Discrimination of delays of reinforcement in aversive conditioning.

<p>(a) The protein level changes of CA125 and LRG1 were confirmed in the larger sample set 2. (b) Marker distributions for the EOC patients with different histological subtypes.</p

Nachrichten aus der Brüder-Gemeine, 1828, no. 05

The Moravian Church's monthly journal of its worldwide activities, including in Labrador, published from 1819-94

Target Proteomic Profiling of Frozen Pancreatic CD24+ Adenocarcinoma Tissues by Immuno-Laser Capture Microdissection and Nano-LC–MS/MS

Cellular heterogeneity of solid tumors represents a common problem in mass spectrometry (MS)-based analysis of tissue specimens. Combining immuno-laser capture microdissection (iLCM) and mass spectrometry (MS) provides a means to study proteins that are specific for pure cell subpopulations in complex tissues. CD24, as a cell surface marker for detecting pancreatic cancer stem cells (CSCs), is directly correlated with the development and metastasis of pancreatic cancer. Herein, we describe an in-depth proteomic profiling of frozen pancreatic CD24⁺ adenocarcinoma cells from early stage tumors using iLCM and LC–MS/MS and a comparison with CD24^– cells dissected from patient-matched adjacent normal tissues. Approximately 40 nL of tissue was procured from each specimen and subjected to tandem MS analysis in triplicate. A total of 2665 proteins were identified, with 375 proteins in common that were significantly differentially expressed in CD24⁺ versus CD24^– cells by at least a 2-fold change. The major groups of the differentially overexpressed proteins are involved in promoting tumor cell migration and invasion, immune escape, and tumor progression. Three selected candidates relevant to mediating immune escape, CD59, CD70, and CD74, and a tumor promoter, TGFBI, were further validated by immunohistochemistry analysis on tissue microarrays. These proteins showed significantly increased expression in a large group of clinical pancreatic adenocarcinomas but were negative in all normal pancreas samples. The significant coexpression of these proteins with CD24 suggests that they may play important roles in the progression of pancreatic cancer and could serve as promising prognosis markers and novel therapeutic targets for this deadly disease

Target Proteomic Profiling of Frozen Pancreatic CD24+ Adenocarcinoma Tissues by Immuno-Laser Capture Microdissection and Nano-LC–MS/MS

Cellular heterogeneity of solid tumors represents a common problem in mass spectrometry (MS)-based analysis of tissue specimens. Combining immuno-laser capture microdissection (iLCM) and mass spectrometry (MS) provides a means to study proteins that are specific for pure cell subpopulations in complex tissues. CD24, as a cell surface marker for detecting pancreatic cancer stem cells (CSCs), is directly correlated with the development and metastasis of pancreatic cancer. Herein, we describe an in-depth proteomic profiling of frozen pancreatic CD24⁺ adenocarcinoma cells from early stage tumors using iLCM and LC–MS/MS and a comparison with CD24^– cells dissected from patient-matched adjacent normal tissues. Approximately 40 nL of tissue was procured from each specimen and subjected to tandem MS analysis in triplicate. A total of 2665 proteins were identified, with 375 proteins in common that were significantly differentially expressed in CD24⁺ versus CD24^– cells by at least a 2-fold change. The major groups of the differentially overexpressed proteins are involved in promoting tumor cell migration and invasion, immune escape, and tumor progression. Three selected candidates relevant to mediating immune escape, CD59, CD70, and CD74, and a tumor promoter, TGFBI, were further validated by immunohistochemistry analysis on tissue microarrays. These proteins showed significantly increased expression in a large group of clinical pancreatic adenocarcinomas but were negative in all normal pancreas samples. The significant coexpression of these proteins with CD24 suggests that they may play important roles in the progression of pancreatic cancer and could serve as promising prognosis markers and novel therapeutic targets for this deadly disease

Evolution of Useless Iron Rust into Uniform α‑Fe₂O₃ Nanospheres: A Smart Way to Make Sustainable Anodes for Hybrid Ni–Fe Cell Devices

The large amount of iron rust yielded in steel industries is undoubtedly a useless and undesired product since its substantial formation and recycle/smelting would give rise to enormous financial costs and environmental pollution issues. To best reuse such rusty wastes, we herein propose a smart and applicable method to convert them into uniform α-Fe₂O₃ nanospheres. Only after a simple and conventional hydrothermal treatment in HNO₃ solution, nearly all of the iron rust can evolve into sphere-like α-Fe₂O₃ products with a typical size of ∼30 nm. When serving as actives for electrochemical energy storage, the <i>in situ</i> generated α-Fe₂O₃ nanospheres exhibit prominent anodic performance, with a maximum specific capacity of ∼269 mAh/g at ∼0.3 A/g, good rate capabilities (∼67.3 mAh/g still retains even at a high rate up to 12.3 A/g), and negligible capacity degradation among 500 cycles. Furthermore, by paring with activated carbons/Ni cathodes, a unique full hybrid Ni–Fe cell is constructed. The assembled full devices can be operated reversibly at a voltage as high as ∼1.8 V in aqueous electrolytes, capable of delivering both high specific energy and power densities with maximum values of ∼131.25 Wh/kg and ∼14 kW/kg, respectively. Our study offers a scalable and effective route to transform rusty wastes into useful α-Fe₂O₃ nanospheres, providing an economic way to make sustainable anodes for energy-storage applications and also a platform to develop advanced Fe-based nanomaterials for other wide potential applications

Overexpression of CD90 (Thy-1) in Pancreatic Adenocarcinoma Present in the Tumor Microenvironment

<div><p>CD90 (Thy-1) plays important roles in oncogenesis and shows potential as a candidate marker for cancer stem cells (CSCs) in various malignancies. Herein, we investigated the expression of CD90 in pancreatic adenocarcinoma (PDAC), with a comparison to normal pancreas and non-malignant pancreatic disease, by immunohistochemical (IHC) analysis of tissue microarrays containing 183 clinical tissue specimens. Statistical analysis was performed to evaluate the correlation between CD90 expression and the major clinicopathological factors after adjustment of age and gender. The IHC data showed that CD90 was significantly overexpressed in PDAC and its metastatic cancers as compared to chronic pancreatitis and benign islet tumors, while it was negative in normal pancreas and 82.7% of adjacent normal pancreas tissues. The abundant CD90 expression was predominantly present in PDAC stroma, such as fibroblasts and vascular endothelial cells, which could serve as a promising marker to distinguish pancreatic adenocarcinoma from normal pancreas and non-malignant pancreatic diseases. Double immunostaining of CD90 with CD24, a CSC marker for PDAC, showed that there was little overlap between these two markers. However, CD90⁺ fibroblast cells were clustered around CD24⁺ malignant ducts, suggesting that CD90 may be involved in the tumor-stroma interactions and promote pancreatic cancer development. Furthermore, CD90 mostly overlapped with α-smooth muscle actin (αSMA, a marker of activated pancreatic stellate cells (PSCs)) in PDAC stroma, which demonstrated that CD90⁺ stromal cells consist largely of activated PSCs. Double immunostaining of CD90 and a vascular endothelial cell marker CD31 demonstrated that CD90 expression on vascular endothelial cells was significantly increased in PDACs as compared to normal pancreas and non-malignant pancreatic diseases. Our findings suggest that CD90 could serve as a promising marker for pancreatic adenocarcinoma where desmoplastic stroma plays an important role in tumor growth and angiogenesis.</p></div

Distribution of CD90 in PDAC of early and late stages evaluated by immunofluorescence staining (<i>green</i>).

<p>DAPI counterstaining was used to visualize nuclei (<i>blue</i>). In early-stage PDACs, CD90 is abundantly expressed on stromal cells, including activated fibroblasts and vascular cells which form the basis for blood vessels (shown in square). Membrane expression of CD90 on the apical cell surface was rarely observed in malignant ducts in late-stage PDACs (marked with a star or arrow). Expression was also observed on endothelial cells (in red circle). Scale bars  = 100 µm.</p

Overexpression of CD90 in the stroma of pancreatic adenocarcinoma (PDAC).

<p>In both early (I and II) and late stages (III and IV) of PDACs, CD90 expression was highly increased, which was abundantly present in the activated stroma, including fibroblasts and vascular endothelial cells. The positive CD90⁺ stromal cells were clustered around the malignant ducts. The circle insert in 3I showed a single layer of CD90⁺ fibroblasts closely localized around tumor duct. The square inserts in 3I–3IV showed strong CD90 expression on vascular endothelial cells in PDAC stage I, II, III and IV, respectively.</p

Double immunofluoresence staining of CD90 (<i>green</i>) and αSMA (<i>red</i>) on PDAC tissues.

<p>DAPI counterstaining was used to visualize nuclei (<i>blue</i>). <i>Yellow</i> or <i>orange</i> represent the co-localization of CD90 and αSMA. (A) A stage I PDAC specimen exhibited a single layer of CD90⁺ activated PSCs (<i>yellow</i>) surrounding the duct-like structure. (B) Higher magnification of the stromal area in PDAC displaying an apparent overlap between CD90 and αSMA (y<i>ellow</i> or <i>orange</i> in the merged images). The IHC result showed that CD90 mostly overlapped with αSMA in PDAC stroma, demonstrating that CD90⁺ stromal cells consist largely of activated PSCs.</p

Clinical pathologic characteristics of the patient samples (n = 163) in TMAs.

<p>Clinical pathologic characteristics of the patient samples (n = 163) in TMAs.</p