Ecological Survey of Avifaunal Resources in University of Port Harcourt, Nigeria

A survey of the avifaunal resources was conducted in the three campuses (Choba, Abuja, and Delta) of the University of Port Harcourt, Nigeria to ascertain their bird species composition, abundance, diversity, and affinity for different tree species. Bird census was carried out on twelve focal trees in each of the three campuses for a period of six months. Shannon-Wiener (H) and Simpson (1 – D) diversity indices were used to measure the diversity of bird species in each of the campuses, while similarity in bird species between campuses was ascertained using Sorensen’s similarity index (SI). Paleontological Statistics (PAST) software was used to obtain a hierarchical classification of the tree species in each campus based on the similarity of bird species sighted on them. A total of 5277 birds belonging to 8 species were encountered in Choba Campus; 3937 belonging to 7 species in Abuja Campus; and 3034 belonging to 8 species in Delta Campus. Choba Campus had the highest bird diversity (H = 0.6623; Simpson 1 – D = 0.3370), followed by Abuja Campus (H = 0.4415; Simpson 1 – D = 0.2217), and Delta Campus (H = 0.1656; Simpson 1 – D = 0.05804). Similarity in bird species composition was highest between Abuja Campus and Delta Campus (SI = 93%) and least between Choba Campus and Delta Campus (SI = 63%). Ploceus cucullatus was the most abundant bird species in the three campuses. In Abuja Campus, Cocus nucifera, Polyalthia longifolia and Terminalia catappa were ecologically the most distant tree species with respect to bird species composition; in Delta Campus, Cocus nucifera, Pinus caribaea, and Polyalthia longifolia, were the most ecologically distant; while Hura crepitans and Polyalthia longifolia were the most ecologically distant in Choba Park. Further investigation is required to ascertain why bird species in the various campuses showed no affinity for Cocus nucifera and Polyalthia longifolia.Key words: University of Port Harcourt, avifauna, abundance, diversity, tree-bird interactio

Enhanced thermodynamic stability of tetragonal-phase field in epitaxial Pb(Zr,Ti)O-3 thin films under a two-dimensional compressive stress

A two-dimensional thermodynamic model was developed to account for the observed difficulty in the fabrication of epitaxial Pb(Zr,Ti)O-3 (PZT) thin films in which tetragonal and rhombohedral phases coexist. The thermodynamic formalism based on the Landau-Devonshire's phenomenological theory predicts the enhanced thermodynamic stability of the tetragonal-phase field under a two-dimensional compressive stress. We have experimentally proved this prediction by fabricating an epitaxially oriented tetragonal PZT thin film on MgO substrate with the target composition corresponding to the bulk morphotropic phase boundary (MPB). (C) 1998 American Institute of Physics.open1160sciescopu

VEGFR2 Expression Correlates with Postnatal Development of Brain Arteriovenous Malformations in a Mouse Model of Type I Hereditary Hemorrhagic Telangiectasia

\ua9 2023 by the authors.Brain arteriovenous malformations (BAVMs) are a critical concern in hereditary hemorrhagic telangiectasia (HHT) patients, carrying the risk of life-threatening intracranial hemorrhage. While traditionally seen as congenital, the debate continues due to documented de novo cases. Our primary goal was to identify the precise postnatal window in which deletion of the HHT gene Endoglin (Eng) triggers BAVM development. We employed SclCreER(+);Eng2f/2f mice, enabling timed Eng gene deletion in endothelial cells via tamoxifen. Tamoxifen was given during four postnatal periods: P1–3, P8–10, P15–17, and P22–24. BAVM development was assessed at 2–3 months using latex dye perfusion. We examined the angiogenic activity by assessing vascular endothelial growth factor receptor 2 (VEGFR2) expression via Western blotting and Flk1-LacZ reporter mice. Longitudinal magnetic resonance angiography (MRA) was conducted up to 9 months. BAVMs emerged in 88% (P1–3), 86% (P8–10), and 55% (P15–17) of cases, with varying localization. Notably, the P22–24 group did not develop BAVMs but exhibited skin AVMs. VEGFR2 expression peaked in the initial 2 postnatal weeks, coinciding with BAVM onset. These findings support the “second hit” theory, highlighting the role of early postnatal angiogenesis in initiating BAVM development in HHT type I mice

Thermodynamic theory of stress distribution in epitaxial Pb(Zr, Ti)O-3 thin films

A phenomenological thermodynamic model has been developed to account for the effects of the film thickness on various properties of ferroelectric thin films. To this end, we have suitably incorporated a position-dependent stress distribution function into the elastic Gibbs function. Various physical properties can be predicted as a function of the film thickness using this modified thermodynamic formalism. A comparison of the theoretical predictions with experimental values of the average strain and the para-ferro transition temperature indicates that the tensile stress caused by the cubic-tetragonal displacive phase transition dominates over the compressive thermal stress in the epitaxially oriented tetragonal Pb(Zr, Ti)O-3 thin films. (C) 1999 American Institute of Physics. [S0003-6951(99)05546-1].open1158sciescopu

Endothelial Depletion of Acvrl1 in Mice Leads to Arteriovenous Malformations Associated with Reduced Endoglin Expression

Rare inherited cardiovascular diseases are frequently caused by mutations in genes that are essential for the formation and/ or function of the cardiovasculature. Hereditary Haemorrhagic Telangiectasia is a familial disease of this type. The majority of patients carry mutations in either Endoglin (ENG) or ACVRL1 (also known as ALK1) genes, and the disease is characterized by arteriovenous malformations and persistent haemorrhage. ENG and ACVRL1 encode receptors for the TGF beta superfamily of ligands, that are essential for angiogenesis in early development but their roles are not fully understood. Our goal was to examine the role of Acvrl1 in vascular endothelial cells during vascular development and to determine whether loss of endothelial Acvrl1 leads to arteriovenous malformations. Acvrl1 was depleted in endothelial cells either in early postnatal life or in adult mice. Using the neonatal retinal plexus to examine angiogenesis, we observed that loss of endothelial Acvrl1 led to venous enlargement, vascular hyperbranching and arteriovenous malformations. These phenotypes were associated with loss of arterial Jag1 expression, decreased pSmad1/5/8 activity and increased endothelial cell proliferation. We found that Endoglin was markedly down-regulated in Acvrl1-depleted ECs showing endoglin expression to be downstream of Acvrl1 signalling in vivo. Endothelial-specific depletion of Acvrl1 in pups also led to pulmonary haemorrhage, but in adult mice resulted in caecal haemorrhage and fatal anaemia. We conclude that during development, endothelial Acvrl1 plays an essential role to regulate endothelial cell proliferation and arterial identity during angiogenesis, whilst in adult life endothelial Acvrl1 is required to maintain vascular integrity

Correlated memory resistor in epitaxial NdNiO3 heterostructures with asymmetrical proton concentration

The electronic devices using correlated transition metal oxides are the promising candidates to overcome the limitation of the current electronics due to the rich electronic phases and the extreme sensitivities. Here, we report proton-based resistive switching memory that uses correlated oxides, i.e., epitaxial NdNiO3 heterostructure with asymmetrical concentration of protons (H+) to obtain multilevel states. By designing such metal-NdNiO3-metal device structures with asymmetrical proton concentration, we demonstrate that the correlated oxides exhibit resistive switching by ionic transport of protons at the metal-hydrogenated NdNiO3 (H-NNO) interface. This finding will guide the development of energy-efficient switching devices for non-volatile memory and neuromorphic applications.open1184sciescopu

Histone Acetylation-Mediated Regulation of the Hippo Pathway

The Hippo pathway is a signaling cascade recently found to play a key role in tumorigenesis therefore understanding the mechanisms that regulate it should open new opportunities for cancer treatment. Available data indicate that this pathway is controlled by signals from cell-cell junctions however the potential role of nuclear regulation has not yet been described. Here we set out to verify this possibility and define putative mechanism(s) by which it might occur. By using a luciferase reporter of the Hippo pathway, we measured the effects of different nuclear targeting drugs and found that chromatin-modifying agents, and to a lesser extent certain DNA damaging drugs, strongly induced activity of the reporter. This effect was not mediated by upstream core components (i.e. Mst, Lats) of the Hippo pathway, but through enhanced levels of the Hippo transducer TAZ. Investigation of the underlying mechanism led to the finding that cancer cell exposure to histone deacetylase inhibitors induced secretion of growth factors and cytokines, which in turn activate Akt and inhibit the GSK3 beta associated protein degradation complex in drug-affected as well as in their neighboring cells. Consequently, expression of EMT genes, cell migration and resistance to therapy were induced. These processes were suppressed by using pyrvinium, a recently described small molecule activator of the GSK 3 beta associated degradation complex. Overall, these findings shed light on a previously unrecognized phenomenon by which certain anti-cancer agents may paradoxically promote tumor progression by facilitating stabilization of the Hippo transducer TAZ and inducing cancer cell migration and resistance to therapy. Pharmacological targeting of the GSK3 beta associated degradation complex may thus represent a unique approach to treat cancer. © 2013 Basu et al

Cholesterol and the risk of grade-specific prostate cancer incidence: evidence from two large prospective cohort studies with up to 37 years' follow up

<b>Background</b> High cholesterol may be a modifiable risk factor for prostate cancer but results have been inconsistent and subject to potential "reverse causality" where undetected disease modifies cholesterol prior to diagnosis.<p></p> <b>Methods</b> We conducted a prospective cohort study of 12,926 men who were enrolled in the Midspan studies between 1970 and 1976 and followed up to 31st December 2007. We used Cox-Proportional Hazards Models to evaluate the association between baseline plasma cholesterol and Gleason grade-specific prostate cancer incidence. We excluded cancers detected within at least 5 years of cholesterol assay.<p></p> <b>Results</b> 650 men developed prostate cancer in up to 37 years' follow-up. Baseline plasma cholesterol was positively associated with hazard of high grade (Gleason score[greater than or equal to]8) prostate cancer incidence (n=119). The association was greatest among men in the 4th highest quintile for cholesterol, 6.1 to <6.69 mmol/l, Hazard Ratio 2.28, 95% CI 1.27 to 4.10, compared with the baseline of <5.05 mmol/l. This association remained significant after adjustment for body mass index, smoking and socioeconomic status.<p></p> <b>Conclusions</b> Men with higher cholesterol are at greater risk of developing high-grade prostate cancer but not overall risk of prostate cancer. Interventions to minimise metabolic risk factors may have a role in reducing incidence of aggressive prostate cancer

Densification of the interlayer spacing governs the nanomechanical properties of calcium-silicate-hydrate

Calciuam-silicate-hydrate (C-S-H) is the principal binding phase in modern concrete. Molecular simulations imply that its nanoscale stiffness is 'defect-driven', i.e., dominated by crystallographic defects such as bridging site vacancies in its silicate chains. However, experimental validation of this result is difficult due to the hierarchically porous nature of C-S-H down to nanometers. Here, we integrate high pressure X-ray diffraction and atomistic simulations to correlate the anisotropic deformation of nanocrystalline C-S-H to its atomic-scale structure, which is changed by varying the Ca-to-Si molar ratio. Contrary to the 'defect-driven' hypothesis, we clearly observe stiffening of C-S-H with increasing Ca/Si in the range 0.8 ≤ Ca/Si ≤ 1.3, despite increasing numbers of vacancies in its silicate chains. The deformation of these chains along the b-axis occurs mainly through tilting of the Si-O-Si dihedral angle rather than shortening of the Si-O bond, and consequently there is no correlation between the incompressibilities of the a- and b-axes and the Ca/Si. On the contrary, the intrinsic stiffness of C-S-H solid is inversely correlated with the thickness of its interlayer space. This work provides direct experimental evidence to conduct more realistic modelling of C-S-H-based cementitious material