Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field.

https://biblio.ugent.be/publication/8555786/file/8555788.pdf

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

In 2009, the Nomenclature Committee on Cell Death (NCCD) proposed a set of recommendations for the definition of distinct cell death morphologies and for the appropriate use of cell death-related terminology, including 'apoptosis', 'necrosis' and 'mitotic catastrophe'. In view of the substantial progress in the biochemical and genetic exploration of cell death, time has come to switch from morphological to molecular definitions of cell death modalities. Here we propose a functional classification of cell death subroutines that applies to both in vitro and in vivo settings and includes extrinsic apoptosis, caspase-dependent or -independent intrinsic apoptosis, regulated necrosis, autophagic cell death and mitotic catastrophe. Moreover, we discuss the utility of expressions indicating additional cell death modalities. On the basis of the new, revised NCCD classification, cell death subroutines are defined by a series of precise, measurable biochemical features.

/pdf/molecular-definitions-of-cell-death-subroutines-q5g428rlyi.pdf

Molecular definitions of cell death subroutines: recommendations of the Nomenclature Committee on Cell Death 2012

Practice guidelines in acute pancreatitis.

https://www.spg.pt/wp-content/uploads/2015/11/2013-ACG_Guideline_AcutePancreatitis_September_2013.pdf

American College of Gastroenterology guideline: management of acute pancreatitis.

Autophagy is a mechanism by which cellular material is delivered to lysosomes for degradation, leading to the basal turnover of cell components and providing energy and macromolecular precursors. Autophagy has opposing, context-dependent roles in cancer, and interventions to both stimulate and inhibit autophagy have been proposed as cancer therapies. This has led to the therapeutic targeting of autophagy in cancer to be sometimes viewed as controversial. In this Review, we suggest a way forwards for the effective targeting of autophagy by understanding the context-dependent roles of autophagy and by capitalizing on modern approaches to clinical trial design.

/pdf/targeting-autophagy-in-cancer-2pjcn0h04a.pdf

Targeting autophagy in cancer

Pathophysiology of systemic inflammatory response syndrome and multiorgan dysfunction syndrome in acute pancreatitis

Diagnosis and Management of Chronic Pancreatitis

A 60-year-old man presented with recurrent abdominal pain and weight loss for 6 months. Abdominal imaging showed a large vascular lesion in the head and neck of pancreas suggestive of arteriovenous malformation (AV malformation). Endoscopic ultrasound was done which showed features of AV malformation with no evidence of pancreatic malignancy. Surgery was planned for definitive treatment of malformation. Digital subtraction angiography with angioembolization was done prior to surgery to reduce vascularity of the lesion. He recovered after a pylorus preserving pancreaticoduodenectomy. Histopathology of the resected specimen confirmed the pancreatic AV malformation. There has been no recurrence at 2 years of follow-up.

A case of pancreatic AV malformation in an elderly man.

UNLABELLED Sclerotherapy results in significant local complications, both immediate and delayed. This study was designed to examine the esophageal pathophysiology underlying these complications. METHODS We prospectively evaluated esophageal transit, motility abnormalities and gastroesophageal reflux (GER) with barium studies and esophageal functional scintigraphy in 24 patients (20 men, 4 women; mean age 33 +/- 12.4 yr) before sclerotherapy (Phase I), after two sessions (Phase II), following variceal eradication (Phase III) and 4 wk later (Phase IV). RESULTS Varices were obliterated after 5.6 +/- 1.9 sessions of intravariceal sclerotherapy performed weekly with 1% polidocanol (17.3 ml per session). There was no baseline Phase I dysmotility or reflux. Phase II studies recorded a marked delay of esophageal global and segmental (mid and distal) transit time in 98.2% of patients by scintigraphy and 90% by barium studies. Incoordinate contractions and aperistalsis were observed in 0, 66.7%, 58.3% and 33.8% of patients from Phases I-IV studies, respectively. Barium studies revealed tertiary waves and reverse peristalsis in 0, 50%, and 75% of patients from Phases I-III; strictures were observed in 0, 1, and 3 patients during Phases I-III. GER was detected scintigraphically in 0, 58.3%, 25% and 16.6% during Phases I-IV sequentially. In contrast, barium studies grossly underestimated GER (0, 5% and 15% at phases I-III). CONCLUSION There was strong concordance between esophageal symptoms, transit, motility abnormalities and GER (p < 0.05). Variceal eradication (Phases III and IV) was associated with a gradual recovery of esophageal symptoms, ulcers and all abnormal scintigraphic parameters. Sclerosant-induced chemical esophagitis in association with peptic esophagitis due to gross reflux following sclerotherapy possibly can explain the symptoms in most patients.

http://jnm.snmjournals.org/content/36/8/1363.full.pdf

Pramod Kumar Garg

Papers

Pathophysiology of systemic inflammatory response syndrome and multiorgan dysfunction syndrome in acute pancreatitis

Diagnosis and Management of Chronic Pancreatitis

A case of pancreatic AV malformation in an elderly man.

Effect of Endoscopic Variceal Sclerotherapy on Esophageal Motor Functions and Gastroesophageal Reflux

Foreign body in the esophagus mimicking esophageal carcinoma.