626 research outputs found
Marceli Januszewicz, syn Marcina. Sylwetka artysty z Wilnem w tle
No full textThis article is dedicated to the painter Marceli Januszewicz (1805 – after 1864) and his family. Having come to study in Vilnius from Podolia at a young age, he devoted many years to drawing the city\u27s monuments. His father Marcin Januszewicz (c. 1780 – after 1842) also studied at Vilnius University under Franciszek Smuglewicz and Jan Rustem; he was known as a talented copyist and picture restorer. The third artist in the family, Stanislaw (1834 – after 1864), son of Marceli, was born in Vilnius and was a talented draughtsman who copied his father\u27s works in his youth. Marceli Januszewicz\u27s life path, which led him to a school in the provincial town of Molodechno, which had a fatal impact on the artist\u27s fate, is discussed most extensively.
Biographies of the artists from the Januszewicz family have been supplemented with new data obtained in the archives, some facts or dates have been clarified and made more precise. An important discovery is that Martin Januszewicz\u27s real name was Marceli, which he used in his personal documents, while in university circles he was called Marcin. This fact is important for the interpretation of the source material.
The second part of the article is dedicated to a discussion of the works of Marceli Januszewicz the younger, questions of authorship and the presentation of newly attributed works to him. Watercolors from the series “Antiquities of the City of Vilnius" are discussed in the context of the artist\u27s relationship with Eustachy Tyszkiewicz. Summarizing the data from various sources, it can be concluded that although Januszewicz was not a member of the Archaeological Commission, he maintained close ties with the activities of the Museum of Antiquities.Artykuł poświęcony jest malarzowi Marcelemu Januszewiczowi (1805–po 1864) i jego rodzinie. Przyjechawszy na studia do Wilna z Podola w młodym wieku, wiele lat poświęcił na rysowanie zabytków miasta. Jego ojciec Marcin Januszewicz (ok 1780–po 1842) również studiował na Uniwersytecie Wileńskim u Franciszka Smuglewicza i Jana Rustema; znany był jako utalentowany kopista i konserwator obrazów. Trzeci artysta z rodziny – Stanisław (1834–po 1864), syn Marcela, urodził się w Wilnie, był utalentowanym rysownikiem, który w młodości kopiował prace ojca. Najobszerniej omówiona została droga życiowa Marcela Januszewicza, która doprowadziła go do szkoły w prowincjonalnym Mołodecznie, co miało fatalny wpływ na losy artysty.
Biografie twórców z rodziny Januszewiczów zostały uzupełnione o nowe dane pozyskane w archiwach, a niektóre fakty lub daty wyjaśniono i doprecyzowano. Istotnym odkryciem jest to, że prawdziwym imieniem Marcina Januszewicza było Marceli, którego używał w dokumentach osobistych, natomiast w środowisku uniwersyteckim nazywano go Marcinem. Fakt ten jest istotny dla interpretacji materiału źródłowego.
Druga część artykułu poświęcona jest omówieniu twórczości Marcela Januszewicza młodszego, kwestiom autorstwa oraz prezentacji nowo przypisanych mu dzieł. Akwarele z cyklu Starożytności miasta Wilna omawiane są w kontekście związków artysty z Eustachym Tyszkiewiczem. Podsumowując dane z różnych źródeł, można stwierdzić, że choć Januszewicz nie był członkiem Komisji Archeologicznej, miał bliskie związki z działalnością Muzeum Starożytności.
Marceli Januszewicz, syn Marcina. Sylwetka artysty z Wilnem w tle
No full textArtykuł poświęcony jest malarzowi Marcelemu Januszewiczowi (1805–po 1864) i jego rodzinie. Przyjechawszy na studia do Wilna z Podola w młodym wieku, wiele lat poświęcił na rysowanie zabytków miasta. Jego ojciec Marcin Januszewicz (ok 1780–po 1842) również studiował na Uniwersytecie Wileńskim u Franciszka Smuglewicza i Jana Rustema; znany był jako utalentowany kopista i konserwator obrazów. Trzeci artysta z rodziny – Stanisław (1834–po 1864), syn Marcela, urodził się w Wilnie, był utalentowanym rysownikiem, który w młodości kopiował prace ojca. Najobszerniej omówiona została droga życiowa Marcela Januszewicza, która doprowadziła go do szkoły w prowincjonalnym Mołodecznie, co miało fatalny wpływ na losy artysty.
Biografie twórców z rodziny Januszewiczów zostały uzupełnione o nowe dane pozyskane w archiwach, a niektóre fakty lub daty wyjaśniono i doprecyzowano. Istotnym odkryciem jest to, że prawdziwym imieniem Marcina Januszewicza było Marceli, którego używał w dokumentach osobistych, natomiast w środowisku uniwersyteckim nazywano go Marcinem. Fakt ten jest istotny dla interpretacji materiału źródłowego.
Druga część artykułu poświęcona jest omówieniu twórczości Marcela Januszewicza młodszego, kwestiom autorstwa oraz prezentacji nowo przypisanych mu dzieł. Akwarele z cyklu Starożytności miasta Wilna omawiane są w kontekście związków artysty z Eustachym Tyszkiewiczem. Podsumowując dane z różnych źródeł, można stwierdzić, że choć Januszewicz nie był członkiem Komisji Archeologicznej, miał bliskie związki z działalnością Muzeum Starożytności.
The genetic basis of pheochromocytoma
No full textUntil very recently, the majority of hereditary pheochromocytomas were related to the MEN 2 and the VHL. In rare instances, hereditary pheochromocytoma was reported in patients with NF1. In addition, nonsyndromic hereditary pheochromocytomas have been reported. Recently, three more genes (SDHD, SDHB, and SDHC) which are all related subunits of the mitochondrial complex II have been identified to cause susceptibility to pheochromocytoma and/or paraganglioma. Hence, mutation analysis of VHL, RET, SDHB, and SDHD is generally recommended in patients with pheochromocytoma regardless of their family history or other features suggestive for a hereditary form. Mutation analysis should start with VHL and RET. However, in the presence of extra-adrenal pheochromocytoma, it may be more useful to screen for VHL, SDHD and SDHB mutations. It is of interest that various different genes can lead to one type of tumor formation. A common pathway (i.e. oxygen sensing) has been shown for VHL and SDHX. However, although several genes that are involved in the pathogenesis of hereditary pheochromocytoma are known, the precise molecular steps in tumorigenesis are widely unknown. In addition, recent data in MEN 2 pheochromocytomas point to a 'second hit' mechanism as a trigger for tumor formation. The molecular pathogenesis of sporadic pheochromocytomas remains obscure [114]
Beta-blocker bashing and downgrading in hypertension management: a fashionable trend representing a matter of concern
No full textGenetic and clinical investigation of pheochromocytoma: a 22-year experience, from Freiburg, Germany to international effort.
No full textAlthough deceptively simple, the etio-pathogenesis of pheochromocytoma represents a clinical and molecular genetic investigative challenge. Here, we summarize, from a historical point of view, the 22-year-long studies initiated at the University of Freiburg, which developed from a local experience to a national and finally an international effort. All research activities are translational and clinical and hence, registry based and intended to improve the outcome of the patients, whether by improved detection, prevention, or treatment. Major clinical steps are the prospective study on hormone tests and imaging techniques for adrenal and extra-adrenal abdominal tumors as well as the concept of organ sparing and endoscopic tumor resection. Further, we introduced 18-fluoro-dopa positron emission tomography. Population-based registries were used in order to identify germline mutations in the susceptibility genes VHL, RET, SDHB, and SDHD in non-syndromic pheochromocytoma. We differentiated distinct clinical features of paraganglioma syndromes associated with SDHB and SDHD gene mutations. Finally, we identified predictors and prevalence of paraganglioma syndromes associated with mutations of the SDHC gene
Malignant Hypertension:A Systemic Cardiovascular Disease: JACC Review Topic of the Week.
No full textMalignant hypertension (MHT) is a hypertensive emergency with excessive blood pressure (BP) elevation and accelerated disease progression. MHT is characterized by acute microvascular damage and autoregulation failure affecting the retina, brain, heart, kidney, and vascular tree. BP must be lowered within hours to mitigate patient risk. Both absolute BP levels and the pace of BP rise determine risk of target-organ damage. Nonadherence to the antihypertensive regimen remains the most common cause for MHT, although antiangiogenic and immunosuppressant therapy can also trigger hypertensive emergencies. Depending on the clinical presentation, parenteral or oral therapy can be used to initiate BP lowering. Evidence-based outcome data are spotty or lacking in MHT. With effective treatment, the prognosis for MHT has improved; however, patients remain at high risk of adverse cardiovascular and kidney outcomes. In this review, we summarize current viewpoints on the epidemiology, pathogenesis, and management of MHT; highlight research gaps; and propose strategies to improve outcomes
Computational assessment of fibromuscular dysplasia-related renal artery stenosis
No full textBackground: Fibromuscular dysplasia (FMD) is a potentially curable cause of renovascular hypertension, primarily affecting middle-aged women. Percutaneous angioplasty is the recommended treatment for patients with hemodynamically significant renal artery stenosis (RAS). However, no established non-invasive method currently exists to estimate the pressure drop across stenosis and assess its hemodynamic impact. This study aimed to assess the clinical applicability of an image-based computational fluid dynamic (CFD) pipeline, functioning as a digital twin of the renal vasculature, for non-invasive assessment of fractional flow reserve (FFR) and trans-stenotic pressure drop in patients with FMD-related RAS. Methods: This retrospective study included 10 middle-aged women: six with FMD-related stenosis (two focal and four multifocal), two with atherosclerotic RAS and two healthy volunteers. For each subject, a patient-specific 3D surface model of the renal vasculature was reconstructed from medical images and CFD simulations were performed using Simvascular. FFR and trans-stenotic pressure drop were assessed across each renal artery. Results: The imaged-based CFD pipeline was feasible for all 10 subjects. A wide range of FFR (0.57 – >0.95) and pressure drops (11–73 mmHg) was observed across subjects, depending on the phenotype and severity of stenosis. The computed pressure drops and FFR values were consistent with the clinical decision on revascularization (AUC = 0.988), supporting the diagnostic relevance of the model. Conclusion: The proposed pipeline represents a promising non-invasive approach to assess the hemodynamic significance of RAS due to FMD. As a digital twin for personalized cardiovascular medicine, it could serve as valuable tool for selecting patients requiring angioplasty and predicting revascularization outcomes
Cardiac Phenotypes in Secondary Hypertension: JACC State-of-the-Art Review
No full textSeveral forms of secondary hypertension carry a high risk of cardiac morbidity and mortality. Evaluation of cardiac phenotypes in secondary hypertension provides a unique opportunity to study underlying hormonal and biochemical mechanisms affecting the heart. We review the characteristics of cardiac dysfunction in different forms of secondary hypertension and clarify the mechanisms behind the higher prevalence of heart damage in these patients than in those with primary hypertension. Attention to the specific clinical/biochemical phenotypes of these conditions may assist clinicians to screen for and confirm secondary forms of hypertension. Thereby, early signs of heart damage can be recognized and monitored, allowing individualized treatment to delay or prevent evolution toward more advanced disease
Subtype diagnosis, treatment, complications and outcomes of primary aldosteronism and future direction of research: a position statement and consensus of the Working Group on Endocrine Hypertension of the European Society of Hypertension
No full text: Primary aldosteronism is a frequent cause of secondary hypertension requiring a specific pharmacological treatment with mineralocorticoid receptor antagonist or with unilateral adrenalectomy. These treatments have shown to reduce the excess of cardiovascular risk characteristically associated with this disease. In part I of this consensus, we discussed the procedures for the diagnosis of primary aldosteronism. In the present part II, we address the strategies for the differential diagnosis of primary aldosteronism subtypes and therapy. We also discuss the evaluation of outcomes and provide suggestions for follow-up as well as cardiovascular and metabolic complications specifically associated with primary aldosteronism. Finally, we analyse the principal gaps of knowledge and future challenges for research in this field
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