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Sea urchins play a key role in the marine environment, contributing to maintain a balance in benthic ecosystems. Toxopneustes roseus acts as a regulator of rhodolith beds and is a key species as a bioturbation promoter, while Rhyncholampas pacificus moderates the detritus content of sediment through various mechanisms and contributes to accelerating the circulation of organic matter. However, nothing is known about their early development, so the objective of this research is to characterize the embryonic and larval development of specimens of the two species from the southern Mexican Pacific and identify the causes that produce their differences. The embryonic development of T. roseus lasted approximately 20 ​h; the echinopluteus larva appeared at 23 ​h and culminated in around 12 days with an eight-armed larva. Metamorphosis was reached at 18 days. The embryonic development of R. pacificus lasted about 15 ​h; the larva emerged at 20 ​h and culminated in about two days with an eight-armed larva. The metamorphosis was completed in 9 days. The reproductive output of both species determines their development time and the structure of their larvae; therefore, the energy of R. pacificus is invested in reaching metamorphosis earlier to ensure that its larvae, which are not very abundant, settle and recruit to the population. Regarding T. roseus, the longest permanence in the plankton is efficiently maintained by its numerous larvae through the presence of mobile arms and the shift of the swimming function to the epauletes. This is the first work that characterizes the early development of a species of the genus Toxopneustes and of the only living species of the genus Ryncholampas. The information generated in this work is essential to gaining knowledge about these groups of echinoids, especially the effect of the environment on their early development., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Flunixin meglumine is a nonsteroidal anti-inflammatory drug (NSAID) widely used in veterinary medicine. It is indicated to treat inflammatory processes, pain, and pyrexia in farm animals. In addition, it is one of the few NSAIDs approved for use in dairy cows, and consequently gives rise to concern regarding its milk residues. The ABCG2 efflux transporter is induced during lactation in the mammary gland and plays an important role in the secretion of different compounds into milk. Previous reports have demonstrated that bovine ABCG2 Y581S polymorphism increases fluoroquinolone levels in cow milk. However, the implication of this transporter in the secretion into milk of anti-inflammatory drugs has not yet been studied. The objective of this work was to study the role of ABCG2 in the secretion into milk of flunixin and its main metabolite, 5-hydroxyflunixin, using Abcg2 (-/-) mice, and to investigate the implication of the Y581S polymorphism in the secretion of these compounds into cow milk. Correlation with the in vitro situation was assessed by in vitro transport assays using Madin-Darby canine kidney II cells overexpressing murine and the two variants of the bovine transporter. Our results show that flunixin and 5-hydroxyflunixin are transported by ABCG2 and that this protein is responsible for their secretion into milk. Moreover, the Y581S polymorphism increases flunixin concentration into cow milk, but it does not affect milk secretion of 5-hydroxyflunixin. This result correlates with the differences in the in vitro transport of flunixin between the two bovine variants. These findings are relevant to the therapeutics of anti-inflammatory drugs., (Copyright © 2019 by The American Society for Pharmacology and Experimental Therapeutics.)

Targeted cognitive training (TCT) of auditory processing enhances higher-order cognition in schizophrenia patients. TCT performance gains can be detected after 1 training session. As a prelude to a potential clinical trial, we assessed a pharmacological augmentation of cognitive therapy (PACT) strategy by testing if the psychostimulant, amphetamine, augments TCT gains in auditory processing speed (APS) in schizophrenia patients and healthy subjects (HS). HS and schizophrenia patients were tested in a screening session (test 1), followed by a double-blind crossover design (tests 2-3), comparing placebo vs amphetamine (10 mg; 7 d between tests). On each test day, 1 hour of Posit Science "Sound Sweeps" training was bracketed by 2- to 4-minute pre- and post-training assessments of APS. Training consisted of a speeded auditory time-order judgment task of successive frequency modulation sweeps. Auditory system "learning" (APS post- vs pre-training) was enhanced by amphetamine (main effect of drug: P < .002; patients: d = 0.56, P < .02; HS: d = 0.39, nonsignificant), and this learning was sustained for at least 1 week. Exploratory analyses assessed potential biomarker predictors of sensitivity to these effects of amphetamine. Amphetamine enhances auditory discrimination learning in schizophrenia patients. We do not know whether gains in APS observed in patients after 1 hour of TCT predict clinical benefits after a full course of TCT. If amphetamine can enhance the therapeutic effects of TCT, this would provide strong support for a "PACT" treatment paradigm for schizophrenia., (© The Author 2016. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oup.com.)

The study characterizes the interaction between BCRP/ABCG2 and moxidectin by means of cellular transport, and pharmacokinetic studies in Bcrp1 (-/-) and wild-type mice. Milbemycin moxidectin ([(3)H]-moxidectin) was tested for its ability to be transported across MCDK-II epithelial monolayer cultures transfected with BCRP. In a second approach, accumulation assays by BCRP-expressing Xenopus laevis oocytes were carried out. Finally, pharmacokinetic studies were performed in order to establish the role of the transporter in milk secretion and tissue distribution. The efflux was negligible in polarized cells but moxidectin was efficiently transported in BCRP-expressing X. laevis oocytes. The transport was blocked by an acridone derivative, a novel BCRP inhibitor. Moxidectin secretion into breast milk was decreased in Bcrp1-knockout mice and the milk to plasma ratio was 2-fold higher in wild-type mice after i.v. administration. Drug accumulation in intestinal content, bile, and intestine was higher in wild-type mice but the plasma concentration was not different. Moxidectin is identified as a BCRP substrate since its Bcrp1-mediated secretion into breast milk and the involvement of Bcrp1 in intestinal and bile secretion has been demonstrated. This interaction has pharmacokinetic and toxicological consequences. The most important toxicological consequences of the interaction between BCRP and moxidectin may be related with the presence of drug residues in milk.

Enzymatic activity was analyzed in the soleus, gastrocnemius (red and white) and plantaris muscles of acutely exercised rats after long-term administration of Panax ginseng extract in order to evaluate the protective role of ginseng against skeletal muscle oxidation. Ginseng extract (3, 10, 100, or 500 mg/kg) was administered orally for three months to male Wistar rats weighing 200 +/- 50 g before exercise and to non-exercised rats (N = 8/group). The results showed a membrane stabilizing capacity of the extract since mitochondrial function measured on the basis of citrate synthase and 3-hydroxyacyl-CoA dehydrogenase activities was reduced, on average, by 20% (P < 0.05) after exercise but the activities remained unchanged in animals treated with a ginseng dose of 100 mg/kg. Glutathione status did not show significant changes after exercise or treatment. Lipid peroxidation, measured on the basis of malondialdehyde levels, was significantly higher in all muscles after exercise, and again was reduced by about 74% (P < 0.05) by the use of ginseng extract. The administration of ginseng extract was able to protect muscle from exercise-induced oxidative stress irrespective of fiber type.

Retinitis pigmentosa (RP) is a degenerative disorder affecting the outer segment of the retina and leading to night blindness and progressive visual field loss. The rhodopsin gene encodes a photolabile pigment located in the rod outer segments constituting around 80-90% of its protein content and is the initiation point for the visual cascade upon absorption of a single photon. Seventy-five unrelated, isolated RP families in the Basque Country, with at least one affected member, were diagnosed at our hospital after ophthalmic examination and electroretinogram analysis. The patients received genetic counselling according to their individual case based on their clinical diagnosis. The modes of inheritance found from pedigree studies were the following: 20% (15/75) were classified as autosomal dominant retinitis pigmentosa (ADRP), 17.33% (13/75) were autosomal recessive (ARRP), 2.66% (2/75) were unclassified (NC), and 60% (45/75) were sporadic cases (SCRP). From these families, 75 unrelated and affected index cases together with 22 affected relatives and 42 unaffected relatives were screened for mutations in the rhodopsin gene by GC clamped denaturing gradient gel electrophoresis. Our results showed that five ADRP, three ARRP, 15 SCRP, and one NC families had alterations in this gene. Only three of these alterations, that is 4% (3/75) (95% CL 0-8), appeared to be responsible for the disease. This represents a lower percentage than the 10% previously reported.