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This paper proposes an innovative approach to analyse the energy behaviour of complex kinetic shading systems. Although several studies have analysed this topic, many are focused only on certain aspects or on simple shading systems due to a lack of tools for running reliable energy simulations on complex systems. This study aims to develop and validate a tool based on Python and EnergyPlus that can consider the continuous nature of the energy simulation and analyse complex kinetic systems. Simply providing an EnergyPlus model and a model of the shading configurations, the algorithm provides as output a comparison sheet to evaluate the performance of the system. The paper provides a description of the tools and studies focused on this topic; subsequently, a methodological insight is presented to explain the workflow, its validation, and the algorithm developed. Finally, the algorithm is tested on a case study to analyse a kinetic shading system. Abbreviations: DSF: Dynamic Shading File; EDSM: Equivalent Dynamic Shading Model; EMS: Energy Management System; ESSM: Equivalent Static Shading Model; Gf: Incident irradiance; Gf max: Incident irradiance threshold; PV: Photovoltaic; ST1/2/3: State 1/2/3; SSM: Static Shading Model; SF: Sunlit Fraction; SSF: Static Shading File; To: Outdoor temperature; To max 1/2: Outdoor temperature threshold 1/2; Tsol: Solar transmittance.

ObjectivesThe objective of this study is to evaluate ChatGPT’s accuracy and reliability in answering complex medical questions related to occupational health and to explore the implications and limitations of AI in occupational health medicine while providing recommendations for future research in this area and informing decision-makers about AI impact in healthcare.MethodsA group of physicians was enlisted to create a dataset of questions and answers on Italian occupational medicine legislation. They were divided into two teams, each assigned to a different subject area. ChatGPT was used to generate answers for each question with/without legislative context. The doctors evaluatedhumanand generated answers in blind, with both teams reviewing each other’s work.ResultsOccupational physicians perform better than ChatGPT in generating accurate questions on a 5-point likert score, while ChatGPT with access to legislative context is comparable to professional doctors in providing complete answers. Still, we found that users tend to prefer answers generated by humans, indicating that while ChatGPT is useful, users still value the opinions of occupational medicine professionals.ConclusionsThe study evaluated ChatGPT’s effectiveness in occupational medicine and identified crucial factors for its responsible use. It emphasizes ongoing dialogue and reflection for AI development in healthcare. ChatGPT provides 24/7 assistance to occupational physicians, increasing efficiency and reducing costs, monitoring workers’ health, and offering personalized service. It has the potential to transform occupational medicine and create safer work environments.

Context The pathogenesis of nephrolithiasis in primary hyperparathyroidism (PHPT) remains to be elucidated. The latest guidelines suggest parathyroidectomy in patients with asymptomatic PHPT with hypercalciuria (> 400 mg/d) and increased stone risk profile. Objective The objective of this work is to evaluate the association of urinary stone risk factors and nephrolithiasis in patients with asymptomatic sporadic PHPT and its clinical relevance. Design A total of 157 consecutive patients with sporadic asymptomatic PHPT were evaluated by measurement of serum and 24-hour urinary parameters and kidney ultrasound. Results Urinary parameters were tested in the univariate analysis as continuous and categorical variables. Only hypercalciuria and hypomagnesuria were significantly associated with nephrolithiasis in the univariate and multivariate analysis adjusted for age, sex, body mass index, estimated glomerular filtration rate, parathyroid hormone, 25-hydroxyvitamin D, serum calcium, and urine volume (odds ratio, OR 2.14 [1.10-4.56]; P = .04; OR 3.06 [1.26-7.43]; P = .013, respectively). Hypomagnesuria remained associated with nephrolithiasis in the multivariate analysis (OR 6.09 [1.57-23.5], P = .009) even when the analysis was limited to patients without concomitant hypercalciuria. The urinary calcium/magnesium (Ca/Mg) ratio was also associated with nephrolithiasis (univariate OR 1.62 [1.27-2.08]; P = .001 and multivariate analysis OR 1.74 [1.25-2.42], P = .001). Hypomagnesuria and urinary Ca/Mg ratio had a better, but rather low, positive predictive value compared with hypercalciuria. Conclusions Hypomagnesuria and urinary Ca/Mg ratio are each associated with silent nephrolithiasis and have potential clinical utility as risk factors, besides hypercalciuria, for kidney stones in asymptomatic PHPT patients. The other urinary indices that have been commonly thought to be associated with kidney stones in PHPT are not supported by our results.

Objectives: This study aimed to demonstrate how to estimate the value of health gain after patients with a multisystem disease achieve a condition-specific composite response endpoint. Methods: Data from patients treated in routine practice with an exemplar multisystem disease (systemic lupus erythematosus) were extracted from a national register (British Isles Lupus Assessment Group Biologics Register). Two bespoke composite response endpoints (Major Clinical Response and Improvement) were developed in advance of this study. Difference-in-differences regression compared health utility values (3-level version of EQ-5D; UK tariff) over 6 months for responders and nonresponders. Bootstrapped regression estimated the incremental quality-adjusted life-years (QALYs), probability of QALY gain after achieving the response criteria, and population monetary benefit of response. Results: Within the sample (n = 171), 18.2% achieved Major Clinical Response and 49.1% achieved Improvement at 6 months. Incremental health utility values were 0.0923 for Major Clinical Response and 0.0454 for Improvement. Expected incremental QALY gain at 6 months was 0.020 for Major Clinical Response and 0.012 for Improvement. Probability of QALY gain after achieving the response criteria was 77.6% for Major Clinical Response and 72.7% for Improvement. Population monetary benefit of response was £1 106 458 for Major Clinical Response and £649 134 for Improvement. Conclusions: Bespoke composite response endpoints are becoming more common to measure treatment response for multisystem diseases in trials and observational studies. Health technology assessment agencies face a growing challenge to establish whether these endpoints correspond with improved health gain. Health utility values can generate this evidence to enhance the usefulness of composite response endpoints for health technology assessment, decision making, and economic evaluation.

The study of chromogenic materials and systems is particularly promising for innovative, transparent building envelopes, with thermo-optical properties adaptable to surrounding environmental conditions. This work spots light on the multiple effects of photochromic glazing on the energy consumption of buildings and on the impact that such technologies would have on the visual comfort of occupants. To our knowledge, this is the first work dealing with building integration of spirooxazine-based photochromic films. This experimental and theoretical work aims helping to fill this gap by reporting the results of a study concerning the spirooxazine photochromic molecules, integrated in transparent matrices of polymethylmethacrylate. This work discloses the potential of specific photochromic materials, especially as a function of spectral peculiarities. The figures of merit of this technology have been studied by assuming its integration in an ideal multi-storey office building, and by studying the effects in terms of energy consumption and visual comfort and proposing a comparison with several static commercial glazing technologies. The photochromic glazing demonstrated to offer significant reduction of energy use for cooling, compared to a clear glass (with yearly saving of 4079 kWh, on the Southern facade), and for artificial lighting (with a saving of 3711 kWh), if compared to the commercial solar control glazing. Furthermore, the dynamic behaviour of the photochromic glazing represented the best choice in terms of visual comfort.

PET radioligands targeted to translocator protein (TSPO) offer a highly sensitive and specific means of imaging joint inflammation in rheumatoid arthritis (RA). Through high expression of TSPO on activated macrophages, TSPO PET has been widely reported in several studies of RA as a means of imaging synovial macrophages in vivo. However, this premise does not take into account the ubiquitous expression of TSPO. This study aimed to investigate TSPO expression in major cellular constituents of RA pannus-monocytes, macrophages, fibroblastlike synoviocytes (FLS cells), and CD4-positive (CD4+) T lymphocytes (T cells)-to more accurately interpret TSPO PET signal from RA synovium. Methods: Three RA patients and 3 healthy volunteers underwent PET of both knees using the TSPO radioligand 11C-PBR28. Through 3H-PBR28 autoradiography and immunostaining of synovial tissue in 6 RA patients and 6 healthy volunteers, cellular expression of TSPO in synovial tissue was evaluated. TSPO messenger RNA expression and 3H-PBR28 radioligand binding was assessed using in vitro monocytes, macrophages, FLS cells, and CD4+ T cells. Results:11C-PBR28 PET signal was significantly higher in RA joints than in healthy joints (average SUV, 0.82 ± 0.12 vs. 0.03 ± 0.004; P < 0.01). Further, 3H-PBR28-specific binding in synovial tissue was approximately 10-fold higher in RA patients than in healthy controls. Immunofluorescence revealed TSPO expression on macrophages, FLS cells, and CD4+ T cells. The in vitro study demonstrated the highest TSPO messenger RNA expression and 3H-PBR28-specific binding in activated FLS cells, nonactivated M0 macrophages, and activated M2 reparative macrophages, with the least TSPO expression being in activated and nonactivated CD4+ T cells. Conclusion: To our knowledge, this study was the first evaluation of cellular TSPO expression in synovium, with the highest TSPO expression and PBR28 binding being found on activated synovial FLS cells and M2 macrophages. TSPO-targeted PET may therefore have a unique sensitivity in detecting FLS cells and macrophage-predominant inflammation in RA, with potential utility for assessing treatment response in trials using novel FLS-cell-targeted therapies.

Some of the more relevant interventions that are proposed in Italy to foster economic growth and markedly reduce its public debt are here analysed. Conditional on general and specific measures (structural reforms, public investments not ncluded in the ratio debt/GDP, additional investments, reduction of the tax wedge, depreciation of the euro against US dollar), simulations of economic growth rates and usual fiscal parameters are made. The only intervention that in the long run seems to foster country’s economy and at the same time drastically reduce its public debt is the devaluation of euro. It must be accompanied by the continuous pursuit of reforms that operate in a general form on the whole system.

Thermal performances of window frames and glazing represent a field of growing research efforts - worldwide - aiming to reduce energy consumption and achieve indoor comfort. A combination of newly designed super-insulated window frames and innovative glazing technologies may enhance the performance of windows. Aerogel-based “thermal breaks” for window frames, coupled with high-performing glazing, may lead to significant energy saving. In this work, yearly energy use for heating and cooling were assessed in several locations, for building models equipped with innovative technologies, for glazing and frames. The results of numerical simulations confirmed the opportunities offered by new technologies.

The complement component C1q is known to play a controversial role in the pathogenesis of systemic lupus erythematosus, but the underlying mechanisms remain poorly understood. Intraperitoneal injection of pristane induces a lupus-like syndrome whose pathogenesis implicates the secretion of type I IFN by CD11b+ Ly6Chigh inflammatory monocytes in a TLR7-dependent fashion. C1q was also shown to influence the secretion of IFN-α. In this study, we explored whether C1q deficiency could affect pristane-induced lupus. Surprisingly, C1qa−/− mice developed lower titers of circulating Abs and milder arthritis compared with the controls. In keeping with the clinical scores, 2 wk after pristane injection the peritoneal recruitment of CD11b+ Ly6Chigh inflammatory monocytes in C1qa−/− mice was impaired. Furthermore, C1q-deficient pristane-primed resident peritoneal macrophages secreted significantly less CCL3, CCL2, CXCL1, and IL-6 when stimulated in vitro with TLR7 ligand. Replenishing C1q in vivo during the pristane-priming phase rectified this defect. Conversely, pristane-primed macrophages from C3-deficient mice did not show impaired cytokine production. These findings demonstrate that C1q deficiency impairs the TLR7-dependent chemokine production by pristane-primed peritoneal macrophages and suggest that C1q, and not C3, is involved in the handling of pristane by phagocytic cells, which is required to trigger disease in this model.

Sulfasalazine has long been used for the treatment of rheumatoid arthritis and is often chosen as a first-line treatment. Here, we report a case of sulfasalazine-induced autoimmune thrombocytopenia and review the mechanisms behind drug-induced immune thrombocytopenia (DITP) and the approach to its diagnosis and management.

Objectives. The aim was to investigate whether the signalling lymphocyte activation molecule (SLAM) signalling pathways contribute to LN and whether SLAM receptors could be valuable biomarkers of disease activity. Methods. Peripheral blood mononuclear cells from 30National Research Ethics Service SLE patients with biopsy-proven LN were analysed by flow cytometry. Clinical measures of disease activity were assessed. The expression of the SLAM family receptors on T-cell subpopulations [CD4, CD8 and double negative (DN) T cells] was measured and compared between lupus patients with active renal disease and those in remission. Results. The frequency of CD8 T cells expressing SLAMF3, SLAMF5 and SLAMF7 was significantly lower in LN patients who were in remission. In contrast, these subsets were similar in patients with active renal disease and in healthy individuals. Patients with active nephritis had an increased percentage of circulating monocytes, consistent with a potential role played by these cells in glomerular inflammation. Changes in the frequency of DN T cells positive for SLAMF2, SLAMF4 and SLAMF7 were observed in lupus patients irrespective of the disease activity. We detected alterations in the cellular expression of the SLAM family receptors, but these changes were less obvious and did not reveal any specific pattern. The percentage of DN T cells expressing SLAMF6 could predict the clinical response to B-cell depletion in patients with LN. Conclusion. Our study demonstrates altered expression of the SLAM family receptors in SLE T lymphocytes. This is consistent with the importance of the SLAM-associated pathways in lupus pathogenesis.

This paper surveys some relevant contributions to the economic literature on co-integrating vector autoregressive (VAR) models [vector error correction mechanisms (VECMs)], emphasizing their usefulness for economic policy. It further discusses some theoretical aspects that are necessary for a complete understanding of their potential. The theoretical introduction of the co-integrating VAR model is followed by an illustration of its applications to monetary policy, fiscal policy and exchanges rates as well as in establishing the effects of structural bilateral shocks between countries (the so-called global VAR, or GVAR, models). Special attention is paid to the VECM capacities of being used in conjunction with dynamic stochastic general equilibrium models and of jointly specifying the short- and long-run dynamics, thus representing the steady-state of economic systems (by means of the co-integration relations) and the short-run dynamics around it.

A theoretical model is developed for the ratio primary-surplus/GDP that a Country has to attain over a given number of years, to lower its public debt from the present value to one a-priori fixed. Such a ratio depends on the average interest rate paid on the outstanding stock of debt as well as inflation and real growth rates. The ratio primary-surplus/GDP is then determined for Germany, Greece and Italy, supposing that 20 years are necessary for lowering the debt to 60% of GDP, as indicated in the Budget Pact approved by 25 EU member States. Results are reported in graphs and show how the German debt can be easily diminished, whilst debts in Greece and Italy can be reduced with a greater difficulty.

The 129-derived Sle16 is a susceptibility locus for systemic autoimmunity when present on the C57BL/6 (B6) background. Genetic analysis of a (129×B6)F2 cross identified a region from the B6 chromosome 3 (Sle18) with positive linkage to antinuclear Abs. In this study, we have generated a B6 congenic strain harboring the 129 allele of Sle18 and intercrossed this line with the lupus-prone B6.129-Sle16 strain. The presence of the 129-Sle18 allele in the B6.129-Sle16Sle18 double congenic mice suppressed the development of Sle16-mediated autoantibody production and ameliorated the renal pathology. The 129-Sle18 locus rectified the B cell abnormalities detected in the B6.129-Sle16 mice, such as the reduction in the percentage of marginal zone B and B1a cells and the increased number of germinal centers. The B6.129-Sle16Sle18 spleens still displayed an increased percentage of activated T and B cells. However, in the B6.129-Sle16Sle18 strain the percentage of naive T cells was equivalent to that in B6.129-Sle18 and B6 mice and these cells showed a reduced proliferative response to anti-CD3 stimulation compared with B6.129-Sle16 T cells. There was a significant increase in the percentage of CD4+FoxP3+regulatory T cells in all congenic strains. These cells had normal regulatory function when tested in vitro. Thus, 129-Sle18 represents a novel, non-MHC lupus-suppressor locus probably operating as a functional modifier of B cells that, in combination with other factors, leads to lupus resistance. Further characterization of this locus will help to uncover the immune mechanism(s) conferring protection against lupus.

Epistatic interactions between the non-autoimmune strains 129 and C57BL/6 (B6), used for generating gene-targeted animals, can induce a lupus-like disease. Genome-wide scan analyses of testcross progeny between these two strains have identified several lupus susceptibility loci, with the strongest linkage to the production of autoantibodies (auto-Abs) displayed by an interval on chromosome 1 of 129 origin (Sle16). However, the contribution of B6 loci to the lupus phenotype remained unknown. We used a congenic approach to deduce the contribution to the autoimmune traits of the B6 genomic interval on chromosome 3 (Sle18), previously shown to be linked to antinuclear Ab production. This interval, when transferred on a 129 background (a strain termed 129.B6-Sle18), promoted auto-Ab production targeting a broad spectrum of autoantigens, expansion of activated CD4(+)T and B cells and mild glomerulonephritis. Surprisingly, these immunological and serological defects were accompanied by a significant increase in the percentage of regulatory T cells (Tregs; CD4(+) Foxp3(+)). However, these cells, that expressed lower levels of Foxp3, had no impaired regulatory function when tested in vitro. These findings illustrate further the efficacy of congenic dissection for functional characterisation of individual lupus susceptibility loci and highlight the contribution of loci derived from non-autoimmune strains to the disease pathogenesis.

Extensive evidence indicates that genetic predisposition is a central element in susceptibility to systemic lupus erythematosus both in humans and animals. We have previously shown that a congenic line carrying a 129-derived chromosome 1 interval on the C57BL/6 background developed humoral autoimmunity. To further dissect the contribution to autoimmunity of this 129 interval, we have created six subcongenic strains carrying fractions of the original 129 region and analyzed their serological and cellular phenotypes. At 1 year of age the congenic strain carrying a 129 interval between the microsatellites D1Mit15 (87.9 cM) and D1Mit115 (99.7 cM) (B6.129chr1b) had high levels of autoantibodies, while all the other congenic lines were not significantly different from the C57BL/6 controls. The B6.129chr1b strain displayed only mild proliferative glomerulonephritis despite high levels of IgG and C3 deposited in the kidneys. FACS analysis of the spleens revealed that the B6.129chr1b mice had a marked increase in the percentage of activated T cells associated with a significant reduction in the proportion of CD4+CD25high regulatory T cells. Moreover, this analysis showed a significantly reduced percentage of marginal zone B cells that preceded autoantibody production. Interestingly the 129chr1b-expressing bone marrow-derived macrophages displayed an impaired uptake of apoptotic cells in vitro. Collectively, our data indicate that the 129chr1b segment when recombined on the C57BL/6 genomic background is sufficient to induce loss of tolerance to nuclear Ags. These findings have important implication for the interpretation of the autoimmune phenotype associated with gene-targeted models.

The present work deals with a mechanistic model of visbreaking (VB) process. It allows satisfactory predictions of feed and products, amounts and properties overcoming the typical limitations of the empirical models (for instance, in terms of flexibility, extrapolability and so on). The mechanistic VB modeling was initially performed by taking into account just two macro-classes of pseudo-components, paraffins and aromatics [Dente, M., Bozzano, G., & Rossi, M. (1993). Reactor modelling of the visbreaking process. In Proceedings of the first conference on chemical and process engineering , Florence (p. 163); Dente, M., Bozzano, G., & Bussani, G., (1997). A comprehensive program for visbreaking simulation: Products amount and their properties prediction. Computers and Chemical Engineering, 21 , 1125; Bozzano, G., Dente, M., Sugaya, M., & McGreavy C., (1998). The characterization of residual hydrocarbon fractions with model compounds retaining the essential information, preprints of Symposia, Vol. 43, No. 3 , 216th ACS National Meeting—Boston, (p. 653)]. More recently, new experimental data related to the visbreaking of highly naphthenic residues have induced to extend the model by including naphthenic components (and their primary products, like cyclo-olefines). The importance of this extension in VB modeling is here described and underlined. Particularly it is discussed the effect of naphthenes presence on VB residue stability, against asphaltenes flocculation.

Early implementation of home care and 30 day readmissions in65 years Veneto region patients discharged for heart failure and with disability.The effectiveness of Home care (HC) on preventing rehospitalizations in patients discharged for heart failure (HF) are uncertain.The aim of the study was to measure the impact of HC on early rehospitalizations of patients discharged for HF and with disabilities.Cohort retrospective study on65 years patients, discharged at home and with a Barthel index50. Variables considered were: previous hospitalizations for ischaemic cardiopathy ad/or chronic obstructive pulmonary disease, number of hospital admissions in the previous year, length of index hospitalization; outcomes considered were: hospital readmissions and days of hospitalizations 30 days from hospital discharge in patients with or without a home care visit within two days from hospital discharge.Of the 5.094 patients (60%85 years), 14.8% received a HC visit within 2 days from discharge (43.7% from a nurse); 18.3% of patients (933) were readmitted within one month. In multivariate analyses an HC access within 2 days did not reduce the risk for readmission (although with better results in younger males but not in older women). An early HC visit reduced the days of hospital stay in males of all ages (65-74 years IRR 0.53 CI 95% 0.37-0.75; 75-84 years IRR 0.71 CI95% 0.60-0.83; 85+ years IRR 0.79 CI 95% 0.67-0.93) while in75 years females there was a significant increase.An early HC visit (within two days from discharge) may have positive effects on males, but not in older women, possibly for the coexistence of socio-economic factors.

Fc gamma RIIB-deficient mice generated in 129 background (Fc gamma RIIB(129)(-/-)) if back-crossed into C57BL/6 background exhibit a hyperactive phenotype and develop lethal lupus. Both in mice and humans, the Fc gamma r2b gene is located within a genomic interval on chromosome 1 associated with lupus susceptibility. In mice, the 129-derived haplotype of this interval, named Sle16, causes loss of self-tolerance in the context of the B6 genome, hampering the analysis of the specific contribution of Fc gamma RIIB deficiency to the development of lupus in Fc gamma RIIB(129)(-/-) mice. Moreover, in humans genetic linkage studies revealed contradictory results regarding the association of "loss of function" mutations in the Fc gamma r2b gene and susceptibility to systemic lupus erythematosis. In this study, we demonstrate that Fc gamma RIIB(-/-) mice generated by gene targeting in B6-derived ES cells (Fc gamma RIIB(B6)(-/-)), lacking the 129-derived flanking Sle16 region, exhibit a hyperactive phenotype but fail to develop lupus indicating that in Fc gamma RIIB(129)(-/-) mice, not Fc gamma RIIB deficiency but epistatic interactions between the C57BL/6 genome and the 129-derived Fc gamma r2b flanking region cause loss of tolerance. The contribution to the development of autoimmune disease by the resulting autoreactive B cells is amplified by the absence of Fc gamma RIIB, culminating in lethal lupus. In the presence of the Yaa lupus-susceptibility locus, Fc gamma RIIB(B6)(-/-) mice do develop lethal lupus, confirming that FcgRIIB deficiency only amplifies spontaneous autoimmunity determined by other loci. The Journal of Immunology, 2011, 187: 1304-1313.

Objective It has been reported that a single dose of human C-reactive protein (CRP) can prevent and reverse the renal damage in murine models of spontaneous lupus, as well as the rapid-onset immune complex disease induced in the accelerated nephrotoxic nephritis (ANTN) model. This study was undertaken to attempt to replicate these observations using a highly purified and fully characterized human CRP preparation. Methods (NZB × NZW)F1 (NZB/NZW) mice were treated with a single 200-μg subcutaneous injection of CRP or control reagents either before disease onset at 4 months of age or when high-grade proteinuria was present at 7 months of age. Mice were monitored at least monthly for proteinuria and autoantibody levels. ANTN was induced by preimmunizing C57BL/6 mice with sheep IgG, followed 5 days later by injection of sheep anti-mouse glomerular basement membrane antibody and CRP or control reagents. Renal disease was assessed by regular urinalysis and histologic evaluation. Results CRP treatment of NZB/NZW mice, either early or late in the disease, had no effect on proteinuria, autoantibody titers, or survival. CRP administration did not reduce renal injury or alter disease in the ANTN model. Human serum amyloid P component, a pentraxin protein that is very closely related to CRP, similarly had no effect. Conclusion Our completely negative observations do not confirm that human CRP has reproducible antiinflammatory or immunomodulatory effects in these murine models, nor do they support the suggestion that CRP might be useful for therapy of lupus or immune complex–mediated nephritis.

Morgagni hernia is a rare cause of diaphragmatic hernia. There are few reports of laparoscopic repair in the literature. Tension-free hernia closure with synthetic mesh reduces recurrence but occasionally results in complications, such as visceral stricture, erosion or perforation. We report a case of successful laparoscopic repair of a very large symptomatic Morgagni hernia in a 78-year-old patient, treated by positioning a gradually resorbable mesh made from porcine SIS (Surgisis Soft Tissue Graft device--Cook Inc, Bloomington, Ind). After surgery, the patient reported an immediate, marked improvement in clinical symptoms. During the postoperative course, pleural and pericardial leakage occurred. The pleural leakage was immediately drained with thoracentesis, and the pericardial leakage was treated conservatively. No other complications occurred after patient discharge. One year later, the patient was in very good general condition. No recurrence was documented with abdominal CT scan, which also demonstrated connective tissue proliferation that was progressively replacing the prosthesis. Laparoscopic repair is a safe, efficacious procedure for the treatment of diaphragmatic hernia, and presents all the advantages of minimally invasive surgery. The use of new types of material featuring marked biocompatibility and gradual reabsorbability characteristics offers considerable benefits.

Membranoproliferative glomerulonephritis (MPGN) type II (dense deposit disease) is an inflammatory renal disease characterized by electron-dense deposits and complement C3 on the glomerular basement membrane. There is no effective therapy. We investigated the role of C5 activation in a model of MPGN that develops spontaneously in complement factor H-deficient mice (Cfh−/−). At 12 months there was a significant reduction in mortality, glomerular cellularity, neutrophil numbers, and serum creatinine levels inCfh−/−mice deficient in C5. Excessive glomerular neutrophil numbers, frequently seen in patients with MPGN during disease flares, were also observed inCfh−/−mice after the administration of an antiglomerular basement membrane antibody. This exaggerated injurious phenotype was absent inCfh−/−mice deficient in C5 but not inCfh−/−mice deficient in C6, indicating a key role for C5 activation in the induction of renal lesions. Importantly, the renal injury was completely reversed inCfh−/−mice pretreated with an anti-murine C5 antibody. These results demonstrate an important role for C5 in both spontaneous MPGN and experimentally induced nephritis in factor H-deficient mice and provide preliminary evidence that C5 inhibition therapy might be useful in human MPGN type II.

Systemic lupus erythematosus (SLE) is characterised by the production of autoantibodies against ubiquitous antigens, especially nuclear components. Evidence makes it clear that the development of these autoantibodies is an antigen-driven process and that immune complexes involving DNA-containing antigens play a key role in the disease process. In rodents, DNase I is the major endonuclease present in saliva, urine and plasma, where it catalyses the hydrolysis of DNA, and impaired DNase function has been implicated in the pathogenesis of SLE. In this study we have evaluated the effects of transgenic over-expression of murine DNase I endonucleases in vivo in a mouse model of lupus. We generated transgenic mice having T-cells that express either wild-type DNase I (wt.DNase I) or a mutant DNase I (ash.DNase I), engineered for three new properties – resistance to inhibition by G-actin, resistance to inhibition by physiological saline and hyperactivity compared to wild type. By crossing these transgenic mice with a murine strain that develops SLE we found that, compared to control non-transgenic littermates or wt.DNase I transgenic mice, the ash.DNase I mutant provided significant protection from the development of anti-single-stranded DNA and anti-histone antibodies, but not of renal disease. In summary, this is the first study in vivo to directly test the effects of long-term increased expression of DNase I on the development of SLE. Our results are in line with previous reports on the possible clinical benefits of recombinant DNase I treatment in SLE, and extend them further to the use of engineered DNase I variants with increased activity and resistance to physiological inhibitors.

This work presents five structural co-integrating VAR models used to describe the economies of France, Germany, Italy, the Netherlands and Spain in the years 1983-1998 and to analyse their economic policies. Shortrun dynamics move around the long-run structure, represented by money, goods and capital market equilibrium conditions. The fitting of the reference theoretical model to the data is not imposed a priori but empirically tested. Long- and short-run properties of models highlight deep heterogeneities in the economic structures and in the monetary policy transmission mechanism among the countries. Germany plays a dominant role in the European economy and, together with the Netherlands, seems to have formed an economic area where the money, goods and capital markets are integrated. France is linked to this area, while Italy turns out to be less integrated. Finally, Spain seems to be completely disjoined.

Using an aggregate econometric model for the EU we investigate by simulation methods some dynamic paths of the European economy in the next five years under alternative hypotheses concerning the growth of world demand, the European currency/USD exchange rate, and the monetary policy.

Background Recent researches suggested a role of microchimerism in the pathogenesis of systemic sclerosis and Graft Versus Host Disease. Objectives Aim of the present study was to evaluate whether fetal microchimerism plays a role in the pathogenesis of Sjogren’s syndrome (SS). Methods We looked for male microchimerism in minor salivary glands tissue from 6 women with SS and at least one male pregnancy or miscarriage. SS diagnosis was made according to EEC criteria. As control we used DNA from minor salivary biopsy of 3 women with SS and female pregnancies only, 1 woman with SS without previous pregnancies and 2 healthy women, one with a male pregnancy and one with a female pregnancy. We assayed by PCR for a specific Y chromosome sequence, SRY, and for the homologous gene of Amelogenin. Results We didn’t find male DNA neither in the tissue from women with SS and male pregnancy nor in the controls. Conclusion This preliminary study doesn’t support the hypothesis of a role of microchimerism in the pathogenesis of Sjogren’s syndrome, however further analysis should be performed to better clarify the hypothetical association between microchimerism and SS.

We present the structure and properties of an aggregate model for the European Union, consisting of 34 equations estimated on annual data aggregated over the twelve-member EU, ranging from 1960 to 1997. Estimation was performed by a two-stage procedure taking into account the possible presence of structural breaks in the long-run parameters and allowing for nonlinearity and simultaneity of the dynamic equations. The estimated equations have a very good fit and pass a number of diagnostic tests, suggesting that EU-wide behavioural equations can be defined in a meaningful way. Simulation experiments show that the model is an agile and effective tool for the study of the European economy at an aggregate level. In particular, the model is shown to improve over previous aggregate explanations of the European economy, in that its dynamic multipliers provide a better account of the European unemployment and inflation dynamics in the last decade.

There are many similarities between graft versus host disease (GVHD) and some rheumatic autoimmune diseases, such as systemic sclerosis (SSc), Sjogren's syndrome (SS), and primary biliary cirrhosis. Bianchi et al reported that fetal cells could survive in the maternal circulation for up to 27 years after parturition. This phenomenon is called fetal microchimerism.1 Some observations led the hypothesis that persistent fetal cells in the maternal circulation could mediate a graft versus host reaction, resulting in autoimmune disease. It is known that during a chronic GVHD, a Sjogren-like syndrome, is often observed: a salivary gland biopsy sample from patients with chronic GVHD showed lymphocytic infiltration, similar to that found in SS.2 Nlson and colleagues have studied male fetal microchimerism in skin lesions …

Systemic lupus erythematosus (SLE) is characterised by the production of autoantibodies against ubiquitous antigens, especially nuclear components. Evidence makes it clear that the development of these autoantibodies is an antigen-driven process and that immune complexes involving DNA-containing antigens play a key role in the disease process. In rodents, DNase I is the major endonuclease present in saliva, urine and plasma, where it catalyses the hydrolysis of DNA, and impaired DNase function has been implicated in the pathogenesis of SLE. In this study we have evaluated the effects of transgenic over-expression of murine DNase I endonucleases in vivo in a mouse model of lupus. We generated transgenic mice having T-cells that express either wild-type DNase I (wt.DNase I) or a mutant DNase I (ash.DNase I), engineered for three new properties – resistance to inhibition by G-actin, resistance to inhibition by physiological saline and hyperactivity compared to wild type. By crossing these transgenic mice with a murine strain that develops SLE we found that, compared to control non-transgenic littermates or wt.DNase I transgenic mice, the ash.DNase I mutant provided significant protection from the development of anti-single-stranded DNA and anti-histone antibodies, but not of renal disease. In summary, this is the first study in vivo to directly test the effects of long-term increased expression of DNase I on the development of SLE. Our results are in line with previous reports on the possible clinical benefits of recombinant DNase I treatment in SLE, and extend them further to the use of engineered DNase I variants with increased activity and resistance to physiological inhibitors.