Anatomical variations of pancreatic head and uncinate process are rarely encountered in clinical practice. These variations are primarily attributed to the complex development of the pancreas. An unduly enlarged uncinate process of the pancreas overlapping the third part of duodenum was discovered during dissection. This malformation of the pancreatic uncinate process was considered to be due to excessive fusion between the ventral and dorsal buds during embryonic development. On further dissection, an avascular pancreatico-duodenal fold guarding the pancreatico-duodenal recess was observed. The enlarged uncinate process can cause compression of neurovascular structures and also cause compression of adjoining viscera. The pancreatico-duodenal recess becomes a potential site for internal herniation. This case is of particular interest to the gastroenterologists and surgeons performing surgical resections. Precise knowledge of embryogenesis of such pancreatic anomalies is necessary for understanding and thus treating many diseases of the pancreas.
Duodenum ; Embryonic Development ; Female ; Head ; Hypertrophy ; Pancreas* ; Pregnancy ; Viscera

Psoriasis is a common inflammatory skin disease with complex etiology and chronic progression. To provide novel insights into the regulatory molecular mechanisms of the disease, we performed RNA sequencing analysis of 14 pairs of skin samples collected from patients with psoriasis. Subsequent pathway analysis and extraction of the transcriptional regulators governing psoriasis-associated pathways was executed using a combination of the MetaCore Interactome enrichment tool and the cisExpress algorithm, followed by comparison to a set of previously described psoriasis response elements. A comparative approach allowed us to identify 42 core transcriptional regulators of the disease associated with inflammation (NFκB, IRF9, JUN, FOS, SRF), the activity of T cells in psoriatic lesions (STAT6, FOXP3, NFATC2, GATA3, TCF7, RUNX1), the hyperproliferation and migration of keratinocytes (JUN, FOS, NFIB, TFAP2A, TFAP2C) and lipid metabolism (TFAP2, RARA, VDR). In addition to the core regulators, we identified 38 transcription factors previously not associated with the disease that can clarify the pathogenesis of psoriasis. To illustrate these findings, we analyzed the regulatory role of one of the identified transcription factors (TFs), FOXA1. Using ChIP-seq and RNA-seq data, we concluded that the atypical expression of the FOXA1 TF is an important player in the disease as it inhibits the maturation of naive T cells into the (CD4+FOXA1+CD47+CD69+PD-L1(hi)FOXP3−) regulatory T cell subpopulation, therefore contributing to the development of psoriatic skin lesions.
Humans ; Inflammation ; Keratinocytes ; Lipid Metabolism ; Psoriasis* ; Response Elements ; Sequence Analysis, RNA ; Skin ; Skin Diseases ; T-Lymphocytes ; Transcription Factors