Adhesive Glycoprotein Research Articles

ANALYSIS OF IMMUNOEXPRESSION OF ESTROGEN RECEPTOR BETA AND EXTRACELLULAR MATRIX METALLOPROTEINASE INDUCER (EMMPRIN) ON TESTICULAR SEMINOMAS NONRECURRENCE AND RECURRENCE

The most common malignancy of testis is seminoma with prognosis that is not always good because of high recurrence rate and death cases. Extracellular matrix metalloproteinase inducer (EMMPRIN) is a glycoprotein adhesion molecules which plays a role in tumor cell invasion and metastasis as evidenced by immunohistochemistry method in several types of tumor cells and tissue that shows the correlation to the clinical progessivity.This study was conducted by observational descriptive analytics with each seven cases of seminoma nonrecurrences and recurrences diagnosed histopathologically from Dr.Hasan Sadikin Hospital, Advent Hospital and St.Borromeus Hospital in Bandung. This study shows that immunoexpression of estrogen receptor beta is not higher in testicular seminoma recurrence compared with nonreccurence. There was no higher imunoexpression of EMMPRIN receptor on testicular seminoma recurrence compared with nonrecurrence; besides, there was no relationship between immunoexspression of estrogen receptor beta and EMMPRIN in testicular seminoma nonrecurrence and recurrence.In conclusion, immunoexpression estrogen receptor beta expressed in all testicular seminoma, so that the patient could be given an alternative therapy and immunoexspression EMMPRIN, cannot be used to predict a recurrence in patients with seminoma who has received complete therapy. Keywords: EMMPRIN, Estrogen Receptor Beta, Seminoma Testis nonrecurrence and recurrence

The transmembrane heparan sulphate proteoglycan syndecan-4 is involved in establishment of the lamellar structure of the annulus fibrosus of the intervertebral disc.

The annulus fibrosus of the intervertebral disc unites adjacent vertebral bodies along the length of the spine and provides tensile resistance towards compressive, twisting and bending movements arising through gait. It consists of a nested series of oriented collagenous lamellae, arranged in cross-ply circumferentially around the nucleus pulposus. The organisation of oriented collagen in the annulus is established during foetal development by an identical arrangement of oriented fibroblasts that are precisely organised into cell sheets, or laminae. These provide a template for ordered deposition of extracellular matrix material on cell surfaces, by means of a poorly understood mechanism involving the actin cytoskeleton. In this study, we investigate the role of two cell surface heparan sulphate proteoglycans (HSPGs), glypican-6 and syndecan-4, in the matrix assembly process in the developmental rat intervertebral disc. We compare their expression patterns with those of heparan sulphate and the interactive, cell-surface adhesive glycoprotein, fibronectin, and relate these to the stage-specific collagenous architectures present within the annulus at both light and electron microscopic levels. We show that both proteoglycans are strongly associated with the development, growth and aging of the intervertebral disc. Furthermore, the immunohistochemical labelling patterns suggest that syndecan-4, in particular, plays a potentially-significant role in annulus formation. We propose that this HSPG mediates interaction between the actin cytoskeleton and nascent extracellular matrix in the lamellar organisation of annulus tissue. These data add considerably towards an understanding of how cells organise and maintain complex, oriented extracellular matrices and has particular clinical relevance to the fields of tissue engineering and repair.

Fibronectin unfolded by adherent but not suspended platelets: An in vitro explanation for its dual role in haemostasis

Fibronectin (FN), a dimeric adhesive glycoprotein, which is present both in plasma and the extracellular matrix can interact with platelets and thus contribute to platelet adhesion and aggregation. It has been shown that FN can decrease platelet aggregation but enhance platelet adhesion, suggesting a dual role of FN in haemostasis. The prevalent function(s) of FN may be determined by its fibril form. To explore the suggested dual role of this adhesive protein for haemostasis in further detail, we now tested for any differences of adherent and suspended platelets with regard to their effect to unfold and assemble FN upon interaction. Platelet aggregation and adhesion assays were performed using washed platelets in the presence of exogenous FN. Addition of plasma FN reduced platelet aggregation in response to collagen or PMA by 50% or 25% but enhanced platelet adhesion onto immobilized collagen, as compared to control experiments. Analyses by fluorescence resonance energy transfer (FRET) demonstrated that adherent platelets but not suspended platelets were capable of unfolding FN during 3h incubation. Fluorescence microscopy and deoxycholate (DOC) solubility assays demonstrated that FN fibrils formed only on the surfaces of adherent platelets. In addition, platelets adherent onto FN revealed a significantly higher activity of specific Src phosphorylation (pY418) than platelets in suspension. These data suggest (1) that the function of FN in haemostasis is prevalent to its assembly, unfolding and subsequent fibril formation on the surface of adherent platelets and (2) that outside-in signaling contributes to the interaction of platelets and FN.

The stability of hygroscopic compounds in orb-web spider viscous thread

Each of the droplets that form an orb-weaving spider's viscous capture thread are composed of a viscoelastic glycoprotein glue core that is surrounded by an aqueous layer and supported by a pair of protein axial fibers. Low molecular weight organic and inorganic compounds within the aqueous layer confer droplet hygroscopicity, thereby maintaining the glycoprotein's adhesion and extensibility and ensuring that the axial fibers remain supercontracted. These materials also cause droplet volume to change in response to ambient humidity. This study examined the viscous threads of Argiope aurantia Lucas 1833, a species found in exposed, low humidity habitats, and Neoscona crucifera (Lucas 1838), a nocturnal species found in high humidity forest edge habitats. An earlier study showed the former species' threads to be more hygroscopic than those of the latter. When aged and exposed to chemical fixatives, the hygroscopicity of A. aurantia threads decreased, while that of N. crucifera threads was unaffected. Fixation eliminated the extensibility of both species' droplets. However, droplet adhesion, as measured by the deflection angle of a thread's axial lines just prior to droplet extension or, in the case of fixed droplets, droplet pull-off, was unaffected. These findings indicate that the compounds that confer greater hygroscopicity to A. aurantia viscous threads are more susceptible to chemical fixatives than those in the aqueous layer of N. crucifera droplets.

The stability of hygroscopic compounds in orb-web spider viscous thread

Each of the droplets that form an orb-weaving spider's viscous capture thread are composed of a viscoelastic glycoprotein glue core that is surrounded by an aqueous layer and supported by a pair of protein axial fibers. Low molecular weight organic and inorganic compounds within the aqueous layer confer droplet hygroscopicity, thereby maintaining the glycoprotein's adhesion and extensibility and ensuring that the axial fibers remain supercontracted. These materials also cause droplet volume to change in response to ambient humidity. This study examined the viscous threads of Argiope aurantia Lucas 1833, a species found in exposed, low humidity habitats, and Neoscona crucifera (Lucas 1838), a nocturnal species found in high humidity forest edge habitats. An earlier study showed the former species' threads to be more hygroscopic than those of the latter. When aged and exposed to chemical fixatives, the hygroscopicity of A. aurantia threads decreased, while that of N. crucifera threads was unaffected. Fixation eliminated the extensibility of both species' droplets. However, droplet adhesion, as measured by the deflection angle of a thread's axial lines just prior to droplet extension or, in the case of fixed droplets, droplet pull-off, was unaffected. These findings indicate that the compounds that confer greater hygroscopicity to A. aurantia viscous threads are more susceptible to chemical fixatives than those in the aqueous layer of N. crucifera droplets.

TgrC1 Has Distinct Functions in Dictyostelium Development and Allorecognition.

The cell adhesion glycoproteins, TgrB1 and TgrC1, are essential for Dictyostelium development and allorecognition, but it has been impossible to determine whether their pleiotropic roles are due to one common function or to distinct functions in separate pathways. Mutations in the respective genes, tgrB1 and tgrC1, abrogate both development and allorecognition and the defects cannot be suppressed by activation of the cyclic AMP dependent protein kinase PKA, a central regulator of Dictyostelium development. Here we report that mutations in genes outside the known PKA pathway partially suppress the tgrC1-null developmental defect. We separated the pleiotropic roles of tgrC1 by testing the effects of a suppression mutation, stcinsA under different conditions. stcAins modified only the developmental defect of tgrC1– but not the allorecognition defect, suggesting that the two functions are separable. The suppressor mutant phenotype also revealed that tgrC1 regulates stalk differentiation in a cell-autonomous manner and spore differentiation in a non-cell-autonomous manner. Moreover, stcAins did not modify the developmental defect of tgrB1–, but the less robust phenotype of tgrB1– obscures the possible role of stcA relative to tgrB1.

Peptide therapies for ocular surface disturbances based on fibronectin-integrin interactions.

The condition of the corneal epithelium is a critical determinant of corneal transparency and clear vision. The corneal epithelium serves as a barrier to protect the eye from external insults, with its smooth surface being essential for its optical properties. Disorders of the corneal epithelium include superficial punctate keratopathy, corneal erosion, and persistent epithelial defects (PEDs). The prompt resolution of these disorders is important for minimization of further damage to the cornea. Currently available treatment modalities for corneal epithelial disorders are based on protection of the ocular surface in order to allow natural healing to proceed. PEDs remain among the most difficult corneal conditions to treat, however. On the basis of characterization of the pathobiology of PEDs at the cell and molecular biological levels, we have strived to develop new modes of treatment for these defects. These treatments rely on two key concepts: provision of a substrate, such as the adhesive glycoprotein fibronectin, for the attachment and migration of corneal epithelial cells, and activation of these cells by biological agents such as the combination of substance P and insulin-like growth factor-1 (IGF-1). Central to both approaches is the role of the fibronectin-integrin system in corneal epithelial wound healing. Determination of the minimum amino acid sequences required for the promotion of corneal epithelial wound closure by fibronectin (PHSRN) and by substance P (FGLM-amide) plus IGF-1 (SSSR) has led to the development of peptide eyedrops for the treatment of PEDs that are free of adverse effects of the parent molecules.

Role of F3/contactin expression profile in synaptic plasticity and memory in aged mice

We have recently shown that overexpression of the F3/contactin adhesive glycoprotein (also known as Contactin-1) promotes neurogenesis in adult hippocampus, which correlates with improved synaptic plasticity and memory. Because F3/contactin levels physiologically decrease with age, here, we aim at investigating whether its overexpression might counteract the cognitive decline in aged animals. For this we use 20- to 24-month-old TAG/F3 transgenic mice in which F3/contactin overexpression is driven by regulatory sequences from the gene encoding the transient axonal glycoprotein TAG-1 throughout development. We show that aged TAG/F3 mice display improved hippocampal long-term potentiation and memory compared with wild-type littermates. The same mice undergo a decrease of neuronal apoptosis at the hippocampal level, which correlated to a decrease of active caspase-3; by contrast, procaspase-3 and Bax as well as the anti-apoptotic and plasticity-related pathway BDNF/CREB/Bcl-2 were rather increased. Interestingly, amyloid-precursor protein processing was shifted toward sAPPα generation, with a decrease of sAPPβ and amyloid-beta levels. Our data confirm that F3/contactin plays a role in hippocampal synaptic plasticity and memory also in aged mice, suggesting that it acts on molecular pathways related to apoptosis and amyloid-beta production.

Von Willebrand Disease in Dental Clinic: An Exclusive Case Report with Review of Literature

ABSTRACT von Willebrand disease (vWD) is the most common type of autosomally inherited bleeding disorder affecting up to 1% of the world's population. The disease represents a range of quantitative and qualitative pathologies of the adhesive glycoprotein, von Willebrand factor (vWF). Since symptoms are often mild, a significant majority of patients remain undiagnosed. In the hemostasis laboratory, the measurement of vWF antigen and ristocetin cofactor activity is key components in the diagnostic algorithm for vWD. With all forms of vWD, however, bleeding episodes can be severe and may require treatment, particularly during or following surgery or dental work. The primary care physician can and should play a role in recognizing the signs and symptoms of vWD and in referring patients for proper management. The treatment of bleeding in vWD involves the use of desmopressin and plasma-derived vWF concentrates and a variety of adjunctive agents. This article gives a detailed description of the case report on a 5-year-old boy who presented with vWD in dental clinic and also imparts the knowledge on back ground, pathophysiology, classification, diagnostic measures and treatment modalities of this fatal bleeding disorder from dental perspective. How to cite this article Aparna M. von Willebrand Disease in Dental Clinic: An Exclusive Case Report with Review of Literature. J Contemp Dent 2015;5(2):107-112

Adhesion glycoprotein CD44 functions as an upstream regulator of a network connecting ERK, AKT and Hippo-YAP pathways in cancer progression.

Targeted therapies are considered to be the future of cancer treatment. However, the mechanism through which intracellular signaling pathways coordinate to modulate oncogenesis remains to be elucidated. In this study, we describe a novel crosstalk among ERK, AKT and Hippo-YAP pathways, with CD44 as an upstream regulator. High cell density leads to activation of ERK and AKT but inactivation of YAP in cancer cells. CD44 modulates cell proliferation and cell cycle but not apoptosis. The expression and activity of cell cycle genes were cooperatively regulated by ERK, AKT and Hippo-YAP signaling pathways through CD44-mediated mechanisms. In addition, CD44 depletion abrogates cancer stem cell properties of tumor initiating cells. Taken together, we described a paradigm where CD44 functions as an upstream regulator sensing the extracellular environment to modulate ERK, AKT and Hippo-YAP pathways which cooperatively control downstream gene expression to modulate cell contact inhibition of proliferation, cell cycle progression and maintenance of tumor initiating cells. Our current study provides valuable information to design targeted therapeutic strategies in cancers.

Hyaluronan Controls the Deposition of Fibronectin and Collagen and Modulates TGF-β1 Induction of Lung Myofibroblasts

The contribution of hyaluronan-dependent pericellular matrix to TGF-β1-driven induction and maintenance of myofibroblasts is not understood. Hyaluronan is an extracellular matrix (ECM) glycosaminoglycan important in cell adhesion, proliferation and migration, and is implicated in myofibroblast formation and maintenance. Reduced turnover of hyaluronan has been linked to differentiation of myofibroblasts and potentiation of lung fibrosis. Fibronectin is a fibril forming adhesive glycoprotein that is also upregulated following induction with TGF-β1. Although they are known to bind each other, the interplay between hyaluronan and fibronectin in the pericellular matrix during myofibroblast induction and matrix assembly is not clear. This study addresses the role of hyaluronan and its interaction with fibrillar matrix components during myofibroblast formation. Hyaluronan and fibronectin were increased and co-localized in the ECM following myofibroblast induction by TGF-β1. Inhibition of hyaluronan synthesis in TGF-β1-induced lung myofibroblasts over a 4day period with 4-methyl umbelliferone (4-MU) further enhanced myofibroblast morphology, caused increased deposition of fibronectin and type I collagen in the ECM, and increased expression of alpha-smooth muscle actin and hyaluronan synthase 2 (HAS2) mRNA. Hyaluronan oligosaccharides or hyaluronidase treatment, which more effectively disrupted the pericellular matrix, had similar effects. CD44 and β1 integrins co-localized in the cell membrane and along some stress fibers. However, CD44 and hyaluronan were specifically excluded from focal adhesions, and associated primarily with cortical actin. Time-lapse imaging of the immediate effects of hyaluronidase digestion showed that hyaluronan matrix primarily mediates attachment of membrane and cortical actin between focal contacts, suggesting that surface adhesion through hyaluronan and CD44 is distinct from focal adhesion through β1 integrins and fibronectin. Fluorescein-labeled hyaluronan bound regularly along fibronectin fibers and co-localized more with β1 integrin and less with CD44. Therefore, the hyaluronan matrix can interfere with the assembly of fibrillar ECM components, and this interplay regulates the degree of myofibroblast formation. These data also suggest that adhesion through hyaluronan matrix impacts cytoskeletal organization, and is potentially part of a clutch mechanism that regulates stick and slip of myofibroblasts by affecting the adhesion to and organization of fibronectin and collagen.

Aberrant P-cadherin expression is associated to aggressive feline mammary carcinomas.

BackgroundCadherins are calcium-dependent cell-to-cell adhesion glycoproteins playing a critical role in the formation and maintenance of normal tissue architecture. In normal mammary gland, E-cadherin is expressed by luminal epithelial cells, while P-cadherin is restricted to myoepithelial cells. Changes in the expression of classical E- and P-cadherins have been observed in mammary lesions and related to mammary carcinogenesis. P-cadherin and E-cadherin expressions were studied in a series of feline normal mammary glands, hyperplastic/dysplastic lesions, benign and malignant tumours by immunohistochemistry and double-label immunofluorescence.ResultsIn normal tissue and in the majority of hyperplastic/dysplastic lesions and benign tumours, P-cadherin was restricted to myoepithelial cells, while 80% of the malignant tumours expressed P-cadherin in luminal epithelial cells. P-cadherin expression was significantly related to high histological grade of carcinomas (p <0.0001), tumour necrosis (p = 0.001), infiltrative growth (p = 0.0051), and presence of neoplastic emboli (p = 0.0401). Moreover, P-cadherin positive carcinomas had an eightfold likelihood of developing neoplastic emboli than negative tumours. Cadherins expression profile in high grade and in infiltrative tumours was similar, the majority expressing P-cadherin, regardless of E-cadherin expression status. The two cadherins were found to be co-expressed in carcinomas with aberrant P-cadherin expression and preserved E-cadherin.ConclusionsThe results demonstrate a relationship between P-cadherin expression and aggressive biological behaviour of feline mammary carcinomas, suggesting that P-cadherin may be considered an indicator of poor prognosis in this animal species. Moreover, it indicates that, in queens, the aberrant expression of P-cadherin is a better marker of mammary carcinomas aggressive behaviour than the reduction of E-cadherin expression. Further investigation with follow-up studies in feline species should be conducted in order to evaluate the prognostic value of P-cadherin expression in E-cadherin positive carcinomas.

Isolation of murine lymph node stromal cells.

Secondary lymphoid organs including lymph nodes are composed of stromal cells that provide a structural environment for homeostasis, activation and differentiation of lymphocytes. Various stromal cell subsets have been identified by the expression of the adhesion molecule CD31 and glycoprotein podoplanin (gp38), T zone reticular cells or fibroblastic reticular cells, lymphatic endothelial cells, blood endothelial cells and FRC-like pericytes within the double negative cell population. For all populations different functions are described including, separation and lining of different compartments, attraction of and interaction with different cell types, filtration of the draining fluidics and contraction of the lymphatic vessels. In the last years, different groups have described an additional role of stromal cells in orchestrating and regulating cytotoxic T cell responses potentially dangerous for the host. Lymph nodes are complex structures with many different cell types and therefore require a appropriate procedure for isolation of the desired cell populations. Currently, protocols for the isolation of lymph node stromal cells rely on enzymatic digestion with varying incubation times; however, stromal cells and their surface molecules are sensitive to these enzymes, which results in loss of surface marker expression and cell death. Here a short enzymatic digestion protocol combined with automated mechanical disruption to obtain viable single cells suspension of lymph node stromal cells maintaining their surface molecule expression is proposed.

Expression and purification of bioactive, low-endotoxin recombinant human vitronectin.

The secreted adhesive glycoprotein vitronectin (VTN) is a multifunctional component of plasma and the extracellular matrix. A high-yielding, inexpensive, low endotoxin source of bioactive recombinant human vitronectin (rhVTN) is highly desirable for in vitro use in diverse cell culture systems ranging from basic research settings to clinical-grade production of human cells. We describe modifications to a previously reported heparin-based affinity chromatography procedure that improve yield and achieve efficient removal of endotoxin from washed and urea-solubilized human VTN inclusion bodies following standard autoinduction of expression in Escherichia coli. This simple procedure makes accessible the low-cost expression and purification of large quantities of bioactive rhVTN using basic equipment and facilitates its use in a spectrum of endotoxin-sensitive applications.

Investigating the regulation of e-cadherin mRNA and protein expression by integrin α3β1 in breast cancer cells.

1104 Background: E-cadherin is an adhesion glycoprotein in epithelial tissues and reduced expression is associated breast cancer metastasis. The cell surface integrin α3β1 is also associated with m...

Abstract 74: Thrombospondin 1 Modulates Arterial Thrombosis via von Willebrand Factor in Mice

Background and Hypothesis: Thrombospondin 1 (TSP1) is a large adhesive glycoprotein that is stored in platelet α-granules. Upon platelet activation, TSP1 is released in large amount (up to 30 μg/mL) in circulation. Previous studies have shown smaller plasma von Willebrand factor (VWF) multimer size in Tsp1 -/- mice compared with wild-type (WT), suggesting that TSP1 protects VWF from excessive proteolysis by ADAMTS13. It remains unclear whether TSP1/VWF axis determines the rate of thrombus growth in injured vessels. We tested the hypothesis that TSP1 modulates arterial thrombosis via VWF. Model and Methods: We generated Vwf -/- / Tsp1 -/- mice and compared with Tsp1 -/- , Vwf -/- and WT mice. Platelet adhesion and susceptibility to thrombosis was assessed in a ferric-chloride injury-induced mesenteric artery thrombosis model. Using high-resolution intravital microscopy, we measured the time to form 1 st thrombus (&gt;20 μm), thrombus growth kinetics and occlusion time in the injured arterioles. Results: We found that the number of fluorescently labeled platelets that adhered transiently to 250μm vessel wall segment within 3-4 min following ferric-chloride injury was similar in Tsp1 -/- mice compared with WT mice. The mean time to form first thrombus was significantly increased in Tsp1 -/- mice compared with WT (9.98±0.52 vs. 7.12±0.55min, P&lt;0.05). The rate of thrombus growth was decreased in Tsp1 -/- mice ( P &lt;0.05 vs. WT). The time to stable occlusion of the mesenteric artery was modestly but significantly prolonged in Tsp1 -/- mice compared with WT mice (15.8±0.59 vs. 13.3±0.63min, P&lt;0.05). Because TSP1 binds to A3 domain of VWF, we investigated TSP1 modulates thrombosis via binding to VWF. Compared to Vwf -/- mice, Vwf -/- / Tsp1 -/ - littermates exhibited similar platelet adhesion, time to form first thrombus, and non-occlusive thrombus growth kinetics, suggesting that TSP1 modulates thrombus growth via VWF. Conclusion: We provide evidence for the first time that TSP1 does not mediate initial platelet adhesion to injured vessel wall but modulates arterial thrombus growth via a mechanism that requires VWF. These results suggest that TSP1 may participate in amplifying platelet aggregation following injury by protecting VWF from excessive cleavage by ADAMTS13.

Gastric cancer patients less than 50 years of age exhibit significant downregulation of E-cadherin and CDX2 compared to older reference populations

PurposeThere is an increasing need to identify molecular markers, which can be used to prognosticate patient populations in gastric cancer. Whereas a significant number have been identified, very few have been characterized in the context of their ability to discriminate between young and old age groups in which a survival difference clearly exists. Material/methodsIn this study, using immunohistochemistry, we evaluated three markers with proven involvement in gastric cancer. The p53 tumor suppressor, the cell adhesion glycoprotein epithelial cadherin (CDH1) and the caudal-related homeobox transcription factor (CDX2) all of these have important roles in the aetiopathogenesis and/or progression of gastric cancer. ResultsAfter adjustments for TNM stage, tumor grade, histopathological characteristics (Lauren classification), we found significant differences in the expression of these proteins, particularly E-cadherin and CDX2 between young and elderly patients. However, these differences did not amount to a significant difference in survival. ConclusionsThis study demonstrates that the protein expression of p53, CDH1 and CDX2 significantly discriminates young patients with gastric cancer who have a better prognostic outlook from older patients, but this difference in expression does not contribute to a survival benefit.

Common Variants in the CDH7 Gene are Associated with Major Depressive Disorder in the Han Chinese Population

Cadherin-7 (CDH7) gene encodes a calcium dependent cell-cell adhesion glycoprotein. Gene loci of cadherins family have been supposed to be involved in the pathogenesis of psychiatric disorders. Recent genome-wide association study also demonstrated that CDH7 was significant associated with bipolar disorder. Due to the fact that the same genetic risk factor can be shared by different kinds of psychiatric disorders, we examined whether CDH7 is also associated with major depressive disorder (MDD) in this study, with a large Han Chinese sample set. We carried out a 2-stage case-control study to examine the association between CDH7 and MDD in the Han Chinese population. Ten tag SNPs were genotyped using Taqman technology in 1,045 MDD patients and 1,520 healthy controls. Single-nucleotide polymorphisms with significance were additionally genotyped in another independent sample set with 576 MDD cases and 576 healthy controls. Among ten genotyped SNPs, rs1444067 and rs12605720 was found to be significantly associated with MDD (rs1444067: P(allele) = 0.00571, OR 0.830, 95 % CI 0.728-0.947; rs12605720: P(allele) = 0.00321, OR 1.245, 95 % CI 1.076-1.441). We successfully replicated these two SNPs association with independent sample sets (rs1444067: P(allele) = 0.00518; rs12605720: P(allele) = 0.0227). Finally we have combined these results by a meta-analysis (rs1444067: P(allele) = 0.000174, OR 0.817; rs12605720: P(allele) = 0.000199, OR 1.255). Our results support CDH7 to be a risk factor of MDD in the Han Chinese population. However, further studies with more markers and independent samples were suggested to validate our findings.

Temperature mediates the effect of humidity on the viscoelasticity of glycoprotein glue within the droplets of an orb-weaving spider's prey capture threads

Sticky viscous prey capture threads retain insects that strike araneoid orb-webs. The threads' two axial fibers support a series of glue droplets, each featuring a core of adhesive viscoelastic glycoprotein covered by an aqueous solution. After sticking, the glue extends, summing the adhesion of multiple droplets, and dissipates some of the energy of a struggling prey. As a day progresses, threads experience a drop in humidity and an increase in temperature, environmental variables that have the potential to alter thread and web function. We hypothesize that thread droplets respond to these opposing environmental changes in a manner that stabilizes their performance, and test this by examining threads spun by Argiope aurantia, a species that occupies exposed, weedy habitats. We confirmed that decreased humidity increases glycoprotein viscosity and found that increased temperature had the opposite effect. To evaluate the combined effect of temperature and humidity on a droplet's ability to transfer adhesive force and dissipate energy, we extended a droplet and measured both the deflection of the axial line supporting the droplet and the duration of its tensive load. The cumulative product of these two indices, which reflects the energy required to extend a droplet, was greatest under afternoon (hot and dry) conditions, less under morning (cool and humid) conditions, and least under hot and humid afternoon conditions. Although the opposing effects of temperature and humidity tend to stabilize glycoprotein performance, A. aurantia thread droplets appear to function optimally during the afternoon, equipping this species to capture large orthopterans, which are most active at this time.

TIRF and Model Blood Vessels Combined to Elucidate the Role of the Cytoskeleton in Platelet Activation

Platelets are cell fragments that play a central role in hemostasis and thrombosis. Typically platelets circulate as thin flat disks; however upon encountering a damaged vessel wall they are recruited to the exposed subendothelial matrix where they adhere and activate. The platelets interact with the exposed matrix proteins via specific adhesive glycoproteins found on the surface of the platelet. Activated platelets have extensive pseudopodia due to a change in the assembly of cytoskeletal proteins such as actin and tubulin. The rearrangement of the cytoskeleton also corresponds with the secretion of granule content leading to the amplification of the platelet stimulation and the formation of a stable platelet-fibrin plug. A popular model assumes that the granules are drawn to the center of the platelet before release occurs, indicating the importance of the cytoskeletal components that drive this centralization leading to the eventual clot formation.In this study we will examine cytoskeletal protein arrangements in granule release using TIRF to study the activated platelets that aggregate on the protein coatings along a microfluidic channel. These protein coatings will include proteins found in damaged vessel walls such as collagen and fibrinogen. TIRF uses an induced evanescent wave created at the interface of a glass and to selectively excite fluorescent molecules located near the interface. Here we will describe the microfluidic channels we used to model blood vessels. By controlling which proteins are coated on the inside of the channels we are able to visualize platelet activation in a more native setting. We will also discuss methods that were used to stain cytoskeletal proteins to reduce the premature activation of the platelets. A better understanding of these models will lead to a greater understanding clot formation.