Über das Verhalten der Membranen von Pflanzenhaaren zu Organischen Farbstoffen

Ohne ZusammenfassungMit 2 Textabbildungen.     

Consumption of Domestic Cat in Madagascar: Frequency,Purpose, and Health Implications

ABSTRACT

The domestic cat Felis catus has a long history of interaction with humans, and is found throughout the world as a household pet and a feral animal. Despite people's often sentimental association with cats, cat meat is sometimes consumed by them; this practice can have important implications for public health. In Madagascar, a least developed country that has experienced recent political instability, cat consumption is known to occur, but remains poorly understood. To improve our understanding of cat consumption practices in Madagascar we interviewed 512 respondents in five towns. We used semi-structured interviews to: 1) clarify the preference for, and prevalence, correlates, and timing of, cat consumption; 2) describe methods used to procure cats for consumption; 3) identify motives for consuming cat meat; and, 4) evaluate to what extent patterns of cat-meat consumption are influenced by taboos. We found that, although cat was not a preferred source of meat, many (34%) Malagasy respondents had consumed cat meat before, with most (54%) of these indicating such consumption occurred in the last decade. We did not detect a link between consumption of cat meat and recent access to meat (a proxy for food security). Cat meat was almost never purchased, but rather was obtained when the owners consumed their own pet cat, as a gift, or by hunting feral cats. Cat meat was usually consumed in smaller towns following cat–human conflict such as attacks on chickens, but in the large capital city, cat meat was procured primarily from road-killed individuals. These results suggest cat-meat consumption is typically an opportunistic means to obtain inexpensive meat, rather than principally serving as a response to economic hardship. These results further suggest cat handling and consumption may present a potential pathway for transmission of several diseases, including toxoplasmosis, that may warrant heightened public health efforts.     

Untersuchungen über die Textur der Zellwände des Parenchyms saftiger Früchte (Mesokarp)

Ohne ZusammenfassungHerrn Prof. Dr. K. Höfler zum 70. Geburtstag gewidmet.     

Impaired macrophage autophagy increases the immune response in obese mice by promoting proinflammatory macrophage polarization

Recent evidence that excessive lipid accumulation can decrease cellular levels of autophagy and that autophagy regulates immune responsiveness suggested that impaired macrophage autophagy may promote the increased innate immune activation that underlies obesity. Primary bone marrow-derived macrophages (BMDM) and peritoneal macrophages from high-fat diet (HFD)-fed mice had decreased levels of autophagic flux indicating a generalized impairment of macrophage autophagy in obese mice. To assess the effects of decreased macrophage autophagy on inflammation, mice with a Lyz2-Cre-mediated knockout of Atg5 in macrophages were fed a HFD and treated with low-dose lipopolysaccharide (LPS). Knockout mice developed systemic and hepatic inflammation with HFD feeding and LPS. This effect was liver specific as knockout mice did not have increased adipose tissue inflammation. The mechanism by which the loss of autophagy promoted inflammation was through the regulation of macrophage polarization. BMDM and Kupffer cells from knockout mice exhibited abnormalities in polarization with both increased proinflammatory M1 and decreased anti-inflammatory M2 polarization as determined by measures of genes and proteins. The heightened hepatic inflammatory response in HFD-fed, LPS-treated knockout mice led to liver injury without affecting steatosis. These findings demonstrate that autophagy has a critical regulatory function in macrophage polarization that downregulates inflammation. Defects in macrophage autophagy may underlie inflammatory disease states such as the decrease in macrophage autophagy with obesity that leads to hepatic inflammation and the progression to liver injury.     

Distinct functions of JNK and c-Jun in oxidant-induced hepatocyte death

Overactivation of c‐Jun N‐terminal kinase (JNK)/c‐Jun signaling is a central mechanism of hepatocyte injury and death including that from oxidative stress. However, the functions of JNK and c‐Jun are still unclear, and this pathway also inhibits hepatocyte death. Previous studies of menadione‐induced oxidant stress demonstrated that toxicity resulted from sustained JNK/c‐Jun activation as death was blocked by the c‐Jun dominant negative TAM67. To further delineate the function of JNK/c‐Jun signaling in hepatocyte injury from oxidant stress, the effects of direct JNK inhibition on menadione‐induced death were examined. In contrast to the inhibitory effect of TAM67, pharmacological JNK inhibition by SP600125 sensitized the rat hepatocyte cell line RALA255‐10G to death from menadione. SP600125 similarly sensitized mouse primary hepatocytes to menadione toxicity. Death from SP600125/menadione was c‐Jun dependent as it was blocked by TAM67, but independent of c‐Jun phosphorylation. Death occurred by apoptosis and necrosis and activation of the mitochondrial death pathway. Short hairpin RNA knockdowns of total JNK or JNK2 sensitized to death from menadione, whereas a jnk1 knockdown was protective. Jnk2 null mouse primary hepatocytes were also sensitized to menadione death. JNK inhibition magnified decreases in cellular ATP content and β‐oxidation induced by menadione. This effect mediated cell death as chemical inhibition of β‐oxidation also sensitized cells to death from menadione, and supplementation with the β‐oxidation substrate oleate blocked death. Components of the JNK/c‐Jun signaling pathway have opposing functions in hepatocyte oxidant stress with JNK2 mediating resistance to cell death and c‐Jun promoting death. J. Cell. Biochem. 113: 3254–3265, 2012. © 2012 Wiley Periodicals, Inc.     

The future of GI and liver research: editorial perspectives. III. JNK/AP-1 regulation of hepatocyte death

Activation of the JNK/activator protein-1 (AP-1)-signaling pathway is a common mediator of hepatocyte death from a variety of stimuli. Although the mechanism by which JNK or AP-1 promotes death is unknown, it results when activation of this signaling pathway is unusually prolonged. Although JNK/AP-1 mediates TNF-induced cell death at or above the level of the mitochondria, the ability of JNK/AP-1 to promote death from necrosis as well as apoptosis suggests that JNK/AP-1 may induce death by several mechanisms. Recognition of JNK/AP-1 signaling as a critical promoter of hepatocyte death raises the possibility that the therapeutic manipulation of this pathway may be effective in the treatment of human liver disease.