Background: Psoriasis vulgaris is a common chronic inflammatory dermatosis. Disorders in keratinocyte proliferation, differentiation, inflammation and immune dysregulation are the major factors implicated in the pathogenesis of psoriasis vulgaris. Methods: The study was performed in skin specimens of 25 patients with psoriasis vulgaris and a control group of 10 individuals without a skin disease. Biopsy specimens from lesional and normal skin were analyzed by immunohistochemical method for expressions of Ki-67, Bcl-2, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL), tumor necrosis factor alpha (TNF-a) and nuclear factor kappa B (NF-kB). In addition, densities of mast cell infiltration were also investigated. Results: Ki-67 and TUNEL indexes and TNF-a and NF-kB expressions were significantly higher in psoriatic epidermis than in normal epidermis (p , 0.05). There was no significant difference at Bcl-2 reactivity between the normal and the psoriatic epidermis (p . 0.05); however, Bcl-2 staining intensity of lymphocytes was higher in psoriatic lesions than in normal dermis (p , 0.05). Additionally, the number of mast cells was significantly higher in psoriatic dermis than in normal skin (p , 0.05). Conclusions: There were several complex factors involved in the pathogenesis of psoriasis. We conclude that cellular damage and apoptosis temporarily coincide with epidermal proliferation during the course of psoriatic hyperplasia. Doger FK, Dikicioglu E, Ergin F, Unal E, Sendur N, Uslu M. Nature of cell kinetics in psoriatic epidermis.

Background/Aim: Epidermal growth factor receptor (EGFR) and vascular endothelial growth factor (VEGF) are frequently encountered with aggressive tumor phenotype and poor prognosis, but the relationship between EGFR/VEGF expression and survival remains unclear. The aim of our study was to further investigate the prognostic value of EGFR and VEGF expression in colon cancer. Materials and Methods: The pathological specimens of 60 colon carcinoma patients were retrospectively evaluated and grouped according to EGFR and VEGF staining intensity and percentage of stained neoplastic cells. A final score was assigned to each case by multiplying percentage and staining score. The patients were stratified into the following categories: negative (score 0), low expression (score 1 or 2), and high expression (score 4). The remaining patient data were filtered out from the institutional cancer database. Results: The mean survival time was 28.93 ± 14.1 (range 2–52) months in the EGFR-negative group, 23.92 ± 14.0 (range 6–46) months in the group with a low EGFR expression, and 17.00 ± 12.8 (range 10–40) months in the group with a high EGFR expression. The median survival time was 27.50 ± 14.7 (range 4–52) months in the VEGF-negative group, 29.33 ± 12.8 (range 6–48) months in the group with a low VGEF expression, and 14.50 ± 14.2 (range 2–40) months in the group with a high VGEF expression. The expression of EGFR and VEGF was not an independent factor that affects survival. Conclusions: The EGFR and VEGF expression rates of colon tumors do not predict the survival. In addition, the EGFR expression in the primary tumor was not predictive of metastatic lymph nodes. The prognostic value of EGFR/VEGF staining may be further questioned.

Laryngeal tuberculosis is a rare presentation of tuberculosis. It can mimic laryngeal carcinoma with its clinical and imaging findings. A 51-year old woman underwent 18F-fluorodeoxyglucose positron emission tomography/computed tomography (PET/CT) imaging for clinically suspected carcinoma of the larynx. PET/CT revealed lung lesions consistent with tuberculosis in additional to hypermetabolic focus on larynx. The patient was histopathologically diagnosed with lung and laryngeal tuberculosis.

Helicobacter pylori colonizes the gastric mucosa in humans and causes chronic gastritis. NF-kappaB has a key role as a mediator in mucosal inflammation. In this study, we examined the expression of NF-kappaB in the antral epithelial cells of H. pylori-infected and H. pylori-uninfected biopsies and examined these processes in relationship with grade and activity of gastritis, density of H. pylori, presence of the intestinal metaplasia, and atrophy. Fifty biopsies (35 H. pylori-positive patients and 15 H. pylori-negative controls) were studied. NF-kappaB immunohistochemical stain was performed. NF-kappaB activity in H. pylori-infected biopsies were markedly enhanced compared with uninflamed biopsies (P = 0.001). We also found positive correlation NF-kappaB expression with severity of gastritis (according to Sydney score) (P = 0.001), activity of gastritis (P = 0.046) and H. pylori load (P < 0.001), and atrophy (P = 0.004). We did not find a significant relationship between NF-kappaB and the presence of intestinal metaplasia (P = 0.355). These findings suggested that expression of NF-kappaB has an important role in H. pylori gastritis.

Although our patient numbers are limited, there is a significant association between IP and HPV. This is the first study showing the cooccurrence of CH and OP with HPV.