Analysis and measurement of a Zener diode voltage-reference

Output voltage sensitivity equations are derived for a zener voltage-reference circuit. The circuit consists of a DC-DC converter, a voltage-resistor current generator, and a zener diode. The performance of the voltage-reference is calculated using the sensitivity equations and compared to measurement data taken from a laboratory model of the circuit. The results are in reasonable agreement. It was concluded that with careful selection of components, two of three major sources of error can be predicted and controlled; these are changes due to input voltage and changes due to temperature. The third, changes due to time, requires calibration against a voltage standard --Abstract, page ii

Civil Justice Reform in the United States — Opportunity for Learning from \u27Civilized\u27 European Procedure Instead of Continued Isolation?

This article reports on present and past efforts at civil justice reform in the United States and assesses the opportunities for learning from Continental models. European jurists have long urged that their American colleagues consider using continental approaches in dealing with the serious problems that afflict the American system of civil justice. A few years back, our colleague Kötz noted that If there is a desire to reform American civil procedure, either by making changes within the adversary system or by developing alternative methods of dispute resolution, the Continental experience may be well worth studying

Civil Justice Reform in the United States — Opportunity for Learning from \u27Civilized\u27 European Procedure Instead of Continued Isolation?

This article reports on present and past efforts at civil justice reform in the United States and assesses the opportunities for learning from Continental models. European jurists have long urged that their American colleagues consider using continental approaches in dealing with the serious problems that afflict the American system of civil justice. A few years back, our colleague Kötz noted that If there is a desire to reform American civil procedure, either by making changes within the adversary system or by developing alternative methods of dispute resolution, the Continental experience may be well worth studying

Why Are U.S. Lawyers Not Learning from Comparative Law?

Address the problem of comparative law in the United States. Explains why comparative law matters. Gives reasons why U.S. lawyers are not learning from comparative law. These include lack of skills, lack of institutional supports, and legal structures that resist comparative law and an attitude that comparative law has little to teach

Autism-Associated Neuroligin-3 Mutations Commonly Impair Striatal Circuits to Boost Repetitive Behaviors

In humans, neuroligin-3 mutations are associated with autism, while in mice the corresponding mutations produce robust synaptic and behavioral changes. However, different neuroligin-3 mutations cause largely distinct phenotypes in mice, and no causal relationship links a specific synaptic dysfunction to a behavioral change. Using rotarod motor learning as a proxy for acquired repetitive behaviors in mice, we found that different neuroligin-3 mutations uniformly enhanced formation of repetitive motor routines. Surprisingly, neuroligin-3 mutations caused this phenotype not via changes in the cerebellum or dorsal striatum, but via a selective synaptic impairment in the nucleus accumbens/ventral striatum. Here, neuroligin-3 mutations increased rotarod learning by specifically impeding synaptic inhibition onto D1-dopamine receptor-expressing but not D2-dopamine receptor-expressing medium spiny neurons. Our data thus suggest that different autism-associated neuroligin-3 mutations cause a common increase in acquired repetitive behaviors by impairing a specific striatal synapse, and thereby provide a plausible circuit substrate for autism pathophysiology

Autism-Associated Neuroligin-3 Mutations Commonly Impair Striatal Circuits to Boost Repetitive Behaviors

In humans, neuroligin-3 mutations are associated with autism, while in mice the corresponding mutations produce robust synaptic and behavioral changes. However, different neuroligin-3 mutations cause largely distinct phenotypes in mice, and no causal relationship links a specific synaptic dysfunction to a behavioral change. Using rotarod motor learning as a proxy for acquired repetitive behaviors in mice, we found that different neuroligin-3 mutations uniformly enhanced formation of repetitive motor routines. Surprisingly, neuroligin-3 mutations caused this phenotype not via changes in the cerebellum or dorsal striatum, but via a selective synaptic impairment in the nucleus accumbens/ventral striatum. Here, neuroligin-3 mutations increased rotarod learning by specifically impeding synaptic inhibition onto D1-dopamine receptor-expressing but not D2-dopamine receptor-expressing medium spiny neurons. Our data thus suggest that different autism-associated neuroligin-3 mutations cause a common increase in acquired repetitive behaviors by impairing a specific striatal synapse, and thereby provide a plausible circuit substrate for autism pathophysiology

Ciliary Proteins Repurposed by the Synaptic Ribbon: Trafficking Myristoylated Proteins at Rod Photoreceptor Synapses

The Unc119 protein mediates transport of myristoylated proteins to the photoreceptor outer segment, a specialized primary cilium. This transport activity is regulated by the GTPase Arl3 as well as by Arl13b and Rp2 that control Arl3 activation/inactivation. Interestingly, Unc119 is also enriched in photoreceptor synapses and can bind to RIBEYE, the main component of synaptic ribbons. In the present study, we analyzed whether the known regulatory proteins, that control the Unc119- dependent myristoylated protein transport at the primary cilium, are also present at the photoreceptor synaptic ribbon complex by using high-resolution immunofluorescence and immunogold electron microscopy. We found Arl3 and Arl13b to be enriched at the synaptic ribbon whereas Rp2 was predominantly found on vesicles distributed within the entire terminal. These findings indicate that the synaptic ribbon could be involved in the discharge of Unc119-bound lipid-modified proteins. In agreement with this hypothesis, we found Nphp3 (Nephrocystin-3), a myristoylated, Unc119- dependent cargo protein enriched at the basal portion of the ribbon in close vicinity to the active zone. Mutations in Nphp3 are known to be associated with Senior–Løken Syndrome 3 (SLS3). Visual impairment and blindness in SLS3 might thus not only result from ciliary dysfunctions but also from malfunctions of the photoreceptor synapse

Air-stable Solid-state Photoluminescence Standards for Quantitative Measurements Based on 4'-phenyl-2,2':6',2''-Terpyridine Complexes with Trivalent Lanthanides

Correct photoluminescence quantum yield (PLQY) determination in the solid state is vital for numerous application fields, such as photovoltaics, solid lighting or the development of phosphors. In order to increase the limited number of suitable standards for such determinations, two new Ln 3+ -based complexes with 4′-phenyl-2,2′ : 6′,2"-terpyridine γ-[Ln 4 (OAc) 12 (ptpy) 2 ] ( 1-Eu with europium and 1-Tb with terbium) are presented. The corresponding complexes show solid-state QYs of 58(4) % and 46(3) %, respectively, exhibiting broadband absorption in the UV range from 380-200 nm. As Ln 3+ ions in general exhibit narrow f - f transitions, spectral regions with a broadness of 20-35 nm can be checked. Both complexes have suitable thermal stability, up to 270 °C, and are stable with respect to air and humidity, for 1-Eu up to 75 % and for 1-Tb up to 53 % relative humidity. These complexes are altogether suitable as standards to increase the reliability of PLQY determination and proposed to be used for a relative PLQY determination in the solid stat

The synaptic ribbon is critical for sound encoding at high rates and with temporal precision.

We studied the role of the synaptic ribbon for sound encoding at the synapses between inner hair cells (IHCs) and spiral ganglion neurons (SGNs) in mice lacking RIBEYE (RBEKO/KO). Electron and immunofluorescence microscopy revealed a lack of synaptic ribbons and an assembly of several small active zones (AZs) at each synaptic contact. Spontaneous and sound-evoked firing rates of SGNs and their compound action potential were reduced, indicating impaired transmission at ribbonless IHC-SGN synapses. The temporal precision of sound encoding was impaired and the recovery of SGN-firing from adaptation indicated slowed synaptic vesicle (SV) replenishment. Activation of Ca2+-channels was shifted to more depolarized potentials and exocytosis was reduced for weak depolarizations. Presynaptic Ca2+-signals showed a broader spread, compatible with the altered Ca2+-channel clustering observed by super-resolution immunofluorescence microscopy. We postulate that RIBEYE disruption is partially compensated by multi-AZ organization. The remaining synaptic deficit indicates ribbon function in SV-replenishment and Ca2+-channel regulation