Computer simulation of syringomyelia in dogs

Syringomyelia is a pathological condition in which fluid-filled cavities (syringes) form and expand in the spinal cord. Syringomyelia is often linked with obstruction of the craniocervical junction and a Chiari malformation, which is similar in both humans and animals. Some brachycephalic toy breed dogs such as Cavalier King Charles Spaniels (CKCS) are particularly predisposed. The exact mechanism of the formation of syringomyelia is undetermined and consequently with the lack of clinical explanation, engineers and mathematicians have resorted to computer models to identify possible physical mechanisms that can lead to syringes. We developed a computer model of the spinal cavity of a CKCS suffering from a large syrinx. The model was excited at the cranial end to simulate the movement of the cerebrospinal fluid (CSF) and the spinal cord due to the shift of blood volume in the cranium related to the cardiac cycle. To simulate the normal condition, the movement was prescribed to the CSF. To simulate the pathological condition, the movement of CSF was blocked

Tumor necrosis factor-α-mediated threonine 435 phosphorylation of p65 nuclear factor-κB subunit in endothelial cells induces vasogenic edema and neutrophil infiltration in the rat piriform cortex following status epilepticus

<p>Abstract</p> <p>Background</p> <p>Status epilepticus (SE) induces severe vasogenic edema in the piriform cortex (PC) accompanied by neuronal and astroglial damages. To elucidate the mechanism of SE-induced vasogenic edema, we investigated the roles of tumor necrosis factor (TNF)-α in blood-brain barrier (BBB) disruption during vasogenic edema and its related events in rat epilepsy models provoked by pilocarpine-induced SE.</p> <p>Methods</p> <p>SE was induced by pilocarpine in rats that were intracerebroventricularly infused with saline-, and soluble TNF p55 receptor (sTNFp55R) prior to SE induction. Thereafter, we performed Fluoro-Jade B staining and immunohistochemical studies for TNF-α and NF-κB subunits.</p> <p>Results</p> <p>Following SE, most activated microglia showed strong TNF-α immunoreactivity. In addition, TNF p75 receptor expression was detected in endothelial cells as well as astrocytes. In addition, only p65-Thr435 phosphorylation was increased in endothelial cells accompanied by SMI-71 expression (an endothelial barrier antigen). Neutralization of TNF-α by soluble TNF p55 receptor (sTNFp55R) infusion attenuated SE-induced vasogenic edema and neuronal damages via inhibition of p65-Thr435 phosphorylation in endothelial cells. Furthermore, sTNFp55R infusion reduced SE-induced neutrophil infiltration in the PC.</p> <p>Conclusion</p> <p>These findings suggest that impairments of endothelial cell functions via TNF-α-mediated p65-Thr 485 NF-κB phosphorylation may be involved in SE-induced vasogenic edema. Subsequently, vasogenic edema results in extensive neutrophil infiltration and neuronal-astroglial loss.</p

Cecum malakoplakia - A tumor-like lesion with coexistent adenocarcinoma

We report the case of a 75-year-old Caucasian male who presented with acute abdomen and fecal leakage from his old appendectomy scar and required exploratory laparotomy. A large cecal mass was found and a right colectomy was performed. At pathology, the neoplastic mass was identified as malakoplakia with a small area corresponding to a moderately differentiated colonic adenocarcinoma. Occurrence of malakoplakia in the cecum, associated with adenocarcinoma, is extremely rare if we take into account the limited number of the reported cases of its coexistence with colonic cancer; our case is the second report of such an entity in the cecum. The unusual presence of fistula to the appendectomy scar may be related to the infiltrative nature of the histiocytes constituting this process. Immunochemical studies can assist in the histopathologic differentiation of malakoplakia from other entities that might represent with this tumor-like configuration

Assessment of JC polyoma virus in colon neoplasms

PURPOSE: Research data have recently emphasized an in triguing association of JC polyoma virus with colon carcinogenesis. Tumorigenicity of JC virus is attributed to the T-antigen of its Mad-1 variant. Controversy arose when another research group did not confirm this association. The purpose of this study was to detect JC virus in a series of colon neoplasms from Greek patients. METHODS: A nested polymerase chain reaction assay was used to detect JC virus in 80 cancerous, 25 adenomatous specimens of large bowel, and 20 colonoscopic biopsy samples from normal patients without colorectal neoplasia. Quantitation of JC virus DNA was performed by real-time polymerase chain reaction. RESULTS: JC polyoma virus nucleotide sequence was detected in 61 percent of colon adenocarcinomas and in 60 percent of adenomas, at a viral load of 9 x 10(3) to 20 x 10(3) copies/mug DNA. Adjacent normal mucosa in 35 positive colon adenocarcinoma specimens, and normal mucosa from six patients of the control group, had low viral loads (50-450 copies/mug DNA). CONCLUSIONS: JC polyoma virus genome is present in colon neoplasms. JC virus detection in adenomas at comparable viral loads to malignant tumors suggests its implication at early steps of colonic carcinogenesis. Taking into consideration other published data, infection of colonic epithelium with JC virus might be a prime candidate for a role in chromosomal and genomic instability

Opening Aeolus&apos; Bag of Winds: Acute Abdominal Pain in a Severely Immunosuppressed Patient

Background Necrotizing enterocolitis (NE) is a necrotizing disease mostly of the ileocecal region. It is a severe and potentially life-threatening complication that can affect patients undergoing chemotherapy for lymphoma. We analyze a case of NE that occurred in a patient with non-Hodgkin&apos;s lymphoma during chemotherapy with concurrent HIV infection. Case Report We present a case of a 37-year-old woman who was admitted to our emergency department because of acute abdominal pain. Her medical history included HIV infection and B-cell immunoblastic lymphoma. For the latter, the patient was receiving rituximab cyclophosphamide hydroxydaunorubicin oncovin vincristine prednisone (R-CHOP) regimen. A complete blood count showed a low leukocyte count (40/mm³) and a low neutrophil count (32/mm³). An exploratory laparotomy with midline incision was performed. Intraoperatively, the cecum and the proximal part of the ascending colon were found to be edematous with the mesocolon being extremely gelatinous without macroscopically identified ischemia. Histopathology revealed a nonspecific infarction necrosis of the bowel wall with multiple ulcerations in the cecum, but no evidence of major vessel thrombosis. The patient had an uneventful postoperative course and was discharged in good condition on the 10th postoperative day. Why Should an Emergency Physician Be Aware of This? To our knowledge, this is the first reported case of NE in a patient with acquired immune-deficiency syndrome who developed the syndrome during an episode of severe neutropenia and was treated surgically. The decision to operate should be balanced between the clinical and laboratory status as well as the operative risk. Physicians should be aware of this complication of chemotherapy, especially in severely immunosuppressed patients, because it could be triggered just by an episode of neutropenia. © 2016 Elsevier Inc

Anastomosing hemangioma: Report of two renal cases and analysis of the literature

Background: Anastomosing hemangioma (AH) is a very rare vascular tumor mimicking angiosarcoma, predominately observed in kidney and less frequently in other organs. We present two new renal cases of AH at opposite ends of the clinical presentation spectrum, provide review of the literature and compare the epidemiological, clinical and pathological profiles of renal and non-renal cases. Case presentation: The first occurred in a 64-year-old woman presented with back pain and the second, a multifocal lesion, in a 47-year-old man with end stage renal disease (ESRD). Histology disclosed a vascular tumor with striking anastomosing pattern, minimal nuclear atypia and locally infiltrative pattern, mimicking superficially angiosarcoma. Extramedullary hematopoiesis, extensive perirenal fat entrapment and increased number of mast cells were additional features in the second lesion. Both patients are well, without disease, 25 and 14 months after diagnosis. Conclusion: Comprehensive review and analysis of the published literature show that the growing number of non-renal AHs exhibits similar epidemiologic, clinical, biologic and histologic characteristics with renal AHs and most mild differences vanish after exclusion of cases associated with ESRD. Better understanding of AH pathogenesis will contribute to optimal treatment choices. © 2017 The Author(s)

Immunological Characteristics of Colitis Associated with Anti-CTLA-4 Antibody Therapy

Anti-CTL4-A therapy is associated with development of colitis. We characterized ipilimumab-associated colitis in nine melanoma patients (6 male, mean age: 55.3-yrs). Median value for diarrhea grade was 2, number of ipilimumab doses 2, and interval since last administration 3-wks. Endoscopic characteristics resembled inflammatory bowel disease and histology revealed predominance of plasmacytes or CD4+ T-cells. We observed significant upregulation of Th1 and Th17 effector pathways (&gt;10-fold increase for IFN-γmRNA, &gt;5-fold for IL-17A, p &lt; 0.01 vs. controls). Significant elevation of FoxP3 was also detected. In conclusion, ipilimumab administration results in elevations of effector lymphocytes and pro-inflammatory mediators in the gut lamina propria. © 2017 Taylor &amp; Francis Group, LLC

Mitosin, a novel marker of cell proliferation and early recurrence in intracranial meningiomas

The expression of mitosin, a novel proliferation-associated molecule was evaluated immunohistochemically in a consecutive series of 47 patients with primary intracranial benign and atypical meningiomas. Mitosin expression was correlated with proliferation markers Ki-67 (MIB-1), proliferating cell nuclear antigen (PCNA), topoisomerase IIa (TopoIIa) and mitotic index, as well as with standard clinicopathological parameters and patient outcome. Seven tumors recurred (14.8%) following gross total resection, within a follow-up period ranging from 21 to 108 months (median 60 months). The higher proliferation indices were obtained with mitosin and PCNA and the lower ones with TopoI?a. Mitosin labeling index (LI) ranged from 0.1 to 57% (median 3%), with a significant overlapping of values between grades. A significant positive correlation was shown between mitosin LI on the one hand and Ki-67 LI (p<0.001), or the mitotic index (p=0.027) on the other. The incidence of recurrence was higher in cases with a mitosin LI higher than 3% (p=0.048). Univariate analysis disclosed mitosin LI (p=0.033) along with the mitotic index (p=0.024) and tumor size (p=0.028) as significant predictors of shortened recurrence-free survival. In multivariate analysis, the labeling indices of mitosin (p=0.035) and Ki-67 (p=0.032), along with tumor size, were shown to provide independent prognostic information, beyond that obtained by standard clinical and pathological parameters. However, as indicated by factor analysis, the prognostic information yielded by mitosin was superior to that provided by the remaining proliferation markers (p=0.041). We conclude that mitosin immunohistochemical expression, although failing to discriminate between benign and atypical meningiomas, may be of use as a novel cell proliferation marker and as a predictor of tumor recurrence