Search

This article discusses the use of Artificial Intelligence (AI) to assess the quality of cleanliness during esophagogastroduodenoscopy, a procedure used to examine the upper gastrointestinal tract. The study used a dataset of 125 HD white-light endoscopy images and trained an AI system to determine the cleanliness of the images. The AI system accurately determined the cleanliness in 73.85% of the images, with better results for certain classes. The system provided its output in less than 20 milliseconds, achieving real-time performance. However, the small size and distribution of the dataset limited the system's performance, and future work should involve acquiring and annotating new images to improve the AI system's performance. [Extracted from the article]

Autism Spectrum Disorders subjects (ASD) are well known to have deficits in social interaction. We recorded simultaneously eye movements and postural sway during exploration of emotional faces in children with ASD and typically developing children (TD). We analyzed several postural and ocular parameters. The results showed that all postural parameters were significantly greater in children with ASD; ASD made significantly fewer saccades and had shorter fixation time than TD, particularly in the eyes, and especially for unpleasant emotions. These results suggest that poor postural control of ASD and their impaired visual strategies could be due to a lack of interest in social cognition, causing a delay in the development of the cortical areas, and thus could have an effect on their postural control.

Abstract Background The gene encoding carboxyl-terminal PDZ ligand of neuronal nitric oxide synthase (NOS1AP) is located on chromosome 1q23.3, a candidate region for schizophrenia, autism spectrum disorders (ASD) and obsessive-compulsive disorder (OCD). Previous genetic and functional studies explored the role of NOS1AP in these psychiatric conditions, but only a limited number explored the sequence variability of NOS1AP. Methods We analyzed the coding sequence of NOS1AP in a large population (n = 280), including patients with schizophrenia (n = 72), ASD (n = 81) or OCD (n = 34), and in healthy volunteers controlled for the absence of personal or familial history of psychiatric disorders (n = 93). Results Two non-synonymous variations, V37I and D423N were identified in two families, one with two siblings with OCD and the other with two brothers with ASD. These rare variations apparently segregate with the presence of psychiatric conditions. Conclusions Coding variations of NOS1AP are relatively rare in patients and controls. Nevertheless, we report the first non-synonymous variations within the human NOS1AP gene that warrant further genetic and functional investigations to ascertain their roles in the susceptibility to psychiatric disorders.

Background and Objectives: Esophageal squamous cell carcinomas (ESCC) are often accompanied by head and neck squamous cell carcinoma (HNSCC) and vice versa. Our study aimed to describe the prevalence of HNSCC in patients with ESCC, the chronology of appearance and the impact on survival., Methods: A retrospective review was carried out through a computerized database of patients diagnosed with ESCC at Hospital Clinic of Barcelona between January 1999 and June 2019. Demographic data, date of ESCC diagnosis, survival time, primary tumor location, diagnosis of HNSCC and chronological relationship were recorded., Results: A total of 231 patients with ESCC confirmed histologically were included in the study with a median age of 64 years (IQR, 56.0-72.0), and 178 (77%) were male. The majority of the patients had a history of smoking and alcohol consumption (69.7% and 60.6%, respectively). The predominant location of ESCC was the middle esophagus (n=124, 53.7%). Forty-one patients (17.7%) had HNSCC: 21 (51.2%) were previous, 14 (34.1%) synchronous and 6 (14.6%) metachronous. All the patients were followed and 196 (84.8%) died with a median survival time of 19 months (IQR, 7-66). There were not statistically significant differences among the living patients and the deceased., Conclusions: In our setting, a 17.7% of patients with ESCC have an associated HNSCC with no significant differences in survival between patients with both ESCC and HNSCC compared to those with only ESCC. However, the implementation of a screening program could allow the detection of a second primary tumor at early stages., (Copyright © 2024 Elsevier España, S.L.U. All rights reserved.)

Background and Objectives: There are few scales with prospective validation for the assessment of the upper gastrointestinal mucosal cleanliness during an esophagogastroduodenoscopy (EGD). The aim of this study was to develop a valid and reproducible cleanliness scale for use during an EGD., Methods: We developed a cleanliness scale (Barcelona scale) with a score (0-2 points) of five segments of the upper gastrointestinal tract with thorough cleaning techniques (esophagus, fundus, body, antrum, and duodenum). First, 125 photos (25 of each area) were assessed, and a score was assigned to each image by consensus among 7 experts endoscopists. Subsequently, 100 of the 125 images were selected and the inter- and intra-observer variability of 15 previously trained endoscopists was evaluated using the same images at two different times., Results: In total, 1500 assessments were performed. In 1336/1500 observations (89%) there was agreement with the consensus score, with a mean kappa value of 0.83 (0.45-0.96). In the second evaluation, in 1330/1500 observations (89%) there was agreement with the consensus score, with a mean kappa value of 0.82 (0.45-0.93). The intra-observer variability was 0.89 (0.76-0.99)., Conclusions: The Barcelona cleanliness scale is a valid measure and reproducible with minimal training. Its application in clinical practice is a significant step to standardize the quality of the EGD., (Copyright © 2023 Elsevier España, S.L.U. All rights reserved.)

Autism spectrum disorders (ASD) are heterogeneous and complex neurodevelopmental conditions that urgently need reliable and sensitive measures to inform diagnosis properly. The Reading the Mind in the Eyes Task (or Eyes Test from now on) is widely used for this purpose. A recent study showed that subcategories of items of the children version of the Eyes Test could be especially discriminative to distinguish ASD and control children. Here, we analyzed the performance on the Eyes Test of 30 high functioning (IQ > 70) adults with ASD and 29 controls from the InFoR cohort multicentric study, using a Generalized Linear Mixed Model. We found that valence and difficulty modulate the performance on the Eyes Test, with easy and positive items being the most discriminative to distinguish ASD and controls. In particular, we suggest this result might be actionable to discriminate ASD patients from controls in subgroups where their overall scores show less difference with controls. We propose for future research the computation of two additional indexes when using the Eyes Test: the first focusing on the easy and positive items (applying a threshold of 70% of correct responses for these items, above which people are at very low risk of having ASD) and the second focusing on the performance gain from difficult to easy items (with a progression of less than 15% showing high risk of having ASD). Our findings open the possibility for a major change in how the Eyes Test is used to inform diagnosis in ASD. LAY SUMMARY: The Eyes Test is used worldwide to inform autism spectrum disorders (ASD) diagnosis. We show here that ASD and neurotypical adults show the most difference in performance on subgroups of items: ASD adults do not improve as expected when comparing easy and difficult items, and they do not show an improvement for items displaying a positive feeling. We advise clinicians to focus on these comparisons to increase the property of the test to distinguish people with ASD from neurotypical adults., (© 2020 The Authors. Autism Research published by International Society for Autism Research and Wiley Periodicals LLC.)

Background: Autism spectrum disorders (ASD) are characterized by abnormal neurodevelopment, genetic, and environmental risk factors, as well as immune dysfunctions. Several lines of evidence suggest alterations in innate immune responses in children with ASD. To address this question in adults with high-functioning ASD (hf-ASD), we sought to investigate the role of natural killer (NK) cells in the persistence of ASD., Methods: NK cells from 35 adults with hf-ASD were compared to that of 35 healthy controls (HC), selected for the absence of any immune dysfunctions, at different time-points, and over a 2-year follow-up period for four patients. The phenotype and polyfunctional capacities of NK cells were explored according to infectious stigma and clinical parameters (IQ, social, and communication scores)., Results: As compared to HC, NK cells from patients with hf-ASD showed a high level of cell activation ( p  < 0.0001), spontaneous degranulation ( p  < 0.0001), and interferon-gamma production ( p  = 0.0004), whereas they were exhausted after in vitro stimulations ( p  = 0.0006). These data yielded a specific HLA-DR + KIR2DL1 + NKG2C + NK-cell signature. Significant overexpression of NKG2C in hf-ASD patients ( p  = 0.0005), indicative of viral infections, was inversely correlated with the NKp46 receptor level ( r  = - 0.67; p  < 0.0001), regardless of the IgG status of tested pathogens. Multivariate linear regression analysis also revealed that expression of the late-activating HLA-DR marker was both associated with structural language ( r  = 0.48; p  = 0.007) and social awareness ( r  = 0.60; p  = 0.0007) scores in adult patients with hf-ASD, while KIR2DL1 expression correlated with IQ scores ( p  = 0.0083)., Conclusions: This study demonstrates that adults with hf-ASD have specific NK-cell profile. Presence of NKG2C overexpression together with high-level activation of NK cells suggest an association with underlying pathogens, a hypothesis warranting further exploration in future studies., Competing Interests: This study is part of clinical trial C07-33 sponsored by Inserm. It was granted approval by local Ethics Committee or “Comité de Protection des Personnes” on 2008 November 14th, authorized by the French authorities (ANSM B80738-70 on 2008 August 11th), and registered in a public trial registry (NCT02628808). All study participants gave their informed written consent to participation, in line with French ethical guidelines.All authors agreed to this manuscript’s publication.Myriam Ly Le-Moal is an employee of the Roche Institute. The other authors report no biomedical financial interests or potential conflicts of interest.Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Autism spectrum disorder (ASD) is a developmental disorder underdiagnosed in adults. To date, no consistent evidence of alterations in brain structure has been reported in adults with ASD and few studies were conducted at that age. We analyzed structural magnetic resonance imaging data from 167 high functioning adults with ASD and 195 controls. We ran our analyses on a discovery (n = 301) and a replication sample (n = 61). The right caudal anterior cingulate cortical thickness was significantly thinner in adults with ASD compared to controls in both the discovery and the replication sample. Our work underlines the relevance of studying the brain anatomy of an adult ASD population.

Despite the high clinical burden, little is known about pathophysiology underlying autism spectrum disorder (ASD). Recent resting-state functional magnetic resonance imaging (rs-fMRI) studies have found atypical synchronization of brain activity in ASD. However, no consensus has been reached on the nature and clinical relevance of these alterations. Here, we addressed these questions in four large ASD cohorts. Using rs-fMRI, we identified functional connectivity alterations associated with ASD. We tested for associations of these imaging phenotypes with clinical and demographic factors such as age, sex, medication status, and clinical symptom severity. Our results showed reproducible patterns of ASD-associated functional hyper- and hypoconnectivity. Hypoconnectivity was primarily restricted to sensory-motor regions, whereas hyperconnectivity hubs were predominately located in prefrontal and parietal cortices. Shifts in cortico-cortical between-network connectivity from outside to within the identified regions were shown to be a key driver of these abnormalities. This reproducible pathophysiological phenotype was partially associated with core ASD symptoms related to communication and daily living skills and was not affected by age, sex, or medication status. Although the large effect sizes in standardized cohorts are encouraging with respect to potential application as a treatment and for patient stratification, the moderate link to clinical symptoms and the large overlap with healthy controls currently limit the usability of identified alterations as diagnostic or efficacy readout., (Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.)

Attention Deficit and Hyperactive Disorder (ADHD) and Autism Spectrum Disorders (ASD) are frequent comorbid neurodevelopmental conditions and the overlap between both disorders remains to be delineated. A more complete understanding of the shared genetic and environmental factors is needed. Using a family-based method, we evaluated the risk of ADHD in a group of relatives with an ASD proband (ASD-) and a group of relatives with an ASD and ADHD proband (ASD+). We enrolled 1245 individuals in the study: 499 probands, their 746 first-degree relatives and 140 controls. We used a multivariate generalized estimating equation (GEE) model, in which the dependent variable was the ADHD diagnosis in the relatives and the independent variable the ASD+ or ASD- in probands. We adjusted for sociodemographic factors (age, sex, IQ) and for the nature of the familial relationship with the affected proband (parent or sibling). Among the probands, there were 287 ASD- and 212 ASD+ individuals. ADHD was more frequent in relatives (19%) than in the control group (7%) (p = 0.001). The risk of ADHD was higher in the ASD+ relatives group than in the ASD- relatives group (GEE model OR 1.58 [95% CI 1.04-2.38], p = 0.032). This result was found in parents (OR 1.96 [95% CI  1.14-3.36], but not in siblings (OR 1.28 [95% CI 0.84-1.94], p = 0.434). Our study provides a representative estimate of the family distribution of ADHD in relatives of ASD probands but supports the modest effect of shared genetic and environmental factors between both disorders.

The current theory implying local, short-range overconnectivity in autism spectrum disorder, contrasting with long-range underconnectivity, is based on heterogeneous results, on limited data involving functional connectivity studies, on heterogeneous paediatric populations and non-specific methodologies. In this work, we studied short-distance structural connectivity in a homogeneous population of males with high-functioning autism spectrum disorder and used a novel methodology specifically suited for assessing U-shaped short-distance tracts, including a recently developed tractography-based atlas of the superficial white matter fibres. We acquired diffusion-weighted MRI for 58 males (27 subjects with high-functioning autism spectrum disorder and 31 control subjects) and extracted the mean generalized fractional anisotropy of 63 short-distance tracts. Neuropsychological evaluation included Wechsler Adult Intelligence Scale IV (WAIS-IV), Communication Checklist-Adult, Empathy Quotient, Social Responsiveness Scale and Behaviour Rating Inventory of Executive Function-Adult (BRIEF-A). In contradiction with the models of short-range over-connectivity in autism spectrum disorder, we found that patients with autism spectrum disorder had a significantly decreased anatomical connectivity in a component comprising 13 short tracts compared to controls. Specific short-tract atypicalities in temporal lobe and insula were significantly associated with clinical manifestations of autism spectrum disorder such as social awareness, language structure, pragmatic skills and empathy, emphasizing their importance in social dysfunction. Short-range decreased anatomical connectivity may thus be an important substrate of social deficits in autism spectrum disorder, in contrast with current models.

Infections and autoimmunity are associated with autism spectrum disorders (ASD), with both strongly influenced by the genetic regulation of the human leukocyte antigen (HLA) system. The relationship between ASD and the HLA genetic diversity requires further investigation. Using a case control design, the distribution of HLA class II-DRB1 and DQB1 alleles, genotypes and haplotypes were investigated in ASD patients, versus healthy controls (HC). ASD patients meeting DSM-IV TR criteria and HC (474 and 350 respectively) were genotyped at medium resolution using a Luminex-based SSO technology. Comparisons of genotypes, allele frequencies associated with a haplotype analysis were performed. Results indicate: (i) the HLA-DRB1 *11-DQB1*07 haplotype was more prevalent in ASD patients, versus HC (Pc = 0.001), partially replicating previous data and possibly linking to gastro-intestinal (GI)-related pro-inflammatory processes, given that this haplotype associates with pediatric celiac disorders; (ii) the HLA-DRB1 *17-DQB1*02 haplotype was higher in HC, versus ASD patients (Pc = 0.002), indicating that this is a protective haplotype. Using the Autism Diagnostic Interview to assess clinical dimensions, higher scores on social (Pc = 0.006) and non-verbal functioning (Pc = 0.004) associated with the DRB1 *11 DQB1*07 haplotype. Our results support HLA involvement in ASD, with possible relevance to GI and gut-brain axis dysregulation.

Autism, learning disabilities and attention deficit/hyperactive disorder are often comorbid disorders. In order to try and find some markers that might be transnosographic, we hypothesized that abnormal postural sway profiles may discriminate children with neurodevelopmental disorders (NDDs) from typically developing children. The aim of our study was thus to compare spatial and temporal measures of the Center of Pressure in three distinct groups of children with NDDs (high functioning autism spectrum disorders, learning disabilities (dyslexia) and attention deficit/hyperactive disorders) and in typically developing children. Postural performances were thus evaluated in 92 children (23 per group, sex-, age- and IQ-matched groups) by using the Multitest Equilibre platform (Framiral ® ). Two viewing conditions (eyes open and eyes closed) were tested on a stable and unstable platform. Results reported similar poor postural instability for the three groups of children with NDDs with respect to the typically developing children, and this was observed for both spatial as well as temporal analysis of displacement of the center of pressure. Such postural instability observed in children with NDDs could be due to impairment in using sensorial inputs to eliminate body sway, probably due to poor cerebellar integration., (Copyright © 2017 ISDN. Published by Elsevier Ltd. All rights reserved.)

The cerebellum is implicated in social cognition and is likely to be involved in the pathophysiology of autism spectrum disorder (ASD). The goal of our study was to explore cerebellar morphology in adults with ASD and its relationship to eye contact, as measured by fixation time allocated on the eye region using an eye-tracking device. Two-hundred ninety-four subjects with ASD and controls were included in our study and underwent a structural magnetic resonance imaging scan. Global segmentation and cortical parcellation of the cerebellum were performed. A sub-sample of 59 subjects underwent an eye tracking protocol in order to measure the fixation time allocated to the eye region. We did not observe any difference in global cerebellar volumes between ASD patients and controls; however, regional analyses found a decrease of the volume of the right anterior cerebellum in subjects with ASD compared to controls. There were significant correlations between fixation time on eyes and the volumes of the vermis and Crus I. Our results suggest that cerebellar morphology may be related to eye avoidance and reduced social attention. Eye tracking may be a promising neuro-anatomically based stratifying biomarker of ASD.

Community-based studies have consistently shown a sex ratio heavily skewed towards males in autism spectrum disorders (ASD). The factors underlying this predominance of males are largely unknown, but the way girls score on standardized categorical diagnostic tools might account for the underrecognition of ASD in girls. Despite the existence of different norms for boys and girls with ASD on several major screening tests, the algorithm of the Autism Diagnosis Interview-Revised (ADI-R) has not been reformulated. The aim of our study was to investigate which ADI-R items discriminate between males and females, and to evaluate their weighting in the final diagnosis of autism. We then conducted discriminant analysis (DA) on a sample of 594 probands including 129 females with ASD, recruited by the Paris Autism Research International Sibpair (PARIS) Study. A replication analysis was run on an independent sample of 1716 probands including 338 females with ASD, recruited through the Autism Genetics Resource Exchange (AGRE) program. Entering the raw scores for all ADI-R items as independent variables, the DA correctly classified 78.9% of males and 72.9% of females (P < 0.001) in the PARIS cohort, and 72.2% of males and 68.3% of females (P < 0.0001) in the AGRE cohort. Among the items extracted by the stepwise DA, four belonged to the ADI-R algorithm used for the final diagnosis of ASD. In conclusion, several items of the ADI-R that are taken into account in the diagnosis of autism significantly differentiates between males and females. The potential gender bias thus induced may participate in the underestimation of the prevalence of ASD in females. Autism Res 2016,. © 2016 International Society for Autism Research, Wiley Periodicals, Inc. Autism Res 2017, 10: 680-689. © 2016 International Society for Autism Research, Wiley Periodicals, Inc., (© 2016 International Society for Autism Research, Wiley Periodicals, Inc.)

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by dysfunctions in social interactions resulting from a complex interplay between immunogenetic and environmental risk factors. Autoimmunity has been proposed as a major etiological component of ASD. Whether specific autoantibodies directed against brain targets are involved in ASD remains an open question. Here, we identified within a cohort an ASD patient with multiple circulating autoantibodies, including the well-characterized one against glutamate NMDA receptor (NMDAR-Ab). The patient exhibited alexithymia and previously suffered from two major depressive episodes without psychotic symptoms. Using a single molecule-based imaging approach, we demonstrate that neither NMDAR-Ab type G immunoglobulin purified from the ASD patient serum, nor that from a seropositive healthy subject, disorganize membrane NMDAR complexes at synapses. These findings suggest that the autistic patient NMDAR-Abs do not play a direct role in the etiology of ASD and that other autoantibodies directed against neuronal targets should be investigated.

Although, the quest to understand emotional processing in individuals with Autism Spectrum Disorders (ASD) has led to an impressive number of studies, the picture that emerges from this research remains inconsistent. Some studies find that Typically Developing (TD) individuals outperform those with ASD in emotion recognition tasks, others find no such difference. In this paper, we move beyond focusing on potential group differences in behaviour to answer what we believe is a more pressing question: do individuals with ASD use the same mechanisms to process emotional cues? To this end, we rely on model-based analyses of participants' accuracy during an emotion categorisation task in which displays of anger and fear are paired with direct vs. averted gaze. Behavioural data of 20 ASD and 20 TD adolescents revealed that the ASD group displayed lower overall performance. Yet, gaze direction had a similar impact on emotion categorisation in both groups, i.e. improved accuracy for salient combinations (anger-direct, fear-averted). Critically, computational modelling of participants' behaviour reveals that the same mechanism, i.e. increased perceptual sensitivity, underlies the contextual impact of gaze in both groups. We discuss the specific experimental conditions that may favour emotion processing and the automatic integration of contextual information in ASD.

Background: Widespread abnormalities in white matter development are frequently reported in cases of autism spectrum disorders (ASD) and could be involved in the disconnectivity suggested in these disorders. Homozygous mutations in the gene coding for fatty-acid 2-hydroxylase (FA2H), an enzyme involved in myelin synthesis, are associated with complex leukodystrophies, but little is known about the functional impact of heterozygous FA2H mutations. We hypothesized that rare deleterious heterozygous mutations of FA2H might constitute risk factors for ASD., Methods: We searched deleterious mutations affecting FA2H, by genotyping 1256 independent patients with ASD genotyped using Genome Wide SNP arrays, and also by sequencing in independent set of 186 subjects with ASD and 353 controls. We then explored the impact of the identified mutations by measuring FA2H enzymatic activity and expression, in transfected COS7 cells., Results: One heterozygous deletion within 16q22.3-q23.1 including FA2H was observed in two siblings who share symptoms of autism and severe cognitive impairment, axial T2-FLAIR weighted MRI posterior periventricular white matter lesions. Also, two rare non-synonymous mutations (R113W and R113Q) were reported. Although predictive models suggested that R113W should be a deleterious, we did not find that FA2H activity was affected by expression of the R113W mutation in cultured COS cells., Conclusions: While our results do not support a major role for FA2H coding variants in ASD, a screening of other genes related to myelin synthesis would allow us to better understand the role of non-neuronal elements in ASD susceptibility.

Melatonin is a powerful antioxidant and a synchronizer of many physiological processes. Alteration in melatonin signaling has been reported in a broad range of diseases, but little is known about the genetic variability of this pathway in humans. Here, we sequenced all the genes of the melatonin pathway -AA-NAT, ASMT, MTNR1A, MTNR1B and GPR50 - in 321 individuals from Sweden including 101 patients with attention-deficit/hyperactivity disorder (ADHD) and 220 controls from the general population. We could find several damaging mutations in patients with ADHD, but no significant enrichment compared with the general population. Among these variations, we found a splice site mutation in ASMT (IVS5+2T>C) and one stop mutation in MTNR1A (Y170X) - detected exclusively in patients with ADHD - for which biochemical analyses indicated that they abolish the activity of ASMT and MTNR1A. These genetic and functional results represent the first comprehensive ascertainment of melatonin signaling deficiency in ADHD., (© 2011 John Wiley & Sons A/S.)

Melatonin is a powerful antioxidant and a synchronizer of many physiological processes. Alteration of the melatonin pathway has been reported in circadian disorders, diabetes and autism spectrum disorders (ASD). However, very little is known about the genetic variability of melatonin receptors in humans. Here, we sequenced the melatonin receptor MTNR1A and MTNR1B, genes coding for MT1 and MT2 receptors, respectively, in a large panel of 941 individuals including 295 patients with ASD, 362 controls and 284 individuals from different ethnic backgrounds. We also sequenced GPR50, coding for the orphan melatonin-related receptor GPR50 in patients and controls. We identified six non-synonymous mutations for MTNR1A and ten for MTNR1B. The majority of these variations altered receptor function. Particularly interesting mutants are MT1-I49N, which is devoid of any melatonin binding and cell surface expression, and MT1-G166E and MT1-I212T, which showed severely impaired cell surface expression. Of note, several mutants possessed pathway-selective signaling properties, some preferentially inhibiting the adenylyl cyclase pathway, others preferentially activating the MAPK pathway. The prevalence of these deleterious mutations in cases and controls indicates that they do not represent major risk factor for ASD (MTNR1A case 3.6% vs controls 4.4%; MTNR1B case 4.7% vs 3% controls). Concerning GPR50, we detected a significant association between ASD and two variations, Delta502-505 and T532A, in affected males, but it did not hold up after Bonferonni correction for multiple testing. Our results represent the first functional ascertainment of melatonin receptors in humans and constitute a basis for future structure-function studies and for interpreting genetic data on the melatonin pathway in patients.

The present study investigated the effects of average growth rate (AGR) levels and age on the number of sperm cells per gram of testis parenchyma and on the gonadal reserve in Landrace (LD) and Large White (LW) boars. In Experiment 1, the effects of breed (LD, LW), level of AGR from birth up to 90 days of age (Level 1: 384 +/- 32 g/day; Level 2: 512 +/- 22 g/day; Level 3: 624 +/- 41 g/day), and age (13, 15, 17, 19 and 21 weeks) on testicular cell concentration were evaluated. Data were analyzed under a 2 x 3 x 4 factorial design. There were significant effects associated with breed (P < 0.001) and age (P < 0.001) but not with AGR (P > 0.05) on sperm cell number per gram of testicular parenchyma. The number of cells increased with age and was greater in LW than in LD young boars, mainly those up to 19 weeks of age. In Experiment 2, the effect of two AGR levels (Level 1: 649-694 g/day; Level 2: 813-885 g/day) from birth up to 100 kg body weight on the number of sperm cells per gram of testis parenchyma and on the gonadal reserve was investigated using 59 purebred LD and LW boars. The boars were castrated at 23, 25, 29 and 33 weeks of age. Age of boars significantly affected gonadal sperm reserve and the number of sperm cells per gram of testicular tissue (P < 0.001). Breed of boars and AGR Levels did not significantly affect number of sperm cells and gonadal sperm reserve (P > 0.05). It was concluded that the number of sperm cells in the testicular tissue of young boars is influenced by their breed and age, but not by the level of their AGR.