Dispersion and ground deposition of radioactive material according to airflow patterns for enhancing the preparedness to N/R emergencies.

The intent of minimizing the impact of the large amount of radioactive material potentially released into the atmosphere in a nuclear event implies preparedness activities. In the early phase and in absence of field observations, countermeasures would largely rely on a previous characterization of the transport and dispersion of radioactive particles and the potential levels of radioactive contamination. This study presents a methodology to estimate the atmospheric transport, dispersion and ground deposition patterns of radioactive particles. The methodology starts identifying the main airflow directions by means of the air mass trajectories calculated by the HYSPLIT model, and, secondly, the dispersion and the ground deposition characteristics associated with each airflow pattern by running the RIMPUFF atmospheric dispersion model. From the basis of these results, different products can be obtained, such as the most probable transport direction, spatial probability distribution of deposition and the geographical probability distribution of deposition above certain predefined threshold. The method is trained on the HYSPLIT trajectories and RIMPUFF simulations during five consecutive years (2012-2016) at the Almaraz Nuclear Power Plant, in Spain. 3644 forward air mass trajectories were calculated (at 00 and 12 UTC, and with duration of 36 h). Eight airflow patterns were identified, and within each pattern, the persistent days, i.e. those days in which trajectories at 00 and 12 UTC grouped into the same airflow pattern, were extracted to simulate the atmospheric dispersion and ground deposition following a hypothetical ISLOCA accident sequence of 35 h. In total, 833 simulations were carried out, in which ground contamination was estimated at cell level on a non-homogeneous geographical grid spacing up to 800 km from Almaraz. The corresponding outcomes show a large variability in the area covered and in deposition values between airflow patterns, which provide comprehensive and oriented information and resources to decision makers to emergency management.

[Low-dose oral contraceptives and pulmonary embolism: a case report]. / Estroprogestinici orali a basso dosaggio ed embolia polmonare: descrizione di un caso clinico.

We have observed a deep venous thrombosis with pulmonary embolism in a young woman receiving low-dose oral contraceptives; this adverse drug effect was not associated with some risk factor and, in particular, with a demonstrable congenital or acquired clotting abnormality. It is reported that EP can induce deep venous thrombosis with different mechanisms, as hemorheological changes with subsequent poor clearance of locally activated clotting factors, or an increase of platelet or leukocytes aggregation, or a direct effect on some clotting factor; furthermore, it is well known that oral contraceptives may induce antibodies to synthetic hormones, with detection of circulating immune complexes, that might produce thrombosis by damaging the vascular endothelium or interfering with clotting factors or platelet aggregation. Moreover, only a familial history of thrombosis or a past history of recurrent deep venous thrombosis, especially in young age, may justify a broad and highly expensive screening of latent clotting abnormalities, that may significantly increase the risk of vascular thrombosis with the use of oral contraceptives.

Complete regression of iatrogenic Kaposi's sarcoma due to corticosteroid treatment in a patient with tubercular pericarditis. A case report.

We report a case of drug-induced Kaposi's sarcoma (KS) on the sole of the right foot in a 71-year-old man, treated for 6 months with corticosteroid therapy (prednisolone 25 mg/day) for pericardial effusion. After corticosteroid withdrawal, a tuberculin skin test became strongly positive and pericardial effusion was considered to be of tubercular origin. The patient remained constantly HIV negative during 14 months of follow-up. Seven months after continuous antitubercular treatment, the KS nodules regressed spontaneously and finally disappeared. Histological studies confirmed the diagnosis of KS and documented its complete regression. Laboratory investigation confirmed prior exposure to CMV, EBV and HSV and suggested drug-induced immunological suppression. Analysis of the HLA system revealed the positivity of locus DR5, associated with classical KS. This case report underscores the relationship between genetic background, environmental factors, drug-induced immunosuppression and the evolution of this peculiar neoplasm.

Familial occurrence in cardiovascular diseases. Cardiovascular involvement in genetic disorders (2).

Current knowledge and assumptions about inheritance of cardiovascular diseases are reported in this review. They are examined from two different points of view. In the first section (familial cardiovascular diseases) discussion centered on main cardiovascular diseases with a definite clinical and pathophysiological feature in which familial occurrence has been extensively demonstrated. The genetic aspects of the primary cardiomyopathies, mitral valve prolapse, arrhythmias and conduction disturbances, long QT syndromes and abnormalities of ventricular repolarization, cardiovascular malformations, coronary artery disease, essential hypertension and rheumatic fever were examined. In this section discussion will be confined to the inherited multisystem disorders involving the cardiovascular system that most frequently occur in clinical practice. Currently known cardiovascular findings in relationship to chromosomal aberrations, connective tissue disorders, metabolic and enzymatic disorders, neuromuscular disorders and other rarer syndromes will be reported.

Familial occurrence in cardiovascular diseases. Familial cardiovascular diseases (1).

Current knowledge and assumptions about inherited cardiovascular diseases are reported in this review. They are examined from two different points of view. In the first section (familial cardiovascular diseases) discussion will center on the main cardiovascular diseases that have a definite clinical and pathophysiological feature in which familial occurrence has been extensively demonstrated. The genetic aspects of the primary cardiomyopathies, mitral valve prolapse, arrhythmias and conduction disturbances, long QT syndromes and abnormalities of ventricular repolarization, cardiovascular malformations, coronary artery disease, essential hypertension and rheumatic fever will be examined. In the second section (cardiovascular involvement in genetic disorders) discussion will be confined to the inherited multisystem disorders involving the cardiovascular system that most frequently occur in clinical practice. Currently known cardiovascular findings in relationship to chromosomal aberrations, connective tissue disorders, metabolic and enzymatic disorders, neuromuscular disorders and other rarer syndromes will be reported.

Antimitochondrial autoantibodies in myocardial hypertrophy: comparison between hypertrophic cardiomyopathy, hypertensive heart disease, and athlete's heart.

Antimitochondrial autoantibodies (AMA) were tested by indirect immunofluorescence in three groups of subjects with different types of myocardial hypertrophy: 35 patients affected with hypertrophic cardiomyopathy (HC), 20 patients with cardiac hypertrophy secondary to essential hypertension, and 35 active endurance athletes with exercise-induced left ventricular hypertrophy. Forty-two healthy subjects served as a control group. Left ventricular hypertrophy was considered a left ventricular mass (LVM) echocardiographically calculated (Devereux formula), exceeding 244 gm or a LVM index exceeding 122 gm/m2 (greater than 2 SD from a previously studied normal population). AMA were found in 15 of 35 (43%) patients with HC and in 6 of 20 (30%) patients with hypertensive heart disease (p less than 0.01); in contrast, AMA were not present in the sera of athletes or in the sera of controls. Although the significance of AMA in subjects with pathologic myocardial hypertrophy has not yet been established, their absence in the sera of athletes strengthens the opinion that cellular changes, as a compensatory response of the myocardium to a work overload, have a physiologic fashion in these cases. Moreover, identification of AMA in the sera of athletes with disproportionate severe left ventricular hypertrophy of uncertain origin may be helpful to ensure a single diagnosis.

Clinical relevance of the electrocardiogram in relatives of patients with hypertrophic cardiomyopathy.

Eighty-nine first-degree relatives of 22 patients with an established diagnosis of hypertrophic cardiomyopathy underwent electrocardiographic and echocardiographic screening. Scalar electrocardiogram was abnormal in 30/89 (33.7%) relatives. Of these thirty, eleven had definite evidence of hypertrophic cardiomyopathy at echo; one had borderline hypertrophy and was considered neither affected nor unaffected; four had questionable signs of hypertrophy. The remaining 14 relatives had normal echo-cardiograms. Fifty-nine relatives (66.3%) had normal electrocardiograms; at echo 3 were considered to have borderline hypertrophy, 16 had questionable signs of hypertrophy and 40 were normal. In relatives of patients with hypertrophic cardiomyopathy an abnormal electrocardiogram may reflect different morphologic conditions: a real hypertrophic cardiomyopathy or a myocardial hypertrophy of uncertain significance. Furthermore, in these categories of subjects, an abnormal electrocardiogram with normal echo must be considered with caution.