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The Normalized Full Gradient (NFG) method which was put forward about 50 years ago has been used for downward continuation of gravity potential data, especially in the former Union of Soviet Socialist Republics. This method nullifies perturbations due to the passage of mass depth during downward continuation. The method depends on the downwards analytical continuation of normalized full gradient values of gravity data. Analytical continuation discriminates certain structural anomalies which cannot be distinguished in the observed gravity field. This method has been used in various petroleum and tectonic studies. The Trapeze method was used for the determination of Fourier coefficients during the application of this method. No other techniques for calculating these coefficients have been used. However, the Filon method was used for the determination of Fourier coefficients during the application of the NFG method in this work. This method, rather than the Trapeze method, should be preferred for indicating abnormal mass resources at the lower harmonics. In this study, the NFG method using the Filon method has been applied the first time to theoretical models of gravity profiles as example field at the Hasankale-Horasan petroleum exploration province where successful results were achieved. Hydrocarbon presence was shown on the NFG sections by the application of NFG downward continuation operations on theoretical models. Important signs of hydrocarbon structure on the NFG section for field and model data at low harmonics are obtained more effectively using this method.

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Type 2 brittle cornea syndrome (BCS2) is an inherited connective tissue disease with a devastating ocular phenotype caused by mutations in the transcription factor PR domain containing 5 (PRDM5) hypothesized to exert epigenetic effects through histone and DNA methylation. Here we investigate clinical samples, including skin fibroblasts and retinal tissue from BCS2 patients, to elucidate the epigenetic role of PRDM5 and mechanisms of its dysregulation in disease. First we report abnormal retinal vascular morphology in the eyes of two cousins with BCS2 (PRDM5 Δ exons 9-14) using immunohistochemistry, and mine data from skin fibroblast expression microarrays from patients with PRDM5 mutations p.Arg590* and Δ exons 9-14, as well as from a PRDM5 ChIP-sequencing experiment. Gene ontology analysis of dysregulated PRDM5-target genes reveals enrichment for extracellular matrix (ECM) genes supporting vascular integrity and development. Q-PCR and ChIP-qPCR confirm upregulation of critical mediators of ECM stability in vascular structures (COL13A1, COL15A1, NTN1, CDH5) in patient fibroblasts. We identify H3K9 di-methylation (H3K9me2) at these PRDM5-target genes in fibroblasts, and demonstrate that the BCS2 mutation p.Arg83Cys diminishes interaction of PRDM5 with repressive complexes, including NuRD complex protein CHD4, and the repressive chromatin interactor HP1BP3, by co-immunoprecipitation combined with mass spectrometry. We observe reduced heterochromatin protein 1 binding protein 3 (HP1BP3) staining in the retinas of two cousins lacking exons 9-14 by immunohistochemistry, and dysregulated H3K9me2 in skin fibroblasts of three patients (p.Arg590*, p.Glu134* and Δ exons 9-14) by western blotting. These findings suggest that defective interaction of PRDM5 with repressive complexes, and dysregulation of H3K9me2, play a role in PRDM5-associated disease.

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