A NEW SUBSPECIES OF RATTUS BARTELS'U (JENTINK) FROM CENTRAL JAVA.

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A NEW RAT FROM JAVA.

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SYSTEMATISCHE UBERSICHT DER BISHER VON JAVA NACHGEWIESENEN VOGEL.

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EINIGE BEMERKU,NGEN UEBER DIE DIFFERENZIERUNG DES RASSENKREISES ALCEDO EURYZON A TEMMINCK.

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EINE NEUE RASSE VON ARBOROPHILA BRUNNEOPECTUS AUS JAVA

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ZUR KENNTNIS DER VERBREITUNG UND ·DER LEBENSWEISE JA VANISCHER SAUGETIERE

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Odderon in baryon-baryon scattering from the AdS/CFT correspondence

Based on the AdS/CFT correspondence, we present a holographic description of various C-odd exchanges in high energy baryon-baryon and baryon-antibaryon scattering, and calculate their respective contributions to the difference in the total cross sections. We predict that, due to the warp factor of AdS_5, the total cross section in pp collisions is larger than in p\bar{p} collisions at asymptotically high energies.Comment: 23 pages, v2: minor changes, to be published in JHE

Effects of Excess Brain-Derived Human α-Synuclein on Synaptic Vesicle Trafficking

α-Synuclein is a presynaptic protein that regulates synaptic vesicle trafficking under physiological conditions. However, in several neurodegenerative diseases, including Parkinson’s disease, dementia with Lewy bodies, and multiple system atrophy, α-synuclein accumulates throughout the neuron, including at synapses, leading to altered synaptic function, neurotoxicity, and motor, cognitive, and autonomic dysfunction. Neurons typically contain both monomeric and multimeric forms of α-synuclein, and it is generally accepted that disrupting the balance between them promotes aggregation and neurotoxicity. However, it remains unclear how distinct molecular species of α-synuclein affect synapses where α-synuclein is normally expressed. Using the lamprey reticulospinal synapse model, we previously showed that acute introduction of excess recombinant monomeric or dimeric α-synuclein impaired distinct stages of clathrin-mediated synaptic vesicle endocytosis, leading to a loss of synaptic vesicles. Here, we expand this knowledge by investigating the effects of native, physiological α-synuclein isolated from the brain of a neuropathologically normal human subject, which comprised predominantly helically folded multimeric α-synuclein with a minor component of monomeric α-synuclein. After acute introduction of excess brain-derived human α-synuclein, there was a moderate reduction in the synaptic vesicle cluster and an increase in the number of large, atypical vesicles called “cisternae.” In addition, brain-derived α-synuclein increased synaptic vesicle and cisternae sizes and induced atypical fusion/fission events at the active zone. In contrast to monomeric or dimeric α-synuclein, the brain-derived multimeric α-synuclein did not appear to alter clathrin-mediated synaptic vesicle endocytosis. Taken together, these data suggest that excess brain-derived human α-synuclein impairs intracellular vesicle trafficking and further corroborate the idea that different molecular species of α-synuclein produce distinct trafficking defects at synapses. These findings provide insights into the mechanisms by which excess α-synuclein contributes to synaptic deficits and disease phenotypes

E NEUE ENTE AUS JAVA

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Risk factors for ulnar nerve compression at the elbow: a case control study

Background. Ulnar nerve compression at the elbow is frequently encountered as the second most common compression neuropathy in the arm. As dexterity may be severely affected, the disease entity can seriously interfere with daily life and work. However, epidemiological research considering the risk factors is rarely performed