Background/Aims: Data about the effects of inflammatory bowel disease (IBD) on various functions of the nervous and cardiovascular systems are limited. In this study, the visual neuronal and cardiovascular functions of patients with IBD were evaluated by measuring visual evoked potentials (VEP) and pulse wave velocity (PWV), respectively. Materials and Methods: There were three study groups: the Crohn's disease (CD) group (n=25), the ulcerative colitis (UC) group (n=30), and a healthy control (C) group (n=25). The exclusion criteria were as follows: patients with IBD were in remission, had no extra-intestinal manifestations of the disease, had no additional chronic disease(s), and had been receiving medical treatment for their IBD without any previous surgical intervention. VEP amplitudes (mV) and the N2 and P2 latencies (ms) were recorded for visual-neuronal analysis of all study groups. For cardiovascular assessment in all study groups, PWV was measured noninvasively as follows: the carotid-femoral PWV with the Complior Colson device (The authors have no conflict of interest.) and the PWV along the aorta with two ultrasound strain-gauge pressure-sensitive transducers (TY-306 Fukuda pressure-sensitive transducers -Fukuda Denshi Co, Tokyo, Japan) fixed transcutaneously over the course of a pair of arteries separated by a known distance. The right femoral and right common carotid arteries were the ones used. Results: The PWV levels of the CD and UC groups were significantly higher than those in the C group (p<0.001). In the bilateral recording of the VEP, the N2 latencies of the CD (p<0.05) and UC (p<0.01) groups were significantly longer than those in the C group. Conclusion: In this study, we showed vascular and visual neuronal impairments at a subclinical stage in patients with both types of IBD.

Thrombotic thrombocytopenic purpura (TTP) is a rare, life-threatening disease characterized by acute episodes of thrombocytopenia and microangiopathic hemolytic anemia occurring due to platelet and von Willebrand factor deposition and hyaline thrombi formation in arterioles and capillaries throughout the body, which results in organ ischemia. TTP can be idiopathic or secondary, and there are several causes of secondary TTP. There is a clinical syndrome resembling TTP that occurs after surgical procedures, so-called "postoperative TTP" (pTTP). In this review, the differential diagnosis, pathogenesis and clinical and laboratory features of pTTP, together with the treatment modalities and outcomes of the patients, are discussed. The pTTP is a diagnosis of exclusion, and disseminated intravascular coagulation, heparin-induced thrombocytopenia and medication-induced effects should be ruled out. As in classical TTP, patients with pTTP should be diagnosed and treated with therapeutic plasma exchange (TPE) as early as possible to reduce their morbidity and mortality. Although rarely seen, surgeons and physicians of all specialties should be alert to the possibility of pTTP, and since pTTP is a life-threatening event that usually can be treated successfully with TPE, especially when diagnosed early in its course, it is critical to recognize and treat pTTP promptly.

Lung cancer is the second most common type of cancer in the world and is the most common cause of cancer-related death in men and women; it is responsible for 1.3 million deaths annually worldwide. It can metastasize to any organ. The most common site of metastasis in the head and neck region is the brain; however, it can also metastasize to the oral cavity, gingiva, tongue, parotid gland and lymph nodes. This article reports a case of small cell lung cancer presenting with metastasis to the facial nerve.

More than half of all brain metastases show infiltrating rather than displacing growth at the macro‐metastasis/organ parenchyma interface (MMPI), a finding associated with shorter survival. The lymphoid enhancer‐binding factor‐1 (LEF1) is an epithelial‐mesenchymal transition (EMT) transcription factor that is commonly overexpressed in brain‐colonizing cancer cells. Here, we overexpressed LEF1 in an in vivo breast cancer brain colonization model. It shortened survival, albeit without engaging EMT at the MMPI. By differential proteome analysis, we identified a novel function of LEF1 as a regulator of the glutathione (GSH) system, the principal cellular redox buffer. LEF1 overexpression also conferred resistance against therapeutic GSH depletion during brain colonization and improved management of intracellular ROS. We conclude that besides EMT, LEF1 facilitates metastasis by improving the antioxidative capacity of epithelial breast cancer cells, in particular during colonization of the brain parenchyma.

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