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Adenosylcobalamin (Ado-[B.sub.12]) is both the cofactor and inducer of ethanolamine ammonia lyase (EA-lyase), a catabolic enzyme for ethanolamine. De novo synthesis of Ado-[B.sub.12] by Salmonella enterica occurs only under anaerobic conditions. Therefore, aerobic growth on ethanolamine requires import of Ado-[B.sub.12] or a precursor (CN-[B.sub.12] or OH-[B.sub.12]) that can be adenosylated internally. Several known enzymes adenosylate corrinoids. The CobA enzyme transfers adenosine from ATP to a biosynthetic intermediate in de novo [B.sub.12] synthesis and to imported CN-[B.sub.12], OH-[B.sub.12], or Cbi (a [B.sub.12] precursor). The PduO adenosyl transferase is encoded in an operon (pdu) for cobalamin-dependent propanediol degradation and is induced by propanediol. Evidence is presented here that a third transferase (EutT) is encoded within the operon for ethanolamine utilization (eut). Surprisingly, these three transferases share no apparent sequence similarity. CobA produces sufficient Ado-[B.sub.12] to initiate eut operon induction and to serve as a cofactor for EA-lyase when [B.sub.12] levels are high. Once the eut operon is induced, the EutT transferase supplies more Ado-[B.sub.12] during the period of high demand. Another protein encoded in the operon (EutA) protects EA-lyase from inhibition by CN-[B.sub.12] but does so without adenosylation of this corrinoid.

When excised inside-out membrane patches are bathed in symmetrical [Cl.sup.-]-rich solutions, the current-voltage (I-V) relationship of macroscopic cystic fibrosis transmembrane conductance regulator (CFTR) [Cl.sup.-] currents inwardly rectifies at large positive voltages. To investigate the mechanism of inward rectification, we studied CFTR [Cl.sup.-] channels in excised inside-out membrane patches from cells expressing wild-type human and murine CFTR using voltage-ramp and step protocols. Using a voltage-ramp protocol, the magnitude of human CFTR [Cl.sup.-] current at +100 mV was 74 [+ or -] 2% (n = 10) of that at -100 mV. This rectification of macroscopic CFTR [Cl.sup.-] current was reproduced in full by ensemble currents generated by averaging single-channel currents elicited by an identical voltage-ramp protocol. However, using a voltage-step protocol the single-channel current amplitude (i) of human CFTR at + 100 mV was 88 [+ or -] 2% (n = 10) of that at--100 mV. Based on these data, we hypothesized that voltage might alter the gating behavior of human CFTR. Using linear three-state kinetic schemes, we demonstrated that voltage has marked effects on channel gating. Membrane depolarization decreased both the duration of bursts and the interburst interval, but increased the duration of gaps within bursts. However, because the voltage dependencies of the different rate constants were in opposite directions, voltage was without large effect on the open probability ([P.sub.o]) of human CFTR. In contrast, the [P.sub.o] of murine CFTR was decreased markedly at positive voltages, suggesting that the rectification of murine CFTR is stronger than that of human CFTR. We conclude that inward rectification of CFTR is caused by a reduction in i and changes in gating kinetics. We suggest that inward rectification is an intrinsic property of the CFTR [Cl.sup.-] channel and not the result of pore block. KEY WORDS: ATP-binding cassette transporter * cystic fibrosis * chloride ion channel * channel gating * voltage dependence

Objective: Women are becoming more prevalent in clinical neuropsychology, but gender bias and disparities persist across multiple professional domains. This study examined potential gender disparities in historical authorship trends across commonly read journals in clinical neuropsychology. Method: Analyses were conducted on 10,531 articles published in six clinical neuropsychology journals from 1985 to 2019. Each author was coded as either a man or a woman using the OpenGenderTracking Project database. Results: On average, women comprised 43.3% (±30.6) of the authors listed in clinical neuropsychology article bylines and were lead and/or corresponding author on 50.3% of these papers. Findings varied by journal, with Child Neuropsychology having the best representation of women across several study metrics. Women comprised an increasing proportion of authors over time and the gender gap in clinical neuropsychology is smaller than was recently reported for the broader field of psychology; nevertheless, the recent rates of women as authors lag behind the prevalence of women in clinical neuropsychology. Encouragingly, gender was not associated with the number of times an article was cited. Articles that included women in leadership roles had significantly more authors overall and specifically more women authors. Conclusions: Women are under-represented as authors in clinical neuropsychology journals, but they are becoming more common and their papers are cited just as frequently as men. Efforts to increase women as research mentors and sponsors may help to further close the publishing gender gap in clinical neuropsychology. [ABSTRACT FROM AUTHOR]

Research describing an improved image restoration algorithm is presented. Using original and diffraction-limited image pairs test results show that the nonlinear algorithm produces super-resolution.

Dysfunction of the cystic fibrosis transmembrane conductance regulator (CFTR) C1- channel is associated with a wide spectrum of disease. In the search for modulators of CFTR, pharmacological agents that interact directly with the CFTR C1-channel have been identified. Some agents stimulate CFTR by interacting with the nucleotide-binding domains that control channel gating, whereas others inhibit CFTR by binding within the channel pore and preventing C1- permeation. Knowledge of the molecular pharmacology of CFTR might lead to new treatments for diseases caused by the dysfunction of CFTR.