Divine Reality and the Principle of Sufficient Reason: A Philosophical Analysis

The cosmological postulation that there cannot be an “effect” without a “cause” is the underlying predicate of the Principle of Sufficient Reason (PSR). PSR states that everything must have a sufficient reason, cause, or foundation. Some theologians consider the above notions to be fideism, preferring to think that God's knowledge is founded on human reason, whereas “intelligent design” is a two-tiered argument that uses design to show the existence of a “Divine Realty” (God). Reality is subjective and is built indirectly depending on human perspective. The paper, therefore, aimed to philosophically analyze the Principle of Sufficient Reason to explain the notion of a divine reality. This analytical philosophical research employs the descriptive and conceptual analysis approaches and reveals that PSR, like other concepts, is not only improbable, but is also contradictory to divine knowledge. It concludes that although PSR uses contradictory terms such as “necessity” and “contingency” and fails to provide adequate justification for the existence of a divine reality, it could be justified that a “Divine Reality” (God or necessary being) must have a “sufficient reason” to exist

Migration and religious socialization in Nigeria: the Fulanization dilemma

Migration has remarkably influenced the development of civilization and the establishment of cultural borders throughout history. In the case of Nigeria, one of the negative impacts of migration has been the violent seizure of ancestral lands by the Fulani as part of a strategy to 'fulanize' and 'Islamize' the Nigerian nation. This study investigates the links between human migration and religious socialization in Africa, particularly Nigeria. The paper employs the descriptive and phenomenological approaches and bases its arguments on the theoretical foundations of Durkheimian and Weberian theories. The paper argues that regional mobility, with its religious socializing effects, affects national politics, government, the economy, and other national domains. It concludes that African countries should include international migration in their plans and national development goals to make their countries safer

Quantification and Distribution of Polynuclear Aromatic Hydrocarbons (PNAs) in Surface Waters in the Vicinity of Kokori Oil Field, Nigeria

The distribution pattern and sources of sixteen PANs listed as priority pollutants were investigated in eight composite water samples using Gas Chromatography (GC) with a Hawlett-Packard model 6890 with 30m x 0.28 capillary column. Analytical observation of the percentage distribution of PNAs concentration in the study area show that SSY(20.12%)>SSX(16.75%)>SSZ(16.01%)>SST(14.43%)>SSW(13.24%)>SSU(12.06%)>SSV(6.84%)>SSA(0.55 %). The observed distribution of genotoxic (Gen.) and carcinogenic (Car.) PNAs and other PNAs in the study area show that the Gen. and Car PNAs recorded 29.58% over other PNAs with 70.42%. The percentage distribution of low PNAs/high PNAs and ratio analysis show that this sources are petrogenic and pyrogenic but dominated with petrogenic PNAs @ JASE

Teaching Basic Science Through Indigenous Practices for Millennium Development Goals

Millennium Development Goals(MD

Meox2 haploinsufficiency increases neuronal cell loss in a mouse model of Alzheimer\u27s disease

Evidence suggests that multiple genetic and environmental factors conspire together to increase susceptibility to Alzheimer\u27s disease (AD). The amyloid cascade hypothesis states that deposition of the amyloid-β (Aβ) peptide is central to AD; however, evidence in humans and animals suggests that Aβ buildup alone is not sufficient to cause neuronal cell loss and cognitive decline. Mouse models that express high levels of mutant forms of amyloid precursor protein and/or cleaving enzymes deposit amyloid but do not show neuron loss. Therefore, a double-hit hypothesis for AD has been proposed whereby vascular dysfunction precedes and promotes Aβ toxicity. In support of this, copy number variations in mesenchyme homeobox 2 (MEOX2), a gene involved in vascular development, are associated with severe forms of AD. However, the role of MEOX2 in AD has not been studied. Here, we tested Meox2 haploinsufficiency in B6.APP/PS1 (B6.APBTg) mice, a mouse model of AD. Despite no overt differences in plaque deposition or glial activation, B6.APBTg mice that carry only one copy of Meox2 (B6.APBTg.Mx−/+) show increased neuronal cell loss, particularly in regions containing plaques, compared with B6.APBTgmice. Neuronal cell loss corresponds with a significant decrease in plaque-associated microvessels, further supporting a synergistic effect of vascular compromise and amyloid deposition on neuronal cell dysfunction in AD

Prefrontal Neurons Encode Actions and Outcomes in Conjunction with Spatial Location in Rats Performing a Dynamic Delayed Non-Match to Position Task

To respond adaptively to change organisms must utilize information about recent events and environmental context to select actions that are likely to produce favorable outcomes. We developed a dynamic delayed nonmatching to position task to study the influence of spatial context on event-related activity of medial prefrontal cortex neurons during reinforcement-guided decision-making. We found neurons with responses related to preparation, movement, lever press responses, reinforcement, and memory delays. Combined event-related and video tracking analyses revealed variability in spatial tuning of neurons with similar event-related activity. While all correlated neurons exhibited spatial tuning broadly consistent with relevant task events, for instance reinforcement-related activity concentrated in locations where reinforcement was delivered, some had elevated activity in more specific locations, for instance reinforcement-related activity in one of several locations where reinforcement was delivered. Timing analyses revealed a limited set of distinct response types with activity time-locked to critical behavioral events that represent the temporal organization of dDNMTP trials. Our results suggest that reinforcement-guided decision-making emerges from discrete populations of medial prefrontal neurons that encode information related to planned or ongoing movements and actions and anticipated or actual action-outcomes in conjunction with information about spatial context

Natural genetic variation determines microglia heterogeneity in wild-derived mouse models of Alzheimer\u27s disease.

Genetic and genome-wide association studies suggest a central role for microglia in Alzheimer\u27s disease (AD). However, single-cell RNA sequencing (scRNA-seq) of microglia in mice, a key preclinical model, has shown mixed results regarding translatability to human studies. To address this, scRNA-seq of microglia from C57BL/6J (B6) and wild-derived strains (WSB/EiJ, CAST/EiJ, and PWK/PhJ) with and without APP/PS1 demonstrates that genetic diversity significantly alters features and dynamics of microglia in baseline neuroimmune functions and in response to amyloidosis. Results show significant variation in the abundance of microglial subtypes or states, including numbers of previously identified disease-associated and interferon-responding microglia, across the strains. For each subtype, significant differences in the expression of many genes are observed in wild-derived strains relative to B6, including 19 genes previously associated with human AD including Apoe, Trem2, and Sorl1. This resource is critical in the development of appropriately targeted therapeutics for AD and other neurological diseases

Meox2 haploinsufficiency increases neuronal cell loss in a mouse model of Alzheimer\u27s disease

Evidence suggests that multiple genetic and environmental factors conspire together to increase susceptibility to Alzheimer\u27s disease (AD). The amyloid cascade hypothesis states that deposition of the amyloid-β (Aβ) peptide is central to AD; however, evidence in humans and animals suggests that Aβ buildup alone is not sufficient to cause neuronal cell loss and cognitive decline. Mouse models that express high levels of mutant forms of amyloid precursor protein and/or cleaving enzymes deposit amyloid but do not show neuron loss. Therefore, a double-hit hypothesis for AD has been proposed whereby vascular dysfunction precedes and promotes Aβ toxicity. In support of this, copy number variations in mesenchyme homeobox 2 (MEOX2), a gene involved in vascular development, are associated with severe forms of AD. However, the role of MEOX2 in AD has not been studied. Here, we tested Meox2 haploinsufficiency in B6.APP/PS1 (B6.APBTg) mice, a mouse model of AD. Despite no overt differences in plaque deposition or glial activation, B6.APBTg mice that carry only one copy of Meox2 (B6.APBTg.Mx−/+) show increased neuronal cell loss, particularly in regions containing plaques, compared with B6.APBTgmice. Neuronal cell loss corresponds with a significant decrease in plaque-associated microvessels, further supporting a synergistic effect of vascular compromise and amyloid deposition on neuronal cell dysfunction in AD