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Hypophysitis is defined as inflammation of the pituitary gland that is primary or secondary to a local or systemic process. Differential diagnosis is broad (including primary tumors, metastases, and lympho-proliferative diseases) and multifaceted. Patients with hypophysitis typically present with headaches, some degree of anterior and/or posterior pituitary dysfunction, and enlargement of pituitary gland and/or stalk, as determined by imaging. Most hypophysitis causes are autoimmune, but other etiologies include inflammation secondary to sellar tumors or cysts, systemic diseases, and infection or drug-induced causes. Novel pathologies such as immunoglobulin G4-related hypophysitis, immunotherapy-induced hypophysitis, and paraneoplastic pituitary-directed autoimmunity are also included in a growing spectrum of this rare pituitary disease. Typical magnetic resonance imaging reveals stalk thickening and homogenous enlargement of the pituitary gland; however, imaging is not always specific. Diagnosis can be challenging, and ultimately, only a pituitary biopsy can confirm hypophysitis type and rule out other etiologies. A presumptive diagnosis can be made often without biopsy. Detailed history and clinical examination are essential, notably for signs of underlying etiology with systemic manifestations. Hormone replacement and, in selected cases, careful observation is advised with imaging follow-up. High-dose glucocorticoids are initiated mainly to help reduce mass effect. A response may be observed in all auto-immune etiologies, as well as in lymphoproliferative diseases, and, as such, should not be used for differential diagnosis. Surgery may be necessary in some cases to relieve mass effect and allow a definite diagnosis. Immunosuppressive therapy and radiation are sometimes also necessary in resistant cases.

Background Meningiomas are heterogeneous, with differences in anatomical, histopathological, and clinical characteristics. Such spatial variability in meningioma biology is thought to result from differences in the expression of critical developmental regulators. We hypothesized that the variability in meningioma biology would follow gradients such as in embryology and tested a cohort of 366 meningiomas for histopathological and immunohistochemical gradients. Methods The medical records from 366 patients treated for meningiomas from 2003 to 2016 were retrospectively analyzed for age, gender, anatomical localization, recurrence-free survival, overall survival, histopathological diagnosis, and immunohistochemistry findings for 6 markers: epithelial membrane antigen (EMA), progesterone receptor (PR), CD34, S100, p53, and Ki-67 labeling index. Results EMA, PR, S100, p53, and CD34 were expressed in 94%, 73%, 49%, 26%, and 23% of the tumors, respectively. p53 expression correlated positively with Ki-67 and World Health Organization (WHO) grade (rτ = 0.31 and rτ = 0.4, respectively). PR positivity correlated inversely with S100, p53, Ki-67, and WHO grade (rτ = −0.19, rτ = −0.14, rτ = −0.15, and rτ = −0.16, respectively). All secretory meningiomas were positive for EMA and PR and negative for S100, and this pattern exhibited a rostrocaudal gradient. The overall proportion of EMA+PR+S100− cases was significantly lower in the cranial vault (30.3%) than in the skull base (45.89%; P = 0.021). The proportion of WHO grade II-III tumors was greater in cranial vault than in skull base meningiomas. Conclusions Unsupervised methods detected an association between the anatomical location and tumor biology in meningiomas. Unlike the categorical associations that former studies had indicated, the present study revealed a rostrocaudal gradient in both the cranial vault and the skull base, correlating with human developmental biology.

Tuberculosis is an important pathological entity in developing countries with increased incidence. Non-osseous spinal cord tuberculomas can be found as extradural, intradural extramedullary, or intramedullary lesions. It has been estimated that intradural spinal tuberculomas comprise only 2–5% of central nervous system tuberculomas. A 31-year-old woman presented with a 2-month history of progressive paraparesis. Magnetic resonance imaging revealed an intradural, extramedullary lesion at L3-S2 levels with high contrast enhancement. Following operation, pathological examination of the lesion revealed granulomas with multinucleated and Langhans-type giant cells, and caseation necrosis typical of a tuberculoma. In the differential diagnosis of cauda equina lesions, primary intradural extramedullary tuberculomas should be considered as a rare entity

The single nucleotide polymorphism rs55705857, located in a non-coding but evolutionarily conserved region at 8q24.21, is strongly associated with IDH-mutant glioma development and was suggested to be a causal variant. However, the molecular mechanism underlying this association has remained unknown. With a case control study in 285 gliomas, 316 healthy controls, 380 systemic cancers, 31 other CNS-tumors, and 120 IDH-mutant cartilaginous tumors, we identified that the association was specific to IDH-mutant gliomas. Odds-ratios were 9.25 (5.17–16.52; 95% CI) for IDH-mutated gliomas and 12.85 (5.94–27.83; 95% CI) for IDH-mutated, 1p/19q co-deleted gliomas. Decreasing strength with increasing anaplasia implied a modulatory effect. No somatic mutations were noted at this locus in 114 blood-tumor pairs, nor was there a copy number difference between risk-allele and only-ancestral allele carriers. CCDC26 RNA-expression was rare and not different between the two groups. There were only minor subtype-specific differences in common glioma driver genes. RNA sequencing and LC-MS/MS comparisons pointed to significantly altered MYC-signaling. Baseline enhancer activity of the conserved region specifically on the MYC promoter and its further positive modulation by the SNP risk-allele was shown in vitro. Our findings implicate MYC deregulation as the underlying cause of the observed association., Scientific Reports, 6, ISSN:2045-2322

Aim: The major part of tissue damage occurs upon reperfusion and is mediated by activated neutrophils that releaseoxygen free radicals. Following hind-limb ischemia/reperfusion, lung injury due to neutrophil infiltration and oxygenfree radicals has been demonstrated. Previous studies have shown that this injury can be prevented pharmacologically.Iloprost is a long acting stable analog of prostacyclin. The aim of this study is to test the effect of iloprost in prevention oflung injury due to lower limb ischemia/reperfusion.Material and Methods: Through a midline laparotomy infrarenal abdominal aorta was approached and cross-clampedin 20 male Spraque-Dawley rats for 2 hours. At the time of declamping Group I animals (n=8) received iloprost (0,1µg/kg/min) and Group II animals (n=8) received normal saline (0,1ml/kg/min) continously for 4 hours. Third group was the shamgroup (n=4). The lung tissue assays were performed for measurement of lipid peroxidation end product malondealdehydeand also total glutathione. Lung tissues were also examined histopathologically under light microscopy.Results: The malondealdehyde levels in the iloprost group were significantly lower than the control group (p0,05). Histopathologicalexamination revealed that the structure of the lung tissue was preserved in the iloprost group whereas lung tissue of thecontrol group had evidence of injury.Conclusion: Our results suggest that iloprost reduces the production of oxygen free radicals and prevents lung injury dueto lower limb ischemia reperfusion. Amaç: İskemi ve bunu takip eden reperfüzyon dönemi sonrasında ortaya çıkan doku hasarı büyük ölçüde reperfüzyon_x000D_ sırasında gerçekleşir. Aktive olmuş nötrofillerden salınan serbest oksijen radikalleri bu hasarda önemli rol oynarlar. Alt_x000D_ ekstremite iskemi-reperfüzyonu sonrasında görülen akciğer hasarında nötrofil infiltrasyonunun ve serbest oksijen_x000D_ radikallerinin önemi gösterilmiştir. Bu hasarı farmakolojik olarak önlemek için birçok çalışma yapılmıştır. İloprost, uzun_x000D_ etkili bir prostasiklin analoğudur. Çalışmanın amacı, alt ekstremite iskemi reperfüzyonu sonrası ortaya çıkan akciğer_x000D_ hasarını önlemedeki iloprostun etkisini araştırmaktır._x000D_ Gereç ve Yöntemler: Çalışmada 20 adet Spraque-Dawley cinsi erkek sıçan kullanıldı. Orta hattan yapılan laparotomi ile abdominal_x000D_ aortaya ulaşıldı. Grup I (n=8) ve Grup II (n=8) de bulunan deneklerin infrarenal aortalarına 2 saat boyunca kross klemp uygulandı._x000D_ Klemp kaldırıldığı sırada Grup I’de bulunan deneklere 0,1 g/kg/dk dozunda iloprost ve Grup II’de bulunan deneklere 0,1ml/kg/_x000D_ dk serum fizyolojik sürekli infüzyon şeklinde 4 saat boyunca verildi. Grup III(n=4) sham grubu olarak belirlendi. Denekler 4. saatin_x000D_ sonunda sakrifiye edilerek akciğer dokuları çıkarıldıve biyokimyasal ve histopatolojik inceleme yapıldı._x000D_ Bulgular: İloprost verilen grupta malondealdehyde seviyeleri kontrol grubuna göre istatistiksel olarak anlamlı derecede_x000D_ düşük bulundu (p0.05)._x000D_ Histopatolojik incelemede, iloprost verilen grupta akciğer dokusunun korunmuş olduğu gözlenirken kontrol grubunda_x000D_ akciğer doku harabiyeti tespit edilmiştir._x000D_ Sonuç: Sonuçlarımız alt ekstremite iskemi-reperfüzyonu sonrasında ortaya çıkan akciğer hasarının önlenmesinde_x000D_ iloprostun serbest oksijen radikal oluşumunu azaltarak etkili olduğunu göstermektedir.