Multiple routes of communication within the amygdala-mPFC network: A comparative approach in humans and macaques.

The network formed by the amygdala (AMG) and the medial Prefrontal Cortex (mPFC), at the interface between our internal and external environment, has been shown to support some important aspects of behavioral adaptation. Whether and how the anatomo-functional organization of this network evolved across primates remains unclear. Here, we compared AMG nuclei morphological characteristics and their functional connectivity with the mPFC in humans and macaques to identify potential homologies and differences between these species. Based on selected studies, we highlight two subsystems within the AMG-mPFC circuits, likely involved in distinct temporal dynamics of integration during behavioral adaptation. We also show that whereas the mPFC displays a large expansion but a preserved intrinsic anatomo-functional organization, the AMG displays a volume reduction and morphological changes related to specific nuclei. We discuss potential commonalities and differences in the dialogue between AMG nuclei and mPFC in humans and macaques based on available data.

Overexpression of squamous cell carcinoma antigen in idiopathic pulmonary fibrosis: clinicopathological correlations.

BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a chronic progressive disorder with a poor prognosis. Epithelial instability is a crucial step in the development and progression of the disease, including neoplastic transformation. Few tissue markers for epithelial instability have been reported in IPF. Squamous cell carcinoma antigen (SCCA) is a serine protease inhibitor typically expressed by dysplastic and neoplastic cells of epithelial origin, more often in squamous cell tumours. At present, no information is available on its expression in IPF. METHODS: SCCA and transforming growth factor beta (TGFbeta) expression in surgical lung biopsies from 22 patients with IPF and 20 control cases was examined. An in vitro study using A549 pneumocytes was also conducted to investigate the relationship between SCCA and TGFbeta expression. SCCA and TGFbeta epithelial expression was evaluated by immunohistochemistry and reverse transcription-PCR (RT-PCR). SCCA values were correlated with different pathological and clinical parameters. Time course analysis of TGFbeta expression in A549 pneumocytes incubated with different SCCA concentrations was assessed by real time RT-PCR. RESULTS: SCCA was expressed in many metaplastic alveolar epithelial cells in all IPF cases with a mean value of 24.9% while it was seen in only two control patients in up to 5% of metaplastic cells. In patients with IPF, SCCA correlated positively with extension of fibroblastic foci (r = 0.49, p = 0.02), expression of TGFbeta (r = 0.78, p<0.0001) and with carbon monoxide transfer factor decline after 9 months of follow-up (r = 0.59, p = 0.01). In vitro experiments showed that incubation of cultured cells with SCCA induced TGFbeta expression, with a peak at 24 h. CONCLUSION: Our findings provide for the first time a potential mechanism by which SCCA secreted from metaplastic epithelial cells may exert a profibrotic effect in IPF. SCCA could be an important biomarker in this incurable disease.

Favorable tissue effects of quantum molecular resonance device (Vesalius) compared with standard electrocautery. A novel paradigm in lung surgery.

BACKGROUND: Electrosurgical devices are largely employed in thoracic surgery but their use is burdened by extensive necrosis and second intention healing. METHODS: A rat model of thoracotomy was performed on 46 adult male rats using a standard electrocautery or a new quantum molecular resonance (QMR) instrument called Vesalius. Skin, muscle and lung specimens were obtained immediately and 2 weeks after surgery to evaluate acute and late effects. RESULTS: Both in the short- and long-term study, Vesalius produced less severe tissue damage than that of standard electrocautery. CONCLUSIONS: The use of the QMR device may provide an alternative to gold-standard electrosurgical devices in thoracic surgery.

[Intra-articular treatment with the TNF-alpha antagonist, etanercept, in severe diffuse pigmented villonodular synovitis of the knee]. / Trattamento intra-articolare con l'antagonista del TNFalpha etanercept nella sinovite villo-nodulare pigmentosa diffusa del ginocchio.

Pigmented villonodular synovitis (PVNS) is a rare pre-malignant disease that require aggressive treatment as surgical synovectomy, eventually followed by radiosynovectomy. Nevertheless, the disease often reoccurs after these treatments. To determine the safety and efficacy of intra-articular (IA) TNFalpha blockade with etanercept (ETN), before extended arthroscopic synovectomy, in severe PVNS of the knee, two patients, (a 26-year-old man with B27+ undifferentiated spondylarthropathy and a 32-year-old femal with seronegative oligoarthritis), affected by diffuse knee PVNS (diagnosis made by histological examination), resistant to IA corticosteroid injections and to repeated arthroscopic synovectomy, were submitted, after protocol approval by human research committee and patient's written informed consent to intra-articular etanercept (IA-ETN) treatment with a different dosage schedule: 12.5 mg weekly IA-ETN injection for 4 weeks, followed by extended arthroscopic synovectomy and of 25 mg IA-ETN injection for 4 weeks, respectively. Previous DMARDs treatment was continued in stable appropriate doses. Any adverse events were recorded throughout the study. The following parameters were considered as clinical endpoints: 1) Knee Joint Index (KJI: range 0-14); 2) Thompson index (THI: range 0-9) At the study entry and at the end of follow-up, high frequency ultrasound grey scale synovial thickening (US-ST) was also assessed. No adverse events were observed due to IA-ETN and to arthroscopic synovectomy. Marked improvement of knee disease activity over time and sustained functional recover was obtained. US-ST evaluation before treatment initiation and at the end of follow-up confirmed the regression of knee joint synovial proliferation.