다중혈관 관상동맥 환자에서 y-문합을 이용하여 양쪽 내흉동맥만을 사용한 우회술의 조기 성적

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes.

For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure flux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy.

Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation, it is imperative to target by gene knockout or RNA interference more than one autophagy-related protein. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways implying that not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular assays, we hope to encourage technical innovation in the field.

/pdf/guidelines-for-the-use-and-interpretation-of-assays-for-ijf2t30pbq.pdf

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction

Lipid peroxidation can be described generally as a process under which oxidants such as free radicals attack lipids containing carbon-carbon double bond(s), especially polyunsaturated fatty acids (PUFAs). Over the last four decades, an extensive body of literature regarding lipid peroxidation has shown its important role in cell biology and human health. Since the early 1970s, the total published research articles on the topic of lipid peroxidation was 98 (1970–1974) and has been increasing at almost 135-fold, by up to 13165 in last 4 years (2010–2013). New discoveries about the involvement in cellular physiology and pathology, as well as the control of lipid peroxidation, continue to emerge every day. Given the enormity of this field, this review focuses on biochemical concepts of lipid peroxidation, production, metabolism, and signaling mechanisms of two main omega-6 fatty acids lipid peroxidation products: malondialdehyde (MDA) and, in particular, 4-hydroxy-2-nonenal (4-HNE), summarizing not only its physiological and protective function as signaling molecule stimulating gene expression and cell survival, but also its cytotoxic role inhibiting gene expression and promoting cell death. Finally, overviews of in vivo mammalian model systems used to study the lipid peroxidation process, and common pathological processes linked to MDA and 4-HNE are shown.

/pdf/lipid-peroxidation-production-metabolism-and-signaling-234bwmyps5.pdf

Lipid peroxidation: production, metabolism, and signaling mechanisms of malondialdehyde and 4-hydroxy-2-nonenal.

The glutathione S-transferases (GST) represent a major group of detoxification enzymes. All eukaryotic species possess multiple cytosolic and membrane-bound GST isoenzymes, each of which displays distinct catalytic as well as noncatalytic binding properties: the cytosolic enzymes are encoded by at least five distantly related gene families (designated class alpha, mu, pi, sigma, and theta GST), whereas the membrane-bound enzymes, microsomal GST and leukotriene C, synthetase, are encoded by single genes and both have arisen separately from the soluble GST. Evidence suggests that the level of expression of GST is a crucial factor in determining the sensitivity of cells to a broad spectrum of toxic chemicals. In this article the biochemical functions of GST are described to show how individual isoenzymes contribute to resistance to carcinogens, antitumor drugs, environmental pollutants, and products of oxidative stress.A description of the mechanisms of transcriptional and posttranscriptional regulat...

The glutathione S-transferase supergene family: regulation of GST and the contribution of the isoenzymes to cancer chemoprotection and drug resistance.

A series of 2-aryl-7-(3-oxo-2H-[1,4]-benzoxazin-6-yl)pyrazolo[1,5-a]pyrimidines (8a-d and 9a-d) have been synthesized and evaluated for COX-2-inhibitor activity.

Synthesis of 2‐Aryl‐7‐(3‐oxo‐2H‐[1,4]‐benzoxazin‐6‐yl)pyrazolo[1,5‐a]pyrimidines as Potential COX‐2‐Inhibitors.

Synthesis of 2‐Aminophenyl‐5‐phenyl‐4‐[3‐oxo‐1,4‐benzoxazin‐6‐yl]thiazoles (VI) as Potential COX‐2 Inhibitors

The association of serum antioxidatns and lipids was studied in 350 urban individuals with an age range of 40–76 years, in comparison with a control rural sample of equal size. Glutathione Peroxidase (GPx) activity was found to be significantly higher in urban population when compared to rural population. Urban population were characterised by elevated levels of serum cholesterol (SC), low density lipoprotein cholesterol (LDLC) and triglycerides (TG) in comparison with rural population. In urban females both tocopherol (T) and GPx were negatively related with age. The serum lipid levels were found to be increased with age in urban population when compared to rural population. Further the correlation coefficients revealed that LDLC positively (.285:P<.05), and TG inversely (−.512:P<.05) related to ascorbic acid (AA), and an inverse association of SC (−.625:P<.05), high density lipoprotein cholesterol (HDLC) (−.369:P<.05) and LDLC (−.532:P<.05) with T in urban population. In rural population GPx shown a good positive correlation with lipid levels. The results of this study revealed that accumulation of lipids with unaltered antioxidants may be the consequence of urbanization.

Relationship between serum antioxidants and lipids among rural and urban populations

Natural Products Targeting Clinically Relevant Enzymes of Eicosanoid Biosynthesis Implicated in Inflammation and Cancer

The frogs belonging to the speciesRana hexadactyla (Lesson) were subjected to localised muscular exercise and training. The muscular exercise induced decreased proteolysis and elevated soluble and structural protein fractions of the brain. The amino acid oxidations were inhibited resulting into elevated amino acid content. The training programme seems to develop improved ammonia detoxificatory mechanism in the brain. The possible correlation between the training programme and structural organisation of the brain was suggested.

Pallu Reddanna

Papers

Synthesis of 2‐Aryl‐7‐(3‐oxo‐2H‐[1,4]‐benzoxazin‐6‐yl)pyrazolo[1,5‐a]pyrimidines as Potential COX‐2‐Inhibitors.

Synthesis of 2‐Aminophenyl‐5‐phenyl‐4‐[3‐oxo‐1,4‐benzoxazin‐6‐yl]thiazoles (VI) as Potential COX‐2 Inhibitors

Relationship between serum antioxidants and lipids among rural and urban populations

Natural Products Targeting Clinically Relevant Enzymes of Eicosanoid Biosynthesis Implicated in Inflammation and Cancer

Effect ofin vivo muscular stimulations VII: Some aspects of ammonia metabolism of amphibian brain during muscular exercise and training