In this paper we critically reexamine some of the long standing beliefs regarding self-similarity and long range dependence (LRD) on the Internet. Power law tails have been conjectured to be a cause of LRD. In this paper, we reexamine the claims regarding heavy tails. We first examine the generative models for the heavy tail phenomena, both in terms of the fragility of some proposed mechanisms to modeling perturbations as well as the weak statistical evidence for the mechanisms. Next, we take a look at some of the implications of LRD in key performance aspects of Internet algorithms. Finally, we present an alternative model explaining the LRD phenomena of Internet traffic. We argue that the multiple time-scale nature of the generation of traffic and transport protocols make the observation of LRD inevitable.

The cytoplasmic coat protein complex-II (COPII) is evolutionarily conserved machinery that is essential for efficient trafficking of protein and lipid cargos. How the COPII machinery is regulated to meet the metabolic demand in response to alterations of the nutritional state remains largely unexplored, however. Here, we show that dynamic changes of COPII vesicle trafficking parallel the activation of transcription factor X-box binding protein 1 (XBP1s), a critical transcription factor in handling cellular endoplasmic reticulum (ER) stress in both live cells and mouse livers upon physiological fluctuations of nutrient availability. Using live-cell imaging approaches, we demonstrate that XBP1s is sufficient to promote COPII-dependent trafficking, mediating the nutrient stimulatory effects. Chromatin immunoprecipitation (ChIP) coupled with high-throughput DNA sequencing (ChIP-seq) and RNA-sequencing analyses reveal that nutritional signals induce dynamic XBP1s occupancy of promoters of COPII traffic-related genes, thereby driving the COPII-mediated trafficking process. Liver-specific disruption of the inositol-requiring enzyme 1α (IRE1α)-XBP1s signaling branch results in diminished COPII vesicle trafficking. Reactivation of XBP1s in mice lacking hepatic IRE1α restores COPII-mediated lipoprotein secretion and reverses the fatty liver and hypolipidemia phenotypes. Thus, our results demonstrate a previously unappreciated mechanism in the metabolic control of liver protein and lipid trafficking: The IRE1α-XBP1s axis functions as a nutrient-sensing regulatory nexus that integrates nutritional states and the COPII vesicle trafficking. COPII | metabolic sensing | XBP1s | nutrient availability | liver steatosis T he cytoplasmic coat protein complex-II (COPII) is evolutionarily conserved secretory machinery that is essential for cellular protein and lipid trafficking through cargo sorting and vesicle formation at the endoplasmic reticulum (ER) (1-4). The vast majority of proteins and lipids exported from the ER require the COPII secretory machinery. The assembly of COPII-coated vesicles for facilitating the transport of cellular cargos has been demonstrated to be a highly complex process (1-6). Activated small GTPase SAR1 localizes to the specialized ER exit sites and initiates the COPII coat assembly, by first recruiting the inner coat formed by the heterodimer SEC23/SEC24, followed by the outer coat heterotetramer SEC13/SEC31, to deform the ER membrane and eventually produce carrier vesicles (2, 4, 7-9). Mutations in COPII components or accessory factors have been implicated in several human genetic diseases, including chylomicron retention disease, congenital dyserythropoietic anemia type II, and cranio-lenticulosutural dysplasia (10-14). However, it remains largely unexplored how the COPII machinery is regulated to meet the cellular secretory demand in response to various physiological stimuli.As a metabolically active tissue, the liver possesses a remarkable adaptive capacity to secrete lipids and proteins according to...

Pure BiFeO3, Bi2Fe4O9, and BiFeO3/Bi2Fe4O9 heterostructure nanofibers were successfully synthesized by a facile wet chemical process followed by an electrospinning technique. Compared with the pure BiFeO3 and Bi2Fe4O9 nanofibers, the introduction of Bi2Fe4O9 in the BiFeO3 makes its absorption edge red shift to absorb much more visible light, and improves its separation efficiency of photogenerated carrier. Besides, the as-obtained BiFeO3/Bi2Fe4O9 nanofibers exhibit higher photocatalytic activity in both the degradation of Rhodamine B and H2 evolution from water under visible-light irradiation. The BiFeO3/Bi2Fe4O9 nanofibers exhibited about 2.7 times and 2.0 times higher H2 evolution than that of pure BiFeO3 and pure Bi2Fe4O9 samples, respectively. The possible photoreactive mechanism of the BiFeO3/Bi2Fe4O9 nanofibers was carefully investigated according to the results of photocatalytic and photoelectric performance, and a Z-scheme mechanism was proposed. Such BiFeO3/Bi2Fe4O9 heterostructure and its composing strategy may bring new insight into the designing of highly efficient visible-light-responsible photocatalysts.

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