PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 2761525

[Liver failure after hepatic resection].

H Shimada·A Matsuba·S Nimoto·H Fujita·G Nakagawara·S Tsuchiya
View original source ↗Export metadata ↓

Abstract

Pathophysiology of hepatic resection in 89 cases was investigated from the point of endotoxemia and phagocytic function in order to clarify the mechanism of postoperative liver failure. In the control group (n = 44) and the bile stasis group (n = 9) plasma endotoxin increased to 22 to 160pg/ml early after operation and decreased thereafter: but in the liver failure group (n = 10) it increased higher corresponding to high risk operation and the massive bleeding or anastomosis leakage. In control and bile stasis groups phagocytic K value, serum CH50, plasma fibronectin decreased to half of the preoperative level on the first postoperative day, and later improved. In liver failure group these levels decreased but never improved. Liver failure group was characterized by an irreversible platelets count decrease corresponding to the increase of serum bilirubin level. It was concluded that endotoxemia in the presence of a self defence system dysfunction is thought to be a trigger for organ failure.

Explore related subjects

Complement System ProteinsEndotoxinsFibronectinsHepatectomyHumansLiver DiseasesLiver NeoplasmsPlatelet CountPostoperative ComplicationsEnglish AbstractJournal ArticleResearch Support, Non-U.S. Gov't

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

H Shimada, A Matsuba, S Nimoto, H Fujita, G Nakagawara, S Tsuchiya. 1989. [Liver failure after hepatic resection].. https://pubmed.ncbi.nlm.nih.gov/2761525/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

High-throughput amplification fragment length polymorphism (htAFLP) analysis identifies genetic lineage markers but not complement phenotype-specific markers in Moraxella catarrhalis.

Comparative high-throughput amplified fragment length polymorphism (htAFLP) analysis was performed on a set of 25 complement-resistant and 23 complement-sensitive isolates of Moraxella catarrhalis in order to determine whether there were complement phenotype-specific markers within this species. The htAFLP analysis used 21 primer-pair combinations, generating 41 364 individual fragments and 2273 fragment length polymorphisms, with an average of 862 polymorphisms per isolate. Analysis of polymorphism data clearly indicated the presence of two phylogenetic lineages and 40 (2%) lineage-specific polymorphisms. However, despite the presence of 361 (16%) statistically significant complement phenotype-associated polymorphisms, no single marker was 100% complement phenotype-specific. Furthermore, no complement phenotype-specific marker was found within different phylogenetic lineages. These findings agree with previous results indicating that the complement resistance phenotype within M. catarrhalis is probably defined by multiple genes, although not all of these genes may be present within all M. catarrhalis isolates.

Complement System Proteins↗
PubMed2006

Differential mucosal susceptibility in HIV-1 transmission and infection.

HIV infection occurs primarily through mucosal surfaces, indicating that protection at mucosal sites may be crucial in prevention and treatment. The host innate and adaptive immune elements provide a level of protection, which differs between mucosal compartments, and appears to be most successful in the oral environment, where transmission is rare. In addition to the distinct oral mucosal architecture and cellular constituents, oral fluids, unlike other mucosal secretions, are rarely a vehicle for HIV infection. Multiple soluble factors may contribute to this antiviral activity, including neutralizing antibodies, secretory leukocyte protease inhibitor (SLPI), antiviral peptides such as defensins and cystatins, glycoproteins including thrombospondin and lactoferrin, and complement components. Understanding the antiviral activities of these and other potential resistance factors is becoming increasingly important in attempts to design treatments in the era of HAART resistance. In this regard, the mechanism of anti-HIV action of SLPI has recently been further elucidated by the discovery of its binding protein/receptor, which plays a key role in the infection of macrophages and may consequently be a novel therapeutic target. Continued elucidation of the unique features of mucosal HIV immunology is essential for understanding HIV pathogenesis and for developing effective vaccines and therapeutics.

Complement System Proteins↗
PubMed2006

Human monocyte-derived dendritic cells are a source of several complement proteins.

OBJECTIVE: Little is known about the role of local production of complement components by dendritic cells (DCs) during the generation of specific immune responses. In this study, we demonstrate that human DCs are an extrahepatic source of several soluble complement proteins. METHODS: Reverse transcriptase polymerase chain reaction (RT-PCR) and Western blot were used to evaluate the expression and production of several complement proteins. RESULTS: We show that DCs produce C3, C5, C9, Factor (F)I, FH, FB, FD and properdin at levels similar to macrophages. Treatment of DCs with lipopolysaccharide (LPS) promoted an increase in the expression of C3 and FI mRNAs and a decrease in C5 mRNA, while C9, FH, FB, FD and properdin mRNA levels were not affected. Treatment with interleukin (IL) -1 or dexamethasone induced a modest increase in C3 mRNA levels and did not affect the expression of other complement components. CONCLUSION: DCs are a source of complement proteins whose synthesis may be regulated in response to different inflammatory stimuli.

Complement System Proteins↗