scholarly journals A rare complication in a Covid-19 positive patient with sigmoid colon cancer-hemoperitoneum due to gallbladder necrosis following micro-thrombosis

2021 ◽  
pp. 317-323
Author(s):  
Mihai Faur ◽  
Andrei Moisin ◽  
Calin Mohor ◽  
Dan Sabau
Keyword(s):  
Rare Complication ◽  
Interleukin 1 ◽  
Rapid Onset ◽  
Point Of View ◽  
Sigmoid Colon Cancer ◽  
Sensory Level ◽  
Level Control ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Viral Respiratory

Covid-19, also known as acute respiratory syndrome 2019-nCoV, severe acute respiratory syndrome (SARS) 2, and Wuhan pneumonia, is a viral respiratory disease caused by a SARS-associated coronavirus (SARS-CoV2). The most serious complications of Covid-19 are due to the development of micro-thrombosis in various organs and systems as a result of the high levels of pro-inflammatory cytokines (tumor necrosis factor alpha, interleukin 1 and 6) which initiate the activation of coagulation and the generation of thrombin. Several studies demonstrated the poor outcome of Covid-19-infected patients who underwent surgery, suggesting that surgery may accelerate and exacerbate Covid-19 progression. We report the case of an 81-year-old patient admitted as an emergency with Covid-19 pneumonia, hemoperitoneum, ischemic acute cholecystitis and obstructive sigmoid cancer. Cholecystectomy, pneumoperitoneal lavage, and Hartmann operation were performed under combined epidural-spinal anesthesia. This technique has some advantages compared to spinal and epidural techniques, such as: rapid onset of analgesia and the possibility of obtaining the desired sensory level, control of the anesthetic block, and ensuring postoperative analgesia. The unfavorable outcome of this case is due to the occurrence of the cytokine storm and coagulation disorders, with the change in the related biological constants, both from a biochemical and systemic point of view.

Pancreatic beta-cell-selective production of tumor necrosis factor-alpha induced by interleukin-1

Diabetes ◽  
1993 ◽  
Vol 42 (7) ◽  
pp. 1026-1031 ◽  
Author(s):  
K. Yamada ◽  
N. Takane ◽  
S. Otabe ◽  
C. Inada ◽  
M. Inoue ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Beta Cell ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Pancreatic Beta Cell ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

Differential effects of cytokines on thermosensitive neurons in guinea pig preoptic area slices

1991 ◽  
Vol 261 (5) ◽  
pp. R1096-R1103 ◽  
Author(s):  
M. Shibata ◽  
C. M. Blatteis
Keyword(s):  
Guinea Pig ◽  
Preoptic Area ◽  
Interleukin 1 ◽  
Interleukin 1 Beta ◽  
Necrosis Factor Alpha ◽  
Firing Rates ◽  
Artificial Cerebrospinal Fluid ◽  
Cold Sensitive ◽  
Factor Alpha ◽  
Necrosis Factor

This study was undertaken to determine whether the reported different courses of the febrile responses to the cytokines interleukin-1 beta (IL-1), interferon-alpha 2 (IFN), and tumor necrosis factor-alpha (TNF) might have neuroelectrophysiological correlates. The reactions of individual thermosensitive neurons in the preoptic area (POA) were evaluated by recording their extracellular single-unit firing rates (FR) in slices of guinea pig POA perfused with artificial cerebrospinal fluid (aCSF), human recombinant IL-1 (50-500 ng), IFN (1,000-8,000 U), and TNF (400-5,000 ng) (all doses per min/ml aCSF); thermosensitivity was assessed by FR responses to changes of perfusate temperature (32-42 degrees C). Overall, these cytokines depressed the FR of warm-sensitive units and excited those of cold-sensitive units, in agreement with expectations. However, the responses of individual neurons treated with two or all three cytokines were dissimilar: 61% of the units tested reacted differentially to two or three cytokines, 32% exhibited identical responses, and 7% had no response to any cytokine. These results support the possibility that IL-1, IFN, and TNF may affect not the same but rather distinct neurons functionally connected to common pyrogenic effectors. Thus they suggest that differential neuronal substrates may be utilized by each cytokine to exert its pyrogenic effect.

scholarly journals Inflammatory cytokines induce synthesis and secretion of gro protein and a neutrophil chemotactic factor but not β2-microglobulin in human synovial cells and fibroblasts

1989 ◽  
Vol 259 (2) ◽  
pp. 585-588 ◽  
Author(s):  
E E Golds ◽  
P Mason ◽  
P Nyirkos
Keyword(s):  
Interleukin 1 ◽  
Human Fibroblasts ◽  
Chemotactic Factor ◽  
Synovial Cells ◽  
Necrosis Factor Alpha ◽  
Normal Human ◽  
Neutrophil Chemotactic Factor ◽  
Factor Alpha ◽  
Beta 2 Microglobulin ◽  
Necrosis Factor

Exposure of human synovial cells and fibroblasts in monolayer culture to interleukin 1 results in prominent secretion of proteins with Mr values of 6000 and 7000. By N-terminal sequence analysis, the Mr-6000 protein is identified as the protein encoded by a recently described gro mRNA. The Mr-7000 protein is identical to a neutrophil chemotactic factor released from monocytes. Stimulation of normal human fibroblasts with tumour necrosis factor alpha also results in expression and secretion of these two proteins. In addition to these cytokine-induced proteins, we have identified beta 2-microglobulin as an Mr-8000 protein constitutively secreted by synovial cells.

NF-IL6 and AP-1 cooperatively modulate the activation of the TSG-6 gene by tumor necrosis factor alpha and interleukin-1

1994 ◽  
Vol 14 (10) ◽  
pp. 6561-6569
Author(s):  
L Klampfer ◽  
T H Lee ◽  
W Hsu ◽  
J Vilcek ◽  
S Chen-Kiang
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Human Fibroblasts ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Normal Human ◽  
Factor Alpha ◽  
Necrosis Factor

Tumor necrosis factor alpha (TNF-alpha) and interleukin-1 (IL-1) activate transcription of the TSG-6 gene in normal human fibroblasts through a promoter region (-165 to -58) that encompasses an AP-1 and a NF-IL6 site. We show by deletion analysis and substitution mutagenesis that both sites are necessary for activation by TNF-alpha. Activation by IL-1 requires the NF-IL6 site and is enhanced by the AP-1 site. These results suggest that the NF-IL6 and AP-1 family transcription factors functionally cooperate to mediate TNF-alpha and IL-1 signals. Consistent with this possibility, IL-1 and TNF-alpha markedly increase the binding of Fos and Jun to the AP-1 site, and NF-IL6 activates the native TSG-6 promoter. Activation by NF-IL6 requires an intact NF-IL6 site and is modulated by the ratio of activator to inhibitor NF-IL6 isoforms that are translated from different in-frame AUGs. However, the inhibitor isoform can also bind to the AP-1 site and repress AP-1 site-mediated transcription. The finding that the inhibitor isoform antagonizes activation of the native TSG-6 promoter by IL-1 and TNF-alpha suggests that NF-IL6 has a physiologic role in these cytokine responses. Thus, the functionally distinct NF-IL6 isoforms cooperate with Fos and Jun to positively and negatively regulate the native TSG-6 promoter by TNF-alpha and IL-1.

scholarly journals Keratinocyte growth factor, tumor necrosis factor-alpha and interleukin-1 beta gene expression in cultured fibroblasts and keratinocytes from burned patients

2013 ◽  
Vol 28 (8) ◽  
pp. 551-558 ◽  
Author(s):  
Alfredo Gragnani ◽  
Bruno Rafael Müller ◽  
Ismael Dale Contrim Guerreiro da Silva ◽  
Samuel Marcos Ribeiro de Noronha ◽  
Lydia Masako Ferreira
Keyword(s):  
Gene Expression ◽  
Tumor Necrosis ◽  
Keratinocyte Growth Factor ◽  
Interleukin 1 ◽  
Interleukin 1 Beta ◽  
Necrosis Factor Alpha ◽  
Cultured Fibroblasts ◽  
Factor Alpha ◽  
Beta Gene ◽  
Necrosis Factor
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