Filariasis of the Axilla in a Patient Returning from Travel Abroad: A Case Report

Background: The term filariasis comprises a group of parasitic infections caused by helminths belonging to different genera in the superfamily Filaroidea. The human parasites occur mainly in tropical and subtropical regions, but filariae are also found in temperate climates, where they can infect wild and domestic animals. Humans are rarely infected by these zoonotic parasites. Patients and Methods: A 55-year-old patient presented with a new-onset, subcutaneous, non-tender palpable mass in the right axilla. Ultrasonography showed a 1.3-cm, solid, singular encapsulated node. Sonography of the breast on both sides, axilla and lymphatic drainage on the left side, lymphatic drainage on the right side, and mammography on both sides were without pathological findings. The node was excised under local anesthesia as the patient refused minimal invasive biopsy. Results: On histopathological examination, the tail of a parasite of the group of filariae was found. The patient revealed that she had stayed in Africa and Malaysia for professional reasons. 6 months before the time of diagnosis, she had also suffered from a fever and poor general condition after a trip abroad. The patient was referred for further treatment to the Institute for Tropical Medicine at the University of Dusseldorf, where a treatment with ivermectin was conducted on the basis of positive staining with antibodies against filariae. Conclusion: Our case demonstrates the importance of interdisciplinary collaboration between breast center, pathology, and other specialties such as microbiology and tropical medicine

ХУЛІГАНСТВО ТА ЙОГО ХАРАКТЕРИСТИКА

Abstract BACKGROUND: Temporal lobe gray-white matter abnormalities (GWMA) are frequent morphological aberrances observed on MRI in patients with temporal lobe epilepsy (TLE) in addition to hippocampal sclerosis (HS). OBJECTIVE: To study the influence of temporal pole GWMA on clinical characteristics and seizure outcome in patients with HS operated on for TLE. METHODS: A cohort of 370 patients undergoing surgery for intractable TLE was prospectively collected in an epilepsy surgery data base. Clinical characteristics and seizure outcome of all 58 TLE patients with identified HS and GWMA (group 1) were compared with those of a matched control group of 58 HS patients without GWMA (group 2). Both groups were further subdivided into patients undergoing transsylvian selective amygdalohippocampectomy (sAH) and anterior temporal lobectomy with amygdalohippocampectomy (ATL). RESULTS: The HS plus GWMA patients were significantly younger at epilepsy onset than those without GWMA. In the HS plus GWMA group, 41% of patients were younger than 2 years when they experienced their first seizure in contrast to only 17% of patients with pure HS (P = .004). Seizure outcome was not statistically different between the 2 groups: 75.9% of the patients in group 1 were seizure free (Engel class I) compared with 81% of patients in group 2. Seizure outcome in both groups was about equally successful with selective amygdalohippocampectomy and anterior temporal lobectomy (ns). CONCLUSION: Limited and standard resections in TLE patients with HS are equally successful regardless of the presence of GWMA

Mucosal atrophy in collagenous colitis: a case report

<p>Abstract</p> <p>Background</p> <p>Mucosal atrophy as a potential cause of impaired colonic compliance has not yet been described as a complication in Collagenous Colitis (CC).</p> <p>Case presentation</p> <p>We present a 51-year-old female patient with a 20-year history of diarrhea and diagnosed with CC ten years prior to her presentation. We reviewed reports from three colonoscopies performed after the diagnosis. Overall 12 biopsies obtained in the last two colonoscopies were re-analyzed by two pathologists blinded to the aim of the study. Besides the typical histological findings of CC, the endoscopic appearance was normal, and no histological signs of atrophy were found during the first colonoscopy. Surprisingly, the second and third colonoscopy revealed a region of advanced segmental mucosal atrophy in the cecum with the mucosal height normalizing toward the transverse colon. This pattern of atrophy was inversely related to the pattern of sub-epithelial collagen deposition, which increased toward the rectum.</p> <p>Conclusion</p> <p>If no chance occurrence, our observation supports the idea that additional factors, probably luminal in nature, may be co-responsible for the mucosal atrophy in this case. Thus, mucosal atrophy in the proximal colon appears to be a new candidate among the growing list of rare complications associated with long standing CC.</p

Ezrin Mediates Tethering of the γ-Aminobutyric Acid Transporter GAT1 to Actin Filaments Via a C-Terminal PDZ-Interacting Domain

A high density of neurotransmitter transporters on axons and presynaptic boutons is required for the efficient clearance of neurotransmitters from the synapse. Therefore, regulators of transporter trafficking (insertion, retrieval, and confinement) can play an important role in maintaining the transporter density necessary for effective function. We determined the interactions that confine GAT1 at the membrane by investigating the lateral mobility of GAT1-yellow fluorescent protein-8 (YFP8) expressed in neuroblastoma 2a cells. Through fluorescence recovery after photobleaching, we found that a significant fraction (~50%) of membrane-localized GAT1 is immobile on the time scale investigated (~150 s). The mobility of the transporter can be increased by depolymerizing actin or by interrupting the GAT1 postsynaptic density 95/Discs large/zona occludens 1 (PDZ)-interacting domain. Microtubule depolymerization, in contrast, does not affect GAT1 membrane mobility. We also identified ezrin as a major GAT1 adaptor to actin. Förster resonance energy transfer suggests that GAT1-YFP8 and cyan fluorescent (CFP) tagged ezrin (ezrin-CFP) exist within a complex that has a Förster resonance energy transfer efficiency of 19% ± 2%. This interaction can be diminished by disrupting the actin cytoskeleton. In addition, the disruption of actin results in a >3-fold increase in γ-aminobutyric acid uptake, apparently via a mechanism distinct from the PDZ-interacting protein. Our data reveal that actin confines GAT1 to the plasma membrane via ezrin, and this interaction is mediated through the PDZ-interacting domain of GAT1

Massive hypercoagulable state despite full-dose anticoagulant treatment in a patient with occult malignancy: considerations concerning chemotherapy without definitive diagnosis

A 55-year-old female patient presented with recurrent deep venous thrombosis and pulmonary embolism while on oral anticoagulant treatment using the vitamin K antagonist phenprocoumon. Hypercoagulable state was regarded to be paraneoplastic, but no underlying malignancy could be identified despite extensive screening for cancer, including gastroscopy and colonoscopy, a bone marrow biopsy, thoracoabdominal CT scans with subsequent biopsies of possibly malignant findings, octreotide scintigraphy, skeletal scintigraphy and gynaecological screening. In the course of her hospital stay she developed progressive right cardiac insufficiency due to the formation of new thromboses despite aggressive anticoagulant treatment and died of right-sided heart failure. The autopsy showed a poorly differentiated adenocarcinoma in the middle lobe of the right lung. In addition, pulmonary lymphangiosis carcinomatosa, pleural and pericardial carcinosis, and lymph node metastases and osteoblastic vertebral body metastases were shown

Tuberous-sclerosis complex-related cell signaling in the pathogenesis of lung cancer

Background: Hamartin (TSC1) and tuberin (TSC2), encoded by the tuberous sclerosis complex (TSC) genes, form a tumor- suppressor heterodimer which is implicated in PI3K- Akt signaling and acts as a functional inhibitor of the mammalian target of rapamycin (mTOR). Dysregulation of mTOR has been assigned to carcinogenesis and thus may be involved in cancer development. We have addressed the role of hamartin, phospho- tuberin (p- TSC2) and phospho- mTOR (p- mTOR) in a series of non- small cell lung cancer (NSCLC) and small cell lung cancer (SCLC) samples. Methods: We collected 166 NSCLC and SCLC samples for immunohistochemical studies and performed western blot analyses in NSCLC and SCLC cell lines as well as comparative analyses with EGFR phosphorylation and downstream effectors. Results: In cell lines we found an inverse correlation between hamartin and p-mTOR expression. In surgical specimens cytoplasmic hamartin expression was observed in more than 50% of adenocarcinoma (AC) and squamous cell carcinoma (SCC) compared to 14% of SCLC. P-mTOR and p-TSC2 staining was found in a minority of cases. There was a significant correlation between p-EGFR Tyr-1068, p-EGFR Tyr-992 and hamartin, and also between p-mTOR and p-EGFR Tyr-1173 in AC. In SCC an inverse correlation between hamartin and p-EGFR Tyr-992 was detected. Phosphorylation of TSC2 was associated with expression of MAP-Kinase. Hamartin, p-TSC2 and p-mTOR expression was not dependant of the EGFR mutation status. Hamartin expression is associated with poorer survival in SCC and SCLC. Conclusions: Our findings confirm the inhibitory role of the tuberous sclerosis complex for mTOR activation in lung cancer cell lines. These results reveal hamartin expression in a substantial subset of NSCLC and SCLC specimens, which may be due to EGFR signaling but is not dependant on EGFR mutations. Our data provide evidence for a functional role of the tuberous sclerosis complex in lung cancer

KDM5C Is Overexpressed in Prostate Cancer and Is a Prognostic Marker for Prostate-Specific Antigen-Relapse Following Radical Prostatectomy

Currently, few prognostic factors are available to predict the emergence of castration-resistant prostate cancer and no curative options are available. Epigenetic gene regulation has been shown to trigger prostate cancer metastasis and androgen independence. Histone lysine demethylases (KDMs) are epigenetic enzymes that can remove both repressive and activating histone marks. KDM5 family members are capable of removing the histone H3 Lysine 4 dimethylation-activating mark, rendering them potential players in the down-regulation of tumor suppressors and suggesting that their activity could repress oncogenes. Here, we systematically investigated KDM5C expression patterns in two independent radical prostatectomy cohorts (822 prostate tumors in total) by immunohistochemistry. Positive nuclear KDM5C staining was significantly associated with a reduced prostate-specific antigen relapse-free survival. Our study confirmed that nuclear KDM5C expression is an independent prognostic parameter. Most strikingly, the prognostic value of nuclear KDM5C expression for progression-free survival was exclusively pronounced for the Gleason group 7. In addition, KDM5C knockdown resulted in growth retardation of prostate cancer cells in vitro and induced regulation of several proliferation-associated genes. Our data indicate that KDM5C is functionally involved in proliferation control of prostate cancer cells and might represent a novel attractive therapy target. Moreover, overexpression of KDM5C is an independent new predictive marker for therapy failure as determined by biochemical recurrence in patients after prostatectomy