Abstract-Diabetes management is a key factor in preventing clinical complications in type 1 diabetes (T1D) patients, where the use of manual or automatic insulin therapies are designed and implemented to counteract the effects of diabetes. However, a good glucose control may perform poorly if any therapy condition changes suddenly or over time, without the patient's awareness. This phenomenon can seriously compromise the patient's health and is usually attributed to uncertainty in the T1D models used to this end.Some simulation tools have been successfully designed to develop strategies for automated control in T1D patients; one of them even has the Food and Drug Administration's (FDA) approval to be used for pre-clinical testing replacing animal experiments. However, none have explicitly included uncertainty as part of their simulation results.This work proposes a simulation tool named Glu4Pred that includes different sources of uncertainty as well as intra-patient variability to predict a more comprehensive dynamics of the glucose-insulin system. The Glu4Pred tool allows to define a complex scenario of several days or meals, where the patient's variability and several sources of uncertainty are simulated obtaining as a result an envelope of glucose traces. This is achieved using different mathematical interval models of the glucose-insulin system. Furthermore, the tool includes a risk index outcome that quantifies the risk of experiencing different grades of hypo-or hyperglycemia in the postprandial state from interval simulation. As a result, a new computational tool integrating several sources of uncertainty through interval simulation, that can support the design of decision-aid systems for insulin therapy and glucose control in T1D, was developed.

Background Primary central nervous system vasculitis (PCNSV) is an uncommon condition in which vascular inflammatory lesions are limited to the brain and spinal cord. Diagnostic criteria include a newly acquired neurological deficit that is unexplained by other processes and angiographic or central nervous system (CNS) biopsy features of vasculitis. In contrast secondary central nervous system vasculitis (SCNSV) is vascular inflammation in which CNS involvement is due to diverse causes. Objectives To investigate the clinical, laboratory, neuroimaging characteristics and treatment in Primary Central Nervous System Vasculitis (PCNSV) versus Secondary Central Nervous System Vasculitis (SCNSV). Methods We studied twenty female patients with central nervous system vasculitis (CNS) during a period of 3 years in a tertiary level center. The clinical manifestations, laboratory, neuroimaging diagnosis and treatment were analyzed. Patients were divided in PCNSV and SCNSV. Biopsy CNS was performed in 3 patients. Results We studied 10 PCNSV and 10 SCNSV patients: systemic lupus erythematous 5, systemic sclerosis (SSc) 4, Sjogren syndrome (SS) 1. Mean age in the PCNSV was 26±5 years and SCNSV 47±7years. Clinical manifestation in PCNSV versus SCNSV were: headache 90% vs 60% (NS), fatigue 80% versus 40% (<0.01), paresthesias 90% versus 80% (NS), motor deficit 20%vs 80% (0.01) and ischemic event 40% vs 40% (NS) respectively. The Antinuclear antibodies (ANA’s) were positive 100% in SCNCV vs 20% (<0.001), anti-DNA was present in 100% (<0.01) in SLE patients with SCNSV, hypocomplementemia was 80% in patients with SCNSV and 22% PCNSV (<0.01). Anti Scl-70 were present in 2 patients with SSc, and anti Ro in patients with SS Cerebral spinal fluid (CSF) was negative for infection, neoplastic process and the proteins were elevated in all cases. MRI showed periventricular and subcortical hyperintense lesions in both groups; however, theses lesions were more frequent in SCNSV. Initial treatment was methylprednisolone pulse followed by monthly cyclophosphamide. Maintenance treatment was prednisone (0.5mg/kg/day) alone in 100% of PCNSV cases and in 60% of SCNSV cases, and prednisone plus azathioprine in 40% of SCNSV cases. Recurrence was present in 20% in PCNSV (20%) and in SCNSV (30%).CNS biopsies showed vasculitis. Conclusions PCNSV had lower frequency of motor deficit, as well as lower ANA’s, and hypocomplementemia in comparison with SCNSV; an increase of CSF proteins was observed in all patients. MRI showed more periventricular and subcortical hyperintense lesions in SCNSV than PCNCV. All patients responded successfully to treatment with steroids plus cyclophosphamide. Early recognition and treatment may reduce poor outcomes. References Salvarini C, Brown RD Jr, Hunder GG. Adult primary central nervous system vasculitis: an update. curr Opin Rheumatol 2012;24:46-52 Salvarini C, Brown RD Jr, Calamia KT, Christianson TJ, Weigand SD, Miller DV, Giannini C, Meschia JF, Huston J3rd, Hunder GG Primary central nervous system vasculitis: an...

Background Primary central nervous system vasculitis (PCNSV) is a challenging clinical problem due to itsnon- specific signs and symptoms, inaccessibility of the central nervous system (CNS) tissue for pathologic examination, lack of efficient non-invasive diagnostic tests and the relative rarity of it presentation. Secondary central nervous system vasculitis (SCNSV) occurs in association with autoimmune rheumatic diseases (ARD), infections, lymphoproliferative diseases, drug abuse, and systemic vasculitis. Objectives To compare the initial clinical, laboratory and imaging features in primary central nervous system vaculitis (PCNSV) versus secondary central nervous system vasculitis (SCNSV) and follow-up after treatment with intravenous cyclophosphamide (IV CYC) plus methylprednisolone (MP). Methods Neurological (focal and non-focal manifestations), laboratory (cerebrospinal fluid and immunological tests) and neuroimaging findings were analyzed in PCNSV and SCNSV patients. Both groups received at onset MPplus IV CYC during 6 months, followed by bimonthly IV CYC plus oral glucocorticosteroids (CGS) for 12 months. All the patients were followed for 36 months. Results Thirty patients were included (12 PCNSV and 18 SCNSV). Focal and non- focal manifestations were similar in both groups (p=NS); headache being the most frequent manifestation in both groups. Fatigue, myalgias, arthralgias, neuropathy low leukocytes and platelets, elevatederythrocyte sedimentation rate, positive ANA, anti ds-DNA, ANCA, low complement, and rheumatoid factor were more frequent in SCNSV (p<0.05). In cerebrospinal fluid (CSF) pleocytosis and proteins were higher in PCNSV (p<0.05). Periventricular and subcortical hyperintense lesions were observed incranial magnetic resonance imaging in both vasculitides. Cerebral angiography and angioresonance showed narrowing of vasculature in both groups. After treatment, Kaplan-Meier survival curve showed higher relapse free survival in PCNSV (p<0.05). Conclusions There are significant differences in the clinical manifestations, laboratory, and CSF findings between PCNSV and SCNSV. After treatment with IV CYC and GCS patients with PCNSV had higher relapse-free survival than SCNSV. Disclosure of Interest None Declared

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