بهروز وثوقی,تصاویر بهروز وثوقی,بیوگرافی بهروز وثوقی
بیوگرافی بهروز وثوقی، قیصر سینمای ایران

نام اصلی: خلیل وثوقی

زمینه فعالیت: سینما، تئاتر، دوبله

تولد: ۲۰ اسفند ۱۳۱۶

محل زندگی: کالیفرنیا سان‌فرانسیسکو

سال‌های فعالیت: ۱۳۴۰ تا کنون

همسرها:  گوگوش (۱۳۵۵–۱۳۵۴)

خیام,زندگینامه خیام,زندگی نامه خیام نیشابوری
زندگینامه خیام نیشابوری

نام اصلی: غیاث‌الدین ابوالفتح عمر بن ابراهیم خیام نیشابوری

زمینه فعالیت: ریاضیات، اخترشناسی، شعر

فلسفه، دین، تاریخ،گاه‌شماری، موسیقی

تولد: ۲۸ اردیبهشت ۴۲۷

درگذشت:   ۱۲ آذر ۵۱۰

محل زندگی: حیره، نیشابور

بخشی از مقاله انگلیسی:

۱٫ Introduction

Given the increase in obesity rates along with the increased frequency of consuming food away from home (Bowman and Vinyard, 2004), the focus on restaurants efforts to promote healthier eating has received much attention (Glanz et al., 2007; Koplan and Brownell, 2010). Nutrition information is sometimes provided and/or required on restaurant menus to help people make healthy choices when they eat out (U.S. Food and Drug Administration, 2013); however, researchers have reported inconsistent effects of nutrition information on customers selecting healthful menu items at restaurants (Elbel et al., 2009; Harnack and French, 2008; Yamamoto et al., 2005). In contrast, other researchers have emphasized the role of psychological factors in food selection (Jun et al., 2014; Senauer, 2001). The theory of planned behavior is one of the most popular theoretical frameworks for investigating how the psychological factors of attitude, subjective norms, perceived behavioral control, and behavior intention affect people’s eating behaviors (e.g., Dunn et al., 2011; Kassem et al., 2003; Vermeir and Verbeke, 2008). However, the TPB has received criticism in two respects: its assumptions and conceptualization of some components. With respect to assumptions, the TPB has been criticized because of the focus on rational decision making although not all behavioral decisions are made based on a rational consideration of the behavior’s advantage and disadvantage (Gibbons et al., 1998; Ohtomo and Hirose, 2007). In particular, food selections are not determined only through deliberative reasoning processes but instead, people sometimes choose whatever they want to eat without rational consideration. To investigate this type of reactive decision making process, prototype images and behavioral willingness have been most frequently used (Gibbons et al., 2009). Although behavioral willingness does prove to be a determinant of actual behavior, like behavioral intention in the TPB, behavioral willingness tends to be shaped by a reactive response to a social context. Prototype image refers to the perceptions a person has about the typical person who engages in a given behavior, and it is one of the determinants of behavioral willingness (Gibbons et al., 2009). For example, Spijkerman et al. (2004) reported that when people had positive perceptions of smokers, they were likely to be willing to smoke themselves; this relationship could be explained by the reactive decision-making approach. Some researchers have alleged that the TPB’s components, in particular attitudes and subjective norms, are not adequately conceptualized (Rise et al., 2008; Taut and B ˘ aban, 2012; Tuu et al., 2008). Critics have charged that the TPB focuses only on cognitive aspects of attitude (i.e., cognitive attitudes) and on social norms related to others’ approval/disapproval regarding a certain behavior (i.e., injunctive norms) thereby suggesting that the concept of attitudes should be examined through both cognitive attitudes and affective attitudes (e.g., feelings/emotions) (e.g., Taut and B ˘ aban, 2012 ˘ ), and the concept of subjective norms through both injunctive norms and descriptive norms (e.g., what most people do) (e.g., Tuu et al., 2008). Despite these criticisms, there are limited studies attempting to remedy such shortcomings of the TPB in the domain of healthy eating behavior. Moreover, to the best of our knowledge, there have been no studies done in restaurant settings that have used this theoretical argument. To address these criticisms, this study investigated the applicability of an extended theory of planned behavior in the domain of customers’ healthful menu item selection by deploying an on-line survey to restaurant consumers. This study had two objectives. The first was to investigate both rational and reactive (or unintentional) behavioral decision processes in selection of healthful menu items at restaurants by adding both prototype image and behavioral willingness to the TPB. The second objective was to test the extended TPB by subdividing the components of attitudes into affective and cognitive attitudes and the component of social norms into injunctive and descriptive norms. Therefore this study contributed to and extended the existing literature by examining the roles of these constructs in people’s selection of healthful menu items at casual dining restaurants.

بهروز وثوقی,تصاویر بهروز وثوقی,بیوگرافی بهروز وثوقی
بیوگرافی بهروز وثوقی، قیصر سینمای ایران

نام اصلی: خلیل وثوقی

زمینه فعالیت: سینما، تئاتر، دوبله

تولد: ۲۰ اسفند ۱۳۱۶

محل زندگی: کالیفرنیا سان‌فرانسیسکو

سال‌های فعالیت: ۱۳۴۰ تا کنون

همسرها:  گوگوش (۱۳۵۵–۱۳۵۴)

خیام,زندگینامه خیام,زندگی نامه خیام نیشابوری
زندگینامه خیام نیشابوری

نام اصلی: غیاث‌الدین ابوالفتح عمر بن ابراهیم خیام نیشابوری

زمینه فعالیت: ریاضیات، اخترشناسی، شعر

فلسفه، دین، تاریخ،گاه‌شماری، موسیقی

تولد: ۲۸ اردیبهشت ۴۲۷

درگذشت:   ۱۲ آذر ۵۱۰

محل زندگی: حیره، نیشابور

بخشی از مقاله انگلیسی:

lncRNAs are common regulators of gene expression

lncRNAs are common in both prokaryotic and eukaryotic genomes; up to 72% of all human and mouse genes are found to be influenced by regulation by RNA molecules [7]. Regulatory transcripts can be either cis- or trans-acting, and occur in intronic, intragenic and other untranslated regions of the genome. Their targets can be either coding or non-coding (i.e. other regulatory RNAs), and can positively (concordant regulation) or negatively (discordant regulation) modify the expression or processing of their target genes. cis-lncRNAs are homologous with their targets and arise from the same genomic region, but from the opposite strand (these are often termed natural antisense transcripts), whereas translncRNAs share incomplete homology with their targets and arise from distant regions of the genome [8]. The orientation of cis-regulatory transcripts to their targets can be 5 to 5 (head-to-head; Figure 1a), 3 to 3 (tail-to-tail; Figure 1B) or fully overlapping, with one gene contained within the region coding the other (Figure 1C). Trans-regulatory transcripts are usually non-overlapping, scince they are from distinct genomic regions.

Mechanisms of lncRNA regulation

There are several proposed mechanisms of action for lncRNAs (Figure 2), which bring plasticity, adaptability and reactivity to genomic architecture and fine control over gene expression. In addition to the mechanisms outlined below, lncRNAs have also been reported to be subject to other mechanisms, including RNA editing, RNA interference, RNA masking, transcriptional interference and protein kinase R activation in some cases [9,10].

Epigenetic regulation

lncRNAs may act as scaffold molecules, to deliver regulatory proteins to loci where they are required. Examples of this type of lncRNA are ANRIL and HOTAIR. The ANRIL antisense transcript is coded for on the opposite strand of the CDKN2A/CDKN2B loci, and causes its effects by binding to and recruiting the CBX7 (chromobox 7) subunit of the PRC1 (Polycomb repressive complex 1) and PRC2. These complexes serve to direct H3K27me (methylation of histone H3 at Lys-27) at the target loci, resulting in the silencing of sense transcripts expressed from this region [11,12]. Similarly, HOTAIR binds to and recruits the PRC2 and the LSD1 (lysine-specific demethylase 1) protein, which is a component of the CoREST (co-repressor for element-1-silencing transcription factor) complex. Again, this brings about specific alterations in the methylation status and the nature of the chromatin surrounding the HOTAIR targets in the HOXD gene cluster [13]. HOXD genes such as HOXD13 direct morphogenesis in all multicellular organisms, and disruption to their expression has been associated with breast cancer [13] and developmental disorders [14].

بخشی از مقاله انگلیسی:

Introduction

Mitochondria are double-membrane-bound organelles present in all nucleated eukaryotic cells, and are responsible for numerous cellular processes, including calcium homeostasis, iron–sulphur cluster biogenesis, apoptosis, and the production of cellular energy (ATP) by oxidative phosphorylation (OXPHOS) [1,2]. With bacterial origins, a historical symbiotic relationship evolved during which mitochondria became normal constituents of eukaryotic cells [3]. Their ancestry remains apparent from their own multicopy genetic material [mitochondrial DNA (mtDNA)], with copy number varying greatly between individuals and across different tissues from the same individual. The 16.6-kb circular mtDNA molecule encodes 13 subunits of the OXPHOS components, 22 mitochondrial tRNAs, and two subunits of the mitoribosomes [4]. Additionally, the mitoproteome requires a further ∼۱۳۰۰ nuclear-encoded proteins for producing, assembling or supporting the five multimeric OXPHOS complexes (I–V) and ancillary mitochondrial processes [5]. It stands to reason that mitochondrial dysfunction can result from either mtDNA or nuclear gene defects, and can occur as a primary, congenital condition or a secondary, age-associated effect attributable to somatic mutation [6]. The umbrella term ‘mitochondrial disease’ refers to a clinically heterogeneous group of primary mitochondrial disorders in which the tissues and organs that are most often affected are those with the highest energy demands. Clinical symptoms can arise in childhood or later in life, and can affect one organ in isolation or be multisystemic [7]; the minimum disease prevalence in adults is ∼۱۲٫۵ per 100 000 [8], and ∼۴٫۷ per 100 000 in children [9]. There is a general lack of genotype–phenotype correlations in many mitochondrial disorders, which means that establishing a genetic diagnosis can be a complicated process, and remains elusive for many patients. This review provides a concise update on three areas where there have been major advances in our understanding in recent years [10], i.e. the molecular genetics, muscle pathology and neuropathology associated with mitochondrial disease, highlighting the range of new techniques that are improving the diagnosis of patients with suspected mitochondrial disease, with the aim of providing options to families at risk of an otherwise incurable condition.

The genetics of mitochondrial disease

Mitochondrial disease caused by mtDNA

Unlike nuclear DNA, which is diploid and follows Mendelian laws of inheritance, mtDNA is exclusively maternally inherited [11]. The multicopy nature of mtDNA gives rise to heteroplasmy, a unique aspect of mtDNA-associated genetics that occurs when there is coexistence of a mix of mutant and wild-type mtDNA molecules (heteroplasmy). In contrast, homoplasmy occurs when all of the mtDNA molecules have the same genotype. Heteroplasmic mutations often have a variable threshold, i.e. a level to which the cell can tolerate defective mtDNA molecules [12]. When the mutation load exceeds this threshold, metabolic dysfunction and associated clinical symptoms occur. Point mutations and large-scale mtDNA deletions represent the two most common causes of primary mtDNA disease, the former usually being maternally inherited, and the latter typically arising de novo during embryonic development.

برچسب ها

تمامی حقوق مطالب برای آی آر 7 محفوظ است و هرگونه کپی برداری بدون ذکر منبع ممنوع می باشد.