To our knowledge, cofilin-1 (spot no. 3) and Rho-GDI-β (spot no. 6) have not been reported as an autoAg in

any disease. Thereby, we next focused on cofilin-1 and Rho-GDI-β for further investigation. First, to confirm antigenicity of cofilin-1, we prepared a recombinant cofilin-1 protein as a fusion find more protein with MBP (cofilin-MBP, Fig. 3a). We separated the purified cofilin-MBP and MBP together by 1D SDS-PAGE and then tested their reactivity to the serum sample of BD6, which had positively reacted to protein spot no. 3 in the screening by 2DE-WB. As a result, BD6 reacted to cofilin-MBP but not to MBP alone (Fig. 3b). This confirmed that protein spot no. 3 was cofilin-1. Similarly, we tried to prepare recombinant proteins for Rho-GDI-β. Unfortunately, however, the recombinant Rho-GDI-β failed buy Buparlisib to be produced in E. coli (data not shown). Next, we determined the prevalence of the anti-cofilin-1-positive patients in various diseases by WB. Specifically, we tested serum samples from 30 patients with BD, 35 patients with RA, 32 patients with SLE and

33 patients with PM/DM. As a result, four (13.3%) patients with BD, two (6.3%) patients with SLE, five (14.3%) patients with RA, and eight (24.2%) patients with PM/DM were found positive for the anti-cofilin-1 autoAbs (Table 4). In PM/DM, although the frequency of anti-cofilin-1 was higher in the PM group (33.3%) than in the DM group (22.2%), the difference was not significant statistically (P= 0.62). Representative results of WB are selleckchem shown in Figure 3b. This indicates that the existence of the anti-cofilin-1 autoAbs is not specific for BD, rather detected at a high frequency in PM/DM, even though the frequency

was not significantly different between the PM/DM and BD groups (P= 0.34). In addition, we compared laboratory parameters between the anti-cofilin-1 autoAbs-positive and -negative patients. The parameters compared included peripheral white blood cell and neutrophil counts, platelet counts, erythrocyte sedimentation rate, serum levels of IgG, IgA, IgM, IgD, and C-reactive protein in the patients with BD (Table 5). However, there was no significant difference. The frequency of occurrence of oral ulceration, uveitis, genital ulceration, and erythema nodosum showed no significant difference. As abnormality of the laboratory data and occurrence of the symptoms are remarkable in the active stage of the BD generally, the anti-cofilin-1 autoAbs do not seem to be correlated with the severity of BD. Also, routine laboratory examinations in the patients with PM/DM did not show a significant difference between the anti-cofilin-1 autoAbs-positive and -negative patients. Representatively, levels of serum creatine phosphokinase were 1502 ± 1303 (IU/L) in the antibody-positive group and 1384 ± 1683 (IU/L) in the -negative group (P= 0.998).

1 [8]. This reporter line was used to screen newly generated mouse-human hybrid antigen-presenting cell lines

for their capacity to https://www.selleckchem.com/products/VX-809.html activate the reporter line in presence of the PAg HMBPP and the PAg-inducing agent zoledronate or the alkylamine sec-butylamine. Mouse-human hybrids are known to successively lose human chromosomes over time in culture. To identify those human chromosome(s) mandatory for PAg presentation, hybrid cells were cloned and tested for induction of reporter cell stimulation in the presence of 1 nM HMBPP. PCR karyotyping showed that loss of human chromosomes 2, 3, 7, 8, 9, 10, 11, 13, 17, 18, 20, 21, and X had no effect on PAg-mediated activation of the reporter cells, while cells without Chr6 failed to induce activation of the reporter cells in the presence of HMBPP or zoledronate. For

reasons so far unknown, 2 of 6 of the Chr6-bearing hybridoma cell lines stimulate the reporter cells in the presence of HMBPP and zoledronate but not in the presence of 2 mM sec-butylamine. This loss of the capacity to stimulate in presence of alkylamine did not correlate with loss of distinct human chromosomes. To test whether Chr6 alone would be sufficient for HMBPP-induced reporter cell activation, we tested Chinese hamster ovary cells monosomal for human Chr6 (CHO Chr6 cells) as presenters. We compared their responses to HMBPP, zoledronate, sec-butylamine or mAb 20.1 using CHO cells, CHO cells transduced with BTN3A1 and CHO Chr6 cells with or without transduced BTN3A1 as antigen-presenting cells. Figure 1 shows that the reporter cells responded Rapamycin purchase to zoledronate and HMBPP in the presence of CHO Chr6 cells. This is in full agreement with the reported requirement of Chr6 for PAg presentation [12]. As previously reported for human cells as PAg-presenters [8, 9, 12], BTN3A1 transduction increased PAg-induced stimulation but only for CHO Chr6 cells (CHO Chr6 BTN3A1). Importantly, CHO cells expressing only the PAg-presenting BTN3A1 molecule (CHO BTN3A1) but lacking Chr6 activated neither in the presence of HMBPP nor zoledronate (Fig. 1A and B). Figure 1C shows that, in the presence of mAb 20.1, CHO Chr6 BTN3A1

cells Olopatadine and even more strikingly CHO BTN3A1 cells massively stimulated the reporter cells. In contrast to our study, Vavassorri et al. [12] showed no data on whether BTN3A1 would be sufficient to render murine cells PAg presenters and Harly et al. [8] only mentioned as an “unpublished observation” that BTN3A1-transduced mouse cells fail to present PAg. However, such a negative result is difficult to interpret unless a suitable positive control is provided. Indeed, it is conceivable that Vγ9Vδ2 T cell-mediated activation requires additional features, e.g. the expression of certain co-stimulatory molecules. Therefore it is important that BTN3A1-transduced CHO and BTN3A1-transduced CHO Chr6 cells induce a strong response to mAb 20.

In addition, string vessels (twisted capillaries) in the cerebral white matter and increased density of CD34-immunoreactive vessels LY2157299 research buy were observed in CS cases. Immunohistochemistry findings for aquaporin 4 indicated no pathological changes in either CS or XP-A cases. Hence, the increased subarachnoid artery space may have caused subdural hemorrhage.

Since such vascular changes were not observed in XP-A cases, the increased density of vessels in CS cases was not caused by brain atrophy. Hence, brain vascular changes may be involved in neurological disturbances in CS. “
“Pituitary adenoma with ossification is a rare histological variant. Previously there have been four cases reported in the literature. Here a case of pituitary prolactin-producing adenoma with bone formation in a 21-year-old woman is described. The patient had irregular menstruation for three years. MRI revealed an unusual 1.5 cm3 ovoid nodule

with partial shell-like structure showing heterogeneous signals. The pre-operative prolactin serum level was 258.78 ng/mL. The patient was operated through the trans-sphenoidal pathway under general anesthesia. Histologically, Trametinib mw the tumor was parenchymal and mostly replaced by the well-differentiated lamellar bony tissue. Sheets of tumor cells interweaved with the mature lamellar bone trabeculae showing no cellular atypia. The cytoplasm

of the adenoma cells was slightly eosinophilic and the myelo-adipose metaplastic foci were also found within the parenchyma. Immunohistochemical staining of tumor cells showed positive expressions of prolactin, synaptophysin and chromogranin A in the cytoplasm of the tumor cells. Meanwhile, negative expressions of S-100, epithelial membrane antigen, GFAP and other pituitary hormones were also demonstrated. As a rare histological variant of pituitary adenoma, the current case of pituitary prolactin producing adenoma with ossification is reported. It is speculated that the ossification Tacrolimus (FK506) may be derived from the osteo-metaplasia of mesenchymal fibroblasts resulting from the effects of both secondary ischemia by the outgrowth of the tumor and/or the autocrine effect of prolactin in this case. The bony shell structure may limit the growth of pituitary adenoma. “
“Medulloblastoma is a primitive neuroectodermal tumor, which originates in the cerebellum, presumably due to the alterations of some neurogenetic elements. Sirtuin 1 (SIRT1), a class III histone deacetylase (HDAC), regulates differentiation of neuronal stem cells but its status in medulloblastomas remains largely unknown. The current study aimed to address this issue by checking SIRT1 expression in noncancerous cerebellar tissues, medulloblastoma tissues and established cell lines.

4). As expected, the percentage of CFSElow cells — that is those that had divided in the host

— was higher in the BM than in spleen and LNs of B6 mice (Fig. 4A). In both IL-15 KO and IL-15Rα KO mice, the percentage of CFSElow cells was low, without differences among the three organs examined (Fig. 4A). A pronounced CD127 downmodulation by donor WT CFSE+ cells was observed only in the BM of B6 mice (Fig. 4B). To investigate whether in B6 mice the lower CD127 membrane expression by BM CD44high CD8+ T cells was related with a higher fraction of proliferating cells in this organ [[10-12]], we performed a more detailed analysis on CFSElow and CFSEhigh cells (Supporting Information Fig. 2 and Fig. 4C). Within each organ, we found that CFSElow cells had a lower

Selleckchem Rucaparib CD127 MFI as compared with CFSEhigh cells. More importantly, within each of the two populations, BM cells had a lower CD127 membrane expression as compared with those in either spleen or LNs (Fig. 4C). Our results on genetically deficient mice show that IL-15 is required for homeostatic proliferation and CD127 downmodulation in the BM by conventional WT CD44high CD8+ T cells. Our analysis on adoptive transfers into WT mice shows that both undivided cells (CFSEhigh) and cells which had recently divided (CFSElow) Talazoparib molecular weight have a lower CD127 membrane expression in BM than in spleen and LNs. Our next question was whether low membrane CD127 expression by BM CD44high CD8+ T cells was due to decreased CD127 mRNA level [[6]]. We performed real-time PCR analysis of CD127 mRNA expression by fluorescence-activated cell sorter (FACS)-sorted highly purified CD44high CD8+ T cells from either spleen or BM

of WT mice and found that CD127 mRNA amount was lower in the BM (Fig. 5). In this group of experiments, cells from LNs were not included due to low cell yields. As a control for suppression of CD127 mRNA transcription, Etofibrate we incubated purified splenic CD8+ T cells with either medium or IL-15 for an overnight (Fig. 5). Real-time PCR results were in agreement with northern blot analysis on purified spleen and BM CD8+ T cells (data not shown). We were unable to perform similar analysis in IL-15 KO mice due to low cell yields (average percentages ± SD of BM TCR+CD8+ cells were 0.30 ± 0.12 in IL-15 KO and 2.59 ± 0.53 in WT, N = 5 per group, p ≤ 0.01). To directly address the molecular mechanisms regulating CD127 gene expression, we used a CD127 genetically modified mouse strain (CD127tg) generated by the Ashwell’s laboratory (National Institutes of Health, Bethesda, MD, USA) [[30]]. This strain has a CD127 transgene under the control of human CD2 promoter, leading to CD127 transgene high expression in T cells and unresponsiveness to the normal transcriptional regulation acting on the endogenous gene. We confirmed that CD127tg is a suitable tool for our experiments by showing that CD127tg CD8+ T cells are unresponsive to IL-15 effect on CD127 expression.

However, a direct immunostimulatory effect of anthelmintic treatment cannot be excluded (53) and may be stronger in hair lambs. “
“Urinary catheters are standard medical devices utilized in both hospital and nursing home settings, but are associated with a high frequency of catheter-associated R788 price urinary tract infections (CAUTI).

In particular, biofilm formation on the catheter surface by uropathogens such as Klebsiella pneumoniae causes severe problems. Here we demonstrate that type 1 and type 3 fimbriae expressed by K. pneumoniae enhance biofilm formation on urinary catheters in a catheterized bladder model that mirrors the physico-chemical conditions present in catheterized patients. Furthermore, we show that both fimbrial types are able to functionally compensate for each other during biofilm formation on urinary catheters. In situ monitoring of fimbrial expression revealed that neither of the two fimbrial types is expressed when cells are grown planktonically. Interestingly, during biofilm formation on catheters, both fimbrial types are expressed, suggesting that they are both important in promoting

biofilm formation on catheters. Additionally, transformed into and expressed by a nonfimbriated Escherichia coli strain, both fimbrial types significantly increased biofilm formation on catheters compared with the wild-type E. coli strain. The widespread Cell press occurrence of the two fimbrial

Selleck PD332991 types in different species of pathogenic bacteria stresses the need for further assessment of their role during urinary tract infections. “
“The extravasation of CD4+ effector/memory T cells (TEM) across the blood-brain barrier (BBB) is a crucial step in the pathogenesis of experimental autoimmune encephalomyelitis (EAE)or multiple sclerosis (MS).Endothelial ICAM-1 and ICAM-2 are essential for CD4+ TEM cells crawlingon the BBBprior todiapedesis. Here, weinvestigated the influence of cell surface levels of endothelial ICAM-1 in determining the cellular route of CD4+ TEM-cell diapedesis across cytokine treatedprimary mouse BBB endothelial cells under physiological flow. Inflammatory conditions inducing high levels of endothelial ICAM-1 promoted rapid initiation of transcellulardiapedesis of CD4+ T cells across the BBB, while intermediate levels of endothelial ICAM-1 favored paracellular CD4+T-celldiapedesis.Importantly, the route of T-celldiapedesis across the BBB was independent of loss of BBB barrier properties. Unexpectedly, a low number of CD4+ TEM cells was found to cross the inflamed BBB in the absence of endothelial ICAM-1 and ICAM-2 via an obviously alternatively regulated transcellular pathway.In vivo, this translated tothe development of ameliorated EAE in ICAM-1null//ICAM-2−/−C57BL/6J mice.

Activated glia have been shown to be both necessary and sufficient for enhanced nociception [13]. Specifically, microglia activation is one of the most common

and earliest features of most neuroinflammatory disorders [15,16] and CNS pathologies [17–19]. We have reported increased activation of astrocytes and microglia in spinal cord tissue of a CRPS patient when compared to control tissue [20]. In man, CNS microglia is thought to arise during gestation from mesodermal/mesenchymal sources [21]. Normally, CNS microglia can replenish with little or no need of repopulation from circulating bone marrow-derived progenitors [21]. However, in disease conditions, blood-derived Selleckchem Afatinib monocytes/macrophages are recruited into the CNS and differentiate into microglia [22,23]. A recent study demonstrated that, following nerve injury, blood monocytes/macrophages infiltrate the CNS and differentiate into functional microglia Selleck SCH727965 at the involved segmental spinal level, resulting in hypersensitivity and chronic pain [24]. Human peripheral blood monocytes can be subdivided into two subgroups based on their expression of cell surface markers: one expressing CD14, but not CD16 (CD14+CD16-) and the other expressing both CD14 and CD16 (CD14+CD16+) [25]. Both subgroups produce similar levels of proinflammatory cytokines. However, CD14+CD16+

monocytes produce much lower levels of the anti-inflammatory cytokine interleukin (IL)-10, suggesting that these cells constitute a proinflammatory subtype [26]. Increased proportions of the CD14+CD16+ subgroup have been described in disease states including sepsis, acquired immunodeficiency disease syndrome, rheumatoid arthritis, systemic lupus erythematosus and active sarcoidosis [25,27–30]. The primary aim of this study was to evaluate Racecadotril the proportion of proinflammatory CD14+CD16+ monocytes as well as the levels of several plasma cytokines in blood from patients afflicted with CRPS compared to age- and gender-matched healthy control individuals. All subjects were enrolled after giving informed consent as approved by the Drexel University College

of Medicine Institutional Review Board (IRB). CRPS patients were recruited from the pain clinic of Drexel University School of Medicine and fulfilled the International Association for the Study of Pain (IASP) diagnostic criteria for CRPS [31]. Healthy control subjects were recruited from the general public. The exclusion criteria for all subjects included: pregnancy, recent infection, lupus erythematosus, HIV/AIDS, rheumatoid arthritis, recent extracorporeal circulation (haemodialysis, bypass surgery, plasmapheresis), bone marrow transplant, immunosuppressive therapy, blood disorders (anaemia, leukaemia), thymectomy or sarcoidosis. All CRPS patients received a complete neurological examination and pain evaluation.

live vaccine and pathogenic strains of B. abortus using the in vitro murine BMDC model. This would provide additional information on the potential of IR or HK vaccines for human use. Based on our data, which demonstrated that while HK and IR strain RB51 induced upregulation of costimulatory molecules, but not TNF-α or IL-12 production, the question remains as to whether live vs. HK or IR strains can also upregulate T-cell function and ultimately protect against challenge. On comparing Brucella, with other live strains of intracellular organisms such as Listeria monocytogenes (Muraille et al., 2005) and Chlamydia trachomatis (Rey-Ladino et al., 2005), live strains induced higher levels of DC maturation

compared with their HK or UV-IR forms, respectively. Roscovitine LEE011 nmr Muraille et al. (2005) and Tsunetsugu-Yokota et al. (2002) showed that the T-lymphocytes primed by HK Listeria or Mycobacterium pulsed DCs did not fully differentiate and that only infection with live organisms induced long-term CD8+ T-cell-mediated immunity. Additionally, only live Listeria and Bacillus Calmette-Guerin strains of Mycobacterium protected against challenge (Muraille et al., 2005). On comparing our data with results from other laboratories, we found that our data were in contrast

with the data presented by Zwerdling et al. (2008) and Macedo et al. (2008). Their results showed that DC–cytokine secretion was not dependent on bacterial viability and HK B. abortus strain 2308 (at 108 or 109 bacteria mL−1) induced DC maturation and TNF-α and IL-12 secretion in a dose-dependent

fashion. The probable reasons for this discrepancy could be the lower DC (5 × 105 cells mL−1), HK and IR Selleck Ponatinib cell concentrations used in our study. Our studies with live bacteria do support that live bacteria induce a dose-dependent upregulation of DC costimulatory molecule expression and cytokine production (Surendran et al., 2010). In this study, there was a dose-dependent response between 1 : 10 and 1 : 100 for HK and IR, but while higher doses stimulated more costimulatory molecule expression, neither the HK or the IR strains induced DC cytokine production at the doses tested here. With live strains, there appears to be a threshold of DC activation needed for cytokine production (Surendran et al., 2010). In this study, for an appropriate comparison between strains, we used the same doses of live, HK and IR strains RB51 and 2308 for infecting the DCs. Besides the differences in DC activation and function reported by Macedo et al. (2008) and Zwerdling et al. (2008), our results were also different from those reported by Vemulapalli (Sanakkayala et al., 2005) and Datta (Datta et al., 2006). Vemulapalli and colleagues, found that both HK and IR strain RB51 induced similar DC activation and IR vs. HK strain RB51 induced increased IL-12 secretion correlating with protection against strain 2308.

copper-dependent enzymes with critical functions in antioxidant defences, in mitochondrial energy production, and in iron metabolism are affected in blood and muscles of patients with profound copper deficiency leading to myeloneuropathy. Homeostatic mechanisms are strongly activated to increase intracellular copper retention. “
“S. Yamashita, E. Kimura, N. Tawara, H. Sakaguchi, T. Nakama, Y. Maeda, T. Hirano, M. Uchino and Y.

Ando (2013) Neuropathology and Applied Neurobiology39, 406–416 Optineurin is potentially associated with TDP-43 and involved in the pathogenesis of inclusion body myositis Olaparib Aims: Increasing evidences suggest a similarity in the pathophysiological mechanisms of neuronal cell death in amyotrophic lateral sclerosis (ALS) and myofibre degeneration in sporadic inclusion body myositis (sIBM). The aim of this study is to elucidate the involvement of ALS-causing proteins

in the pathophysiological mechanisms in sIBM. Methods: Skeletal muscle biopsy specimens of five patients with sIBM, two with oculopharyngeal muscular dystrophy (OPMD), three with polymyositis (PM), three with dermatomyositis (DM), three with neurogenic U0126 muscular atrophy, and three healthy control subjects were examined. We analysed the expression and localization of familial ALS-causing proteins, including transactive response DNA binding protein-43 (TDP-43), fused in sarcoma/translocated in liposarcoma (FUS/TLS), Cu/Zn superoxide dismutase (SOD1) and optineurin (OPTN) by immunohistochemistry. Results: TDP-43, OPTN and, to a lesser extent, FUS/TLS were more frequently accumulated in the cytoplasm in patients with sIBM and OPMD than in patients with PM, DM, neurogenic muscular atrophy, or healthy control subjects. SOD1 was accumulated in a small percentage of myofibres in patients Phosphoprotein phosphatase with sIBM and OPMD, and to a very small extent in patients with PM and DM. Confocal microscopy imaging showed that TDP-43 proteins more often colocalized with OPTN than with FUS/TLS, p62 and

phosphorylated Tau. Conclusions: These findings suggest that OPTN in cooperation with TDP-43 might be involved in the pathophysiological mechanisms of skeletal muscular degeneration in myopathy with rimmed vacuoles. Further investigation into these mechanisms is therefore warranted. “
“Despite the blood–brain barrier (BBB) the human CNS is continuously screened by blood-derived immunological cells. In certain brain areas the local BBB configuration grants passage of large molecules, whereas others are better shielded. We investigated whether these regional BBB compositions are paralleled by differences in the degree of cellular immunosurveillance by investigating tissue from 23 normal human brains for several CD markers, FoxP3, granzyme B, and perforin.

We describe a technique utilizing the DIEP

flap skin paddle for immediate nipple reconstruction at the time of mastectomy and reconstruction, Tanespimycin solubility dmso eliminating the need for delayed reconstruction and limiting donor site morbidity by concealing the donor site below the mastectomy skin flaps. In the six cases described performed between 2010 and 2012 (mean with 53 years; range 46–59 years), there have been no complications to the flap or the nipple postoperatively, nor has there been a need for further nipple revisions for 6 months. The nipple position relative to the flap breast mound has remained unchanged for up to 6 months. The immediate nipple reconstruction does not significantly lengthen operative time, requiring approximately 30 additional operative minutes per nipple. Immediate nipple reconstruction utilizing the DIEP flap can be a cost-effective and feasible technique for recreating a natural-appearing and aesthetic nipple in select patients. © 2012 Wiley Periodicals, Inc. Microsurgery, 2013. “
“This case describes the use of the medial plantar artery flap used to

cover Dorsomorphin cell line a lateral foot wound in a 19-year-old male with a history of spina bifida. The original operative plan was for coverage with a medial plantar flap based distally on retrograde flow through the lateral plantar artery; however, this had to be revised intraoperatively as his vascular anatomy was not adequate to support a flap of this type. Thus, advancement with rotation modification of the

conventional medial plantar flap was performed with good results. At 2-month follow-up, the patient’s flap had fully healed, he returned to full weight-bearing status, and he had gross sensation in the sole of his foot. This case illustrates the use of the well-described medial plantar flap by rotating and advancing the flap for reconstruction of defects of the foot. © 2012 Wiley Resveratrol Periodicals, Inc. Microsurgery, 2012. “
“Reconstruction of complex mid back wounds is challenging due to the patient comorbidities and scarcity of reliable regional flap alternatives. Four consecutive cases treated with perforator based V-Y advancement flaps are reported. An effective repair was achieved in all the patients and the mean follow up period was 28 months. Our results indicate the efficacy of adipocutaneous flaps in complex spinal soft tissue repair and may help to refine the relevant algorhythm. © 2011 Wiley-Liss, Inc. Microsurgery, 2011. “
“Soft tissue coverage in the distal lower extremity remains a significant challenge. While free flaps are often utilized for larger defects, local perforator-based propeller flaps may be ideal for smaller wounds requiring coverage. Propeller flaps can provide excellent form and function for both traumatic and atraumatic defects with minimal donor site morbidity but can have concerning rates of flap loss.

These findings are interesting click here and surprising because they revealed that infants as young as 4 months of age are sensitive to several depth cues (e.g., T- and Y-junctions) that are fundamental for perceiving shape. In addition, this work established that the ability to detect inconsistencies in global object structure is present early and that selective attention to particular visual information may guide young infants’ oculomotor exploration of novel objects. In the present

study, we asked whether the perception of an impossible figure would also evoke increased manual exploration of these displays during a reaching task with older infants. Recent studies using a picture-grasping task with 9-month-olds have demonstrated that infants in this age group typically engage in manual investigation of depicted objects (DeLoache, Pierroutsakos, & Uttal, 2003; DeLoache, Pierroutsakos,

Uttal, Small molecule library nmr Rosengren, & Gottlieb, 1998; Pierroutsakos & DeLoache, 2003; Yonas, Granrud, Chov, & Alexander, 2005). For example, when presented with a realistic photograph of an object, infants touch, rub, and sometimes even grasp at the depicted object. And, as the degree of realism decreases in the depicted objects (e.g., black and white photo versus line drawing), so too does the frequency of manual gestures initiated toward those displays (Pierroutsakos & DeLoache, 2003). This behavior does not reflect an inability to perceive the difference between depicted and real objects: When given a choice between

a real object and a picture of it, infants virtually always reach for the real one (DeLoache et al., 1998). Rather, it appears that infants explore depicted objects because they are not fully certain about their nature. Perceiving Clostridium perfringens alpha toxin whether or not an object is graspable and within reach involves encoding spatial position coordinates and integrating visual features inherent to the object prior to performing a manual action. Coordinated reaching and object manipulation skills begin to surface around the age of 4 months, and young infants start reaching for graspable objects at about this time (Bertenthal, 1996; von Hofsten, 2004), even reaching in the dark for an object previously seen (Clifton, Perris, & McCall, 1999). Studies of visually guided reaching further reveal a rapid increase in sensitivity to pictorial depth information in static image displays. Between the ages of 5 and 7 months, infants show increased reaching to the nearer-appearing object in the display, which indicates that infants can perceive pictorial depth from information provided by linear perspective (Yonas, Cleaves, & Pettersen, 1978; Yonas, Elieff, & Arterberry, 2002), surface occlusion (Granrud & Yonas, 1984), surface illumination (Granrud, Yonas, & Opland, 1985), and cast shadows (Yonas & Granrud, 2006).