bluuebunny/crossref_metadata_2025_split huggingface dataset:
The effect of social networks and social support on common mental disorders following specific life events
Authors: Maulik P. K. , Eaton W. W. , Bradshaw C. P. 
Published: November 2009

Maulik PK, Eaton WW, Bradshaw CP. The effect of social networks and social support on common mental disorders following specific life events.Objective: This study examined the association between life events and common mental disorders while accounting for social networks and social supports.Method: Participants included 1920 adults in the Baltimore Epidemiologic Catchment Area Cohort who were interviewed in 1993–1996, of whom 1071 were re‐interviewed in 2004–2005. Generalized estimating equations were used to analyze the data.Results: Social support from friends, spouse or relatives was associated with significantly reduced odds of panic disorder and psychological distress, after experiencing specific life events. Social networks or social support had no significant stress‐buffering effect. Social networks and social support had almost no direct or buffering effect on major depressive disorder, and no effect on generalized anxiety disorder and alcohol abuse or dependence disorder.Conclusion: The significant association between social support and psychological distress, rather than diagnosable mental disorders, highlights the importance of social support, especially when the severity of a mental health related problem is low.
Skin metastasis: a pathologist's perspective
Authors: Hussein Mahmoud Rezk Abdelwahed 
Published: November 2009

Skin metastasis is defined as the spread of malignant cells from a primary malignancy to the skin. It is one manifestation of systemic spread of cancer. The tumor cells originate either from an internal malignancy or from a primary skin cancer. This study presents a literature review concerning these issues as well as this author's experience encountered throughout 19 years of surgical pathology and dermatopathology practice. Several conclusions are evident. Generally, skin metastases are encountered in 0.7–9% of all patients with cancer and as such the skin is an uncommon site of metastatic disease when compared to other organs. There is usually a long‐time lag between the diagnosis of the primary malignancy and the recognition of the skin metastases. However, these metastases may be the first indication of the clinically silent visceral malignancies. The regional distribution of the skin metastasis, although not always predictable, is related to the location of the primary malignancy and the mechanism of metastatic spread. The relative frequency of skin metastasis correlates with the type of primary cancer, which occurs in each sex. For instance, lung and breast carcinomas are the most common primaries that send skin metastasis in men and women, respectively. The head and neck region and the anterior chest are the areas of greatest predilection in men. The anterior chest wall and the abdomen are the most commonly involved sites in women. Skin metastases usually appear as non‐specific groups of discrete firm painless nodules that emerge rapidly without any explanation. They vary in size from so tiny as to be of ‘miliary lesions' to as large as ‘Hen’s egg size’. Some skin metastasis may mimic specific dermatological conditions such as cutaneous cyst, dermatofibroma, pyogenic granuloma, hemangioma, papular eruptions, herpes zoster eruptions, rapidly infiltrating plaques, alopecic patches, cellulitis and erysipelas. Histologically, the skin metastases usually show features reminiscent of the primary malignancy, but with variable degrees of differentiation. Molecularly, skin metastasis is an organized, non‐random and organ‐selective process orchestrated by interaction among several heterogeneous molecules, which are largely unknown. Metastasis to the skin is often a pre‐terminal event that heralds poor outcome.Hussein MRA. Skin metastasis: a pathologist's perspective.
Study on bioactive compounds of in vitro cultured Calculus Suis and natural Calculus Bovis1
Authors: WAN Tien‐Chun , CHENG Fu‐Yuan , LIU Yu‐Tse , LIN Liang‐Chuan , SAKATA Ryoichi 
Published: November 2009

ABSTRACTThe purpose of the study was to investigate bioactive compounds of in vitro cultured Calculus Suis and natural Calculus Bovis obtained as valuable by‐products from animals used for meat production. The results showed that the components of natural Calculus Bovis were rich in bilirubin and biliverdin and had higher content of essential amino acids. The major amino acids of in vitro cultured Calculus Suis were identified as glycine, alanine, glutamic acid and aspartic acid, and those for natural Calculus Bovis were found to be glutamic acid, aspartic acid, proline, and arginine. The methionine and cysteine contents of precursors for glutathione in natural Calculus Bovis were significantly higher than those of in vitro cultured Calculus Suis. The mineral contents of zinc, iron and manganese of natural Calculus Bovis were significantly higher than those of in vitro cultured Calculus Suis. The major bile acids in both products were cholic acid and dehydrocholic acid, respectively. The chenodeoxycholic and ursodeoxycholic acid content of in vitro cultured Calculus Suis was significantly higher than that of natural Calculus Bovis.
Oral administration of Lactobacillus plantarum Lq80 and Megasphaera elsdenii iNP‐001 induces efficient recovery from mucosal atrophy in the small and the large intestines of weaning piglets
Authors: YOSHIDA Yoko , TSUKAHARA Takamitsu , USHIDA Kazunari 
Published: November 2009

ABSTRACTWeaning causes atrophy of intestinal mucosa and a drop of IgA protection in piglets which increases vulnerability to pathogenic infections. Probiotic lactobacilli may support recovery from such weaning stresses. Butyrate‐produce bacteria may support the growth of colonic mucosa. Megasphaera elsdenii, a lactate‐utilizing butyrate producer, may help butyrate production particularly when combined with lactobacilli. Weaned piglets (Experiment 1: 20 days old, Experiment 2: 28 days old) were orally dosed once a day with either (L) 1010 (cell/dose) L. plantarum Lq80, or (LM) 1010 (cell/dose) Lq80 with 109 (cell/dose) M. elsdenii iNP‐001. Lq80 was contained in capsules resistant to gastric digestion. M. elsdenii was contained in capsules resistant to gastric and intestinal digestion. An untreated control (C) was also prepared. After 2 weeks of administration, L. plantarum enhanced the recovery from the villous atrophy in both experiments. The rectal and colonic IgA tended to be higher in L and LM than in C in Experiment 1. Colonic butyrate was higher in LM than in the others in Experiment 1. The thickness of the colonic mucosa was greater in LM than in the others in Experiment 1. In early weaned piglets, the effects of L. plantarum and M. elsdenii were clear.
Collagenous Extracellular Matrix of Cartilage Submitted to Mechanical Forces Studied by Second Harmonic Generation Microscopy
Authors: Werkmeister Elisabeth , De Isla Natalia , Netter Patrick , Stoltz Jean‐François , Dumas Dominique 
Published: November 2009

AbstractOsteoarthritis is a degenerative pathology leading to degradation of the extracellular matrix (ECM). Similar effects can be visualized when applying mechanical or biochemical constraints on cartilaginous tissue. Here, we characterized modification of the ECM appearing under mechanical compression and/or biochemical action (hypoxia environment, nitric oxide and collagenase action). In recent decades, multiphoton microscopy has proved its interest for observing living, thick and opaque biological tissues. Thus, the main components of the cartilaginous ECM can be observed without fluorescent labeling. In particular, the collagen network emits strong second harmonic generation (SHG) signal which could be collected at half of the excitation wavelength. Combining autofluorescence and SHG signal detection enables to obtain complementary structural information. Here, we proved that multiphoton microscopy represents an appropriate tool for ex vitro cartilage imaging. First, we showed that SHG signal specifically comes from collagen (collagenase digestion). Further, we verified that the use of an appropriate band‐pass filter enables to reject the autofluorescence from the ECM. Once this specificity was shown, we followed modification of the cartilage ECM submitted to mechanical or biochemical constraints (compression, enzymatic digestion). By performing textural analysis of SHG images (Haralick’s method), we showed the restructuration of the collagen network according to constraints.
Quantum Dot‐mediated Photoproduction of Reactive Oxygen Species for Cancer Cell Annihilation
Authors: Chen Ji‐Yao , Lee Yee‐Man , Zhao Dan , Mak Nai‐Ki , Wong Ricky Ngok‐Shun , Chan Wing‐Hong , Cheung Nai‐Ho 
Published: November 2009

AbstractWhile semiconductor quantum dots produce little singlet oxygen, they may undergo Type I photoreactions to produce other reactive oxygen species (ROS) to kill cells. CdTe quantum dots coated with thioglycolic acid were used to test that possibility. Some thiol ligands were purposely removed to regenerate the surface electron traps that were passivated by the ligand. This allowed photoinduced electrons to dwell on the surface long enough to be gathered by nearby oxygen molecules to produce ROS. The photocytotoxicity of these quantum dots was tested on nasopharyngeal carcinoma cells. Photokilling was shown to be drug and light dose dependent. Using 0.6 μm quantum dots for incubation and 4.8 J cm−2 for irradiation, about 80% of the cells were annihilated. These quantum dots promised to be potent sensitizers for photoannihilation of cancer cells.
Variation inPseudonocardiaantibiotic defence helps govern parasite‐induced morbidity inAcromyrmexleaf‐cutting ants
Authors: Poulsen Michael , Cafaro Matías J. , Erhardt Daniel P. , Little Ainslie E. F. , Gerardo Nicole M. , Tebbets Brad , Klein Bruce S. , Currie Cameron R. 
Published: November 2009

SummaryHost–parasite associations are potentially shaped by evolutionary reciprocal selection dynamics, in which parasites evolve to overcome host defences and hosts are selected to counteract these through the evolution of new defences. This is expected to result in variation in parasite‐defence interactions, and the evolution of resistant parasites causing increased virulence. Fungus‐growing ants maintain antibiotic‐producingPseudonocardia(Actinobacteria) that aid in protection against specialized parasites of the ants' fungal gardens, and current evidence indicates that both symbionts have been associated with the ants for millions of years. Here we examine the extent of variation in the defensive capabilities of the ant–actinobacterial association againstEscovopsis(parasite‐defence interactions), and evaluate how variation impacts colonies of fungus‐growing ants. We focus on five species ofAcromyrmexleaf‐cutting ants, crossing 12 strains ofPseudonocardiawith 12 strains ofEscovopsisin a Petri plate bioassay experiment, and subsequently conduct subcolony infection experiments using resistant and non‐resistant parasite strains. Diversity in parasite‐defence interactions, including pairings where the parasites are resistant, suggests that chemical variation in the antibiotics produced by different actinobacterial strains are responsible for the observed variation in parasite susceptibility. We evaluate the role this variation plays showing that infection of ant subcolonies with resistant parasite strains results in significantly higher parasite‐induced morbidity with respect to garden biomass loss. Our findings thus further establish the role ofPseudonocardia‐derived antibiotics in helping defend the ants' fungus garden from the parasiteEscovopsis, and provide evidence that small molecules can play important roles as antibiotics in a natural system.
Siah Proteins: Novel Drug Targets in the Ras and Hypoxia Pathways
Authors: House Colin M. , Möller Andreas , Bowtell David D.L. 
Published: November 2009

Abstract
The Siah (seven in absentia homolog) family of RING-domain proteins are components of ubiquitin ligase complexes, targeting proteins for proteasomal degradation. Siah family members have been reported to function in Ras, estrogen, DNA-damage, and hypoxia response pathways. Although earlier reports implicated Siah proteins as tumor suppressors, recent studies in mouse models have shown that Siah inhibition impairs tumor growth and metastasis. Given their central role in oncogenic and angiogenic pathways, Siah proteins are attractive novel therapeutic targets in cancer. [Cancer Res 2009;69(23):8835–8]
Extracellular Signal–Regulated Kinase Signaling Pathway Regulates Breast Cancer Cell Migration by Maintaining slug Expression
Authors: Chen Haoming , Zhu Genfeng , Li Yong , Padia Ravi N. , Dong Zheng , Pan Zhixing K. , Liu Kebin , Huang Shuang 
Published: November 2009

Abstract
Cell migration is a critical step in cancer cell invasion. Recent studies have implicated the importance of the extracellular signal–regulated kinase (ERK) signaling pathway in cancer cell migration. However, the mechanism associated with ERK-regulated cell migration is poorly understood. Using a panel of breast cancer cell lines, we detected an excellent correlation between ERK activity and cell migration. Interestingly, we noticed that a 48-hour treatment with U0126 [specific mitogen-activated protein/ERK kinase (MEK)-1/2 inhibitor] was needed to significantly inhibit breast cancer cell migration, whereas this inhibitor blocked ERK activity within 1 hour. This observation suggests that ERK-dependent gene expression, rather than direct ERK signaling, is essential for cell migration. With further study, we found that ERK activity promoted the expression of the activator protein-1 (AP1) components Fra-1 and c-Jun, both of which were necessary for cell migration. Combination of U0126 treatment and Fra-1/c-Jun knockdown did not yield further reduction in cell migration than either alone, indicating that ERKs and Fra-1/c-Jun act by the same mechanism to facilitate cell migration. In an attempt to investigate the role of Fra-1/c-Jun in cell migration, we found that the ERK-Fra-1/c-Jun axis regulated slug expression in an AP1-dependent manner. Moreover, the occurrence of U0126-induced migratory inhibition coincided with slug reduction, and silencing slug expression abrogated breast cancer cell migration. These results suggest an association between ERK-regulated cell migration and slug expression. Indeed, cell migration was not significantly inhibited by U0126 treatment or Fra-1/c-Jun silencing in cells expressing slug transgene. Our study suggests that the ERK pathway regulates breast cancer cell migration by maintaining slug expression. [Cancer Res 2009;69(24):9228–35]
Intrinsic Gene Expression Profiles of Gliomas Are a Better Predictor of Survival than Histology
Authors: Gravendeel Lonneke A.M. , Kouwenhoven Mathilde C.M. , Gevaert Olivier , de Rooi Johan J. , Stubbs Andrew P. , Duijm J. Elza , Daemen Anneleen , Bleeker Fonnet E. , Bralten Linda B.C. , Kloosterhof Nanne K. , De Moor Bart , Eilers Paul H.C. , van der Spek Peter J. , Kros Johan M. , Sillevis Smitt Peter A.E. , van den Bent Martin J. , French Pim J. 
Published: November 2009

Abstract
Gliomas are the most common primary brain tumors with heterogeneous morphology and variable prognosis. Treatment decisions in patients rely mainly on histologic classification and clinical parameters. However, differences between histologic subclasses and grades are subtle, and classifying gliomas is subject to a large interobserver variability. To improve current classification standards, we have performed gene expression profiling on a large cohort of glioma samples of all histologic subtypes and grades. We identified seven distinct molecular subgroups that correlate with survival. These include two favorable prognostic subgroups (median survival, &gt;4.7 years), two with intermediate prognosis (median survival, 1–4 years), two with poor prognosis (median survival, &lt;1 year), and one control group. The intrinsic molecular subtypes of glioma are different from histologic subgroups and correlate better to patient survival. The prognostic value of molecular subgroups was validated on five independent sample cohorts (The Cancer Genome Atlas, Repository for Molecular Brain Neoplasia Data, GSE12907, GSE4271, and Li and colleagues). The power of intrinsic subtyping is shown by its ability to identify a subset of prognostically favorable tumors within an external data set that contains only histologically confirmed glioblastomas (GBM). Specific genetic changes (epidermal growth factor receptor amplification, IDH1 mutation, and 1p/19q loss of heterozygosity) segregate in distinct molecular subgroups. We identified a subgroup with molecular features associated with secondary GBM, suggesting that different genetic changes drive gene expression profiles. Finally, we assessed response to treatment in molecular subgroups. Our data provide compelling evidence that expression profiling is a more accurate and objective method to classify gliomas than histologic classification. Molecular classification therefore may aid diagnosis and can guide clinical decision making. [Cancer Res 2009;69(23):9065–72]
The Human Ortholog of Granulocyte Macrophage Colony-Stimulating Factor and Interleukin-2 Fusion Protein Induces Potent Ex vivo Natural Killer Cell Activation and Maturation
Authors: Penafuerte Claudia , Bautista-Lopez Norma , Mohamed-Rachid Boulassel , Routy Jean-Pierre , Galipeau Jacques 
Published: November 2009

Abstract
Natural killer (NK) cells are appealing cellular pharmaceuticals for cancer therapy because of their innate ability to recognize and kill tumor cells. Therefore, the development of methods that can enhance the potency in their anticancer effect would be desirable. We have previously shown that a murine granulocyte macrophage colony-stimulating factor (GM-CSF)/interleukin 2 (IL-2) fusion protein displays novel antitumor properties in vivo compared with both cytokines in combination due to recruitment of NK cells. In the present work, we have found that human ortholog of the GM-CSF/IL-2 fusion protein (a.k.a. hGIFT2) induces robust NK cell activation ex vivo with significant secretion of RANTES and a 37-fold increase in IFNγ production when compared with either IL-2 or GM-CSF single cytokine treatment or their combination. Moreover, hGIFT2 upregulates the expression of NK cell activating receptors NKp44, NKp46, and DNAM-1 (CD226), as well as CD69, CD107a, and IL-2Rβ expression. In addition, hGIFT2 promotes NK cell maturation, based on the downregulation of CD117 expression and upregulation of CD11b. This phenotype correlates with significantly greater cytotoxicity against tumor cells. At the molecular level, hGIFT2 leads to a potent activation of Janus-activated kinases (JAK) downstream of both IL-2 and GM-CSF receptors (JAK1 and JAK2, respectively) and consequently leads to a hyperphosphorylation of signal transducers and activators of transcription (STAT)1, STAT3, and STAT5. In conclusion, hGIFT2 fusokine possesses unique biochemical properties distinct from IL-2 and GM-CSF, constitutes a novel and potent tool for ex vivo NK cell activation and maturation, and may be of use for cancer cell immunotherapy. [Cancer Res 2009;69(23):9020–8]
In Benign Barrett's Epithelial Cells, Acid Exposure Generates Reactive Oxygen Species That Cause DNA Double-Strand Breaks
Authors: Zhang Hui Ying , Hormi-Carver Kathy , Zhang Xi , Spechler Stuart J. , Souza Rhonda F. 
Published: November 2009

Abstract
Cells that sustain double-strand breaks (DSB) can develop genomic instability, which contributes to carcinogenesis, and agents that cause DSBs are considered potential carcinogens. We looked for evidence of acid-induced DNA damage, including DSBs, in benign Barrett's epithelial (BAR-T) cell lines in vitro and in patients with Barrett's esophagus in vivo. In BAR-T cells, we also explored the mechanisms underlying acid-induced DNA damage. We exposed BAR-T cells to acid in the presence of a fluorescent probe for reactive oxygen species (ROS) and in the presence or absence of disodium 4,4′-diisothiocyanatostilbene-2,2′-disulfonate (which prevents intracellular acidification) and N-acety-l-cysteine (a scavenger of ROS). DSBs were detected by Western blotting and immunofluorescence for histone H2AX phosphorylation and by CometAssay. During endoscopy in patients with Barrett's esophagus, we took biopsy specimens from the metaplastic mucosa before and after esophageal perfusion with 0.1 N HCl for 3 min and sought DSBs by Western blotting for histone H2AX phosphorylation. In BAR-T cells, acid exposure resulted in ROS production and caused a time-dependent increase in levels of phospho-H2AX that continued for at least 48 h. Pretreatment with disodium 4,4′-diisothiocyanatostilbene-2,2′-disulfonate or N-acety-l-cysteine prevented the acid-induced increase in phospho-H2AX levels. DSBs also were detected in biopsy specimens of Barrett's metaplasia following esophageal acid perfusion in all of 6 patients with Barrett's esophagus. Acid exposure causes DSBs in Barrett's epithelial cells through ROS produced as a consequence of intracellular acidification. These findings suggest that acid can be considered a carcinogen in Barrett's esophagus. [Cancer Res 2009;69(23):9083–9]
Phase II Study of Dasatinib in Patients with Metastatic Castration-Resistant Prostate Cancer
Authors: Yu Evan Y. , Wilding George , Posadas Edwin , Gross Mitchell , Culine Stephane , Massard Christophe , Morris Michael J. , Hudes Gary , Calabrò Fabio , Cheng Shinta , Trudel Géralyn C. , Paliwal Prashni , Sternberg Cora N. 
Published: November 2009

Abstract
Purpose: Antiproliferative and antiosteoclastic activity from preclinical models show potential for dasatinib, an oral SRC and SRC family kinase inhibitor, as a targeted therapy for patients with prostate cancer. This phase II study investigated the activity of dasatinib in patients with metastatic castration-resistant prostate cancer (CRPC).
Experimental Design: Chemotherapy-naive men with CRPC and increasing prostate-specific antigen were treated with dasatinib 100 or 70 mg twice daily. Endpoints included changes in prostate-specific antigen, bone scans, measurable disease (Response Evaluation Criteria in Solid Tumor), and markers of bone metabolism. Following Prostate Cancer Working Group 2 guidelines, lack of progression according to Response Evaluation Criteria in Solid Tumor and bone scan was determined and reported at 12 and 24 weeks.
Results: Forty-seven patients were enrolled and received dasatinib (initial dose 100 mg twice daily, n = 25; 70 mg twice daily, n = 22), of whom 41 (87%) had bone disease. Lack of progression was achieved in 20 (43%) patients at week 12 and in 9 (19%) patients at week 24. Of 41 evaluable patients, 21 (51%) patients achieved ≥40% reduction in urinary N-telopeptide by week 12, with 33 (80%) achieving some level of reduction anytime on study. Of 15 patients with elevated urinary N-telopeptide at baseline, 8 (53%) normalized on study. Of 40 evaluable patients, 24 (60%) had reduction in bone alkaline phosphatase at week 12 and 25 (63%) achieved some reduction on study. Dasatinib was generally well tolerated and treatment-related adverse events were moderate.
Conclusions: This study provides encouraging evidence of dasatinib activity in bone and reasonable tolerability in chemotherapy-naive patients with metastatic CRPC. (Clin Cancer Res 2009;15(23):7421–8)