Adenoviral mediated expression of anti-inflammatory progranulin by placental explants modulates endothelial cell activation by decrease of ICAM-1 expression.

Introduction: Functional disorders of the villous trophoblast may result in preeclampsia through the release of endothelial activating substances. Progranulin is an anti-inflammatory, pro-angiogenic cytokine with TNF-α antagonizing activity. The trophoblastic expression of progranulin is increased during preeclampsia.

MiR-205-5p and miR-342-3p cooperate in the repression of the E2F1 transcription factor in the context of anticancer chemotherapy resistance.

High rates of lethal outcome in tumour metastasis are associated with the acquisition of invasiveness and chemoresistance. Several clinical studies indicate that E2F1 overexpression across high-grade tumours culminates in unfavourable prognosis and chemoresistance in patients. Thus, fine-tuning the expression of E2F1 could be a promising approach for treating patients showing chemoresistance.

Unraveling a tumor type-specific regulatory core underlying E2F1-mediated epithelial-mesenchymal transition to predict receptor protein signatures.

Cancer is a disease of subverted regulatory pathways. In this paper, we reconstruct the regulatory network around E2F, a family of transcription factors whose deregulation has been associated to cancer progression, chemoresistance, invasiveness, and metastasis. We integrate gene expression profiles of cancer cell lines from two E2F1-driven highly aggressive bladder and breast tumors, and use network analysis methods to identify the tumor type-specific core of the network.

E2F1 induces miR-224/452 expression to drive EMT through TXNIP downregulation.

Malignant melanoma is highly lethal due to its aggressive invasive properties and metastatic dissemination. The transcription factor E2F1 is crucial for melanoma progression through poorly understood mechanisms. Here, we show that the miR-224/miR-452 cluster is significantly increased in advanced melanoma and invasive/metastatic cell lines that express high levels of E2F1.

[Changes to the classification of Eating Disorders in DSM-5].

The fifth revision of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) resulted in substantial changes with regard to the classification of Eating Disorders. In DSM-5, Feeding and Eating Disorders are for the first time subsumed in a single category. The Binge Eating Disorder (BED) was established as the third classical eating disorder in addition to Anorexia Nervosa (AN) and Bulimia Nervosa (BN).

The relationship between premorbid body weight and weight at referral, at discharge and at 1-year follow-up in anorexia nervosa.

Body mass index (BMI) is one of the most important outcome predictors in patients with anorexia nervosa (AN). A low premorbid BMI percentile calculated by the patients recalled premorbid weight and the height at first admission has been found to predict the BMI at first inpatient admission. In this study, we sought to confirm this relationship.

Clinical problems encountered in the treatment of adolescents with anorexia nervosa.

The conceptualization of anorexia nervosa (AN) depends on the diagnostic criteria. Most patients with teenage onset AN seem to remit within 3-10 years depending on the definitions of recovery. The mortality of adolescent onset anorexia nervosa (AN) has fortunately decreased over the last two decades.

The E2F1-miRNA cancer progression network.

The transcription factor E2F1 exhibits dual properties, acting as a tumor suppressor and oncogene. Cellular stress such as DNA damage or mitogenic signaling leads to the activation of E2F1 as a mediator of apoptosis in the context of a conserved cellular anti-tumorigenic safeguard mechanism. However in highly aggressive chemoresistant tumors like malignant melanoma and prostate/bladder cancer it switches off this role and acts as promoter of cancer progression.

Anorexia nervosa.

We first discuss current diagnostic issues concerning the classification of anorexia nervosa (AN) by reference to the proposed criteria of the fifth version of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). We strongly welcome the changes in the latest revision of DSM-5 (update April 2012), which in our opinion partially solve the previously delineated classification problems. Nevertheless, we still miss a standard or reference(s) for the weight criterion including the delineation between a healthy and unhealthy underweight, a better operationalization of observable behaviors including symptoms of disordered eating, readily accessible cognitions and a better allowance for cross-cultural aspects in the proposed DSM-5 classification of AN.

Dissection of cell context-dependent interactions between HBx and p53 family members in regulation of apoptosis: a role for HBV-induced HCC.

Chronic hepatitis B virus (HBV) infection is the major risk for hepatocellular carcinomas (HCC). HBV X protein (HBx) and p53 tumor suppressor family interactions may be crucial for HCC induction. We compared p53 and p73 interactions with HBx in normal and HCC tumor cell lines differing in their p53 status.

Do the currently proposed DSM-5 criteria for anorexia nervosa adequately consider developmental aspects in children and adolescents?

The purpose of this article is to discuss the proposed criteria of the fifth version of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) for anorexia nervosa (AN) and to compare these with an alternative proposal which is based on a broader conception of the AN phenotype (Hebebrand and Bulik, in press). The proposed DSM-5 criteria seem to only insufficiently resolve the problems inherent to the current classification of AN because (1) the A criterion does not include a reference to allow the clinician to decide if the (young) patient meets the weight criterion, (2) the AN patient first must have evolved the cognitive capacity for complex abstract reasoning in order to fulfill the criteria B and C (Bravender et al. in Eur Eat Disord Rev 18:79-89, 2010), (3) physical symptoms of starvation including the neuroendocrine dysfunction characteristic of AN are not a diagnostic requirement, and (4) the subtypes are not helpful for classification of younger patients who almost all have the restricting type.

School avoidance from the point of view of child and adolescent psychiatry: symptomatology, development, course, and treatment.

Background: A considerable percentage of children and adolescents who avoid school have mental illnesses. This article reviews the typical manifestations, classification, development, course, and treatment of school-avoiding behavior.

Methods: Based on a selective review of recent literature, we present findings on the psychopathologically relevant features of school-avoiding children and adolescents, including psychiatric diagnoses, developmental, family-related, and psychological test variables.

Functional interplay between E2F1 and chemotherapeutic drugs defines immediate E2F1 target genes crucial for cancer cell death.

The E2F1 transcription factor enhances apoptosis by DNA damage in tumors lacking p53. To elucidate the mechanism of a potential cooperation between E2F1 and chemotherapy, whole-genome microarrays of chemoresistant tumor cell lines were performed focusing on the identification of cooperation response genes (CRG). This gene class is defined by a synergistic expression response upon endogenous E2F1 activation and drug treatment.

[A good care of students in their residency (PJ students)--a win-win-situation].

The provision of good mentors and education to medical students in their residency (PJ students) bears three essential advantages: 1) If the students feel themselves in good hands, they will co-operate effectively, thereby reducing the burden of the medical staff. 2) Contented students are potential advertisers for other interns, clinical trainees, medical students in residency and Ph.D.

Transcriptional repression of the prosurvival endoplasmic reticulum chaperone GRP78/BIP by E2F1.

The endoplasmic reticulum chaperone GRP78/BIP plays a central role in the prosurvival machinery, and its enhanced expression has been implicated in drug resistance, carcinogenesis, and metastasis. E2F1, as part of an antitumor safeguard mechanism, promotes apoptosis regardless of functional p53. Using cells that are defective in p53, we show that E2F1 represses GRP78/BIP at the transcriptional level, and this requires its DNA binding domain.

Val103Ile polymorphism of the melanocortin-4 receptor gene (MC4R) in cancer cachexia.

Background: At present pathogenic mechanisms of cancer cachexia are poorly understood. Previous evidence in animal models implicates the melanocortin-4 receptor gene (MC4R) in the development of cancer cachexia. In humans, MC4R mutations that lead to an impaired receptor function are associated with obesity; in contrast, the most frequent polymorphism (Val103Ile, rs2229616; heterozygote frequency approximately 2%) was shown to be negatively associated with obesity.