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We wanted to ask whether the rhythmic pattern of shoot elongation should be taken into account for the micropropagation ofCitrus aurantiumL. and whetherin vitroculture altered the rhythmic properties. It has been established in the present work that (1) where and when the axillary buds are excised with respect to the elongation cycle are of importance to optimize micropropagation and (2) the infradian rhythmic growth pattern of micropropagated plants is maintained with a period of 45.8d not significantly different from that of plants derived from seeds (42.4d). [ABSTRACT FROM AUTHOR]

A multicentre controlled trial was carried out to determine the optimal dosage of a 2/1 combination of captopril plus hydrochlorothiazide (HCTZ) in mild hypertension at three doses against placebo in a 6 week double-blind trial. The number of patients was 111:27 received placebo; 26 were treated with captopril 25 mg plus HCTZ 12.5 mg (25/12.5); 25 with captopril 50 mg plus HCTZ 25 mg (50/25); and 33 with captopril 100 mg plus HCTZ 50 mg (100/50). A significant fall in blood pressure was seen in all four groups, but was greater with the active treatments. The percentage of patients who were normalized [diastolic blood pressure (DBP) less than or equal to 90 mm Hg] or good responders (10% fall in DBP) increased as a function of the dose. At Day 21, the antihypertensive effect of 50/25 was similar to that of 100/50, but greater than that of captopril 25-HCTZ 12.5. At Day 42, the antihypertensive effects of the three doses were similar. Tolerance data showed a higher incidence of side-effects with 100/50 than with the other dosages. Thus, 50/25 appeared to be the optimal dosage for the control of mild hypertension. [ABSTRACT FROM AUTHOR]

Pharmacological, genetic and expression studies implicate N-methyl-D-aspartate (NMDA) receptor hypofunction in schizophrenia (SCZ). Similarly, several lines of evidence suggest that autism spectrum disorders (ASD) could be due to an imbalance between excitatory and inhibitory neurotransmission. As part of a project aimed at exploring rare and/or de novo mutations in neurodevelopmental disorders, we have sequenced the seven genes encoding for NMDA receptor subunits (NMDARs) in a large cohort of individuals affected with SCZ or ASD (n=429 and 428, respectively), parents of these subjects and controls (n=568). Here, we identified two de novo mutations in patients with sporadic SCZ in GRIN2A and one de novo mutation in GRIN2B in a patient with ASD. Truncating mutations in GRIN2C, GRIN3A and GRIN3B were identified in both subjects and controls, but no truncating mutations were found in the GRIN1, GRIN2A, GRIN2B and GRIN2D genes, both in patients and controls, suggesting that these subunits are critical for neurodevelopment. The present results support the hypothesis that rare de novo mutations in GRIN2A or GRIN2B can be associated with cases of sporadic SCZ or ASD, just as it has recently been described for the related neurodevelopmental disease intellectual disability. The influence of genetic variants appears different, depending on NMDAR subunits. Functional compensation could occur to counteract the loss of one allele in GRIN2C and GRIN3 family genes, whereas GRIN1, GRIN2A, GRIN2B and GRIN2D appear instrumental to normal brain development and function.

Nowadays, there is a huge contrast between the scarcity of French-speaking publications concerning early-onset obsessive compulsive disorder and the prevalence of this illness according to the most recent publications. We present herein the epidemiological and clinical results of a vast national survey called “ABC-TOC” from which we extracted the complete data emanating from 36 children and adolescent aged from 6 to 15 years old.This study reveals that obsessive compulsive disorder in this age group is characterised by the plurality of many obsessions and concomitant compulsions whose evolution remains unstable and fluctuating, and is often marked by irritability and conduct disorders in the foreground. Moreover, there is an outstanding comorbid pathology: bipolar disorder (17.4% of the patients) preceded by a cyclothymic temperament, which is strongly related to a high suicidal risk: more than one third of the subjects of this study had suicidal ideations and 3 of them (9.7%) have attempted suicide several times since the OCD onset. [ABSTRACT FROM AUTHOR]

Aim: The aim of this paper is to describe the clinical features of COVID‐19‐related encephalopathy and their metabolic correlates using brain 2‐desoxy‐2‐fluoro‐D‐glucose (FDG)‐positron‐emission tomography (PET)/computed tomography (CT) imaging. Background and purpose: A variety of neurological manifestations have been reported in association with COVID‐19. COVID‐19‐related encephalopathy has seldom been reported and studied. Methods: We report four cases of COVID‐19‐related encephalopathy. The diagnosis was made in patients with confirmed COVID‐19 who presented with new‐onset cognitive disturbances, central focal neurological signs, or seizures. All patients underwent cognitive screening, brain magnetic resonance imaging (MRI), lumbar puncture, and brain 2‐desoxy‐2‐fluoro‐D‐glucose (FDG)‐positron‐emission tomography (PET)/computed tomography (CT) (FDG‐PET/CT). Results: The four patients were aged 60 years or older, and presented with various degrees of cognitive impairment, with predominant frontal lobe impairment. Two patients presented with cerebellar syndrome, one patient had myoclonus, one had psychiatric manifestations, and one had status epilepticus. The delay between first COVID‐19 symptoms and onset of neurological symptoms was between 0 and 12 days. None of the patients had MRI features of encephalitis nor significant cerebrospinal fluid (CSF) abnormalities. SARS‐CoV‐2 RT‐PCR in the CSF was negative for all patients. All patients presented with a consistent brain FDG‐PET/CT pattern of abnormalities, namely frontal hypometabolism and cerebellar hypermetabolism. All patients improved after immunotherapy. Conclusions: Despite varied clinical presentations, all patients presented with a consistent FDG‐PET pattern, which may reflect an immune mechanism. [ABSTRACT FROM AUTHOR]

Background Patients with schizophrenia display significant working memory and executive deficits. In patients with obsessive-compulsive disorder (OCD), several studies suggest that working memory dysfunction may be one of the causes of compulsive checking behaviors. Hence, this study aimed at assessing whether patients with schizophrenia were impaired on an image comparison task used to measure checking behaviors, and whether the origin and profile of impairment on this task was different between schizophrenia and OCD. Methods Eye movement recordings were used to assess the checking behavior of 24 patients with schizophrenia and 24 control participants who had to decide whether two images were different or identical. The verbal and visuo-spatial components of participants’ working memory were measured using the reading span and backward location span tests. Results Compared to controls, patients with schizophrenia had reduced working memory spans and showed excessive checking behavior when comparing the two images. However, the intensity of their checking behavior was not significantly related to their working memory deficits. Conclusions Several recent studies demonstrated that the excessive checking behaviors displayed by patients with OCD were related to working memory dysfunction. The absence of a relationship between the excessive checking behavior of patients with schizophrenia and their working memory deficits suggests that checking behaviors do not have the same origin in the two disorders. [ABSTRACT FROM AUTHOR]

Schizophrenia is a chronic illness with a progressive course that can be marked by resistance to antipsychotic treatment. This can make therapeutic support challenging for the practitioner, with results that are partial and unsatisfactory. In the literature, treatment with high-dose olanzapine (> 20 mg/day) appears to be a good alternative to clozapine, the gold standard for treatment-resistant schizophrenia. In the present observational prospective study, we studied the clinical and biological profiles of patients treated with olanzapine doses up to 100 mg/day. In total, 50 patients were clinically and biologically assessed. We found a linear relationship between oral dose and serum concentration (Pearson's r = 0.83, p < 0.001) with effects of tobacco (p < 0.05) and of coffee and tea consumption (p < 0.01). Tolerance seemed to be good regardless of dose. No link was found between concentration and efficiency. Despite a nonexhaustive assessment of pharmacokinetic parameters, not least pharmacogenetic data (e.g., genotyping of cytochrome P450-1A2 or glycoprotein P Abcb1a), pharmacokinetic aspects alone cannot account for why the disease may sometimes be resistant to 20 mg of olanzapine but respond to higher doses. A nuclear imaging study exploring brain occupancy by high-dose olanzapine, coupled with the abovementioned pharmacokinetic assessment, may prove a relevant experimental paradigm for studying the pathophysiological mechanisms of resistant schizophrenia. [ABSTRACT FROM AUTHOR]