We present experimental evidence of the existence of cell variability in terms of threshold light dose for Hep G2 (liver cancer cells) cultured. Using a theoretical model to describe the effects caused by successive photodynamic therapy (PDT) sessions, and based on the consequences of a partial response we introduce the threshold dose distribution concept within a tumor. The experimental model consists in a stack of flasks, and simulates subsequent layers of a tissue exposed to PDT application. The result indicates that cells from the same culture could respond in different ways to similar PDT induceddamages. Moreover, the consequence is a partial killing of the cells submitted to PDT, and the death fraction decreased at each in vitro PDT session. To demonstrate the occurrence of cell population modification as a response to PDT, we constructed a simple theoretical model and assumed that the threshold dose distribution for a cell population of a tumor is represented by a modified Gaussian distribution.Microscopic image (100×) of a necrosis caused by PDT in a rat liver. The edge is the depth of necrosis

Total retocolectomy with ileal pouch-anal anastomosis (IPAA) is the surgery of choice for patients with ulcerative colitis (UC) that are refractory to clinical treatment. Pouchitis is one of the most common complications after this procedure. Defects in autophagy have been reported in inflammatory bowel diseases. However, there are no studies on the IP. Therefore, we studied markers for autophagy in the IP mucosa of UC and FAP patients comparing them to controls with a normal distal ileum. Sixteen patients with IP in "J" shape, asymptomatic and with endoscopically normal IP were evaluated. The control group consisted of eight patients with normal colonoscopy. There was a significant decrease in the transcriptional levels of ATG5, MAP1LC3A and BAX in the FAP group. There was also a decrease in the protein level of Beclin-1 in the UC and FAP compared to the control group. Although the LC3II levels by immunoblot were higher in the UC group, LC3/p62 co-localization were lower in the immunofluorescence analysis in the UC and FAP compared to the control group. Corroborating these results, there was an increase of p62 by immunoblot in the UC group. These findings indicated a modulation of macroautophagy markers in the IP, which may explain the mucosa inflammation predisposition.Ulcerative colitis (UC) is a chronic intestinal inflammation that can affect the large intestine and rectum. Its etiology is not completely established. Familial adenomatous polyposis (FAP) is an autosomal dominant disease which affects young individuals and is associated with the formation of multiple polyps in the large intestine and rectum, which invariably implies a greater risk of cancer 1,2 . Both diseases, despite being different, may require the same surgical procedure. The ileal pouch-anal anastomosis (IPAA) is the elective procedure of choice in the surgical management of refractory UC, and FAP with many polyps in the rectum 3 . The main complication after this procedure is the pouch inflammation (pouchitis) that can affect up to 45 percent of patients who are submitted to IPAA for UC, and only five percent of the FAP patients who undergo the same procedure 4 . This suggests that constitutive differences between UC and FAP pouches have a critical role in its pathogenesis.Pouchitis develops only after ileostomy closure, when the pouch mucosa starts to be exposed to the fecal stream 5 . The distinct immunological aspects of the different inflammatory bowel diseases (IBD), specifically UC, which involve impaired innate and adaptive responses, associated to genetic susceptibility, environmental factors, and intestinal microbiota may be involved in the pouch inflammation etiology 5,6 . Autophagy is an evolutionarily conserved catabolic pathway that consists of selective degradation of cellular components and a homeostatic mechanism that protects cells exposed to stress situations (toxins, starvation) 7,8 . There are three primary forms of authophagy: macroautophagy, microautophagy and chaperone-mediated autophagy (CMA) 9 . Although there ar...

There was cognitive impairment of PWE and it was significantly associated with QEEG, which suggests that QEEG measures may contribute to the understanding of physiopathological events and as a marker for cognitive alterations in epilepsy.

BackgroundDifferential diagnosis of inflammatory bowel disease is often very challenging. Paracoccidioidomycosis is a fungal disease that can mimic manifestations of Crohn’s disease.Case presentationWe report a case of a 13-year-old Caucasian boy with abdominal pain for 1.5 years associated with nausea, diarrhea, and weight loss of 10 kg. He presented increased C-reactive protein and an increased erythrocyte sedimentation rate. A colonoscopy showed deep serpiginous ulcers throughout his entire colon and rectum, which suggested Crohn’s disease. He received one dose of infliximab, which is an anti-tumor necrosis factor-α, and showed no improvement. After the second dose, he got worse and started to have bloody diarrhea. A new colonoscopy was performed and pathological examination revealed ulcerative chronic inflammation with non-caseating granulomas and fungal structures (budding forms) compatible with Paracoccidioides brasiliensis. He underwent intravenously administered and then orally administered trimethoprim-sulfamethoxazole treatment. Due to drug intolerance, he was treated with amphotericin B and itraconazole, then he showed clinical improvement and mucosal healing with good outcome.ConclusionParacoccidioidomycosis must be part of the differential diagnosis of inflammatory bowel diseases in endemic areas and must be excluded before starting immunosuppressive therapy.