Infections during gestation and the consequent maternal immune activation (MIA) increase the risk of developing neuropsychiatric disorders in infants and throughout life, including autism spectrum disorders (ASD). ASD is a neurodevelopmental disorder that affects three times more males than females and is mainly characterized by deficits in social communication and restricted interests. Consistent findings also indicate that ASD patients suffer from movement disorders, although these symptoms are not yet considered as diagnosis criteria. Here we used the double-stranded RNA analog polyinosinic:polycytidylic acid (poly I:C) MIA animal model of ASD in mice and explored its effects in males and females on social and motor behavior. We then investigated brain areas implicated in controlling and coordinating movements, namely the nigro-striatal pathway, motor cortex and cerebellum. We show that male mice are more affected by this treatment than females as they show reduced social interactions as well as motor development and coordination deficits. Reduced numbers of Purkinje cells in the cerebellum was found more widespread and within distinct lobules in males than in females. Moreover, a reduced number of neurons was found in the motor cortex of males only. These results suggest that females are better protected against developmental insults leading to ASD symptoms in mice. They also point to brain areas that may be targeted to better manage social and motor consequences of ASD.

We have previously shown that environmental enrichment decreases the activating and rewarding effects of the psychostimulant cocaine and increases resistance to the neurotoxic effect of the Parkinson-inducing drug MPTP. These effects were accompanied by an increase in the striatal expression of the neurotrophin BDNF, an increase in the striatal levels of delta-Fos B and by a decrease in striatal levels of the dopamine transporter, the main molecular target for cocaine and MPTP. Here, we used cDNA arrays to investigate the effects of rearing mice in enriched environments from weaning to adulthood on the profile of expression of genes in the striatum focusing on genes involved in intracellular signalling and functioning. We found that mice reared in an enriched environment show several alterations in the levels of mRNA coding for proteins involved in cell proliferation, cell differentiation, signal transduction, transcription and translation, cell structure and metabolism. Several of these findings were further confirmed by real-time quantitative PCR and, in the case of protein kinase C lambda, also by western blot. These findings are the first description of alterations in striatal gene expression by an enriched environment. The striatal gene expression regulation by environment that we report here may play a role in the resistance to the effects of drugs of abuse and dopaminergic neurotoxins previously reported.

Maxillofacial trauma (MFT) is a serious health problem and in Saudi Arabia is mainly caused by road traffic accidents (RTAs). MFT commonly associated with injuries to the face, head, and jaws and may cause soft tissue lacerations and bruises. MFT can also cause fatal blood loss and airway obstruction. The objective of this review was to determine the prevalence of MFT, identify the major causative factors in males and females in the main cities of Saudi Arabia.

To analyze the incidence of maxillofacial fractures due to motor vehicle accidents in Dubai, as well as age, sex, etiology, patterns, treatment, and complications. To compare the findings with similar studies and provide recommendations for the prevention and management of these fractures.

Contrasting findings were reported in several animal models with a Shank3 mutation used to induce various autism spectrum disorder (ASD) symptoms. Here, we aimed at investigating behavioral, cellular, and molecular consequences of a C-terminal (frameshift in exon 21) deletion in Shank3 protein in mice, a mutation that is also found in clinical conditions and which results in loss of major isoforms of Shank3. A special focus was made on cerebellar related parameters.

Emergency surgical treatment has been challenging and the risk of blood contamination has been high, which is a concern among the medical and dental fraternity. The risk outweighs the benefits in these unprecedented times if proper screening and inactivation of blood products are not performed. Pathogen reduction technologies incorporate various modalities for the inactivation of blood products mainly related to blood transfusion. Oral surgical procedures and periodontal surgeries use platelet-rich fibrin for various regenerative procedures that amplify the prognosis positively. The use of blood products for various treatments could result in contamination, a factor which should be significant attention. The objective of this study was to review the role of pathogen reduction technology in inactivating pathogens in blood products and its use in oral and periodontal surgical procedures. The literature presented in the study is from original studies from a period of 2000 to 2020 which was sourced from Medline, PubMed, and Cochrane central databases. Relevant published papers and in-press papers that provided information were identified and selected. The studies presented have shown data related to implementation of pathogen reduction technologies in relation to the severe acute respiratory syndrome, Middle East respiratory syndrome, and its possible implementation in coronavirus disease-2019 (COVID-19). The paper reviews the various technologies offered and the possibility to eradicate pathogens found in routine blood products, used in oral and periodontal surgical procedures. In all probability, the use of pathogen reduction technology might offer a ray of light to contain the spread among dental treatment procedures.

The aim of this study was to systematically review all COVID-19 publications to summarize the clinical features, assess comorbidities, prevalence, and disease outcomes.

Intrastriatal embryonic ventral mesencephalon grafts have been shown to integrate, survive, and reinnervate the host striatum in clinical settings and in animal models of Parkinson's disease. However, this ectopic location does not restore the physiological loops of the nigrostriatal pathway and promotes only moderate behavioral benefits. Here, we performed a direct comparison of the potential benefits of intranigral versus intrastriatal grafts in animal models of Parkinson's disease. We report that intranigral grafts promoted better survival of dopaminergic neurons and that only intranigral grafts induced recovery of fine motor skills and normalized cortico-striatal responses. The increase in the number of toxic activated glial cells in host tissue surrounding the intrastriatal graft, as well as within the graft, may be one of the causes of the increased cell death observed in the intrastriatal graft. Homotopic localization of the graft and the subsequent physiological cell rewiring of the basal ganglia may be a key factor in successful and beneficial cell transplantation procedures.

Injury to the human central nervous system can lead to devastating consequences due to its poor ability to self-repair. Neural transplantation aimed at replacing lost neurons and restore functional circuitry has proven to be a promising therapeutical avenue. We previously reported in adult rodent animal models with cortical lesions that grafted fetal cortical neurons could effectively re-establish specific patterns of projections and synapses. The current study was designed to provide a detailed characterization of the spatio-temporal in vivo development of fetal cortical transplanted cells within the lesioned adult motor cortex and their corresponding axonal projections. We show here that as early as 2 weeks after grafting, cortical neuroblasts transplanted into damaged adult motor cortex developed appropriate projections to cortical and subcortical targets. Grafted cells initially exhibited characteristics of immature neurons, which then differentiated into mature neurons with appropriate cortical phenotypes where most were glutamatergic and few were GABAergic. All cortical subtypes identified with the specific markers CTIP2, Cux1, FOXP2, and Tbr1 were generated after grafting as evidenced with BrdU co-labeling. The set of data provided here is of interest as it sets biological standards for future studies aimed at replacing fetal cells with embryonic stem cells as a source of cortical neurons.

Autism Spectrum Disorder (ASD) is a progressive neurodevelopmental disorder mainly characterized by deficits in social communication and stereotyped behaviors and interests. Here, we aimed to investigate the state of several key players in the dopamine and glutamate neurotransmission systems in the valproic acid (VPA) animal model that was administered to E12.5 pregnant females as a single dose (450 mg/kg). We report no alterations in the number of mesencephalic dopamine neurons or in protein levels of tyrosine hydroxylase in either the striatum or the nucleus accumbens. In females prenatally exposed to VPA, levels of dopamine were slightly decreased while the ratio of DOPAC/dopamine was increased in the dorsal striatum, suggesting increased turn-over of dopamine tone. In turn, levels of D1 and D2 dopamine receptor mRNAs were increased in the nucleus accumbens of VPA mice suggesting upregulation of the corresponding receptors. We also report decreased protein levels of striatal parvalbumin and increased levels of p-mTOR in the cerebellum and the motor cortex of VPA mice. mRNA levels of mGluR1, mGluR4, and mGluR5 and the glutamate receptor subunits NR1, NR2A, and NR2B were not altered by VPA, nor were protein levels of NR1, NR2A, and NR2B and those of BDNF and TrkB. These findings are of interest as clinical trials aiming at the dopamine and glutamate systems are being considered.

Dietary supplementations with n-3 polyunsaturated fatty acid (PUFA) have been explored in autism spectrum disorder (ASD) but their efficiency and potential in ameliorating cardinal symptoms of the disease remain elusive. Here, we compared a n-3 long-chain (LC) PUFA dietary supplementation (n-3 supp) obtained from fatty fish with a n-3 PUFA precursor diet (n-3 bal) obtained from plant oils in the valproic acid (VPA, 450 mg/kg at E12.5) ASD mouse model starting from embryonic life, throughout lactation and until adulthood. Maternal and offspring behaviors were investigated as well as several VPA-induced ASD biological features: cerebellar Purkinje cell (PC) number, inflammatory markers, gut microbiota, and peripheral and brain PUFA composition. Developmental milestones were delayed in the n-3 supp group compared to the n-3 bal group in both sexes. Whatever the diet, VPA-exposed offspring did not show ASD characteristic alterations in social behavior, stereotypies, PC number, or gut microbiota dysbiosis while global activity, gait, peripheral and brain PUFA levels as well as cerebellar TNF-alpha levels were differentially altered by diet and treatment according to sex. The current study provides evidence of beneficial effects of n-3 PUFA based diets, including one without LCPUFAs, on preventing several behavioral and cellular symptoms related to ASD.

In dentistry, occupational contact dermatitis may affect dental professionals along with technicians, nurses, and patients. Changes to dental practice in recent years have altered the reported frequencies of allergens causing contact dermatitis in both dental professionals and dental patients. In the current cross-sectional study, we used a structured questionnaire and clinical examinations to examine the prevalence of self-reported hand eczema among United Arab Emirates (UAE). The relationship between subjective skin discomfort and latex, composite/bonding, or other dental materials also was explored. A structured questionnaire was designed to analyze the prevalence of skin conditions among dental professionals and study its implication in gender, occupation, and age groups. The questionnaire included information about skin symptoms, atopy, occupational experience, and other background factors like respiratory symptoms, work history and methods, and exposure at work. It was distributed to 550 randomly selected dental healthcare professionals. Out of 550 dental healthcare workers contacted, 434 responded giving a response rate of 79%. The prevalence of dry and rough skin on the hands was highest (45%). There was a total of 29 cases of allergic contact dermatitis, 15 cases of contact urticaria, 12 cases of irritating contact dermatitis, and 1 incidence of onychomycosis among the 100 dental healthcare professionals who reported having dermatitis on their hands, forearms, or faces due to their daily dental chores. Rubber chemicals and natural rubber latex (NRL) in protective gloves used by dentists, as well as dental-restorative plastic materials (methylacrylates), were the most common causes of allergy. Dry skin and hand eczema were more common among dental healthcare professionals. Plastic gloves or NRL gloves with a low protein content are recommended for dental work. Skin exposure to methylacrylates or latex should be avoided.

Myocardial work (MW) is a new echocardiographic tool with a high sensitivity to detect early and subtle alterations of myocardial function. We aimed to evaluate the late effects of anthracyclines by assessing the global and segmental MW and intraventricular mechanical dispersion from speckle tracking echocardiography in childhood lymphoma survivors (CLS).

The neuropeptide Y (NPY) is widely expressed in the central nervous system and has been shown to stimulate neurogenesis in the hippocampus and the olfactory epithelium. Here, we demonstrate that intracerebroventricular injection of NPY stimulates proliferation of neural precursors in the mice subventricular zone (SVZ), one the most neurogenic areas of the brain. Newly generated neuroblasts migrate through the rostral migratory stream to the olfactory bulb and also directly to the striatum, as evidenced by BrdU labelling and cell phenotyping. Using knock-out mice, specific NPY receptor agonists and antagonists, we report that this neuroproliferative effect is mediated by the Y1 receptor subtype that we found to be highly expressed in the SVZ both at the mRNA and protein levels. Our data suggest that stimulating endogenous SVZ neural stem cells by NPY may be of a potential interest in cell replacement based therapies of neurodegenerative diseases affecting the striatum such as Huntington's disease.

Early environmental enrichment (EE) produces several changes in gene expression in the brain and confers protection against the behavioral, neurochemical and molecular effects of repeated administration of drugs of abuse. Because the endogenous cannabinoid system (ECS) is known to play an important role in the rewarding effects of drugs, we investigated whether the positive effects of early exposure to EE are associated with changes in the expression of genes encoding for proteins that belong to the ECS in C57 mice. Using in situ hybridization, we compared the expression of the cannabinoid receptor CB1, fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MGL) enzymes in brain regions involved in drug addiction in mice reared in either EE or standard environments (SE) from weaning until adulthood. We found that EE increases CB1 mRNA levels in the hypothalamus and in the basolateral amygdala but decreased them in the basomedial amygdala. Similarly, we found that FAAH mRNA levels are higher in the hypothalamus and the basolateral amygdala of EE mice compared to SE mice, with no change in the basomedial amygdala. In contrast, MGL mRNA levels were not affected by EE in any of the areas analyzed. The regional selectivity of EE-induced changes may indicate that early exposure to EE induces changes in the ECS that could result in reduced responses to stress, as confirmed in EE mice in a novelty-induced suppression of feeding test, and, ultimately, in resistance to addiction.

The primary motor cortex (M1) is involved in fine voluntary movements control. Previous studies have shown the existence of a dopamine (DA) innervation in M1 of rats and monkeys that could directly modulate M1 neuronal activity. However, none of these studies have described the precise distribution of DA terminals within M1 functional region nor have quantified the density of this innervation. Moreover, the precise role of DA on pyramidal neuron activity still remains unclear due to conflicting results from previous studies regarding D2 effects on M1 pyramidal neurons. In this study we assessed in mice the neuroanatomical characteristics of DA innervation in M1 using unbiased stereological quantification of DA transporter-immunostained fibers. We demonstrated for the first time in mice that DA innervates the deep layers of M1 targeting preferentially the forelimb representation area of M1. To address the functional role of the DA innervation on M1 neuronal activity, we performed electrophysiological recordings of single neurons activity in vivo and pharmacologically modulated D2 receptor activity. Local D2 receptor activation by quinpirole enhanced pyramidal neuron spike firing rate without changes in spike firing pattern. Altogether, these results indicate that DA innervation in M1 can increase neuronal activity through D2 receptor activation and suggest a potential contribution to the modulation of fine forelimb movement. Given the demonstrated role for DA in fine motor skill learning in M1, our results suggest that altered D2 modulation of M1 activity may be involved in the pathophysiology of movement disorders associated with disturbed DA homeostasis.

Motor impairments are amongst the earliest and most consistent signs of autism spectrum disorders but are not used as diagnostic criteria. In addition, the relationship between motor and cognitive impairments and their respective neural substrates remain unknown.

This study was aimed to investigate the potential neuroprotective effect of neuropeptide Y (NPY) on the survival of dopaminergic cells in both in vitro and in animal models of Parkinson's disease (PD). NPY protected human SH-SY5Y dopaminergic neuroblastoma cells from 6-hydroxydopamine-induced toxicity. In rat and mice models of PD, striatal injection of NPY preserved the nigrostriatal dopamine pathway from degeneration as evidenced by quantification of (1) tyrosine hydroxylase (TH)-positive cells in the substantia nigra pars compacta, levels of (2) striatal tyrosine hydroxylase and dopamine transporter, (3) dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) as well as (4) rotational behavior. NPY had no neuroprotective effects in mice treated with Y(2) receptor antagonist or in transgenic mice deficient for Y(2) receptor suggesting that NPY effects are mediated through this receptor. Stimulation of Y(2) receptor by NPY triggered the activation of both the ERK1/2 and Akt pathways but did not modify levels of brain derived neurotrophic factor (BDNF) or glial cell line-derived neurotrophic factor. These results open new perspectives in neuroprotective therapies using NPY and suggest potential beneficial effects in PD.