Colleen Nofi

78 statements · 3 topics

Etiologies (Gastroschisis/NEC/Atresia/Volvulus) · guest expert Intestinal Rehab · guest expert

Featured statements

Necrotizing entercolitis or neck is a devastating gastrointestinal disease impacting premature infants whose pathophysiology is driven by a multitude of complex pathways that are not completely understood.
quote · Etiologies (Gastroschisis/NEC/Atresia/Volvulus)
Once released from the cell, CRP becomes extracellular CIRP or ECIRP, where it then acts as a damp by enhancing the release of cytokines and chemokines, and amplifying the inflammatory cascade.
quote · Etiologies (Gastroschisis/NEC/Atresia/Volvulus)
Once released from the cell, extracellular CIRP acts as a DAMP by enhancing the release of cytokines and chemokines and amplifying the inflammatory cascade
clinical · Intestinal Rehab
MOP3-treated pups had significantly reduced fluorescence intensity indicating protection of the intestinal barrier compared to vehicle-treated NEC pups
clinical · Intestinal Rehab
Reduction in eCIRP with MOP3 treatment correlated with reduction in systemic inflammatory markers including IL-6 and TNF-alpha
clinical · Necrotizing Enterocolitis
MOP3 (MFGE8 derived oligopeptide 3) is an eCIRP scavenging peptide that removes eCIRP from circulation to reduce inflammation
clinical · Necrotizing Enterocolitis

Nothing matches these filters — clear the search or widen the filters.

Colleen's statements about Etiologies (Gastroschisis/NEC/Atresia/Volvulus) 26 statements

Open the Etiologies (Gastroschisis/NEC/Atresia/Volvulus) collection →

Dr. Colleen Nofi - Best of the Best in Pediatric Surgery 2025

Quotation Necrotizing entercolitis or neck is a devastating gastrointestinal disease impacting premature infants whose pathophysiology is driven by a multitude of complex pathways that are not completely understood. Open
Statement Necrotizing enterocolitis is a devastating gastrointestinal disease impacting premature infants whose pathophysiology is driven by complex pathways that are not completely understood Open
Statement NEC has limited treatment options and an unacceptably high morbidity and mortality risk Open
Statement Under biologic conditions, CIRP is found inside the cell where it acts as an RNA chaperone protein Open
Statement In states of cellular stress such as sepsis, CIRP escapes outside the cell Open
Quotation Once released from the cell, CRP becomes extracellular CIRP or ECIRP, where it then acts as a damp by enhancing the release of cytokines and chemokines, and amplifying the inflammatory cascade. Open
Statement Once released from the cell, extracellular CIRP acts as a DAMP by enhancing the release of cytokines and chemokines and amplifying the inflammatory cascade Open
Statement MOP3 (MFGE8 derived oligopeptide 3) is an eCIRP scavenging peptide that removes eCIRP from circulation to reduce inflammation Open
Statement CIRP knockout protected pups from NEC severity with preservation of intestinal villi architecture Open
Statement CIRP knockout mice subjected to NEC showed reduced intestinal inflammation as measured by mRNA levels of IL-6 and TNF-alpha in the small bowel Open
Statement CIRP knockout pups had reduced fluorescent dextran leakage indicating preserved intestinal barrier function compared to wild-type NEC pups Open
Statement CIRP knockout pups subjected to NEC had 100% survival whereas wild-type pups had only 65% survival in the same model under the same conditions Open
Quotation Remarkably, in the same model under the same conditions, there was 100% survival for CRP knockout pups subjected to neck, whereas the survival was only 65% for wild type pups. Open
Statement MOP3 treatment reduced circulating eCIRP levels in NEC pups compared to vehicle Open
Statement Reduction in eCIRP with MOP3 treatment correlated with reduction in systemic inflammatory markers including IL-6 and TNF-alpha Open
Statement MOP3 treatment protected against NEC severity with preservation of intestinal villi Open
Statement MOP3 treatment reduced intestinal inflammation in NEC as measured by mRNA levels of IL-6 and TNF-alpha Open
Statement MOP3-treated pups had significantly reduced fluorescence intensity indicating protection of the intestinal barrier compared to vehicle-treated NEC pups Open
Statement Murine pups subjected to NEC and treated with MOP3 had 80% survival compared to only 50% survival in vehicle-treated pups Open
Quotation When we compared overall survival of murine pups subjected to the neck model, we found a significant improvement in survival, up to 80% in pups treated with MP3, compared to only 50% for vehicle treated pups. Open
Statement MOP3 protects against NEC pathogenesis by scavenging eCIRP and preventing deleterious downstream impacts Open
Statement eCIRP exacerbates NEC pathogenesis by increasing inflammation and intestinal injury Open
Statement MOP3 is effective in other models of ischemia-reperfusion injury in the gut Open
Statement The therapeutic benefit of MOP3 is not at the same level as complete CIRP knockdown Open
Statement The murine NEC model uses a 4-day protocol with continuous stressors including LPS, formula gavage, and hypoxia Open
Statement MOP3 treatment was administered once per day at the beginning of the model, ongoing with the NEC insult Open
Colleen's statements about Intestinal Rehab 26 statements

Open the Intestinal Rehab collection →

Dr. Colleen Nofi - Best of the Best in Pediatric Surgery 2025

Statement Necrotizing enterocolitis is a devastating gastrointestinal disease impacting premature infants whose pathophysiology is driven by complex pathways that are not completely understood Open
Quotation Necrotizing entercolitis or neck is a devastating gastrointestinal disease impacting premature infants whose pathophysiology is driven by a multitude of complex pathways that are not completely understood. Open
Statement NEC has limited treatment options and an unacceptably high morbidity and mortality risk Open
Statement Under biologic conditions, CIRP is found inside the cell where it acts as an RNA chaperone protein Open
Statement In states of cellular stress such as sepsis, CIRP escapes outside the cell Open
Quotation Once released from the cell, CRP becomes extracellular CIRP or ECIRP, where it then acts as a damp by enhancing the release of cytokines and chemokines, and amplifying the inflammatory cascade. Open
Statement Once released from the cell, extracellular CIRP acts as a DAMP by enhancing the release of cytokines and chemokines and amplifying the inflammatory cascade Open
Statement MOP3 (MFGE8 derived oligopeptide 3) is an eCIRP scavenging peptide that removes eCIRP from circulation to reduce inflammation Open
Statement CIRP knockout protected pups from NEC severity with preservation of intestinal villi architecture Open
Statement CIRP knockout mice subjected to NEC showed reduced intestinal inflammation as measured by mRNA levels of IL-6 and TNF-alpha in the small bowel Open
Statement CIRP knockout pups had reduced fluorescent dextran leakage indicating preserved intestinal barrier function compared to wild-type NEC pups Open
Statement CIRP knockout pups subjected to NEC had 100% survival whereas wild-type pups had only 65% survival in the same model under the same conditions Open
Quotation Remarkably, in the same model under the same conditions, there was 100% survival for CRP knockout pups subjected to neck, whereas the survival was only 65% for wild type pups. Open
Statement MOP3 treatment reduced circulating eCIRP levels in NEC pups compared to vehicle Open
Statement Reduction in eCIRP with MOP3 treatment correlated with reduction in systemic inflammatory markers including IL-6 and TNF-alpha Open
Statement MOP3 treatment protected against NEC severity with preservation of intestinal villi Open
Statement MOP3 treatment reduced intestinal inflammation in NEC as measured by mRNA levels of IL-6 and TNF-alpha Open
Statement MOP3-treated pups had significantly reduced fluorescence intensity indicating protection of the intestinal barrier compared to vehicle-treated NEC pups Open
Statement Murine pups subjected to NEC and treated with MOP3 had 80% survival compared to only 50% survival in vehicle-treated pups Open
Quotation When we compared overall survival of murine pups subjected to the neck model, we found a significant improvement in survival, up to 80% in pups treated with MP3, compared to only 50% for vehicle treated pups. Open
Statement eCIRP exacerbates NEC pathogenesis by increasing inflammation and intestinal injury Open
Statement MOP3 protects against NEC pathogenesis by scavenging eCIRP and preventing deleterious downstream impacts Open
Statement MOP3 is effective in other models of ischemia-reperfusion injury in the gut Open
Statement The therapeutic benefit of MOP3 is not at the same level as complete CIRP knockdown Open
Statement The murine NEC model uses a 4-day protocol with continuous stressors including LPS, formula gavage, and hypoxia Open
Statement MOP3 treatment was administered once per day at the beginning of the model, ongoing with the NEC insult Open
Colleen's statements about Necrotizing Enterocolitis 26 statements

Open the Necrotizing Enterocolitis collection →

Dr. Colleen Nofi - Best of the Best in Pediatric Surgery 2025

Quotation Necrotizing entercolitis or neck is a devastating gastrointestinal disease impacting premature infants whose pathophysiology is driven by a multitude of complex pathways that are not completely understood. Open
Statement Necrotizing enterocolitis is a devastating gastrointestinal disease impacting premature infants whose pathophysiology is driven by complex pathways that are not completely understood Open
Statement NEC has limited treatment options and an unacceptably high morbidity and mortality risk Open
Statement Under biologic conditions, CIRP is found inside the cell where it acts as an RNA chaperone protein Open
Statement In states of cellular stress such as sepsis, CIRP escapes outside the cell Open
Quotation Once released from the cell, CRP becomes extracellular CIRP or ECIRP, where it then acts as a damp by enhancing the release of cytokines and chemokines, and amplifying the inflammatory cascade. Open
Statement Once released from the cell, extracellular CIRP acts as a DAMP by enhancing the release of cytokines and chemokines and amplifying the inflammatory cascade Open
Statement MOP3 (MFGE8 derived oligopeptide 3) is an eCIRP scavenging peptide that removes eCIRP from circulation to reduce inflammation Open
Statement CIRP knockout protected pups from NEC severity with preservation of intestinal villi architecture Open
Statement CIRP knockout mice subjected to NEC showed reduced intestinal inflammation as measured by mRNA levels of IL-6 and TNF-alpha in the small bowel Open
Statement CIRP knockout pups had reduced fluorescent dextran leakage indicating preserved intestinal barrier function compared to wild-type NEC pups Open
Statement CIRP knockout pups subjected to NEC had 100% survival whereas wild-type pups had only 65% survival in the same model under the same conditions Open
Quotation Remarkably, in the same model under the same conditions, there was 100% survival for CRP knockout pups subjected to neck, whereas the survival was only 65% for wild type pups. Open
Statement MOP3 treatment reduced circulating eCIRP levels in NEC pups compared to vehicle Open
Statement Reduction in eCIRP with MOP3 treatment correlated with reduction in systemic inflammatory markers including IL-6 and TNF-alpha Open
Statement MOP3 treatment protected against NEC severity with preservation of intestinal villi Open
Statement MOP3 treatment reduced intestinal inflammation in NEC as measured by mRNA levels of IL-6 and TNF-alpha Open
Statement MOP3-treated pups had significantly reduced fluorescence intensity indicating protection of the intestinal barrier compared to vehicle-treated NEC pups Open
Quotation When we compared overall survival of murine pups subjected to the neck model, we found a significant improvement in survival, up to 80% in pups treated with MP3, compared to only 50% for vehicle treated pups. Open
Statement Murine pups subjected to NEC and treated with MOP3 had 80% survival compared to only 50% survival in vehicle-treated pups Open
Statement MOP3 protects against NEC pathogenesis by scavenging eCIRP and preventing deleterious downstream impacts Open
Statement eCIRP exacerbates NEC pathogenesis by increasing inflammation and intestinal injury Open
Statement MOP3 is effective in other models of ischemia-reperfusion injury in the gut Open
Statement The therapeutic benefit of MOP3 is not at the same level as complete CIRP knockdown Open
Statement The murine NEC model uses a 4-day protocol with continuous stressors including LPS, formula gavage, and hypoxia Open
Statement MOP3 treatment was administered once per day at the beginning of the model, ongoing with the NEC insult Open