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Males should be more selective when they have a high investment in reproduction, especially in species with biparental or paternal care. In this context, male mate choice can promote size-assortative mating (SAM) when (1) large males win intrasexual disputes, (2) large females are more fecund, and (3) males prefer larger females to smaller ones. In the spider Manogea porracea, males exhibit high reproductive investment by building their webs above those of females and exhibiting extended care of offspring in the absence of females. Under these circumstances, we expect the occurrence of SAM and male preference for large females. Herein, we performed observations and experiments in the field to evaluate the hypotheses that (1) M. porracea mates assortatively by size and (2) SAM is influenced by male mate choice. Furthermore, we measured variables that could affect mating patterns, the sex ratios, and densities of both sexes. Pairing in M. porracea was positively size-assortative in 2012, but not in 2013. Large males won most disputes for mates and preferred larger females, which produced more eggs. The inconsistency in detection of SAM was due to population dynamics, namely variations in sex ratio and population density across the breeding season. Furthermore, we found that the significance of male mate choice on sexual selection of body size in M. porracea strongly depends on the competition intensity for mating opportunities. The traditional sexual selection hypothesis of SAM needs to be reviewed and must include measures of competition intensity.

Tumor angiogenesis is a hallmark of advanced cancers and promotes invasion and metastasis. Over 90% of head and neck squamous cell carcinomas (HNSCC) express angiogenic factors such as vascular endothelial growth factor (VEGF). Several preclinical studies support the prognostic implications of angiogenic markers for HNSCC and currently this is an attractive treatment target in solid tumors. Since radiotherapy is one of the most commonly used treatments for HNSCC, it is imperative to identify the interactions between antiangiogenic therapy and radiotherapy, and to develop combination therapy to improve clinical outcome. The mechanisms between antiangiogenic agents and ionizing radiation are complicated and involve many interactions between the vasculature, tumor stroma and tumor cells. The proliferation and metastasis of tumor cells rely on angiogenesis/blood vessel formation. Rapid growing tumors will cause hypoxia, which up-regulates tumor cell survival factors, such as hypoxia-inducing factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF), giving rise to more tumor proliferation, angiogenesis and increased radioresistance. Thus, agents that target tumor vasculature and new tumor vessel formation can modulate the tumor microenvironment to improve tumor blood flow and oxygenation, leading to enhanced radiosensitivity. In this review, we discuss the mechanisms of how antiangiogenic therapies improve tumor response to radiation and data that support this combination strategy as a promising method for the treatment of HNSCC in the future., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

WNK4, a serine/threonine kinase, plays a critical role in the expression of membrane proteins in the cell surface; however, the underlying mechanism of WNK4 is not clear. Here, we demonstrate that WNK4 inhibits the fusion of plasma membrane delivering vesicle with sorting/recycling endosome through disrupting SNARE formation of syntaxin13, an endosomal t-SNARE and VAMP2, the v-SNARE in plasma membrane delivering vesicle. Their interaction and co-localization were enhanced by hyperosmotic stimulation which is known for WNK4 activation. The kinase domain of WNK4 interacts with the transmembrane domain (TM) of syntaxin13 and this interaction was abolished when the TM was replaced with that of syntaxin16. Interestingly, cell fractionation using sucrose gradients revealed that WNK4 inhibited the formation of the syntaxin13/VAMP2 SNARE complex in the endosomal compartment, but not syntaxin16/VAMP2 or syntaxin13/VAMP7. Syntaxin13 was not phosphorylated by WNK4 and WNK4KI also showed the same binding strength and similar inhibitory regulation on SNARE formation of syntaxin13. Physiological relevance of this mechanism was proved with the expression of NCC (Na(+) C1(-) co-transporter) in the cell surface. The inhibiting activity of WNK4 on surface expression of NCC was abolished by syntaxin13 siRNA transfection. These results suggest that WNK4 attenuates PM targeting of NCC proteins through regulation of syntaxin13 SNARE complex formation with VAMP2 in recycling and sorting endosome., (© 2013.)

Endovascular treatments for catastrophic aortic conditions have gained increasing popularity over the past 20 years. Originally developed for abdominal aortic aneurysms (EVAR), treatment has been modified for use in thoracic aortic repair (TEVAR). As expanding numbers of patients with increasingly intractable conditions and more hostile anatomies are treated, endovascular stent designs are maturing to be suitable for these more demanding situations. This article discusses the engineering considerations that apply to changing stent graft designs for current and evolving thoracic applications. The biological parameters that differentiate thoracic from abdominal aortic environments are outlined. Factors concerning materials, sealing mechanisms, deployment, stent frame architecture, and migration resistance are described, and eagerly awaited potential future developments are summarized., (Copyright © 2013 Elsevier Inc. All rights reserved.)