Recollection-Based Retrieval Is Influenced by Contextual Variation at Encoding but Not at Retrieval

In this article, we investigated the effects of variations at encoding and retrieval on recollection. We argue that recollection is more likely to be affected by the processing that information undergoes at encoding than at retrieval. To date, manipulations shown to affect recollection were typically carried out at encoding. Therefore, an open question is whether these same manipulations would also affect recollection when carried out at retrieval, or whether there is an inherent connection between their effects on recollection and the encoding stage. We therefore manipulated, at either encoding or retrieval, fluency of processing (Experiment 1)—typically found not to affect recollection—and the amount of attentional resources available for processing (Experiments 2 and 3)—typically reported to affect recollection. We found that regardless of the type of manipulation, recollection was affected more by manipulations carried out at encoding and was essentially unaffected when these manipulations were carried out at retrieval. These findings suggest an inherent dependency between recollection-based retrieval and the encoding stage. It seems that because recollection is a contextual-based retrieval process, it is determined by the processing information undergoes at encoding—at the time when context is bound with the items—but not at retrieval—when context is only recovered.     

Regulation of developmental intercellular signalling by intracellular trafficking

Universal trafficking components within the cell can be recruited to coordinate and regulate the developmental signalling cascades. We will present ways in which the intracellular trafficking machinery is used to affect and modulate the outcome of signal transduction in developmental contexts, thus regulating multicellular development. Each of the signalling components must reach its proper intracellular destination, in a form that is properly folded and modified. In many instances, the ability to bring components together or segregate them into distinct compartments within the cell actually provides the switch mechanism to turn developmental signalling pathways on or off. The review will begin with a focus on the signal-sending cells, and the ways in which ligand trafficking can impinge on the signalling outcome, via processing, endocytosis and recycling. We will then turn to the signal-receiving cell, and discuss mechanisms by which endocytosis can affect the spatial features of the signal, and the compartmentalization of components downstream to the receptor.     

Delayed Wound Healing in Heat Stable Antigen (HSA/CD24)-Deficient Mice

Background

Healthy individuals rarely have problems with wound healing. Most skin lesions heal rapidly and efficiently within one to two weeks. However, many medical and surgical complications can be attributed to deficiencies in wound repair. Open wounds have lost the barrier that protects tissues from bacterial invasion and allows the escape of vital fluids. Without expeditious healing, infections become more frequent. The CD24 gene encodes a heavily-glycosylated cell surface protein anchored to the membrane by phosphatidylinositol. CD24 plays an important role in the adaptive immune response and controls an important genetic checkpoint for homeostasis and autoimmune diseases in both mice and humans. We have previously shown that overexpression of CD24 results in increased proliferation and migration rates.

Aim

To examine the role of CD24 in the wound healing process.

Methods

An excisional model of wound healing was used and delayed wound healing was studied in genetically modified heat stable antigen (HSA/CD24)-deficient mice (HSA ^-/-) compared to wild-type (WT) mice.

Results

Large full-thickness skin wounds, excised on the back of mice, exhibited a significant delay in the formation of granulation tissue, and in wound closure when compared to their WTHSA ^+/+ littermates. Wounds were histologically analyzed and scored, based on the degree of cellular invasion, granulation tissue formation, vascularity, and re-epithelialization. Additionally, in stitched wounds, the HSA ^-/- mice failed to maintain their stitches; they did not hold and fell already 24 hours, revealing erythematous wound fields. Re-expression of HSA, delivered by lentivirus, restored the normal healing phenotype, within 24 hours post-injury, and even improved the healing in WT, and in BalbC mice.

Conclusions

Delayed wound-healing in the absence of HSA/CD24 suggests that CD24 plays an important role in this process. Increased expression of CD24, even in the normal state, may be used to enhance wound repair.     

Small angle X-ray scattering of resistant starch type III

Starch fraction, which is resistant to enzymatic digestion, is produced during retrogradation. This fraction, termed resistant starch type III (RSIII), has health benefits such as pre-biotic effects, improving lipid and cholesterol metabolism, and reducing the risk of colon cancer. The work presented in this paper is aimed at investigating the colloidal structure of native high amylose corn starch (HACS) and the RSIII polymorphs produced from it using small angle X-ray scattering. Experimental scattering curves were fitted with appropriate theoretical models such as the "modified lamellar model". Our results show that retrogradation at low temperature leads to formation of polymorph B with crystallinity much lower than that of the granular form, but the lamellas are arranged in long-range periodicity. Conversely, retrogradation at high temperature leads to formation of polymorphs A and V with no defined periodicity. The degree of crystallinity is very low, and the system is better described as a dilute particulate system.     

The expression of interleukin-15 and interleukin-18 by human term placenta is not affected by lipopolysaccharide

The aim of the study was to examine the stimulatory effect of the inflammatory agent lipopolysaccharide (LPS) on the capacity of human term placenta to secrete interleukin (IL)-15 and IL-18. Isolated placental cotyledons from normal human term deliveries were dually perfused for ten hours with perfusion medium alone (n=5) or with perfusion medium containing LPS (1 microg/kg perfused placental tissue) (n=5). Placental tissue was collected from three different placental compartments (amnion, chorion, and placenta) before and after perfusion. The placental tissues collected were homogenized and examined for IL-15 and IL-18 by ELISA. In addition, formalin-fixed and paraffin-embedded sections from term placentas before perfusion were stained by immunohistochemistry to characterize the cellular origin of placental IL-15 and IL-18. Statistical significance was determined using paired/unpaired t-test. p<0.05 was considered significant. Our results show that IL-15 and IL-18 are produced more by chorionic tissue, as compared to the amnion and placental tissues. Moreover, we show that IL-15 and IL-18 are expressed by epithelial cells of the amnion, chorionic cells of the chorion and decidual cells of the decidua. However, IL-15, but not IL-18, was expressed also by syncytiotrophoblasts of the villi. Perfusion of LPS did not affect the capacity of amnion, chorion and placental tissues to secrete IL-15 and IL-18, as compared to control. The expression of IL-15 and IL-18 in the different compartments of the human placenta suggests a possible role for these two cytokines in normal placental development, pregnancy and labor. Moreover, our results indicate that IL-15 and IL-18 are not part of the mechanism of the response of human placenta to LPS.