Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An experimental study was undertaken to evaluate the effects of total parenteral nutrition (TPN) on tumor growth in rats. Sato lung cancer was transplanted subcutaneously in male Donryu rats. Two weeks after inoculation, experimental animals were divided into three groups: Group I (5% G); Group II (21% G, 4% A.A; TPN) received intravenous infusion through cervical vein; Group III rats were maintained on a regular diet. All of the animals were killed on the eighth day. There was a significant increase in tumor volume and tumor weight in both G-II (7.3 +/- 3.9 cm3, 8.7 +/- 6.3 g) and G-III (7.4 +/- 4.6 cm3, 9.7 +/- 5.4 g), as compared with G-I (3.3 +/- 1.4 cm3, 3.7 +/- 1.9 g). In morphometric studies, an average area of tumor cell in G-II was 267 +/- 172 microns2, being significantly larger than in G-I (195 +/- 95 microns2) or G-III (185 +/- 93 microns2). The nuclear diameter of tumor cell was 9.9 +/- 2.2 microns in G-II, 9.2 +/- 1.9 micron in G-III, and 8.5 +/- 1.5 micron in G-I, respectively. Total water balance throughout the experimental period was +84.0 +/- 14.5 ml/100 g BW in G-II, +86.3 +/- 8.2 ml/100 g BW in G-III, and +44.8 +/- 22.5 ml/100 g body weight in G-I, respectively. Increased tumor volume and tumor weight found in G-II may not be due to hyperplasia of each tumor cell, but rather due possibly to water retention in tumor tissue.
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PMID:Does total parenteral nutrition (TPN) really promote tumor growth? A morphometric study. 643 77

NLRP-3 inflammasome is one of several intracellular danger recognition platforms that integrates infectious or non-infectious types of danger into the expression of pro-inflammatory cytokines to set-up inflammation for danger control. NLRP3 activation induces three types of caspase-1-mediated responses: secretion of IL-1beta, secretion of IL-18 and a programmed form of cell death, referred to as pyroptosis. Similar to the well-documented impact of Toll-like receptor-driven danger signalling in kidney disease, evolving data now suggest a similar involvement of the NLRP3 inflammasome in renal inflammation. Here, we discuss the accumulating data on NLRP3 in the kidney: its IL-1beta and IL-18-dependent 'canonical' effects and the current evidence for its 'non-canonical' effects, e.g. in tumor growth factor (TGF)-beta signalling, epithelial-mesenchymal transition and fibrosis. Research in this area will certainly uncover yet unknown aspects of danger signalling in the kidney and how it drives renal inflammation and immunopathology.
Nephrol Dial Transplant 2014 Jan
PMID:Canonical and non-canonical effects of the NLRP3 inflammasome in kidney inflammation and fibrosis. 2402 44