Antti J Metso's research while affiliated with Helsinki University Central Hospital and other places

... The average stroke survival time is 6 to 7 years with many patients enduring physical disability and late cognitive impairment [3][4][5]. Neurological outcomes after stroke depend on numerous factors including age, infarct size and location, genetic factors, as well as the degree of brain repair [6][7][8][9]. Poststroke brain repair involves many events including reestablishing blood-brain barrier (BBB) structure and function [9][10][11][12]. ...

... accessed on 19 February 2022). This duplication was associated with an increased risk of aortic dissection [20] and cervical artery dissection [21] by previous studies. The CNV in patient 2 is absent from dbVar and is therefore considered extremely rare. ...

... The mean patient age studied ranged from 61.4 to 77.8 years (Table 1). LOS, mRS, and mortality were the three outcome measurements most consistently measured across the studies included in this review [7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23]. Anemia was defined using one of four parameters (Table 1). ...

... Using PEGylated liposomal doxorubicin (Caelyx), Keller et al. [427] compared the effi cacy of the liposomal formulation with that of a common regimen in patients with taxane -refractory advanced breast cancer. The regimen scheme was Caelyx (50 mg/m 2 every 28 weeks) or vinorelbine (30 mg/m 2 ) or mitomycin C (10 mg/m 2 every 28 days) plus vinblastine (5 mg/m 2 at days 1,14,28,42). Finally, progression free survival and overall survival were similar for Caelyx and the comparative regimen. ...

... Although underlying collagen vascular disorders that meet diagnostic and genetic criteria is uncommonly found in CeADs (1-5% of spontaneous CeADs), isolated mild connective tissue abnormalities in skeletal, ocular, and skin systems (ie, joint hypermobility or multiple dislocations, easy bruising, poor wound healing or easy bruising) are frequently observed in patients with spontaneous CeAD (50-96%) [23][24][25] Patients with subclinically increased vascular tortuosity or enlarged aortic root diameter are also more prone to have CeAD. 26,27 Hence, most cases of so-called spontaneous CeAD likely occur in the setting of systemic yet poorly defined mild connective tissue disorders. ...

... Nonetheless, gene variants that increase the risk of CeAD follow a similar theme to those of aortic dissection and SCAD, including associations with TGF-β signaling, ECM and cytoskeletal protein genes, and metabolism associated genes. Variants in TGFBR2 (230,231), dual specificity protein phosphatase 22 (DUSP22), (232), LRP1 and PHACTR1 have all been associated with an increased risk of CeAD (233). Variants in ECM protein genes associated with CeAD include those for COL3A1, COL4A1, and COL5A2 and FBN1 (230,232,234,235). ...

... Grond-Ginsbach et al. analyzed the peripheral leukocyte count (white blood cell count; WBC) in a large group of patients (N = 172) with acute SCAD from the Cervical Artery Dissection and Ischemic Stroke Patients study (26). Further, this study also included 348 patients with non-CAD ischaemic stroke and 223 age-and sex-matched healthy controls. ...

... A clinically important fact is that dissections occur simultaneously in multiple brain-supplying arteries in approximately 15% of cases. There can be bilateral dissection of the vertebral arteries or of the internal carotid arteries, or simultaneous dissection of a vertebral artery and an internal carotid artery (19). ...

... Dissection is defined as the separation of arterial wall structural elements that will further form an intramural hematoma in the affected area [12]. It would cause narrowing of the arterial lumen, decreased blood flow, increased chance of embolism formation, and consequently non-ischemic local symptoms [12,13]. Cervicocerebral artery dissection can occur as an extracranial (cervical) or intracranial condition [12]. ...

... Familial occurrence of CeAD is rare (i.e.<1%). 11,28,29 Hence, the presented sample of nine affected duos with familial CeAD, all white Caucasians from Germany or from the German speaking part of Switzerland, provided a unique material for a genetic analysis. The analysis of a large group of unrelated subjects for the ExAC database for comparison was a further strength of this study. ...