Dietary niche overlap and resource partitioning among six steppe passerines of Central Spain using DNA metabarcoding

Trophic niche partitioning is a mechanism that facilitates the coexistence of ecologically similar species by sharing their resource use. However, detailed information of the trophic niche in insectivorous birds is usually limited by the lack of accurate identification of consumed food resources. The use of DNA metabarcoding has proved useful for molecular identification of the taxa present in bird faecal samples. Here, we used this molecular technique to study the diets of six steppe passerine species distributed in two Special Protection Areas in central Spain, and to characterize the dietary niche overlap and the prey composition differences between bird species. In total, we distinguished 112 diet items, covering 39 arthropod families of 13 orders. Although significant dietary differences existed in prey species composition, our results indicated a 74% overlap in steppe bird dietary niche, mostly due to high consumption of abundant arthropod prey such as beetles, grasshoppers and spiders in the breeding season by all bird species. The lowest overlap was found for the dietary niches of the Greater Short-toed Lark Calandrella brachydactyla and Dupont's Lark Chersophilus duponti, a scarce and threatened species, which appeared to be the species with the most distinct dietary niche within the community. Our results make a significant contribution to the knowledge of shrub-steppe bird diets and their trophic interactions, indicating that some extent of interspecific resource partitioning occurs in the study area, notably between Dupont's Lark and the Greater Short-toed Lark. Our study demonstrates the value of DNA metabarcoding in the assessment of passerine diets and provides useful ecological results for the design of biodiversity conservation programmes in the increasingly scarce and threatened steppe habitatsThis study was supported by the European Commission LIFE Ricot ı (LIFE15-NAT-ES-000802) and LIFE Connect Ricot ı (LIFE20-NAT-ES-000133) projects, and the BBVA Foundation Dron Ricot ı project. This is a contribution to the Excellence Network Remedinal 3CM (S2013/MAE2719). Lu ıs P. da Silva and Vanessa A. Mata were funded by Fundac ~ao para a Ci^encia e Tecnologia (FCT) through the research contract CEECIND/02064/ 2017 and 2020.02547.CEECIND, respectivel

An investigation of WNT pathway activation and association with survival in central nervous system primitive neuroectodermal tumours (CNS PNET)

Central nervous system primitive neuroectodermal tumours (CNS PNET) are high-grade, predominantly paediatric, brain tumours. Previously they have been grouped with medulloblastomas owing to their histological similarities. The WNT/β-catenin pathway has been implicated in many tumour types, including medulloblastoma. On pathway activation β-catenin (CTNNB1) translocates to the nucleus, where it induces transcription of target genes. It is commonly upregulated in tumours by mutations in the key pathway components APC and CTNNB1. WNT/β-catenin pathway status was investigated by immunohistochemical analysis of CTNNB1 and the pathway target cyclin D1 (CCND1) in 49 CNS PNETs and 46 medulloblastomas. The mutational status of APC and CTNNB1 (β-catenin) was investigated in 33 CNS PNETs and 22 medulloblastomas. CTNNB1 nuclear localisation was seen in 36% of CNS PNETs and 27% of medulloblastomas. A significant correlation was found between CTNNB1 nuclear localisation and CCND1 levels. Mutations in CTNNB1 were identified in 4% of CNS PNETs and 20% of medulloblastomas. No mutations were identified in APC. A potential link between the level of nuclear staining and a better prognosis was identified in the CNS PNETs, suggesting that the extent of pathway activation is linked to outcome. The results suggest that the WNT/β-catenin pathway plays an important role in the pathogenesis of CNS PNETs. However, activation is not caused by mutations in CTNNB1 or APC in the majority of CNS PNET cases

Accounting and the hope of action

The paper discusses the role of hope in the construction of an accounting technology to realize a program, by looking at a process of choosing non-financial indicators in an effort to achieve healthier workplaces. By exploring the literature dealing with the concept of hope and by drawing on the debate on the relationship between accounting and action, we highlight the features of three hope-related concepts (hopelessness, naıve hope, and reflective hope). We also highlight how these concepts relate to different areas of uncertainty (validity, accuracy, and relevance) in the development of accounting technologies. Evidence collected through participant observation of a team involved in the construction of indicators offers empirical material to investigate the interplay between hopelessness, naıve hope, and reflective hope in relation to uncertainties concerning the link between accounting and action. Beyond analyzing how team members move from a naıve to a reflective hope in making the accounting-action link, the paper shows that among practitioners it is accepted that unintended consequences constitute the rule rather than the exception in the accounting-action link

Myometrial invasion and lymph node metastasis in endometrioid carcinomas: tumor-associated macrophages, microvessel density, and HIF1A have a crucial role

Myometrial invasion is an independent prognostic parameter of the endometrioid carcinomas which correlates with the risk of metastasis to pelvic and/or paraaortic lymph nodes. Recognition of myometrial invasion is sometimes difficult. In fact, myoinvasion is overdiagnosed in routine practice in as many as 25% of the cases. Recently, it has been observed that tumor-associated macrophages stimulate angiogenesis and promote cancer dissemination. Tumor macrophages (CD163), microvessel density (CD31), and hypoxia inducible factor 1 \u3b1 subunit (HIF1A) were investigated in 64 primary endometrioid carcinomas with (50 cases) and without (14 cases) myometrial invasion as well as in the corresponding regional lymph nodes metastases of 20 of the myoinvasive tumors. Endometrioid carcinomas with myometrial invasion showed higher number of CD163-tumor macrophages and greater microvessel density than endometrioid carcinomas without myometrial invasion (P=0.000 and P=0.000, respectively). In carcinomas confined to the corpus uteri (stage I), expression of HIF1A was associated with deep myoinvasion (stage IC) (P=0.006). There was a significant relationship between microvessel density and CD163-macrophages both in the myoinvasive and nonmyoinvasive tumors. On the other hand, high-grade endometrioid carcinomas had more macrophage infiltrates and microvessels than low-grade tumors (P=0.03 and P=0.07). Also, there was a positive correlation between CD163-macrophages and microvessel density in the primary tumors and their corresponding regional lymph node metastases. These findings link increased microvessel proliferation to stromal macrophage infiltrate and suggest that enhanced tumor angiogenesis, triggered by stromal macrophages, regulates the progression of endometrioid carcinomas. The identical stroma microenvironment found in the primary and the corresponding metastatic tumor suggests that tumor stroma response is determined by the intrinsic biology of the tumor

Crossed Cerebellar Diaschisis in Alzheimer's Disease

We describe the phenomenon of crossed cerebellar diaschisis (CCD) in four subjects diagnosed with Alzheimer's disease (AD) according to the National Institute on Aging -Alzheimer Association (NIA-AA) criteria, in combination with 18F-FDG PET and 11C-PiB PET imaging. 18F-FDG PET showed a pattern of cerebral metabolism with relative decrease most prominent in the frontal-parietal cortex of the left hemisphere and crossed hypometabolism of the right cerebellum. 11C-PiB PET showed symmetrical amyloid accumulation, but a lower relative tracer delivery (a surrogate of relative cerebral blood flow) in the left hemisphere. CCD is the phenomenon of unilateral cerebellar hypometabolism as a remote effect of supratentorial dysfunction of the brain in the contralateral hemisphere. The mechanism implies the involvement of the cortico-ponto-cerebellar fibers. The pathophysiology is thought to have a functional or reversible basis but can also reflect in secondary morphologic change. CCD is a well-recognized phenomenon, since the development of new imaging techniques, although scarcely described in neurodegenerative dementias. To our knowledge this is the first report describing CCD in AD subjects with documentation of both 18F-FDG PET and 11C-PiB PET imaging. CCD in our subjects was explained on a functional basis due to neurodegenerative pathology in the left hemisphere. There was no structural lesion and the symmetric amyloid accumulation did not correspond with the unilateral metabolic impairment. This suggests that CCD might be caused by non-amyloid neurodegeneration. The pathophysiological mechanism, clinical relevance and therapeutic implications of CCD and the role of the cerebellum in AD need further investigation

FGFR2 point mutations in 466 endometrioid endometrial tumors: Relationship with MSI, KRAS, PIK3CA, CTNNB1 mutations and clinicopathological features

Mutations in multiple oncogenes including KRAS, CTNNB1, PIK3CA and FGFR2 have been identified in endometrial cancer. The aim of this study was to provide insight into the clinicopathological features associated with patterns of mutation in these genes, a necessary step in planning targeted therapies for endometrial cancer. 466 endometrioid endometrial tumors were tested for mutations in FGFR2, KRAS, CTNNB1, and PIK3CA. The relationships between mutation status, tumor microsatellite instability (MSI) and clinicopathological features including overall survival (OS) and disease-free survival (DFS) were evaluated using Kaplan-Meier survival analysis and Cox proportional hazard models. Mutations were identified in FGFR2 (48/466); KRAS (87/464); CTNNB1 (88/454) and PIK3CA (104/464). KRAS and FGFR2 mutations were significantly more common, and CTNNB1 mutations less common, in MSI positive tumors. KRAS and FGFR2 occurred in a near mutually exclusive pattern (p = 0.05) and, surprisingly, mutations in KRAS and CTNNB1 also occurred in a near mutually exclusive pattern (p = 0.0002). Multivariate analysis revealed that mutation in KRAS and FGFR2 showed a trend (p = 0.06) towards longer and shorter DFS, respectively. In the 386 patients with early stage disease (stage I and II), FGFR2 mutation was significantly associated with shorter DFS (HR = 3.24; 95% confidence interval, CI, 1.35-7.77; p = 0.008) and OS (HR = 2.00; 95% CI 1.09-3.65; p = 0.025) and KRAS was associated with longer DFS (HR = 0.23; 95% CI 0.05-0.97; p = 0.045). In conclusion, although KRAS and FGFR2 mutations share similar activation of the MAPK pathway, our data suggest very different roles in tumor biology. This has implications for the implementation of anti-FGFR or anti-MEK biologic therapies