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Envy is a word signifying an emotion that arises from social comparison and signals that one is outperformed by another person, or group of people, which makes one feel painful inferiority. It originates from the Latin \"invidere\" which means to \"gaze maliciously\". Yet, this emotion does not want to be communicated. It is hard to identify or admit it, partly because of a range of other negative emotions, such as hostility, resentment and rejection that accompany envious feelings. Envy may also trigger admiration that motivates one to \"do better\". However, subjective, historical and philosophical accounts overwhelmingly speak of its negative consequences. Not surprisingly, envy is regarded as a social taboo. Even the traditional scientific community considers envy as a \"second class\" emotion. It is said that envy does not meet the criteria for basic emotions. Only recently, with the paradigmatic shift in modern evolutionary psychology, a new framework was offered and started shedding light onto the emotion nobody likes to feel, think or talk about. This paper presents a review of theoretical considerations, predictions and empirical results, emerging from a relatively small amount of studies that incited a change in the conceptualization of this unwanted and seemingly inept emotion.

The genomes of both human cytomegalovirus (HCMV) and murine cytomegalovirus (MCMV) were first sequenced over 20 years ago. Similar to HCMV, the MCMV genome had initially been proposed to harbor ≈170 open reading frames (ORFs). More recently, omics approaches revealed HCMV gene expression to be substantially more complex comprising several hundred viral ORFs. Here, we provide a state-of-the art reannotation of lytic MCMV gene expression based on integrative analysis of a large set of omics data. Our data reveal 365 viral transcription start sites (TiSS) that give rise to 380 and 454 viral transcripts and ORFs, respectively. The latter include >200 small ORFs, some of which represented the most highly expressed viral gene products. By combining TiSS profiling with metabolic RNA labelling and chemical nucleotide conversion sequencing (dSLAM-seq), we provide a detailed picture of the expression kinetics of viral transcription. This not only resulted in the identification of a novel MCMV immediate early transcript encoding the m166.5 ORF, which we termed ie4 , but also revealed a group of well-expressed viral transcripts that are induced later than canonical true late genes and contain an initiator element (Inr) but no TATA- or TATT-box in their core promoters. We show that viral upstream ORFs (uORFs) tune gene expression of longer viral ORFs expressed in cis at translational level. Finally, we identify a truncated isoform of the viral NK-cell immune evasin m145 arising from a viral TiSS downstream of the canonical m145 mRNA. Despite being ≈5-fold more abundantly expressed than the canonical m145 protein it was not required for downregulating the NK cell ligand, MULT-I. In summary, our work will pave the way for future mechanistic studies on previously unknown cytomegalovirus gene products in an important virus animal model.

Triangularia mangenotti was analyzed for the production of secondary metabolites, resulting in the isolation of known zopfinol (1) and its new derivatives zopfinol B–C (2–4), the 10-membered lactones 7-O-acetylmultiplolide A (5) and 8-O-acetylmultiplolide A (6), together with sordarin (7), sordarin B (8), and hypoxysordarin (9). The absolute configuration of 1 was elucidated by the synthesis of MPTA-esters. Compound 1 showed antimicrobial activity against the Gram-positive bacteria Bacillus subtilis and Staphylococcus aureus and the fungus Mucor hiemalis. While 4 was weakly antibacterial, 3 showed stronger antibiotic activity against the Gram-positive bacteria and weak antifungal activity against M. hiemalis and Rhodotorula glutinis. We furthermore observed the cytotoxicity of 1, 3 and 4 against the mammalian cell lines KB3.1 and L929. Moreover, the new genus Pseudorhypophila is introduced herein to accommodate Triangularia mangenotii together with several species of Zopfiella—Z. marina, Z. pilifera, and Z. submersa. These taxa formed a well-supported monophyletic clade in the recently introduced family Navicularisporaceae, located far from the type species of the respective original genera, in a phylogram based on the combined dataset sequences of the internal transcribed spacer region (ITS), the nuclear rDNA large subunit (LSU), and fragments of the ribosomal polymerase II subunit 2 (rpb2) and β-tubulin (tub2) genes. Zopfiella submersa is synonymized with P. marina due to the phylogenetic and morphological similarity. The isolation of zopfinols 1–4 and sordarins 7–9 confirms the potential of this fungal order as producers of bioactive compounds and suggests these compounds as potential chemotaxonomic markers.

Although previous research suggests that Big Five (BF) and Dark Triad (DT) traits are related to dispositional envy, no studies have simultaneously examined the effects of both groups of traits on an envious disposition operationalised both as a general and dual construct. Moreover, possible mechanisms through which DT trait dimensions may relate to a personal tendency to envy remain obscure. This research presents two studies. First, BF and DT traits were examined as predictors of dispositional envy in a sample of 312 adult participants by using general, malicious, and benign envy scales. Overall, results showed that narcissism, and to a lesser degree Machiavellianism of DT, were the most consistent positive predictors of dispositional envy regardless of the instrument used to measure the construct. Trait neuroticism of BF was a significant positive predictor of an envious disposition measured as a general construct, conscientiousness was a significant negative predictor of envy measured as both a general and malicious disposition, while openness appeared as a weak positive predictor of a benign enviousness. Next, we examined the relationship of DT traits with enviousness in another sample of 233 participants and by using multidimensional measures of DT traits. The results indicated that Entitlement , the lack of Self-sufficiency of the narcissist dimension, and the Machiavellian Cynical view are the most significant factors in predicting dispositional envy . Different associations of BF and DT traits with dispositional envy, measured by distinctive scales, and the links of particular components of the DT traits dimensions with trait envy, were discussed.

Estrogens and antiestrogens influence the G 1 phase of the cell cycle. In MCF-7 breast cancer cells, estrogen stimulated cell cycle progression through loss of the kinase inhibitor proteins (KIPs) p27 and p21 and through G 1 cyclin-dependent kinase (cdk) activation. Treatment with antiestrogen drugs, Tamoxifen or ICI 182780, caused cell cycle arrest, with up-regulation of both p21 and p27 levels, an increase in their binding to cyclin E–cdk2, and kinase inhibition. The requirement for these KIPs in the arrests induced by estradiol depletion or by antiestrogens was investigated with antisense. Antisense inhibition of p21 or p27 expression in estradiol-depleted or antiestrogenarrested MCF-7 led to abrogation of cell cycle arrest, with loss of cyclin E-associated KIPs, activation of cyclin E–cdk2, and S phase entrance. These data demonstrate that depletion of either p21 or p27 can mimic estrogen-stimulated cell cycle activation and indicate that both of these KIPs are critical mediators of the therapeutic effects of antiestrogens in breast cancer.

Herpes simplex virus 1 ( HSV-1 ) infection and stress responses disrupt transcription termination by RNA Polymerase II (Pol II). In HSV-1 infection, but not upon salt or heat stress, this is accompanied by a dramatic increase in chromatin accessibility downstream of genes. Here, we show that the HSV-1 immediate-early protein ICP22 is both necessary and sufficient to induce downstream open chromatin regions (dOCRs) when transcription termination is disrupted by the viral ICP27 protein. This is accompanied by a marked ICP22-dependent loss of histones downstream of affected genes consistent with impaired histone repositioning in the wake of Pol II. Efficient knock-down of the ICP22-interacting histone chaperone FACT is not sufficient to induce dOCRs in ΔICP22 infection but increases dOCR induction in wild-type HSV-1 infection. Interestingly, this is accompanied by a marked increase in chromatin accessibility within gene bodies. We propose a model in which allosteric changes in Pol II composition downstream of genes and ICP22-mediated interference with FACT activity explain the differential impairment of histone repositioning downstream of genes in the wake of Pol II in HSV-1 infection. Herpes simplex virus 1 (HSV-1) infection disrupts transcription termination by RNA Polymerase II. Here, Djakovic et al. identify the immediate-early protein ICP22 protein of HSV-1 to induce open chromatin downstream of genes upon read-through transcription involving the histone chaperone FACT.

Four patients with symptomatic uterine fibroids measuring less than 6 cm underwent laparoscopic ultrasound-guided radiofrequency ablation (RFA) using multiprobe-array electrodes. Follow-up of the treated fibroids was performed with gadolinium-enhanced magnetic resonance imaging (MRI) and patients' symptoms were assessed by telephone interviews. The procedure was initially technically successful in 3 of the 4 patients and MRI studies at 1 month demonstrated complete fibroid ablation. Symptom improvement, including a decrease in menstrual bleeding and pain, was achieved in 2 patients at 3 months. At 7 months, 1 of these 2 patients experienced symptom worsening which correlated with recurrent fibroid on MRI. The third, initially technically successfully treated patient did not experience any symptom relief after the procedure and was ultimately diagnosed with adenomyosis. Our preliminary results suggest that RFA is a technically feasible treatment for symptomatic uterine fibroids in appropriately selected patients.

Trisomy 22 is a rare chromosomal abnormality infrequently detected prenatally. External ear abnormalities, in particular microtia, are often associated with trisomy 22, but prenatal detection of microtia has not been reported in association with trisomy 22. We report a fetus with trisomy 22, with fetal MRI findings of microtia, craniofacial dysmorphism, and polygyria. Fetal MRI is a useful tool for auricular assessment and might have utility in the prenatal detection of chromosomal abnormalities, especially among fetuses with structural anomalies.

Estrogens and antiestrogens influence the G1phase of the cell cycle. In MCF-7 breast cancer cells, estrogen stimulated cell cycle progression through loss of the kinase inhibitor proteins (KIPs) p27 and p21 and through G1cyclin-dependent kinase (cdk) activation. Treatment with antiestrogen drugs, Tamoxifen or ICI 182780, caused cell cycle arrest, with up-regulation of both p21 and p27 levels, an increase in their binding to cyclin E-cdk2, and kinase inhibition. The requirement for these KIPs in the arrests induced by estradiol depletion or by antiestrogens was investigated with antisense. Antisense inhibition of p21 or p27 expression in estradiol-depleted or antiestrogen-arrested MCF-7 led to abrogation of cell cycle arrest, with loss of cyclin E-associated KIPs, activation of cyclin E-cdk2, and S phase entrance. These data demonstrate that depletion of either p21 or p27 can mimic estrogen-stimulated cell cycle activation and indicate that both of these KIPs are critical mediators of the therapeutic effects of antiestrogens in breast cancer.

Estrogens and antiestrogens influence the G 1 phase of the cell cycle. In MCF-7 breast cancer cells, estrogen stimulated cell cycle progression through loss of the kinase inhibitor proteins (KIPs) p27 and p21 and through G 1 cyclin-dependent kinase (cdk) activation. Treatment with antiestrogen drugs, Tamoxifen or ICI 182780, caused cell cycle arrest, with up-regulation of both p21 and p27 levels, an increase in their binding to cyclin E–cdk2, and kinase inhibition. The requirement for these KIPs in the arrests induced by estradiol depletion or by antiestrogens was investigated with antisense. Antisense inhibition of p21 or p27 expression in estradiol-depleted or antiestrogenarrested MCF-7 led to abrogation of cell cycle arrest, with loss of cyclin E-associated KIPs, activation of cyclin E–cdk2, and S phase entrance. These data demonstrate that depletion of either p21 or p27 can mimic estrogen-stimulated cell cycle activation and indicate that both of these KIPs are critical mediators of the therapeutic effects of antiestrogens in breast cancer.