Although many failed surrogate markers are provided in the literature, inflammation may contribute to the outcome of ischemic stroke. In 50 consecutive patients with acute ischemic stroke, in the absence of symptoms and signs of concomitant infection, we evaluated a panel of biomarkers reported to be variably associated with brain ischemia, and correlate their serum level with the brain lesion volume and clinical outcome. Infarct size was calculated on computed tomography (CT) scans by means of the Cavalieri's method. Neurological impairment was scored by using the Glasgow Coma Scale, Glasgow Outcome Scale and National Institutes of Health (NIH) scales at stroke onset and 3-month follow-up. Some markers showed a direct significant correlation with both initial and final NIH scale and with infarct size, particularly tumor necrosis factor alpha (TNF-alpha) (P=0.002), intercellular adhesion molecule-1 (P<0.01) and matrix metalloproteinase-2/9 (P=0.001). In contrast to previous reports, interleukin-6 (IL-6) serum level showed a significant inverse correlation with both final neurological impairment and infarct size (P<0.001). This novel finding allows us suggesting that IL-6, in the context of a complex pro-inflammatory network occurring during stroke, is associated with neuroprotection rather than neurotoxicity in patients with ischemic brain injury. 相似文献
Coenurosis is a central nervous system disease of wild and domestic ruminants caused by Coenurus cerebralis, a bladder worm stage of Taenia multiceps). Even in Sardinia island, this metacestode seems to be widespread in sheep (Scala et al. Vet Parasitol 143(3–4):294–298, 2007) where coenurosis is an important health problem (Varcasia et al. Parasitol Res 99(5):622–626, 2006) the last and unique report of coenurosis in cattle was in 1990 (Cubeddu et al. 1990). In the present paper, a case of bovine coenurosis in Sardinia was described 22 years after the first report with a morphological a biomolecular characterization. A 2-year-old Limousine bull was euthanized in the Bolotana (NU) municipality (Central Sardinia). The remote anamnesis achieved from the farmer reporting that the bull showed neurological symptoms from 1 year of age previously classified as nutritional problems by the farm’s veterinary. The breeder also says that the bull have by self-produced the skull fracture by hitting a gaff in the farm. The skull was opened and the brain removed and carefully examined showing two coenurus cysts containing clear fluid with numerous scoleces both in the right hemisphere. Morphological features of the cysts and mt-DNA sequencing confirm that the parasites were T. multiceps Coenuri. 相似文献
To establish consensus on follow-up (FU) after focal therapy (FT) in renal masses. To formulate recommendations to aid in clinical practice and research.
Methods
Key topics and questions for consensus were identified from a systematic literature research. A Web-based questionnaire was distributed among participants selected based on their contribution to the literature and/or known expertise. Three rounds according to the Delphi method were performed online. Final discussion was conducted during the “8th International Symposium on Focal Therapy and Imaging in Prostate and Kidney Cancer” among an international multidisciplinary expert panel.
Results
Sixty-two participants completed all three rounds of the online questionnaire. The panel recommended a minimum follow-up of 5 years, preferably extended to 10 years. The first FU was recommended at 3 months, with at least two imaging studies in the first year. Imaging was recommended biannually during the second year and annually thereafter. The panel recommended FU by means of CT scan with slice thickness ≤3 mm (at least three phases with excretory phase if suspicion of collecting system involvement) or mpMRI. Annual checkup for pulmonary metastasis by CT thorax was advised. Outside study protocols, biopsy during follow-up should only be performed in case of suspicion of residual/persistent disease or radiological recurrence.
Conclusions
The consensus led to clear FU recommendations after FT of renal masses supported by a multidisciplinary expert panel. In spite of the low level of evidence, these recommendations can guide clinicians and create uniformity in the follow-up practice and for clinical research purposes.
Gut microbiota is represented by different microorganisms that colonize the intestinal tract, mostly the large intestine, such as bacteria, fungi, archaea and viruses. The gut microbial balance has a key role in several functions. It modulates the host’s metabolism, maintains the gut barrier integrity, participates in the xenobiotics and drug metabolism, and acts as protection against gastro-intestinal pathogens through the host’s immune system modulation. The impaired gut microbiota, called dysbiosis, may be the result of an imbalance in this equilibrium and is linked with different diseases, including cancer. While most of the studies have focused on the association between microbiota and gastrointestinal adenocarcinomas, very little is known about gastroenteropancreatic (GEP) neuroendocrine neoplasms (NENs). In this review, we provide an overview concerning the complex interplay between gut microbiota and GEP NENs, focusing on the potential role in tumorigenesis and progression in these tumors.
Genetic hemochromatosis is an autosomal recessive disorder characterized by iron overload and a variety of clinical manifestations such as liver cirrhosis and arthropathy. It is the most common genetic disease of northern European populations. The principal gene responsible for hereditary hemochromatosis, designated HFE, is located on chromosome 6 in the HLA region. The single point mutation 845A, changing cysteine at position 282 to tyrosine (C282Y), in this gene has been identified as the main genetic basis of hereditary hemochromatosis. Two other mutations, 187G, a histidine to aspartate at amino acid 63 (H63D), and 193T, a serine to cysteine at amino acid 65 (S65C), appear to be associated with milder forms of hereditary hemochromatosis. There is a high prevalence of the C282Y mutation in northern European populations, whereas in those of the Mediterranean basin the prevalence seems low and almost absent in Far East countries. This mutation seems usually to occur on the ancestral haplotype 7.1. Accordingly, a Celtic origin of this mutation has been suggested. The aim of this study was to determine the frequency of HFE gene mutations in five geographic regions in Italy. Samples were tested for C282Y, H63D, and S65C mutations of the HFE gene according to methods of each laboratory and the results were standardized with the exchange of typed samples between the different laboratories. In addition, C282Y-positive DNA samples were typed for D6S105 allele 8 and HLA-A3 by ARMS-PCR. We have found that the allele frequency of the C282Y mutation decreases from northeast Italy (Friuli, 6%) to northwest Italy (Piedmont, 4.8%) and to central Italy (Emilia-Romagna, 1.7%). However, this mutation is lacking in the two regions of the Mediterranean basin's center (Sicily and Sardinia). Accordingly, a significant difference in the frequency of the mutation was observed between these Italian regions (P = 0.07 x 10(-3)). In contrast, no difference was observed in allele frequency of H63D in the five Italian regions. Finally, as regards the S65C mutation a very low frequency was observed in Friuli, Emilia-Romagna, and Sardinia, whereas in Sicily and Piedmont we have not found this mutation. In conclusion, these data are consistent with the hypothesis that the C282Y mutation occurred in Caucasian populations of Celtic origin, whereas the H63D mutation is more ancient as demonstrated by the ubiquitous distribution. 相似文献
Some effects of recombinant p14, a protein encoded by the tat gene of immunodeficiency virus type 1 (HIV-1), were investigated on T lymphocytic cell cultures. In particular, we detected p14 adsorption to cells, the rate of cell replication, the expression of fibronectin (FN) and its receptor (FNR) and of cell surface CD4 antigen in HIV-1-infected or uninfected MT-4 and H9 cells, treated with p14. Moreover, we evaluated the proportion of apoptotic cells in uninfected and chronically infected H9 cells in the presence of p14 and the modulation of interferon (IFN) production induced by p14 in PBMC of healthy subjects. The results obtained demonstrate that p14 exerts multifunctional activities on HIV-1 infected and uninfected cells. In particular, this protein interacts in a specific manner with cell surface, especially with that of infected cells, and enhances the expression of FN and FNR but not that of the CD4 lymphocyte antigen. Moreover, p14 increases cell replication, IFN production and can exert a slight modulation of apoptosis. We also propose a model to explain a possible role in HIV-1 infection of the effects of exogenous p14. 相似文献