The role of the 'Natural history of religion' in Hume's critique of religious belief

I argue that Hume's naturalistic explanation of religious belief in the Natural History of Religion has significant epistemic consequences. While he argues in the Dialogues Concerning Natural Religion (and in other works) that belief in God is not justified on the basis of testimony or philosophical argument, this is not enough to show that religious belief is not warranted. In the Natural History, Hume provides a genetic explanation for religious belief. I contend that the explanation of religious belief in the Natural History, given Hume's conclusions in his other works, provides grounds to reject religious belief. Thus, I conclude that the Natural History plays an important role in Hume's overall critique of religion insofar as it is a necessary component in Hume's arsenal against the warrant of religious belief.

The Role of the Polish Military Contingent in the Reconstruction of Ghazni Province

The article outlines the activity of the Polish army as part of NATO operations in Afghanistan. The analysis concerns humanitarian aid in particular, and identifies the most important activities of the PRT (Provincial Reconstruction Team) carried out in the field of reconstruction and security in the city of Ghazni from 2001. The PMC (Polish Military Contingent) worked for the stability of the city, starting in mid-2008. The author concludes that the objectives pursued by the PMC related to the reconstruction of the city of Ghazni increased the level of security of the local community and the overall stability in the region. The methods used in the article (comparative, research, systemic and genetic explanation method) make it possible to examine and present the processes and changes taking place.

Genomic Characterization of a Pediatric Cohort with Non-Malignant Lymphoproliferative Disorders

Introduction: Pediatric non-malignant lymphoproliferative disorders (LPDs) are a clinically and genetically heterogeneous. While transient lymphadenopathy is extremely common and rarely dangerous, long-standing immune dysregulation and lymphoproliferation in children may be life-threatening. Data to guide evaluation and treatment of children with benign LPD are lacking. The primary objective of this study was to define the genomic spectrum and clinical characteristics of a cohort of children with nonmalignant LPD. Identification of the underlying pathogenic mechanisms may facilitate timely interventions and potentially guide optimal therapeutic strategies. Method s: Patients at Texas Children's Hospital and collaborating referral centers who met criteria for non-malignant LPD were offered participation in this study, approved by the Baylor College of Medicine Institutional Review Board. LPD was defined as persistent lymphadenopathy, lymph organ involvement, or lymphocytic infiltration for more than 3 months, with or without chronic or significant EBV infection. Chronic or significant EBV infection was defined as recurrent or persistent EBV viremia more than 3 months, invasive EBV disease, or EBV PCR copies >100,000. All subjects and/or family members provided written informed consent to have their clinical and genetic information published. Genetic testing was performed clinically or through research-based whole-exome sequencing (WES). Results : Fifty-one subjects from 47 different families with non-malignant LPD were identified. Median age at disease presentation was 3.3 years (range 3.9 weeks - 21 years) with nearly equal proportions of males (n = 26) and females (n = 25). Almost half of subjects were Hispanic (49%), and 29% were non-Hispanic white. Fifteen subjects (29%) met HLH-2004 diagnostic criteria for HLH. Twenty-one patients had EBV-associated lymphoproliferative disorders (EBV-LPD) and 6 of the 51 ultimately developed malignancy. Clinical genetic testing was performed in 29 patients, and research-based WES was performed in 44 patients. Potential disease-causing genetic defects were identified in 62% of families. Of these pathogenic variants, targeted therapies may be effective for treatment in at least 10 of the conditions (17 subjects, 33%). Furthermore, genetic results supported potential for curative HSCT in 35% of the patients. Mechanistically, all of the LPD-associated genes could be placed into 1 of 3 categories: 1) defective control of lymphocyte activity; 2) impaired lymphocyte activation, cytoskeletal organization, and apoptosis; and 3) dysregulated inflammation. Ten-year survival for the entire cohort was 72.4% with a median 5.6 years of follow-up (range 0.10 - 26.6). Patients without evidence of a genetic explanation had a lower ten-year survival compared to those patients for whom a genetic explanation was identified (48% versus 82%, respectively, p=0.03). When both EBV-LPD and genetic explanation were considered, the ten-year survival estimate for those with EBV-associated disease and no genetic explanation was significantly worse than those with EBV-associated disease and a genetic explanation (17% vs. 90%; p =0.002). Patients without EBV-associated disease were at lower risk of death than those with EBV-LPD. Evaluating outcomes associated with maximum treatment received, ten-year survival was lowest (25% survival) among those who underwent HSCT. Conclusion s: Pediatric non-malignant LPD represents a group of conditions with high risk of death. WES identified actionable mutations in the majority of LPD cases in this cohort. Early identification of these mutations can guide therapy by confirming diagnosis, revealing molecular targets and/or supporting definitive therapy with stem cell transplant. Disclosures Forbes: Takeda: Consultancy. Jolles:CSL Behring: Consultancy, Honoraria, Research Funding, Speakers Bureau; LFB: Consultancy, Honoraria, Research Funding, Speakers Bureau; UCB Pharma: Consultancy, Other: Drug Safety Committee; Shire/Takeda: Consultancy, Honoraria, Research Funding, Speakers Bureau; Pharming: Consultancy, Honoraria, Research Funding, Speakers Bureau; Octapharma: Consultancy, Honoraria, Research Funding, Speakers Bureau. Heslop:Marker Therapeutics: Equity Ownership, Membership on an entity's Board of Directors or advisory committees; Allovir: Equity Ownership; Gilead Biosciences: Membership on an entity's Board of Directors or advisory committees; Kiadis: Membership on an entity's Board of Directors or advisory committees; Tessa Therapeutics: Membership on an entity's Board of Directors or advisory committees, Research Funding; Cell Medica: Research Funding. Rouce:Novartis: Consultancy, Honoraria; Tessa Therapeutics: Research Funding; Kite, a Gilead Company: Consultancy, Honoraria.

Klasifikasi Bentuk Muka Bumi (Landform) untuk Pemetaan Geomorfologi pada Skala 1:25.000 dan Aplikasinya untuk Penataan Ruang

Sari – Pembuatan peta geomorfologi, khususnya bagi mahasiswa geologi pemeta tugas akhir, dan umumnya bagi para ahli Geologi, kadang-kadang menimbulkan kesulitan pada tahap klasifikasi dan penamaan satuan geomorfologinya. Klasifikasi bentuk muka bumi ini dibuat untuk menjembatani kesulitan tersebut dengan tetap mendasarkan pada penjelasan genetis geologis. Dalam pembagian ini terdapat sembilan satuan bentang alam yang dikontrol baik oleh proses endogen maupun proses eksogen, yang masing-masing terbagi ke dalam beberapa satuan bentuk muka bumi. Kesembilan satuan bentang alam tersebut adalah: 1. Pegunungan Lipatan, 2. Pegunungan Plateau/Lapisan Datar, 3. Pegunungan Sesar, 4. Pegunungan Gunungapi, 5. Karst, 6. Sungai dan Danau, 7. Pantai, Delta dan Laut, 8. Gurun, 9. Glasial.Abstract – The development of geomorphologic map, especially for the students of geology, and also for geologists, faces a major problem in the stage of classifying and naming of its geomorphologic unit. This classification of landform tries to act as a bridge the problem which is still based on geologically genetic explanation. This classification is divided into nine landscape units that controlled by endogenic and/or exogenic processes, and each landscape is divided into several landform units. The landscape units are 1. Folded Mountain, 2. Plateau/Horizontal Layer Mountain, 3. Faulted or Block Mountain, 4. Volcanoes, 5. Karst, 6. River/Fluvial and Lake/Lacustrin, 7. Coastal, Delta and Marine, 8. Desert, 9. Glaciated Region.

First record of leucism for Carollia castanea Allen, 1890 (Phyllostomidae: Carollinae) in southeastern Costa Rica

Carollia castanea se distribuye desde Honduras hasta Venezuela. Casos de leucismo no han sido reportados para esta especie pero si para otros filostómidos. Capturamos un adulto de C. castanea con leucismo en la Zona Protectora Las Tablas. Presentaba despigmentación en la punta de las alas, debajo del antebrazo y en la parte superior del uropatagio, pero las manchas blancas no cubrían una alta porción de la piel. Algunos casos de leucismo en murciélagos han sido explicados por endogamia en poblaciones pequeñas o aisladas, pero esto no está apoyado por evidencia empírica. Nuestro registro es anecdótico, y no podemos ofrecer una explicación ecológica o genética. Proponemos que los casos de leucismo sean evaluados en cada contexto específico y soportado por estudios poblacionales robustos. Carollia castanea is distributed from Honduras to Venezuela. Leucism has not been reported for this species but there are reports for other phyllostomid bats. An adult C. castanea with leucism was captured at Las Tablas Protected Zone, Costa Rica. It presented depigmentation on both wing tips, under the and on the upper part of the uropatagium, however the white patches did not cover a high proportion of its skin. Some leucism cases in bats have been explained by inbreeding in small or isolated population, but it is scarcely supported by empirical evidence. Our record is anecdotal therefore we cannot offer an ecological or even a genetic explanation. We propose that leucism cases should be assessed in each specific context where it is recorded, and supported by robust po­pulation studies.