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To probe CP violation in the leptonic sector using GeV energy neutrino beams in current and future experiments using argon detectors, precise models of the complex underlying neutrino and antineutrino interactions are needed. The E12-14-012 experiment at Jefferson Lab Hall A was designed to perform a combined analysis of inclusive and exclusive electron scatterings on both argon (N=22) and titanium (Z=22) nuclei using GeV-energy electron beams. The measurement on titanium nucleus provides essential information to understand the neutrino scattering on argon, large contribution to which comes from scattering off neutrons. Here we report the first experimental study of electron-titanium scattering as double-differential cross section at beam energy E=2.222 GeV and electron-scattering angle θ=15.541, measured over a broad range of energy transfer, spanning the kinematical regions in which quasielastic scattering and delta production are the dominant reaction mechanisms. The data provide valuable new information needed to develop accurate theoretical models of the electromagnetic and weak cross sections of these complex nuclei in the kinematic regime of interest to neutrino experiments.

A consistent comparison between nonrelativistic and relativistic descriptions of the (e,e'p) reaction is presented. We use the nonrelativistic DWEEPY code and develop a fully relativistic model starting from the effective Pauli reduction for the scattering state and the relativistic mean field theory for the bound state. Results for the 16O(e,e'p) differential cross section and structure functions are compared in various kinematical conditions. A limit in energy of the validity of the nonrelativistic approach is established. The effects of spinor distortion and of the effective momentum approximation for the scattering state are discussed. A satisfactory agreement with data of differential cross sections, structure functions, and polarization observables is achieved., RevTeX, 20pages, 18 figures, submitted to Phys.Rev.C

To compare functional and anatomical outcomes after idiopathic macular pucker removal between eyes that underwent internal limiting membrane (ILM) peeling and eyes that did not.In this multicentric, randomized clinical trial, 60 eyes of 60 patients affected with idiopathic macular pucker were enrolled. Thirty eyes underwent 23-gauge pars plana vitrectomy associated with ILM peeling ("ILM peeling group"), whereas 30 eyes did not undergo ILM peeling ("ILM not peeling group"). Retinal sensitivity, frequency of microscotomas, and all the other microperimetric parameters were tested by MP1 microperimetry. Best-corrected visual acuity was investigated with the Early Treatment Diabetic Retinopathy Study chart. Anatomical outcomes were analyzed with spectral domain optical coherence tomography.After a 12-month follow-up, the mean retinal sensitivity in the 4° central area showed a greater and faster recovery in the ILM not peeling group than in the ILM peeling group (P = 0.041). The number of absolute microscotomas (0 dB) within the 12° central retinal area was significantly higher in the ILM peeling group than in the ILM not peeling group (P = 0.044).The ILM not peeling group seems to show better outcomes than the ILM peeling group as measured by mean retinal sensitivity and number of microscotomas after a 12-month follow-up.

SummaryThe association of cigarette smoking with the development of occlusive vascular disease is firmly established. Unfavourable changes in a series of variables held independent risk factors for the development of vascular lesions (HDL-cholesterol, haematocrit, white blood cell count, fibrinogen and plasminogen activator inhibitor-1 (PAI-1)) are thought to be directly influenced by cigarette smoking. However, the role played by the genotype in the effect of smoking on the above parameters has not been investigated. To control the genotype, we studied the relationship between cigarette smoking and a series of cardiovascular risk factors in 27 monozygotic twin pairs (7 male and 20 female pairs, mean age ± SD: 47.4 ± 12.9 yrs) with a life-long discordance for smoking. Smoking twins had a life-long dose of smoking (Brickman index) of 287.3 ± 241.5. Body mass index, blood pressure, haematocrit, haemoglobin and red blood cell counts, total cholesterol levels and the acute phase reactants α-acid glycoprotein and C-reactive protein were similar in smokers and non-smokers. Triglyceride was higher by 12.6% (9.5-35%, 95% confidence interval, p = 0.02) and HDL-cholesterol lower by 7.5% (0.2-15%, p = 0.04) in the smoking co-twins, who also had 8.4 % (-0.2-17%, p = 0.06) higher white blood cell counts and 4.1% (1.2-7%, p

The role of somatostatin and growth hormone in eye diseases recently became a matter of interest because of its link with proliferative diabetic retinopathy. In diabetic patients the pathologic proliferation of blood vessels as a result of retinal ischemia is a major cause of blindness. The hypoxic portions of the retina release angiogenic factors, stimulating neovascularization. Somatostatin is a natural peptide hormone that affects the release of a number of other hormones, such as growth hormone, glucagon, insulin and gastrin. The somatostatin analog promises to be safe and effective treatment for severe diabetic retinopathy. This compound has been shown to block the local and systemic production of insulin-like growth factor 1 and growth hormone, which promote the angiogenesis and endothelial cell proliferation associated with proliferative retinopathy. Several studies have confirmed that using somatostatin analogs to block insulin-like growth factor 1 production is effective in reducing neovascularization and preventing disease progression to proliferative stage of diabetic retinopathy. Long-acting somatostatin analogs are currently being tested for the treatment of diabetic retinopathy. The development of somatostatin analogs with increased selectivity for receptor subtypes will provide improved outcomes in the management of patients with diabetic retinopathy.

Diabetic retinopathy (DR) is a major cause of blindness in the working population of the Western world and there is no doubt that its prevalence is strongly related to the duration of diabetes and the glycemic control. However, although intensive diabetes management, with the goal of achieving near-normal glycemia, has been shown to prevent and/or delay the onset of DR, there is now ample of evidence that the development of this microangiopathy is a multifactorial process in which genetic, metabolic, haemostatic and growth factors play an important role. Moreover, given the suggestions that immunological mechanisms might have a role in the pathogenesis of diabetic microangiopathy via immune complex deposition, it has been hypothesized that antiphospholipid antibodies (A-Ab) directed against endothelial antigens could be responsible for initiating vascular injury. In particular, not only A-Ab production was found to be increased in patients with overt nephropathy or macroangiopathy but also Lupus Anticoagulant positivity, representing an intersection point between immune and haemostatic alterations, has been highlighted as a potential and additional risk factor in the pathogenesis of microangiopathy in type 1 diabetics. Moreover, given the high levels of activated protein C, endothelin-1 and thrombo-modulin that have been observed in normo-albuminuric and uncomplicated patients, it has been concluded that the vascular endothelium shifts pathologically from an antithrombotic to a prothrombotic state even in the early phases of the disease. This condition was found to be more pronounced in subjects with anticardiolipin positivity and/or high circulating immune complexes concentrations, since they possess the ability not only to induce platelet activation and aggregation but also to activate the complement system via the classical pathway. Therefore, a potential synergism between generation of autoantibodies, haemostatic alterations and endothelial stress has been suggested, a stimulating hypothesis that needs further studies to be clarified in its complexity.

The interpretation of the signals detected by high precision experiments aimed at measuring neutrino oscillations requires an accurate description of the neutrino-nucleus cross sections. One of the key element of the analysis is the treatment of nuclear effects, which is one of the main sources of systematics for accelerator based experiments such as the Long Baseline Neutrino Experiment (LBNE). A considerable effort is currently being made to develop theoretical models capable of providing a fully quantitative description of the neutrino-nucleus cross sections in the kinematical regime relevant to LBNE. The approach based on nuclear many-body theory and the spectral function formalism has proved very successful in explaining the available electron scattering data in a variety of kinematical conditions. The first step towards its application to the analysis of neutrino data is the derivation of the spectral functions of nuclei employed in neutrino detectors, in particular argon. We propose a measurement of the coincidence (e, e'p) cross section on argon. This data will provide the experimental input indispensable to construct the argon spectral function, thus paving the way for a reliable estimate of the neutrino cross sections. In addition, the analysis of the (e, e'p) data will help a number of theoretical developments, like the description of final-state interactions needed to isolate the initial-state contributions to the observed single-particle peaks, that is also needed for the interpretation of the signal detected in neutrino experiments. 28 pages, 4 figures, Proposal PR12-14-012 submitted to the JLAB PAC 42, July 2014

The interpretation of the signals detected by high precision experiments aimed at measuring neutrino oscillations requires an accurate description of the neutrino-nucleus cross sections. One of the key element of the analysis is the treatment of nuclear effects, which is one of the main sources of systematics for accelerator based experiments such as the Long Baseline Neutrino Experiment (LBNE). A considerable effort is currently being made to develop theoretical models capable of providing a fully quantitative description of the neutrino-nucleus cross sections in the kinematical regime relevant to LBNE. The approach based on nuclear many-body theory and the spectral function formalism has proved very successful in explaining the available electron scattering data in a variety of kinematical conditions. The first step towards its application to the analysis of neutrino data is the derivation of the spectral functions of nuclei employed in neutrino detectors, in particular argon. We propose a measurement of the coincidence $(e,e^\prime p)$ cross section on argon. This data will provide the experimental input indispensable to construct the argon spectral function, thus paving the way for a reliable estimate of the neutrino cross sections. In addition, the analysis of the $(e,e^\prime p)$ data will help a number of theoretical developments, like the description of final-state interactions needed to isolate the initial-state contributions to the observed single-particle peaks, that is also needed for the interpretation of the signal detected in neutrino experiments., 28 pages, 4 figures, Proposal PR12-14-012 submitted to the JLAB PAC 42, July 2014

Diabetic retinopathy (DR) is the most frequent complication of diabetes and a leading cause of impaired vision in the Western world. There is general agreement that early diagnosis and treatment of DR can slow its progression and help to prevent blindness. However, as a result of its asymptomatic nature and its etiopathogenesis, which is still unclear due to its multifactorial complexity, DR-related blindness has a growing social impact in industrialized countries. Therefore, in order to gain a better understanding of this serious disease, the author performed an updated 10-year review of risk factors and management of DR in type 1 diabetes.

Aim: To investigate whether acetazolamide, already found to be helpful in decreasing cystoid macular edema in patients with retinitis pigmentosa, was also effective in the treatment of diabetic macular edema in nonproliferative retinopathy. Methods:Two randomized age- and sex-matched groups (cases and controls) of 12 diabetics (five Type 1 and seven Type 2) were selected for this pilot study and graded for retinopathy (Early Treatment of Diabetic Retinopathy Study – Airlie House Classification). Cases were treated with acetazolamide for three months according to a standard protocol. The Early Treatment of Diabetic Retinopathy Study chart was used for assessing far-best corrected visual-acuity, and fluorescein angiography was performed using the Heidelberg Retina Angiograph. The Amsler grid-test and computerized-perimetry (Octopus 2000R) were also performed. Results: Fluorescein-angiographic findings and perimetric data improved significantly (p 0.01). The Amsler grid-test resulted insignificant in our study (p > 0.05). No adverse effects or significant variations in laboratory tests were recorded. Conclusion: Further clinical investigations involving larger numbers of patients and a longer follow-up are required to confirm these preliminary results. However, the present study seems to suggest that acetazolamide could be effective in reducing fluorescein-angiographic findings and improving perimetric data in diabetics with macular edema, even though the mechanism of action remains obscure. Visual-acuity varied only slightly.

AIMS—To investigate whether diabetic retinopathy (DR), already associated with microvascular alterations, ischaemia, and endothelial dysfunction, was also characterised by abnormal modulation of coagulation pathways. METHODS—Plasma samples, collected from 67 type 1 diabetics comparable for age, duration of disease (DD), and metabolic control (MC), were processed for prothrombin degradation products (F1+2) and factor VII coagulant activity (FVII:c). 50 normal subjects served as a control group. The ETDRS-Airlie House Classification of DR was used. RESULTS—A significant correlation between FVII:c and F1+2 plasma concentrations was observed (p 0.05). CONCLUSIONS—These findings pointed out the presence of a hypercoagulable state associated with endothelial dysfunction in patients with insulin dependent diabetes mellitus (IDDM), demonstrated both by increased FVII:c and F1+2 plasma levels. Moreover, the observation of different DR related degrees of procoagulant activity, despite comparable DD and MC, strengthens the hypothesis of multiple risk factors in the pathogenesis of DR.

Purpose. Microvascular alterations, impairment of coagulation, ischemia and diffuse endothelial damage are related to the progression of diabetic retinopathy. Defibrotide has been demonstrated to produce profibrinolytic, cytoprotective and vasofacilatory activities. The aim of the present study was to evaluate the therapeutic effect of Defibrotide in the treatment of nonproliferative diabetic retinopathy. Methods. Two randomized age- and sex-matched groups (cases and controls) of 35 NIDDM patients presenting non-proliferative diabetic retinopathy were included in this study: cases were treated with Defibrotide (800-1600 mg daily) for two years. Results. All tested parameters (ETDRS visual acuity; computerized perimetry; retinography; fluorescein angiography), improved significantly (p

As previously reported in the literature, hyperbaric oxygen delivery seems to modify the natural course of retinitis pigmentosa. In order to evaluate these first encouraging data, 48 affected subjects were separately studied in two subgroups (cases and controls). All patients underwent yearly an ophthalmological examination completed by a maximum amplitude electroretinogram, conducted according to our ‘differential derivation’ system, a new recording technique specifically designed to enhance the signal-to-noise ratio. Oxygen delivery was provided regularly for 90 min daily (2.2 Absolute Atmosphere) in three cycles according to a standard protocol. In the cases, electroretinographic mean values were as follows: at TO (basal) 4.68 ± 3.81 μV; after one year (T1) 8.46 ± 5.71 μV; at two years (T2) 10.7 ± 7.6 μV; at the end of the study (T3) 14.4 ± 11.7 μV. In the controls, electroretinographic mean values were as follows: at T0 4.92 ± 3.05 μV; at T1 5.04 ± 3.07 μV; at T2 3.46 ± 2.77 μV; at T3 2.97 ± 3.61 μV. Amplitudes showed a remarkable (p

The authors present a biomicroscopic evaluation of vitreal alterations in a large group of patients affected by primary retinitis pigmentosa (RP). 286 RP patients (571 eyes), 153 (305 eyes) males and 133 (266 eyes) females, have been studied; the mean age of this whole group was 37.26 + or - 14.93 years (age range: 5-77). Vitreal static and dynamic biomicroscopy was performed on fully dilated pupils by means of a Haag-Streit 900 slit-lamp and high-power positive precorneal lenses (+90 and +78 dpt Volk lenses). Most patients showed floating cottonball-like condensations (26.824%) often associated with fibrillary degeneration (15.88%), while non-pigmentary vitreal particulation was detected in 26.609% of cases and the pigmentary type in 12.017%, respectively. Posterior vitreal detachment was detected alone in only 0.43% of cases while 18.24% of examined eyes showed no vitreal alterations. A high statistical correlation between vitreal aspects and pigmentary grading of the fundus oculi (p = 0.0001), as well as duration of the disease (p = 0.0074), was found; at the same time, no statistical correlation with refractive error was demonstrated (p = 0.47).

Diabetes mellitus is a major cause of blindness in the working population of the Western World. Numerous large, prospective, randomized clinical trials have delineated the current standard prevention and treatment protocols including intensive glycemic and blood pressure control as well as laser photocoagulation for clinically significant macular edema and/or proliferative retinopathy at a high risk for tractional retinal detachment. However, despite all these interventions, vision loss from diabetic retinopathy still occurs at an alarming rate and no data provide an adequate explanation for the serious and rapid involvement of the retinal microcirculation that may be observed in the disease despite a good metabolic control. In fact, there is now ample of evidence that the development of diabetic retinopathy is a multifactorial process where genetic, metabolic and growth factors play an important role. Some biochemical mechanisms, supposed to be involved in the pathogenesis of diabetic retinopathy, have been highlighted in this review.