Pascaart van de zee-custen van Ruslant, Laplant, Finmarcken, Spitsbergen en Nova-zemla - [Yleisnäkymä - Overview]

1 Amsterdam 1664

Nieuwe Kaart van het Koninkryk Zweden, na de laatste ondekkinge - [Yleiskuva - Overview]

Amsterdam : Isaak Trion 1734

Pas caart van de Oost zee verthoonende alle de ghelegentheyt tusschen't Eylandt Rugen en Wiborg - [Yleisnäkymä - Overview]

Amsterdam 1664

Pas caart van de Oost zee. Detalji.

Amsterdam 1664

Pas-kaart van Europa met een gedeelte van de kust van Africa tot aen Cabo verde - [Yleisnäkymä - Overview]

1 Amsterdam 1665

Nieuwe Paskaert voor een Gedeelte van de Oost Zee ... als mede de Kust van Oost Vinlandt - [Yleiskuva - Overview]

Amsterdam : Johannes van Keulen 1692

Havaintoja substantiivien muodostuksesta Henrik Florinuksen sanaston ensiesiintymissä 1678-1693

Summary: Some observations on substantive-formation in the language of Henrik Florinus from the period 1678-1693

Lack of GDAP1 induces neuronal calcium and mitochondrial defects in a knockout mouse model of charcot-marie-tooth neuropathy.

Mutations in GDAP1, which encodes protein located in the mitochondrial outer membrane, cause axonal recessive (AR-CMT2), axonal dominant (CMT2K) and demyelinating recessive (CMT4A) forms of Charcot-Marie-Tooth (CMT) neuropathy. Loss of function recessive mutations in GDAP1 are associated with decreased mitochondrial fission activity, while dominant mutations result in impairment of mitochondrial fusion with increased production of reactive oxygen species and susceptibility to apoptotic stimuli. GDAP1 silencing in vitro reduces Ca2+ inflow through store-operated Ca2+ entry (SOCE) upon mobilization of endoplasmic reticulum (ER) Ca2+, likely in association with an abnormal distribution of the mitochondrial network. To investigate the functional consequences of lack of GDAP1 in vivo, we generated a Gdap1 knockout mouse. The affected animals presented abnormal motor behavior starting at the age of 3 months. Electrophysiological and biochemical studies confirmed the axonal nature of the neuropathy whereas histopathological studies over time showed progressive loss of motor neurons (MNs) in the anterior horn of the spinal cord and defects in neuromuscular junctions. Analyses of cultured embryonic MNs and adult dorsal root ganglia neurons from affected animals demonstrated large and defective mitochondria, changes in the ER cisternae, reduced acetylation of cytoskeletal α-tubulin and increased autophagy vesicles. Importantly, MNs showed reduced cytosolic calcium and SOCE response. The development and characterization of the GDAP1 neuropathy mice model thus revealed that some of the pathophysiological changes present in axonal recessive form of the GDAP1-related CMT might be the consequence of changes in the mitochondrial network biology and mitochondria-endoplasmic reticulum interaction leading to abnormalities in calcium homeostasis.

New biogeographical and morphological information on Physaloptera ngoci Le-Van-Hoa, 1961 (Nematoda: Physalopteridae) in South-east Asian rodents

During a study of the helminth fauna of 1,643 rodents trapped along the Mekong River (Thailand, LaoPeople"s Democratic Republic and Cambodia) in 2008-2011, the spirurid nematode Physaloptera ngoci Le-Van-Hoa,1961 was recovered with an overall prevalence of 2.8%. Based on the original description, it was identified in nine of 23 different Murinae host species and is here reported for the first time from these three countries. A scanning electron microscopy study provides additional morphological data.