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Aim: To define the clinical and histopathological characteristics of primary lacrimal sac lymphoma in a predominantly white population. Methods: Specimens of lacrimal sac lymphoma and follow up data were solicited from members of the Ophthalmic Oncology Task Force of the European Organization for Research and Treatment of Cancer (EORTC) and the European Ophthalmic Pathology Society (EOPS). Specimens were stained with haematoxylin and eosin and an immunohistochemical panel against leucocyte antigens was applied. Diagnosis was reached by consensus of five experienced pathologists according to the World Health Organization classification system. The histopathological findings were correlated with the clinical data. Results: Of 15 primary lacrimal sac lymphomas, five (33%) were diffuse large B cell lymphoma (DLBCL), five (33%) were extranodal marginal zone B cell lymphoma of mucosa associated lymphoid tissue (MALT lymphoma), three were classified as “transitional MALT lymphoma,” being in transition from MALT lymphoma to DLBCL, and two were unclassified B cell lymphomas. Nine of the patients were female, and the median age at the time of diagnosis was 71 years (range 45–95 years). The most frequent presenting symptoms were epiphora (85%), swelling in the region of the lacrimal sac (79%), and dacryocystitis (21%). All but one patient presented in stage I. Systemic spread occurred in three of nine patients (33%). The 5 year overall survival was 65%. Conclusions: DLBCL and MALT lymphoma are equally common in the lacrimal sac in contrast with the remaining periorbital and/or orbital region where MALT lymphoma predominates.

There are two species of the genus Echinococcus, Echinococcus multilocularis (also called alveolar hydatid) and Echinococcus granulosus, characterized by distinct growth features in humans. The main endemic regions for human alveolar echinococcosis (AE) caused by E. multilocularis are Central Europe, Russia, Turkey, Japan, China, eastern France and North America. Human echinococcosis is usually caused by an intrahepatic growth of parasitic larvae. Cerebral occurrence of E. multilocularis disease is rare, accounting for only 1% of cases, and is generally considered to be fatal. This report presents two cases of intracerebral E. multilocularis disease which occurred in two infected patients with AE pulmonary metastases. The anatomical and clinical features are discussed. Our retrospective survey would indicate that surgical treatment should be envisaged whenever possible.

BackgroundEchinococcus multilocularis growth and persistent granuloma, which lead to the development of the severe parasitic disease alveolar echinococcosis (AE), might be caused by abnormal expression of stress-induced proteins, with subsequent abnormalities in T cell activation. Similar to its involvement in tumors, the NKG2D–major histocompatability complex class I chain–related molecules A and B (MICA/B) signaling system could be involved in host-parasite interactions; however, its involvement in helminthic diseases has never been studied MethodsWe studied MICA/B, NKG2D, and transforming growth factor–β (TGF-β) expression on liver sections and measured levels of soluble MICA in serum samples obtained from patients with progressive AE. Livers from healthy and cirrhotic subjects were studied as controls ResultsExpression of MICA/B proteins was strongly enhanced in the hepatocytes and endothelial and bile duct cells; in the CD68+ cells of the periparasitic infiltrate, especially epithelioid and giant cells; and, also, in the metacestode germinal layer. Strong expression of MICA/B in the liver contrasted with low numbers of NK cells and lack of expression of NKG2D on the numerous CD8+ T lymphocytes of the periparasitic infiltrate, as well as with the absence of soluble MICA in serum. TGF-β was strongly expressed by most of the infiltrating lymphocytes ConclusionsSustained expression of MICA/B molecules and TGF-β might lead to modulation of NKG2D with subsequent inhibition of NKG2D-dependent cytotoxicity. Abnormalities of this signaling system could contribute to parasitic evasion of the host’s immunity

Background: Human Papillomavirus (HPV) infection is recognised as aetiological factor of carcinogenesis in oropharyngeal squamous cell carcinomas (OPC). HPV-related OPC respond better to treatments and have a significantly favourable outcome. Epithelial to mesenchymal transition (EMT) implicated in tumour invasion, is a hallmark of a poor prognosis in carcinomas. Methods: We have studied the relationship of EMT markers (E-cadherin, β -catenin and vimentin) with HPV infection (DNA and E6/E7 mRNA detection), p16 INK4a expression and survival outcomes in a cohort of 296 patients with OPC. Results: Among the 296 OPSSC, 26% were HPV positive, 20.3% had overt EMT (>25% of vimentin positive tumour cells). Lower E-cadherin expression was associated with a higher risk of distant metastasis in univariate ( P =0.0110) and multivariate analyses (hazard ratios (HR)=6.86 (1.98; 23.84)). Vimentin expression tends towards worse metastasis-free survival (MFS; HR=2.53 (1.00; 6.41)) and was an independent prognostic factor of progression-free survival (HR=1.55 (1.03; 2.34)). Conclusions: There was a non significant association of EMT with HPV status. This may be explained by a mixed subpopulation of patients HPV positive with associated risk factors (HPV, tobacco and alcohol). Thus, the detection of EMT in OPC represents another reliable approach in the prognosis and the management of OPC whatever their HPV status.

HSV fulminant hepatitis is a rare pathology. Rapid hepatic failure, as a consequence of extended liver damage, has generally been attributed to necrosis. As apoptosis can constitute another way for hepatocytes to die, we decided to investigate whether programmed cell death took place during HSV fulminant hepatitis. Liver sections were obtained from two cases of fulminant herpetic hepatitis as well as from hepatitis B virus and Rickettsia-infected livers. Herpes simplex virus infection was confirmed using in situ hybridization. Apoptosis was assessed by histopathological examination, p53, activated-caspase 3 and Fas immunohistochemistry and TUNEL labeling. We report that the number of cells expressing activated-caspase 3 was largely increased in fulminant herpes simplex virus hepatitis, when compared to livers chronically infected by hepatitis B virus or from a Rickettsial acute hepatitis. Apoptosis of hepatocytes was confirmed by a positive double-staining for activated-caspase 3 and hepatocytes. Finally, the apoptotic process has progressed beyond the step of nuclear DNA cleavage as demonstrated by TUNEL labeling. These data as a whole show that apoptosis is responsible, at least partially, for liver damage during HSV fulminant hepatitis.

BackgroundSignal transducer and activator of transcription 3 (STAT3) has been implicated as an oncogene in several neoplastic diseases. However, the biological effects of STAT3 have not been extensively studied in rectal carcinogenesis.AimsTo evaluate STAT3 activation in advanced rectal cancers and its association with clinicopathological variables and prognosis.MethodsNuclear immunohistochemical expression of phosphorylated STAT3 (p-STAT3) was studied in 104 advanced rectal cancers (T3–T4). All patients were participating in the EORTC 22921 trial to assess whether preoperative chemoradiotherapy followed by postoperative chemotherapy improved overall and progression-free survival.ResultsNuclear p-STAT3 expression was detected in 37.5% of rectal cancer patients. No correlation was observed between p-STAT3 and any clinicopathological variables tested. However, patients with tumours positive for p-STAT3 had significantly improved overall survival.ConclusionThese results highlight an unexpected role for nuclear p-STAT3 expression in advanced rectal cancers and need further investigation to clarify this finding.

In this study, we are concerned with the 237 isotope of neptunium ( 237 Np), which is a by-product of uranium in nuclear reactors. To study ultrastructural lesions induced by this element, a group of rats were injected with a solution of 237 Np-nitrate once a day for 14 weeks. Lesions observed in liver and kidney are described using electron microscopy. Ultrastructural alterations of cellular membranes and intracellular organelles demonstrated the existence of neptunium toxicity. This toxicity was characterized by various lesions, such as cytoplasmic clarification, disappearance of mitochondrial cristae, swollen mitochondria, abnormal condensation of nuclear chromatin, and nuclear fragmentations. This study demonstrated the probable induction of apoptosis by neptunium both in liver and kidneys.Key words: neptunium, apoptosis, contamination, intracellular concentration.

The threefold aim of this experimental study was to test the correlation of cardiac troponin I released to myocardial infarction size and myocardial fixation of anticardiac troponin I antibody and to determine how long after myocardial infarction the measure of cardiac troponin I concentration can evaluate myocardial infarction size. Forty rabbits were assigned either to a control group or to an experimental preconditioned group. Infarction was obtained by tightening a snare around the left anterior descending artery. Serial venous blood samples were drawn for measurement of cardiac troponin I. The rabbits were sacrificed at 72 hours and a histological study was performed to determine the infarct size and the size of the area void of fixation of anticardiac troponin I antibody. There was a linear correlation between the total amount of CTn I released and both infarct size (r=0.45, p<0.02) and the size of the area void of anti-cardiac troponin I antibody (r=0.47, p<0.02). These two sizes were strongly correlated (r=0.95, p<0.02). The hour 9 CTn I sample was the best correlated with both the infarct size (r=0.47, p<0.02) and the size of area void of anticardiac troponin I antibody (r=0.45, p<0.02). Our study shows that: 1) cardiac troponin I release is correlated to both myocardial infarction size and the size of area void of fixation of anticardiac troponin I antibody, 2) the area void of anticardiac troponin I antibody fixation includes the whole ischemic area, and 3) evaluation of myocardial infarction size can be obtained by CTn I concentration as early as the ninth hour.

Background. More than 80 transthyretin (TTR) mutations have been described, most associated with amyloidosis. Peripheral neuropathy is the most common clinical presentation in TTR amyloidosis although the carpal tunnel syndrome (CTS) may be the first symptom and skin can be involved, as transthyretin amyloidosis is a systemic disease. Case report. The 78 year-old proband, belonging to a French family of Italian origin, presented with a 5 year history of peripheral neuropathy in the lower extremities. However, 15 years earlier he had had surgery for bilateral CTS. Amyloidosis was diagnosed on salivary gland and skin biopsies. Immunohistochemistry on skin biopsy was positive using anti-TTR. The proband has 10 siblings, 5 have CTS. Methods. SSCP and direct sequencing of exons 2, 3, and 4 of the TTR gene were done on DNAJ from the proband and his brother who had had CTS. To confirm the mutation a PCR-IMRA was done. Results. SSCP analysis of TTR exons 2, 3, and 4 did not suggest a mutation. Sequence analysis of TTR exon 3 revealed heterozygosity in both subjects for a single base-pair transversion from A to T in codon 78 (TAC-TTC) indicating a tyrosine to phenyiaianine change. The mutation was confirmed by PCR-IMRA. Conclusion. This TTR mutation (Tyr78Phe) is associated with peripheral neuropathy, carpal tunnel syndrome and skin amyloidosis. It is also associated with late onset of the disease.

Complementary examinations including cerebral and ocular magnetic resonance imaging, blood dosage of dopamine and NSE, a renal echography and a renal vessels Doppler, and x-rays of the spinal column were performed. The diagnosis is based on die presence of two or more of the following criteria6: (1) a minimum of six café-au-lait spots; (2) a minimum of two neurofibromas of any type, or a minimum of one plexiform neurofibroma; (3) freckling in the axillary or inguinal region; (4) optic glioma; (5) a minimum of two Lisch nodules; (6) a distinctive osseous lesion (dysplasia of the sphenoid bone or dysplasia or thinning of the long bone cortex); and (J) a first-degree relative with neurofibromatosis 1 according to the preceding criteria. Other ocular manifestations of neurofibromatosis 1 are Lisch nodules, plexiform neurofibroma of the eyelid, anomalies of me orbital bones, hyperplastic intracorneal nerves, uveal ectropion, buphthalmos, choroidal tumor, optic gliomas, and, rarely, retinal hamartomatous lesions.7 Juvenile xanthogranuloma is a minor feature of neurofibromatosis 1 with a frequency estimated at 2%, which is far from that of café-au-lait spots (with a frequency of more than 95%), axillary freckling (65% to 84%), skin neurofibromas (14% to 95%), and Lisch nodules (22% to 96%).8 Despite its relatively low frequency, a diagnosis of ocular juvenile xanthogranuloma in a young child requires at least a full clinical examination and follow-up to screen for other signs of neurofibromatosis 1.