries requiring resection. This literature was largely generated before the widespread acceptance of the importance of damage control laparotomy (DCL). Thus, when such injuries occur in patients initially left in colonic discontinuity after DCL, the question of anastomosis versus stoma becomes more difficult, and there are no data to guide management decisions. The goal of this report is to describe the results of our early experience with delayed anastomosis (DA) after destructive colon injury in the setting of DCL. We reviewed the records of patients with destructive colon injuries at our Level I trauma center over a 5.5-year period for demographics, injury characteristics, and outcome. Studied outcomes included anastomotic leak, intra-abdominal abscess, and colon injury-related death. The decision to proceed with DA was based on individual surgeon opinion at the time of re-exploration. From January 1, 2000 to July 31, 2006, 92 patients sustained colon injury, 55 of which required resection (31 blunt mechanism and 24 penetrating). Twenty-two resections occurred in the setting of DCL. Six of these patients underwent stoma creation and 11 underwent DA. Three died before reoperation, and two had an anastomosis created during the initial DCL. The remaining 33 resections occurred during initial definitive operation, and 21 underwent anastomosis, whereas 12 had a stoma created. Comparing the 11 patients undergoing DA with the 21 undergoing immediate anastomosis, the anastomotic leak rate (0% vs 5%), abscess rate (36% vs 24%), and colon related-death rate (9% vs 0%; all P > 0.05) were similar. Six patients undergoing DA had a right hemicolectomy with ileocolonic anastomosis, four had a segmental left colon resection, and one had a near total abdominal colectomy with ileosigmoid anastomosis. Delayed anastomosis of colon injuries after DCL is safe in selected patients and has a similar complication rate as resection and anastomosis performed during initial definitive operation. DA avoids stoma creation in some patients who are not candidates for anastomosis during initial DCL. To our knowledge, this represents the first reported series of DA after DCL, an area in which further work is needed to carefully define indications for the safe application of this concept.
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Islam, Md Shafiqul, Masatoshi Hori, and Hiroshi Ozaki. "Dextran sulfate sodium-induced colitis mice up-regulated extracellular matrix tenascin-C." Asian Journal of Medical and Biological Research 2, no. 4 (2017): 582–86. http://dx.doi.org/10.3329/ajmbr.v2i4.31000.
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Tenascin-C, an extracellular matrix glycoprotein, expresses high level during embryogenesis and almost absent during the normal postnatal life. However, it is re-appeared in a diverse condition such as tissue injury and in the stroma of various carcinomas. In this study, we investigated the appearance of tenascin-C in dextran sulfate sodium (DSS)-induced colitis in mice. DSS induced colitis mice demonstrated severe mucosal damage, with distortion and loss of crypts, depletion of goblet cells and infiltration of macrophages particularly F4/80 positive macrophages, granulocytes and lymphocytes in the colon tissues. These DSS inflamed colon expressed a high and dense level of tenascin-C in the severe damaged areas, whereas, moderate staining was observed in the moderate inflamed areas. DSS-induced colitis mice significantly increased macrophages infiltration in the colon tissues. These results suggested that tenascin-C extracellular matrix re-appeared in the colon tissues during inflammation.Asian J. Med. Biol. Res. December 2016, 2(4): 582-586
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Lu, C., D. Shah, A. Wijnands, et al. "P085 Expression profiling of Wnt pathway genes in colon biopsies of patients with Ulcerative Colitis." Journal of Crohn's and Colitis 15, Supplement_1 (2021): S186. http://dx.doi.org/10.1093/ecco-jcc/jjab076.214.
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Abstract Background There is an increasing demand of agents that can promote mucosal healing in Inflammatory Bowel Disease (IBD). Wnt/β-catenin signaling plays a critical role in epithelial regeneration and repair, and stimulating regeneration in the damaged epithelium by modulating Wnt signaling has been suggested as a potential treatment option for IBD. To guide development of Wnt modulating therapeutic molecules for IBD, an understanding of how Wnt signaling may be altered in IBD tissues is required. While earlier work showed altered Wnt pathway gene expression in UC tissues, these studies failed to consider disease conditions (moderate vs severe) and patient treatment history on expression of the Wnt family genes. These previous studies utilized RT-qPCR or microarray and did not reveal how Wnt pathway gene expression might be affected specifically in the epithelium and in the adjacent stromal stem cell niche. Here we report our work investigating expression patterns of Wnt pathway genes in UC biopsies from 12 patients with moderate and severe disease. Patients had either received no anti-TNF treatment or had gone through anti-TNF treatment and partially responded to the treatment. Methods Expression of a set of Wnt pathway genes was assessed in UC colon and rectum biopsies by RNAscope in situ hybridization and compared to expression patterns in normal control colon. The genes included the Wnt target genes AXIN2, LGR5 and RNF43, Wnt ligands and the FZD5 and LRP6 receptors enriched in the intestinal epithelium as well as key Wnt signal modulators RSPO1-4. Results Expression of Wnt target genes were mildly reduced in the UC colon epithelium, while their expression in some crypts appeared much lower. Overall expression levels of Wnt pathway genes did not differ between moderate and severe UC colon and Wnt target gene expression was more affected in the anti-TNF treated colons, which may reflect more refractory disease. Expression of FZD5, LRP6 and the key niche factor RSPO2, was reduced in the UC colon. RSPOs are normally expressed in the stromal cells next to the crypt bottom stem cell compartment but this expression pattern was disrupted in the UC colon as a result of immune cell infiltration. Although expression of Wnts was induced in the UC colon tissues, the location of expression was altered due to tissue damage, potentially making the Wnts less accessible to the intestinal stem cells. Conclusion Reduced expression of Wnt receptors, RSPOs and Wnt target genes indicate insufficient Wnt signal induction in the damaged colon epithelium of UC patients. This suggests that repair of the damaged epithelium by Wnt agonist treatment may constitute a new mechanism of action and benefit patients with UC.
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Piper, Clint, Vivian Zhou, Richard Komorowski, et al. "Pathogenic Bhlhe40+ GM-CSF+ CD4+ T cells promote indirect alloantigen presentation in the GI tract during GVHD." Blood 135, no. 8 (2020): 568–81. http://dx.doi.org/10.1182/blood.2019001696.
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Abstract Gastrointestinal (GI) tract involvement is the major cause of morbidity and mortality in acute graft-versus-host disease (GVHD), and pathological damage is largely attributable to inflammatory cytokine production. Recently, granulocyte-macrophage colony stimulating factor (GM-CSF) has been identified as a cytokine that mediates inflammation in the GI tract, but the transcriptional program that governs GM-CSF production and the mechanism by which GM-CSF links adaptive to innate immunity within this tissue site have not been defined. In the current study, we identified Bhlhe40 as a key transcriptional regulator that governs GM-CSF production by CD4+ T cells and mediates pathological damage in the GI tract during GVHD. In addition, we observed that GM-CSF was not regulated by either interleukin 6 (IL-6) or IL-23, which are both potent inducers of GVHD-induced colonic pathology, indicating that GM-CSF constitutes a nonredundant inflammatory pathway in the GI tract. Mechanistically, GM-CSF had no adverse effect on regulatory T-cell reconstitution, but linked adaptive to innate immunity by enhancing the activation of donor-derived dendritic cells in the colon and subsequent accumulation of these cells in the mLNs. In addition, GM-CSF promoted indirect alloantigen presentation, resulting in the accumulation of donor-derived T cells with a proinflammatory cytokine phenotype in the colon. Thus, Bhlhe40+ GM-CSF+ CD4+ T cells constitute a colitogenic T-cell population that promotes indirect alloantigen presentation and pathological damage within the GI tract, positioning GM-CSF as a key regulator of GVHD in the colon and a potential therapeutic target for amelioration of this disease.
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Jia, Mingxi, Wenjing Zhang, Taojin He, et al. "Evaluation of the Genotoxic and Oxidative Damage Potential of Silver Nanoparticles in Human NCM460 and HCT116 Cells." International Journal of Molecular Sciences 21, no. 5 (2020): 1618. http://dx.doi.org/10.3390/ijms21051618.
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Nano Ag has excellent antibacterial properties and is widely used in various antibacterial materials, such as antibacterial medicine and medical devices, food packaging materials and antibacterial textiles. Despite the many benefits of nano-Ag, more and more research indicates that it may have potential biotoxic effects. Studies have shown that people who ingest nanoparticles by mouth have the highest uptake in the intestinal tract, and that the colon area is the most vulnerable to damage and causes the disease. In this study, we examined the toxic effects of different concentrations of Ag-NPs on normal human colon cells (NCM460) and human colon cancer cells (HCT116). As the concentration of nanoparticles increased, the activity of the two colon cells decreased and intracellular reactive oxygen species (ROS) increased. RT-qPCR and Western-blot analyses showed that Ag NPs can promote the increase in P38 protein phosphorylation levels in two colon cells and promote the expression of P53 and Bax. The analysis also showed that Ag NPs can promote the down-regulation of Bcl-2, leading to an increased Bax/Bcl-2 ratio and activation of P21, further accelerating cell death. This study showed that a low concentration of nano Ag has no obvious toxic effect on colon cells, while nano Ag with concentrations higher than 15 μg/mL will cause oxidative damage to colon cells.
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Kapoor, Sabeeta, Elisabetta Damiani, Shan Wang, et al. "BRD9 Inhibition by Natural Polyphenols Targets DNA Damage/Repair and Apoptosis in Human Colon Cancer Cells." Nutrients 14, no. 20 (2022): 4317. http://dx.doi.org/10.3390/nu14204317.
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Epigenetic mechanisms play an important role in the etiology of colorectal cancer (CRC) and other malignancies due, in part, to deregulated bromodomain (BRD) functions. Inhibitors of the bromodomain and extraterminal (BET) family have entered into clinical trials as anticancer agents, and interest has grown in other acetyl ‘reader’ proteins as therapeutic targets, including non-BET member bromodomain-containing protein 9 (BRD9). We report here that overexpression of BRD9 is associated with poor prognosis in CRC patients, and that siRNA-mediated knockdown of BRD9 decreased cell viability and activated apoptosis in human colon cancer cells, coincident with increased DNA damage. Seeking natural compounds as BRD9 antagonists, molecular docking in silico identified several polyphenols such as Epigallocatechin-3-gallate (EGCG), Equol, Quercetin, and Aspalathin, with favorable binding energies, supported by BROMOscan® (DiscoverX) and isothermal titration calorimetry experiments. Polyphenols mimicked BRD9 knockdown and iBRD9 treatment in reducing colon cancer cell viability, inhibiting colony formation, and enhancing DNA damage and apoptosis. Normal colonic epithelial cells were unaffected, signifying cancer-specific effects. These findings suggest that natural polyphenols recognize and target BRD9 for inhibition, and might serve as useful lead compounds for bromodomain therapeutics in the clinical setting.
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Oberreuther-Moschner, Daniela L., Gerhard Jahreis, Gerhard Rechkemmer, and Beatrice L. Pool-Zobel. "Dietary intervention with the probiotics Lactobacillus acidophilus 145 and Bifidobacterium longum 913 modulates the potential of human faecal water to induce damage in HT29clone19A cells." British Journal of Nutrition 91, no. 6 (2004): 925–32. http://dx.doi.org/10.1079/bjn20041108.
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Probiotics reduce the risk of colon cancer by inhibiting carcinogen-induced DNA damage in animals, but there are no analogous data in human subjects. To enhance knowledge of the effects of probiotics in human subjects, we have investigated the genotoxicity of faecal water after dietary intervention with standard yoghurt or with probiotic yoghurt, which included the strains Lactobacillus acidophilus 145 and Bifidobacterium longum 913. Faeces were collected from nine healthy volunteers after intervention with probiotic yoghurt or standard yoghurt. Faecal water was isolated and incubated with human colon tumour cells HT29clone19A. DNA strand breaks, oxidised DNA bases and damage after challenge with H2O2 were determined by micro-gel-electrophoresis. Faecal water was genotoxic in comparison with NaCl, but protected against H2O2-induced DNA strand breaks. The intervention with probiotic yoghurt significantly lowered faecal water genotoxicity compared with standard yoghurt. However, probiotic intervention also increased oxidative damage; this either reflected prooxidative activity or stimulation of endogenous defence systems. Altogether, the balance of effects favoured protection, since faecal water from the probiotic group reduced overall genetic damage. Thus, there was a reduction of strand break-inducing compounds in human faeces after dietary intervention with probiotic bacteria. This protection reflected results from previous studies in carcinogen-exposed animals where probiotics reduced DNA damage in colon cells.
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Xiao, Rijin, Ying Su, Rosalia C. M. Simmen, and Frank A. Simmen. "Dietary soy protein inhibits DNA damage and cell survival of colon epithelial cells through attenuated expression of fatty acid synthase." American Journal of Physiology-Gastrointestinal and Liver Physiology 294, no. 4 (2008): G868—G876. http://dx.doi.org/10.1152/ajpgi.00515.2007.
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Dietary intake of soy protein decreases tumor incidence in rat models of chemically induced colon cancer. We hypothesized that decreased expression of fatty acid synthase (FASN) underlies, in part, the tumor-preventive effects of soy protein, since FASN overexpression characterizes early tumorigenesis. Here, we show that colonic FASN levels are reduced with dietary intake of soy protein isolate (SPI), compared with a control casein diet, in male Sprague-Dawley rats administered the colon carcinogen azoxymethane. SPI consumption resulted in decreased serum insulin levels and decreased azoxymethane-induced tumor suppressor p53 phosphorylation in colon crypt epithelium. To evaluate potential links between insulin and FASN leading to DNA damage, C2BBe1 colon epithelial cells, treated with insulin and/or the carcinogen N-nitroso- N-methylurea (NMU), were evaluated for DNA damage and apoptosis after transfection with control or FASN small interfering RNAs (siRNAs). While the numbers of DNA apurinic/apyrimidinic sites (biomarker of DNA damage) induced by NMU were unaffected by transfection of FASN siRNA, insulin induction of these sites was decreased with FASN knockdown. By contrast, NMU-induced apoptosis of C2BBe1, as well as intestinal epithelial cell (IEC)-6, was enhanced by transfected FASN siRNA. Increased FASN expression in IEC-6 cells by addition of liver X receptor agonist T0901317 did not affect apurinic/apyrimidinic site number, but enhanced cell killing by cerulenin, a FASN inhibitor. Moreover, insulin rescued NMU-treated cells from apoptosis in an FASN-dependent manner. Results suggest that dietary SPI, by decreasing circulating insulin levels and colon FASN expression, attenuates insulin-induced DNA damage and FASN-mediated anti-apoptosis during carcinogenesis, resulting in an overall reduced tumorigenic state.
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Das, Alakesh, Dikshita Deka, Antara Banerjee, and Surajit Pathak. "Evaluating the Anti-proliferative and Apoptotic Role of Atrial Natriuretic Peptide in Colon Cancer Cell Lines." International Journal of Experimental Research and Review 38 (April 30, 2024): 236–45. http://dx.doi.org/10.52756/ijerr.2024.v38.021.
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The use of small peptides and conventional anticancer drugs is gaining importance in oncology as small peptides may help increase chemo or radiation sensitivity. The present study aimed to study the impact of atrial natriuretic peptide (ANP) in reducing colon cancer cell proliferation in primary and metastatic colon cancer cell lines. The proliferation of colon cancer cell lines (SW480 and SW620) was analysed by CCK-8 assay and cell damage was analyzed by lactate dehydrogenase activity. Catalase activity assay was performed to measure the oxidative stress and antioxidant defense mechanisms in SW480 and SW620 cell lines. Subsequently, up or downregulation of cancer-specific gene expression such as BAX, Caspase-3, BCL-2, CDK-6, and PCNA genes were assessed after the treatment of small peptide ANP in SW480 and SW620 colon cancer cell lines. The ANP treatment decreased the colon cancer cell proliferation, upregulated the apoptosis-related gene expression (Caspase-3, BAX), downregulated the anti-apoptotic gene (BCL-2) expression, and proliferation-related genes (CDK-6, PCNA) in SW480 and SW620 colon cancer cell lines, and the differences were found to be statistically significantly. Further, increased levels of catalase in the colon cancer cell lines after ANP-treatment suggested the therapeutic role of ANP. Subsequently, the LDH analysis showed the potential of ANP in inducing colon cancer cell damage. Collectively, the current study clearly shows that ANP is a potential molecule in reducing uncontrolled cancer cell growth. However, additional research using animal models and additional colon cancer cell lines is needed to validate its potential usage in clinical studies.
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Xu, Mengfan, Lili Fu, Junwen Zhang, et al. "Potential of Inactivated Bifidobacterium Strain in Attenuating Benzo(A)Pyrene Exposure-Induced Damage in Colon Epithelial Cells In Vitro." Toxics 8, no. 1 (2020): 12. http://dx.doi.org/10.3390/toxics8010012.
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Long-term exposure to benzo(a)pyrene (BaP) poses a serious genotoxic threat to human beings. This in vitro study investigated the potential of inactivated Bifidobacterium animalis subsp. lactis BI-04 in alleviating the damage caused by BaP in colon epithelial cells. A concentration of BaP higher than 50 μM strongly inhibited the growth of colon epithelial cells. The colon epithelial cells were treated with 50 μM BaP in the presence or absence of inactivated strain BI-04 (~5 × 108 CFU/mL). The BaP-induced apoptosis of the colon epithelial cells was retarded in the presence of B. lactis BI-04 through activation of the PI3K/ AKT signaling pathway, and p53 gene expression was decreased. The presence of the BI-04 strain reduced the intracellular oxidative stress and DNA damage incurred in the colon epithelial cells by BaP treatment due to the enhanced expression of antioxidant enzymes and metabolism-related enzymes (CYP1A1). The data from comet assay, qRT-PCR, and western blot analysis showed that the cytotoxic effects of BaP on colon epithelial cells were largely alleviated because the bifidobacterial strain could bind to this carcinogenic compound. The in vitro study highlights that the consumption of commercial probiotic strain BI-04 might be a promising strategy to mitigate BaP cytotoxicity.
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Ricciardi V, Juan A. "Damage control surgery by transverse colon perforation: case report." MOJ Surgery 11, no. 2 (2023): 110–12. http://dx.doi.org/10.15406/mojs.2023.11.00234.
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Obstruction and perforation due to colorectal cancer represent challenging matters in terms of diagnosis, life-saving strategies, obstruction resolution and oncologic challenge. The outcomes of these different resections when performed in acute clinical situations remain substantially unexplored. Case report: 65 years old diabetic and obese female, with abdominal pain accompanied by the absence of channeling of flatus and bowel movements as well as countless vomiting of low intestinal content, wich is why its refer to the emergency of the IAHULA, Merida Venezuela. Physical examination: tachycardic, tachypneic, with, HR: 130 TA: 90/60, FR: 28m oxygen saturation 89%. Abdomen distended, diminished hydro aerial sounds, painful on palpation, with voluntary muscular defense. An emergency laparotomy show: general fecal peritonitis, perforations of the transverse colon, stenosing sigmoid tumor. For this reason, phase 1 damage control surgery was performed by transversectomy + placement of proximal and distal threads, requiring phase II in an intensive care unit, ventilatory support and vasopressor drugs. Phase III was planned in 48 to 72 hours for probable complete left colectomy, however, the patient died after 18 hours of postoperative. Discussion: damage control surgery has been considered an appropriate approach to the treatment of critically ill patients with severe intra-abdominal sepsis. Conclusion: Abdominal sepsis and a septic shock are both possible as a critical scenarios in patients with perforation and obstruction of the colon secondary tumors and carcinomas, for that reason it is important to know which patient can be selected to a damage control surgery in orden to improve the morbimortality.
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Wen, Lingmiao, Wei Xiong, Guihua Wei, et al. "Differential Response of Ileal and Colonic Microbiota in Rats with High-Fat Diet-Induced Atherosclerosis." International Journal of Molecular Sciences 23, no. 19 (2022): 11154. http://dx.doi.org/10.3390/ijms231911154.
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Growing evidence suggests that gut microbiota are associated with atherosclerosis (AS). However, the functional heterogeneity of each gut segment gives rise to regional differences in gut microbiota. We established a rat model of AS by feeding the rats a high-fat diet for a long period. The pathological and microbiota changes in the ileum and colon of the rats were examined, and correlations between AS and microbiota were analyzed. The aortic mesothelium of the experimental rats was damaged. The intima showed evident calcium salt deposition, indicating that the AS rat model was successfully developed. We noted varying degrees of pathological damage in the ileum and colon of the experimental rats. The 16S rDNA high-throughput sequencing showed significant differences in α-diversity, β-diversity, and microbiota comparisons in the ileum and colon. Furthermore, the ileum and colon of AS rats showed varying degrees of intestinal microbiota disturbance. This article contributes to the study of the relationship between the microbiota in different regions of the gut and AS, and provides new approaches in gut microbiota intervention for the treatment of AS.
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Tortora, Katia, Francesco Vitali, Carlotta De Filippo, Giovanna Caderni, and Lisa Giovannelli. "DNA damage in colon mucosa of Pirc rats, an Apc-driven model of colon tumorigenesis." Toxicology Letters 324 (May 2020): 12–19. http://dx.doi.org/10.1016/j.toxlet.2020.02.002.
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Geller, AJ, JT Newsome, DE Fleischer, EA Montgomery, AM Axelrad, and SB Benjamin. "Bipolar forceps provide adequate cautery, interpretable histologic tissue, and superficial colon damage in canine colon." Gastrointestinal Endoscopy 41, no. 4 (1995): 303. http://dx.doi.org/10.1016/s0016-5107(05)80065-3.
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Greer, Cpt Lauren T., Maj Suzanne M. Gillern, and Maj Amy E. Vertrees. "Article Commentary: Evolving Colon Injury Management: A Review." American Surgeon 79, no. 2 (2013): 119–27. http://dx.doi.org/10.1177/000313481307900221.
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The colon is the second most commonly injured intra-abdominal organ in penetrating trauma. Management of traumatic colon injuries has evolved significantly over the past 200 years. Traumatic colon injuries can have a wide spectrum of severity, presentation, and management options. There is strong evidence that most non-destructive colon injuries can be successfully managed with primary repair or primary anastomosis. The management of destructive colon injuries remains controversial with most favoring resection with primary anastomosis and others favor colonic diversion in specific circumstances. The historical management of traumatic colon injuries, common mechanisms of injury, demographics, presentation, assessment, diagnosis, management, and complications of traumatic colon injuries both in civilian and military practice are reviewed. The damage control revolution has added another layer of complexity to management with continued controversy.
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Liu, Yiwen, Qing Wu, Dongmei Wan, et al. "Expression and Possible Significance of ACE2 in the Human Liver, Esophagus, Stomach, and Colon." Evidence-Based Complementary and Alternative Medicine 2021 (August 25, 2021): 1–9. http://dx.doi.org/10.1155/2021/6949902.
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Angiotensin-converting enzyme 2 (ACE2) has been identified as the key receptor of SARS coronavirus that plays a key role in the pathogenesis of SARS. It is known that ACE2 mRNA can be expressed in most organs. However, the protein expression of ACE2 is not clear yet. To explore the role of ACE2 as a precipitating factor in digestive organ damage in COVID-19, this study investigated the expression of ACE2 protein in the human liver, esophagus, stomach, and colon. The result showed that ACE2 can be expressed in the liver, esophagus, stomach, and colon, which suggests SARS-CoV-2 may enter the digestive system through ACE2 and cause liver damage and gastrointestinal damage. It is hoped that the result of the study will provide a new strategy for the prevention and treatment of digestive organ damage under COVID-19.
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Xia, Cui, Chunhui Duan, Conghui Chen, et al. "The Effects of Electrolytic Multivitamins and Neomycin on Antioxidant Capacity and Intestinal Damage in Transported Lambs." Animals 14, no. 6 (2024): 824. http://dx.doi.org/10.3390/ani14060824.
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Transport stress can cause damage to animals. In this experiment, 60 four-month-old lambs were randomly divided into three groups: CG (basal diet), EG (basal diet + 375 mg/d/lamb electrolytic multivitamin), and NG (basal diet + 200 mg/d/lamb neomycin). The results were as follows: during road transport, in all groups, the levels of SOD, T-AOC, and GSP-Px, and mRNA expressions of CAT, SOD, Nrf2, HO-1, and Bcl-2 in the jejunum and colon decreased (p < 0.01). However, mRNA expressions of Keap1, IL-1β, IL-2, IL-12, Bax, and Caspase3 in the jejunum and colon and the level of MDA increased (p < 0.01). The concentrations of IgA, IgG, and sIgA in the jejunum and colon also decreased (p < 0.01). In the EG and NG, the levels of SOD (p < 0.05) and T-AOC (p < 0.01) increased, and the level of MDA decreased (p < 0.01). However, in the jejunum, the levels of SOD and T-AOC, the concentrations of IgA and IgG, and mRNA expression of Bcl-2 increased (p < 0.05). mRNA expressions of IL-1, IL-2, and Caspase 3 (p < 0.05), and mRNA expression of IL-12 (p < 0.01) decreased. In the colon, SOD activity and the concentration of sIgA increased (p < 0.01). The level of MDA and mRNA expressions of IL-2 and Caspase 3 also decreased (p < 0.05). In the jejunum and colon, mRNA expression of SOD (p < 0.05) and mRNA expression of Nrf2 increased (p < 0.01). mRNA expression of Keap1 (p < 0.05) and Bax (p < 0.01) decreased. In summary, road transport can cause a decrease in antioxidant activity and immunity of lambs and an increase in oxidative damage. Electrolytic multivitamins and neomycin can improve immune function and potentially reduce oxidative damage to the jejunum and colon.
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Sánchez-Garrido, Ana I., Vanessa Prieto-Vicente, Víctor Blanco-Gozalo, et al. "Preventive Effect of Cardiotrophin-1 Administration before DSS-Induced Ulcerative Colitis in Mice." Journal of Clinical Medicine 8, no. 12 (2019): 2086. http://dx.doi.org/10.3390/jcm8122086.
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Ulcerative colitis is a relatively frequent, chronic disease that impacts significantly the patient’s quality of life. Although many therapeutic options are available, additional approaches are needed because many patients either do not respond to current therapies or show significant side effects. Cardiotrophin-1 (CT-1) is a cytokine with potent cytoprotective, anti-inflammatory, and antiapoptotic properties. The purpose of this study was to assess if the administration of CT-1 could reduce colon damage in mice with experimental colitis was induced with 5% dextran sulfate sodium (DSS) in the drinking water. Half of the mice received an i.v. dose of CT-1 (200 µg/kg) 2 h before and 2 and 4 days after DSS administration. Animals were followed during 7 days after DSS administration. The severity of colitis was measured by standard scores. Colon damage was assessed by histology and immunohistochemistry. Inflammatory mediators were measured by Western blot and PCR. CT-1 administration to DSS-treated mice ameliorated both the clinical course (disease activity index), histological damage, inflammation (colon expression of TNF-α, IL-17, IL-10, INF IFN-γ, and iNOS), and apoptosis. Our results suggest that CT-1 administration before induction of colitis improves the clinical course, tissue damage, and inflammation in DSS-induced colitis in mice.
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Prieto-Vicente, Vanessa, Ana I. Sánchez-Garrido, Víctor Blanco-Gozalo, et al. "Cardiotrophin-1 attenuates experimental colitis in mice." Clinical Science 132, no. 9 (2018): 985–1001. http://dx.doi.org/10.1042/cs20171513.
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Cardiotrophin-1 (CT-1) holds potent anti-inflammatory, cytoprotective, and anti-apoptotic effects in the liver, kidneys, and heart. In the present study, the role of endogenous CT-1 and the effect of exogenous CT-1 were evaluated in experimental ulcerative colitis. Colitis was induced in CT-1 knockout and wild-type (WT) mice by administration of dextran sulphate sodium (DSS) in the drinking water during 7 days. CT-1 knockout mice showed higher colon damage and disease severity than WT mice. In addition, CT-1 (200 µg/kg/day, iv) or vehicle (as control) was administered during 3 days to WT, colitic mice, starting on day 4 after initiation of DSS. Disease activity index (DAI), inflammatory markers (tumor necrosis factor α (TNF-α), INFγ, IL-17, IL-10, inducible nitric oxide synthase (iNOS)), colon damage, apoptosis (cleaved caspase 3), nuclear factor κB (NFκB) and STAT-3 activation, and bacterial translocation were measured. Compared with mice treated with DSS, mice also treated with exogenous CT-1 showed lower colon damage, DAI, plasma levels of TNFα, colon expression of TNF-α, INFγ, IL-17, iNOS and cleaved caspase 3, higher NFκB and signal transducer and activator of transcription 3 (STAT3) pathways activation, and absence of bacterial translocation. We conclude that endogenous CT-1 plays a role in the defense and repair response of the colon against ulcerative lesions through an anti-inflammatory and anti-apoptotic effect. Supplementation with exogenous CT-1 ameliorates disease symptoms, which opens a potentially new therapeutic strategy for ulcerative colitis.
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Rybalchenko, V. F., P. S. Rusak, R. M. Boris, S. A. Braginskaya, B. S. Rinzberg, and D. S. Mamontov. "Injury of the recta and colon and perine in children." Paediatric Surgery. Ukraine, no. 2(75) (June 25, 2022): 52–59. http://dx.doi.org/10.15574/ps.2022.75.52.
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Purpose - to improve the treatment of children with traumatic injuries of the rectum, perineum and intestines. Materials and methods. In the clinic of the Department of Pediatric Surgery of the Shupyk National Healthcare University of Ukraine for 30 years, 9 children with traumatic injuries of the rectum, perineum and colon were treated. The age of the patients ranged from 1.5 to 16 years. There were 2 female patients (22.23%) and 7 male patients (77.77%). Results. The study found that among 9 patients who had damage to the rectum, concomitant damage to the descending colon in 1 (11.11%), sigmoid in 1 (11.11%), penetrating into the abdominal cavity in 3 (33.33%), urinary bladder in 1 (11.11%), vagina in 2 (22.22%). In 1 (11.11%) patient, a traumatic injury to the rectal wall was noted. Thus, among 9 patients fatigue was used in 8 (88.89%) children, of which in 3 (33.33%) double-barreled fatigue was initially imposed, requiring the distal colon to be turned off. Primary reconstructive surgeries were performed in 8 (88.89%) patients, and in 1 (11.11%) child with a delay of 2 weeks due to an inflammatory process in the rupture of the rectum and vagina in a 1.5-year-old child. Our own research has shown that the use of suspended or split fatigue on a spur is not an effective method of disconnecting the injured both colon and rectum from the contents. Traumatic damage to the rectum and vagina with rupture of the sphincter apparatus was found in 2 (22.22%) patients. Adhesive obstruction was found in 1 (11.11%) patient. All patients were discharged from the clinic. Conclusions. Visualization of the damage volume should be complete and performed under general anesthesia in the operating room. Surgical treatment of traumatic damage to the perineum of the rectum and colon requires an individual and should be phased: the imposition of a separate or final colostomy, as well as reconstructive and restorative surgery of the perineum, sphincter apparatus with mandatory electromyoidentification of the sphincter apparatus. Treatment of patients with perineal injury due to sexual abuse requires psychological and social rehabilitation. The research was carried out in accordance with the principles of the Helsinki Declaration. The study protocol was approved by the Local Ethics Committee of all participating institutions. The informed consent of the patient was obtained for conducting the studies. No conflict of interests was declared by the authors. Keywords: children, trauma, rectum, perineum, vagina, colon.
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Appleyard, Caroline B., Myrella L. Cruz, Angel A. Isidro, Janelle C. Arthur, Christian Jobin, and Claudio De Simone. "Pretreatment with the probiotic VSL#3 delays transition from inflammation to dysplasia in a rat model of colitis-associated cancer." American Journal of Physiology-Gastrointestinal and Liver Physiology 301, no. 6 (2011): G1004—G1013. http://dx.doi.org/10.1152/ajpgi.00167.2011.
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Evidence supports involvement of microflora in the transition of chronic inflammation to neoplasia. We investigated the protective efficacy of the probiotic VSL#3 in a model of colitis-associated colorectal cancer. Chronic colitis was induced in Sprague-Dawley rats by administration of trinitrobenzene sulfonic acid (TNBS), followed 6 wk later by systemic reactivation. To induce colitis-associated dysplasia and cancer, the animals received TNBS (intravenously) twice a week for 10 wk. One group received VSL#3 in drinking water from 1 wk before colitis induction until death. The colons were examined for damage and presence of dysplasia or cancer. Samples were analyzed for cell proliferation and apoptosis, vitamin D receptor (VDR) expression, angiogenic factors, and presence of alkaline sphingomyelinase or phosphatase. Microbial community composition was evaluated by terminal restriction fragment-length polymorphism analysis of the bacterial 16S rRNA gene. None of the probiotic-treated animals developed carcinoma, and no high-grade dysplasia was found in either the proximal or mid colon. In contrast, 29% of the animals in the control group developed carcinoma in one or more regions of the colon. VSL#3-treated animals had significantly less damage than the vehicle treated-controls in all areas of the colon, and this correlated with decreased richness and diversity of the mucosally adherent microbiota. Treatment with the probiotic increased the antiangiogenic factor angiostatin, VDR expression, and alkaline sphingomyelinase. We concluded that pretreatment with the probiotic VSL#3 can attenuate various inflammatory-associated parameters, delaying transition to dysplasia and cancer, thus offering its potential therapeutic use in patients with long-standing colitis.
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Burger-van Paassen, Nanda, Maria van der Sluis, Janneke Bouma, et al. "Colitis development during the suckling-weaning transition in mucin Muc2-deficient mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 301, no. 4 (2011): G667—G678. http://dx.doi.org/10.1152/ajpgi.00199.2010.
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The mucin Muc2 is the structural component of the colonic mucus layer. Adult Muc2 knockout (Muc2−/−) mice suffer from severe colitis. We hypothesized that Muc2 deficiency induces inflammation before weaning of mother's milk [ postnatal day (P) 14] with aggravation of colitis after weaning (P28). Muc2−/−and wild-type mice were killed at embryonic day 18.5 and P1.5, P7.5, P14, P21, and P28. Colonic morphology, influx of T cells, and goblet cell-specific protein expression was investigated by (immuno)histochemistry. Cytokine and Toll-like receptor (TLR) profiles in the colon were analyzed by quantitative RT-PCR. Muc2−/−mice showed an increased and persistent influx of Cd3ε-positive T cells in the colonic mucosa as of P1.5. This was accompanied by mucosal damage at P28 in the distal colon but not in the proximal colon. At P14, the proinflammatory immune response [i.e., increased interleukin (IL)-12 p35, IL-12 p40, and tumor necrosis factor-α, expression] in the distal colon of Muc2−/−mice presented with an immune suppressive response [i.e., increased Foxp3, transforming growth factor (TGF)-β1, IL-10, and Ebi3 expression]. In contrast, at P28, a proinflammatory response remained in the distal colon, whereas the immune suppressive response (i.e., Foxp3 and TGF-β1 expression) declined. The proximal colon of Muc2−/−mice did not show morphological damage and was dominated by an immune suppressive response at P14 and P28. Interestingly, changes in expression of TLRs and TLR-related molecules were observed in the distal colon at P14 and P28 and in the proximal colon only at P28. Colitis in Muc2−/−mice is limited before weaning by immune suppressive responses and exacerbates in the distal colon after weaning because of the decline in the immune suppressive response.
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Yahia, Doha, Yasmin O. El-Amir, and Mahmoud Rushdi. "Mancozeb fungicide-induced genotoxic effects, metabolic alterations, and histological changes in the colon and liver of Sprague Dawley rats." Toxicology and Industrial Health 35, no. 4 (2019): 265–76. http://dx.doi.org/10.1177/0748233719834150.
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The present study was designed to evaluate genotoxic markers of mancozeb exposure and withdrawal in colon and liver tissues together with histological changes in the gastrointestinal tract of Sprague Dawley rats. Thirty rats were divided into three equal groups; group I: treatment, 250 mg/kg mancozeb dissolved in corn oil administered twice weekly for 7 weeks; group II: withdrawal, the same treatment as group I after which animals were untreated for 5 weeks; group III: control, administered corn oil on the same schedule as group I for 7 weeks. All administrations were by oral gavage. Serum samples were analyzed for biochemical parameters. The comet assay and histopathological examinations were done on liver and colon specimens. The results demonstrated that mancozeb exposure caused significant increases in triglycerides and total cholesterol accompanied by decreases in glucose levels, with extensive DNA damage in liver and colon together with pathological changes in stomach, colon, and liver. Mancozeb withdrawal for 5 weeks improved the lipid and glucose profiles and decreased the degree of DNA damage and changes in the architecture of the stomach, colon, and liver. We concluded that discontinuing exposure to mancozeb fungicide for 5 weeks could ameliorate the adverse effects induced by 7 weeks of exposure to mancozeb. A longer withdrawal time may further reduce the observed genotoxicity.
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Potenza, Lucia, Cinzia Calcabrini, Roberta De Bellis, et al. "Effects of Reactive Oxygen Species on Mitochondrial Content and Integrity of Human Anastomotic Colorectal Dehiscence: A Preliminary DNA Study." Canadian Journal of Gastroenterology 25, no. 8 (2011): 433–39. http://dx.doi.org/10.1155/2011/741073.
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BACKGROUND: Anastomotic dehiscence is one of the most severe complications of colorectal surgery. Gaining insight into the molecular mechanisms responsible for the development of anastomotic dehiscence following colorectal surgery is important for the reduction of postoperative complications.OBJECTIVE: Based on the close relationship between surgical stress and oxidative stress, the present study aimed to determine whether a correlation exists between increased levels of reactive oxygen species and colorectal anastomotic dehiscence.METHODS: Patients who underwent surgical resection for colorectal cancer were divided into three groups: patients with anastomotic dehiscence (group 1); patients without dehiscence who underwent neoadjuvant radiochemotherapy (group 2); and patients without anastomotic dehiscence who did not undergo neoadjuvant radiochemotherapy (group 3). Quantitative polymerase chain reaction and real-time polymerase chain reaction assays were performed to measure nuclear DNA and mitochondrial DNA (mtDNA) content, and possible oxidative damage to nonmalignant colon and rectal tissues adjacent to the anastomoses.RESULTS: mtDNA content was reduced in the colon tissue of patients in groups 1 and 2. Rectal mtDNA was found to be more damaged than colonic mtDNAs in all groups. The 4977 bp common deletion was observed in the mtDNA of tissues from both the colon and rectum of all patients.DISCUSSION: Patients in groups 1 and 2 were more similar to one another than to group 3, probably due to higher levels of reactive oxygen species in the mitochondria; the greater damage found in the rectum suggests that dehiscence originates primarily from the rectal area.CONCLUSIONS: The present study of mtDNA analyses of normal human colon and rectal tissues from patients with colorectal cancer is among the first of its kind.
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Takaba, Junji, Yuji Mishima, Kiyohiko Hatake, and Tadashi Kasahara. "Role of Bone Marrow-Derived Monocytes/Macrophages in the Repair of Mucosal Damage Caused by Irradiation and/or Anticancer Drugs in Colitis Model." Mediators of Inflammation 2010 (2010): 1–11. http://dx.doi.org/10.1155/2010/634145.
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Mucosal damage is a common side effect of many cancer treatments, especially radiotherapy and intensive chemotherapy, which often induce bone marrow (BM) suppression. We observed that acetic acid- (AA-) induced mucosal damage in the colon of mice was worsened by simultaneous treatment with irradiation or 5-FU. However, irradiation 14 days prior to the AA treatment augmented the recovery from mucosal damage, suggesting that the recovery from BM suppression had an advantageous effect on the mucosal repair. In addition, BM transplantation also augmented the recovery from AA-induced mucosal damage. We further confirmed that transplanted BM-derived cells, particularly F4/80+Gr1+“inflammatory” monocytes (Subset 1), accumulated in the damaged mucosal area in the early healing phase, and both of Subset 1 and F4/80+Gr1-“resident” monocytes (Subset 2) accumulated in this area in later phases. Our results suggest that monocytes/macrophages contribute to the mucosal recovery and regeneration following mucosal damage by anticancer drug therapy.
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Dhingra, Priyanka, Alison Obr, Carl Spana, John Dodd, and Paul Kayne. "A NEW APPROACH FOR TREATMENT OF ULCERATIVE COLITIS: A MELANOCORTIN RECEPTOR AGONIST PL8177." Inflammatory Bowel Diseases 30, Supplement_1 (2024): S1—S2. http://dx.doi.org/10.1093/ibd/izae020.003.
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Abstract INTRODUCTION The melanocortin system plays an important role in resolving inflammatory processes. The melanocortin 1 receptor (MC1R)–specific agonist PL8177 has demonstrated MC1R binding affinity and functional activity that mirrors that of α-melanocyte–stimulating hormone. The effect of PL8177 on inflammation, cell population composition, and gene and protein expression was investigated in colons from a dextran sulfate sodium (DSS)–induced rat model of colitis. METHODS Colitis was induced by 5% DSS in drinking water. Rats received vehicle control (placebo) capsules, oral PL8177 capsules (20, 50, and 100 μg per animal), or mesalazine (positive control). Colons were harvested on day 8. Samples were analyzed for cytokines, and by single nuclei RNA-seq and data-independent acquisition tandem mass spectrometry phosphoproteome profiling. Colitis was assessed by diarrhea and rectal bleeding, colon length shortening, colon weight gain, and histopathology. Total colitis index assessed inflammatory damage. RESULTS PL8177 50 μg showed a significant (P&lt;0.05) improvement in colon weight (53% reduction), stool consistency, and fecal occult blood score vs vehicle, and there was significant improvement in the total colitis index for the PL8177 100-μg group vs vehicle. All PL8177 cohorts showed greater improvement in the total colitis index than mesalazine. Mesalazine produced a marked reduction in colon length, but only moderate improvement (35%) in colon weight. Single nuclei RNA-seq showed that in the PL8177 100-μg group, relative cell populations and key gene expression levels were closer to those of healthy controls PL8177 100-μg treatment caused a relative decrease in immune cells and an increase in enterocytes and enteric glial cells compared to vehicle control. Subclustering analysis revealed significant differences between PL8177 100-μg and vehicle populations. Although both showed the presence of macrophages, vehicle-treated colons were primarily M1 macrophages involved in inflammation. In PL8177 100 μg–treated colons, macrophages were primarily pro-resolution M2. Proteomic analysis showed that PL8177-treated colons are more similar to sham colons than to vehicle colons. Also after treatment with PL8177, Smad 2 and 3, proteins known to promote intestinal homeostasis showed expression similar to that seen in the sham group, a result not seen in vehicle-treated colons. DISCUSSION Oral PL8177 treatment showed significant improvement in anatomical markers of colitis vs the vehicle and mesalazine control groups, supporting the aim of treating inflammatory bowel disease (IBD). Transcriptomics and proteomics data show that oral PL8177 treatment causes diseased colons to move toward the healthy state and to resolve inflammation. Resolving inflammation—rather than blocking it—provides the possibility of efficacy coupled with safety in treating IBD.
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Cui, Yujing, Haoyue Guan, Samuel Kumi Okyere, et al. "Microbial Guardians or Foes? Metagenomics Reveal Association of Gut Microbiota in Intestinal Toxicity Caused by DON in Mice." International Journal of Molecular Sciences 26, no. 4 (2025): 1712. https://doi.org/10.3390/ijms26041712.
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The role of gut microbiota has become a research hotspot in recent years; however, whether the gut microbiota are involved in the alleviation or exacerbation of Deoxynivalenol (DON) toxicity has not been fully studied. Therefore, the objective of this study was to investigate whether the gut microbiota are involved in reducing or aggravating the intestinal damage induced by DON in mice. Mice that received or did not receive antibiotic-induced intestinal flora clearance were orally given DON (5 mg kg/bw/day) for 14 days. At the end of the experiment, serum, intestinal tissue samples and colon contents were collected for further analysis. DON caused development of severe histopathological damage, such as necrosis and inflammation of the jejunum and colon in mice without gut microbiota clearance. The levels of tight junction proteins ZO-1 and occludin were reduced in the jejunum and colon of mice without gut microbiota clearance. In addition, the mRNA and protein levels of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) were increased in mice without gut microbiota clearance. The presence of microbiota exacerbate the intestinal damage induced by DON via changes in gut microbiota abundance and production of gut damaging metabolites.
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Palvai, Sandeep, Meenu Mahesh Kuman, and Sudipta Basu. "Hyaluronic acid cloaked oleic acid nanoparticles inhibit MAPK signaling with sub-cellular DNA damage in colon cancer cells." Journal of Materials Chemistry B 5, no. 20 (2017): 3658–66. http://dx.doi.org/10.1039/c7tb00656j.
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Minhas, Dr S. S., Dr J. K. Mahajan, and Dr D. C. Merwaha. "Extensive Abdominal Electric Burn Injury." Indian Journal of Plastic Surgery 24, no. 02 (1991): 034–35. http://dx.doi.org/10.1055/s-0043-1775696.
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Najafi, Masoud, Mohsen Cheki, Gholamreza Hassanzadeh, Peyman Amini, Dheyauldeen Shabeeb, and Ahmed E. Musa. "Protection from Radiation-induced Damage in Rat’s Ileum and Colon by Combined Regimens of Melatonin and Metformin: A Histopathological Study." Anti-Inflammatory & Anti-Allergy Agents in Medicinal Chemistry 19, no. 2 (2020): 180–89. http://dx.doi.org/10.2174/1871523018666190718161928.
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Background: Radiation-induced enteritis and proctitis are common side effects of abdominopelvic cancers among patients that undergo radiotherapy for prostate, colorectal or urinary cancers. Exposure of these tissues to high doses of radiation leads to damage to villous, inflammation, pain, ulcer and bleeding, which may cause malabsorption and gastrointestinal disorders. To date, several procedures such as pharmaceutical treatment have been proposed for protection and mitigation of gastrointestinal toxicity following radiotherapy. Aims: In the current study, we aimed to investigate the possible radioprotection of ileum and colon in rats using a combination of melatonin and metformin. Methods: In this experimental study, 30 male Wistar rats were randomly assigned to six groups: control, melatonin (100 mg/kg) treatment, melatonin (100 mg/kg) plus metformin (100 mg/kg) treatment, radiation (10 Gy to whole body) group, radiation + melatonin (100 mg/kg) treatment, and radiation + melatonin (100 mg/kg) plus metformin (100 mg/kg) treatment. After 3.5 days, rats were sacrificed and their ileum and colon tissues carefully removed. Histopathological evaluations were conducted on these tissue samples. Results: Histological evaluations reported moderate to severe damages to ileum and colon following whole body irradiation. Melatonin administration was able to protect the ileum remarkably, while the combination of melatonin and metformin was less effective. Interestingly, for the colon, melatonin was less effective while its combination with metformin was able to protect against radiation toxicity completely. Conclusion: For the ileum, melatonin was a more effective radioprotector compared to its combination with metformin. However, the combination of melatonin and metformin can be proposed as an ideal radioprotector for the colon.
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Yu, Sirui, Ying Cheng, Jing Yu, Shubei He, Jin Chai, and Qiong Pan. "ORGANIC ANION TRANSPORTER POLYPEPTIDE (OATP) 3A1 AMELIORATES INTESTINAL MUCOSAL DAMAGE IN INFLAMMATORY BOWEL DISEASE." Inflammatory Bowel Diseases 30, Supplement_1 (2024): S65—S66. http://dx.doi.org/10.1093/ibd/izae020.141.
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Abstract BACKGROUND Inflammatory bowel disease (IBD) is a chronic condition characterised by disruption of the colonic mucosal barrier. OATP3A1/SLCO3A1 is a bile acid efflux transporter, alleviating cholestasis-associated liver injury. However, the functional role and regulational mechanism of intestinal OATP3A1 in IBD remain unclear. METHODS The expression and correlation of SLCO3A1 were investigated in the public datasets with IBD patients. Intestinal epithelial cell-specific Slco3a1 knockout (Slco3a1ΔIEC) mice were generated and fed with 4% DSS for functional studies. RESULTS Intestinal SLCO3A1 expression was significantly elevated in the ulcerative colitis (UC) and Crohn's disease (CD) patients, and positively correlated with TNFα, IL1β and MADCAM1. Compared with Slco3a1flox/flox littermates administrated by DSS, Slco3a1ΔIEC mice exhibited exacerbated colitis, characterized by more severe weight loss, enhanced colon shortening and spleen swelling. Interestingly, intestine histology assessments revealed that epithelial Oatp3a1 ablation significantly aggravated extensive disruption of the mucosal epithelium and inflammatory infiltration. The intestinal mucosal barrier function of Slco3a1ΔIEC mice was more severely damaged, as assessed by detecting serum permeated FITC-dextran. Expression of tight junction-associated proteins was decreased in Slco3a1ΔIEC mice. CONCLUSION Our data showed that intestinal OATP3A1 expression was markedly upregulated and exerted a protective role in inflammatory bowel disease. Overexpression of intestinal OATP3A1 may hold potential as a novel approach to alleviate intestinal inflammation- associated mucosal damage. Figure 1 SLCO3A1 mRNA levels in the intestinal tissues of IBD patients and generation of Slco3a1ΔIECmice. (A) SLCO3A1 mRNA expression in patients with active UC or active CD and matched controls, revealed by analyzing databases of RNA-Seq data. (B and C) Pearson’s correlation analysis between SLCO3A1 expression and TNF-α, IL1β, or MADCAM1 in colon biopsy samples from active UC (n = 74) and CD (n = 52) patients. Data were collected from GEO database GSE75214. (D) Schematic diagram of Slco3a1ΔIEC mice. (E) Genotyping of Slco3a1ΔIEC mice using genomic DNA extracted from mice tails. (F) Western blot confirmed the intestine epithelia ablation of OATP3A1 in Slco3a1ΔIEC mice. Figure 2 Effects of intestinal epithelia-specific ablation of OATP3A1 on colitis and mucosal damage in a 4% DSS treatment mouse model of IBD. (A, B) Body weight loss and spleen weight were measured from Slco3a1flox/flox or Slco3a1ΔIEC mice. (C) Serum FITC-dextran level was detected by fluorescence spectrophotometer. (D) Gross morphology images of the colon, and colon length were measured. (E) Representative images of H&E-stained colons, and histopathology analysis of colitis were performed. (F) Immunoblots of colonic lysates on Zo-1, Occludin or Claudin-1(n = 4 for each group). **P &lt; 0.01; ***P &lt; 0.001. n = 5 for Slco3a1flox/flox group; n =6 for Slco3a1ΔIEC group treated with DSS.
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Quan, T. H., N. Hachiya, and Y. Takizawa. "Induction of DNA damage in rat colon mucosal DNA after treatment with a colon carcinogen and/or a colon tumor promoter." Mutation Research/Environmental Mutagenesis and Related Subjects 253, no. 3 (1991): 272. http://dx.doi.org/10.1016/0165-1161(91)90207-o.
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Szweda, M., J. Szarek, M. Lew, A. Szarek-Bęska, and D. Gulda. "Can liquorice extract and herbal solution prevent colonic mucosa damage caused by robenacoxib in dogs?" Polish Journal of Veterinary Sciences 18, no. 4 (2015): 793–98. http://dx.doi.org/10.1515/pjvs-2015-0103.
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Abstract Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used in animals, especially in dogs, to manage pain due to inflammatory disease. This study investigated whether plant drugs can prevent mucosal injury induced by robenacoxib. We used fifteen healthy beagle dogs (7 male and 8 female) aged 4 months, weighing 4.2-5.1 kg at the beginning of the study. Endoscopy and biopsy of the colon were performed before and on the 21 day treatment with robenacoxib (1), robenacoxib, herbal solution with liquorice extract (2), placebo – an empty capsule (3). There were 5 animals in each group. The greatest microscopic damage in the colon was observed in animals which received robenacoxib. Plant drug administration reduced the severity of lesions in the colon when administered with robenacoxib (ARI = – 0.15). Conclusion: concurrent administration of liquorice extract and plant solution with robenacoxib was associated with significant decreased severity of the robenacoxib-induced colonic mucosal lesions.