Morphological classification of genetic diversity in cultivated okra, Abelmoschus esculentus (L) Moench using principal component analysis (PCA) and single linkage cluster analysis (SLCA)

29 okra accessions sourced from different agro-ecological regions in Nigeria and grown during the rainy season of 2007 at Abeokuta (derived savannah) were evaluated for genetic diversity using principal component analysis (PCA) and single linkage cluster analysis (SLCA). The experiment was laid out in a randomized complete block design (RCBD) with five replications. The accessions were classified into six and five cluster groups by PCA and SLCA respectively. The mean contributions of plant height, days to flowering, branches per plant, fresh pod width, mature pod width, fresh pod length, pod weight per plant, pod per plant, seeds per pod, and seed weight per plant were relatively high in the principal axes confirming the major contributions of these traits to seed yield in okra. The first four principal axes accounted for over 60% of the total variation among the 18 characters describing the accessions. Accessions 29, 9 and 14, which appears to be the most diverse may be useful as source for variable characters in okra improvement among the accessions studied been the most distant.Key words: Derived savannah, principal axes, accessions, variation, cluster analysis, okra

TGF-β in progression of liver disease

Transforming growth factor-β (TGF-β) is a central regulator in chronic liver disease contributing to all stages of disease progression from initial liver injury through inflammation and fibrosis to cirrhosis and hepatocellular carcinoma. Liver-damage-induced levels of active TGF-β enhance hepatocyte destruction and mediate hepatic stellate cell and fibroblast activation resulting in a wound-healing response, including myofibroblast generation and extracellular matrix deposition. Being recognised as a major profibrogenic cytokine, the targeting of the TGF-β signalling pathway has been explored with respect to the inhibition of liver disease progression. Whereas interference with TGF-β signalling in various short-term animal models has provided promising results, liver disease progression in humans is a process of decades with different phases in which TGF-β or its targeting might have both beneficial and adverse outcomes. Based on recent literature, we summarise the cell-type-directed double-edged role of TGF-β in various liver disease stages. We emphasise that, in order to achieve therapeutic effects, we need to target TGF-β signalling in the right cell type at the right time

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field