Developing Eco-Friendly 3D-Printing Composite Filament: Utilizing Palm Midrib to Reinforce High-Density Polyethylene Matrix in Design Applications.

Designers actively pursue the use of novel materials and concepts in furniture and interior design. By providing insights into their processing behavior and suitability for 3D-printing processes, this research helps to highlight the potential of using waste materials to create more environmentally friendly and sustainable 3D-printing filaments that can be used in furniture and interior design. Furthermore, the study evaluates the effect of incorporating palm midrib nanoparticles (DPFNPs) to reinforce a high-density polyethylene (HDPE) matrix with different loadings such as 10, 20, 30, 40, and 50 wt.%. The composites were extruded into filaments using a manual extruder, which was then utilized to fabricate 3D-printed specimens using a 3D-printing pen. The effect of adding DPFNPs on the composite's chemical, thermal, and mechanical properties was evaluated, with a particular focus on how these modifications influence the melt flow rate (MFR) and, subsequently, the material's printability. The results revealed that HDPE and filament composites presented similar FTIR spectra. On the other hand, the filament composites presented an increase in the thermal stability and a decrease in the mechanical strength with increasing DPFNP content in the HDPE matrix. The filaments were successfully printed using a 3D-printing pen. Thus, using DPFNPs in the HDPE matrix presents a low-cost alternative for filament production and may expand 3D-printing applications in interior and furniture design with more sustainable materials. Future work will delve into optimizing these composites for improved printability and assessing their recyclability, aiming to broaden their applications in 3D printing and beyond.

Insights into the implication of obesity in hypogonadism among adolescent boys.

OBJECTIVES: This research aimed at uncovering the mechanisms behind obesity-related hypogonadism in adolescent boys and to investigate the association between anthropometric characteristics and testicular functions of these boys. METHODS: This study included 60 adolescent boys (12-18 years) with exogenous obesity (BMI≥95th percentile) and 30 age matched lean controls (BMI=15th-85th percentile). Full clinical examination, anthropometric measurements and pubertal assessment were performed. Laboratory investigations included hemoglobin, hematocrit, lipid panel, LH, FSH, free and total testosterone, inhibin B and estradiol. RESULTS: The results indicated the presence of positive family history of obesity in 85% of obese boys vs. 40% of the lean counterparts. Concerning SBP of obese boys, 7% were hypertensive (95th percentile), 25% were prehypertensive (between 90th and 95th percentiles) while, DBP findings showed that 33% are hypertensive and 33% are prehypertensive. Meanwhile, 13.3% of lean controls were prehypertensive. Anthropometric measurements and lipid profile values revealed a significant difference between obese and lean boys. Compared to obese boys the normal weight boys had higher levels of free testosterone (21.15 ± 2.90 pg/mL vs. 11.38 ± 3.96 pg/mL, p<0.001), total testosterone (10.59 ± 6.63 ng/dL vs. 3.23 ± 1.70 ng/dL, p<0.001), FSH (7.33 ± 3.75 mIU/mL vs. 5.63 ± 3.96 mIU/mL, p=0.026) and inhibin B (83.28 ± 27.66 pg/mL vs. 62.90 ± 17.85 pg/mL, p=0.001) and they registered lower level of estradiol (18.48 ± 7.33 pg/mL vs. 40.20 ± 7.91 pg/mL, p<0.001). In obese boys, BMI SDS significantly correlated with lipid profile and estradiol whereas, it showed significant negative correlation with LH, free and total testosterone and inhibin B. Penile length significantly correlated with LH while it revealed significant negative correlation with cholesterol. CONCLUSIONS: This study evidenced a close association between obesity and hypogonadism in adolescent boys which could be due to the increased estradiol level and decreased T/E2 ratio.

Mitochondrial DNA maintenance defects: potential therapeutic strategies.

Mitochondrial DNA (mtDNA) replication depends on the mitochondrial import of hundreds of nuclear encoded proteins that control the mitochondrial genome maintenance and integrity. Defects in these processes result in an expanding group of disorders called mtDNA maintenance defects that are characterized by mtDNA depletion and/or multiple mtDNA deletions with variable phenotypic manifestations. As it applies for mitochondrial disorders in general, current treatment options for mtDNA maintenance defects are limited. Lately, with the development of model organisms, improved understanding of the pathophysiology of these disorders, and a better knowledge of their natural history, the number of preclinical studies and existing and planned clinical trials has been increasing. In this review, we discuss recent preclinical studies and current and future clinical trials concerning potential therapeutic options for the different mtDNA maintenance defects.

First Record of HAdV-D20 Among Keratoconjunctivitis Patients in Iraq.

Background: Human Adenovirus species D (HAdV-D) was common human viral pathogen especially in eye infection, consists of several types of which HAdV-D8, -D19 and -D37 were common in eye infection. This study includes detection of HAdV-D types implicated in conjunctivitis based on L2 (Penton protein) gene similarity. Methods: Conjunctival swabs were collected from Keratoconjunctivitis patients as eye infection related to adenovirus. Viral nucleic acids were extracted and specific primer pairs for HAdV-D L2 gene (encoding for penton base protein) was used to amplify the target gene and only positive samples were sent to sequencing. Results: The results revealed that only 6 samples give positive results for L2 gene amplification and then sent for sequencing for L2 (penton protein) gene-based typing. The results show that 4 local isolates (S1, S2, S3, S6) were similar to HAdV-D8 and 2 local isolates (S4, S5) were similar to HAdV-D20. Also the results display that the HAdV-37, prominent HAdV-D type of human eye infection, may be variant of HAdV-D20 due to that six variation were seen in S4and S5 local isolates nucleotide sequence in relation to HAdV-D37: T>C at position 14364, A>C at position 14411, T>C at position 14427, C>A at position 14448, G>A at position 14540 and T>C at position 14617, leading to only 2 amino acid change in resulted penton protein: T (Threonine) instead of K (Lysine) at position 204 and N (Asparagine) instead of D (Aspartic acid) at position 247. Conclusion: The current study concludes the possibility of implication of HAdV-D20 in eye infections especially conjunctivitis.

Routine thyroidectomy with total laryngectomy: Is it really indicated? A randomized controlled trial.

BACKGROUND: We investigated the incidence of thyroid gland invasion in patients with advanced laryngeal carcinoma who were treated with total laryngectomy, also the impact of different preoperative and intraoperative predictors on thyroid gland invasion. Moreover, the impact of thyroid gland preservation on the locoregional tumor control and the recurrence rates after surgery were investigated. MATERIALS AND METHODS: This study was conducted over 5 years on 100 patients with advanced laryngeal carcinoma who underwent total laryngectomy. The adopted protocol in our hospital is to perform an ipsilateral thyroid lobectomy if there is subglottic extension, thyroid or cricoid cartilage invasion or true invasion of the thyroid gland. The patients of the study were divided into thyroid sparing and thyroid sacrificing groups. The two groups were compared in terms of demographic data, tumor characteristics, incidence of postoperative hypothyroidism and tumor recurrence. RESULTS: There was no significant difference between groups regarding the tumor profile. Regarding local tumor spread, the only two subsites that showed significant difference is anterior commissure and thyroid cartilage invasion. In the thyroid sacrificing group, invasion of the thyroid gland was proved histopathologically in only one patient. Postoperatively, the incidence of hypothyroidism was significantly higher in the thyroid sacrificing group. However, there was no statistically significant difference between the two groups regarding the incidence of tumor recurrence. CONCLUSION: The incidence of thyroid gland invasion by an advanced laryngeal carcinoma is low. Preservation of the thyroid gland during laryngectomy to reduce the risk of thyroid dysfunction does not affect the oncological control.

Addressing Discrepancies between Experimental and Computational Procedures.

Imaging subject-specific heart valve, a crucial step to its design, has experimental variables that if unaccounted for, may lead to erroneous computational analysis and geometric errors of the resulting model. Preparation methods are developed to mitigate some sources of the geometric error. However, the resulting 3D geometry often does not retain the original dimensions before excision. Inverse fluid-structure interaction analysis is used to analyze the resulting geometry and to assess the valve's closure. Based on the resulting closure, it is determined if the geometry used can yield realistic results. If full closure is not reached, the geometry is adjusted adequately until closure is observed.

Brain Network Analysis of EEG Recordings Can Be Used to Assess Cognitive Function in Teenagers With 15q13.3 Microdeletion Syndrome.

15q13.3 microdeletion syndrome causes a spectrum of cognitive disorders, including intellectual disability and autism. We assessed the ability of the EEG analysis algorithm Brain Network Analysis (BNA) to measure cognitive function in 15q13.3 deletion patients, and to differentiate between patient and control groups. EEG data was collected from 10 individuals with 15q13.3 microdeletion syndrome (14-18 years of age), as well as 30 age-matched healthy controls, as the subjects responded to Auditory Oddball (AOB) and Go/NoGo cognitive tasks. It was determined that BNA can be used to evaluate cognitive function in 15q13.3 microdeletion patients. This analysis also significantly differentiates between patient and control groups using 5 scores, all of which are produced from ERP peaks related to late cortical components that represent higher cognitive functions of attention allocation and response inhibition (P < 0.05).

Clinical trials in mitochondrial disorders, an update.

Mitochondrial disorders comprise a molecular and clinically diverse group of diseases that are associated with mitochondrial dysfunction leading to multi-organ disease. With recent advances in molecular technologies, the understanding of the pathomechanisms of a growing list of mitochondrial disorders has been greatly expanded. However, the therapeutic approaches for mitochondrial disorders have lagged behind with treatment options limited mainly to symptom specific therapies and supportive measures. There is an increasing number of clinical trials in mitochondrial disorders aiming for more specific and effective therapies. This review will cover different treatment modalities currently used in mitochondrial disorders, focusing on recent and ongoing clinical trials.

Hormonal, metabolic and skeletal phenotype of Schaaf-Yang syndrome: a comparison to Prader-Willi syndrome.

BACKGROUND: Nonsense and frameshift mutations in the maternally imprinted, paternally expressed gene MAGEL2, located in the Prader-Willi critical region 15q11-15q13, have been reported to cause Schaaf-Yang syndrome (SYS), a genetic disorder that manifests as developmental delay/intellectual disability, hypotonia, feeding difficulties and autism spectrum disorder. Prader-Willi syndrome (PWS) is a genetic disorder characterised by severe infantile hypotonia, hypogonadotrophic hypogonadism, early childhood onset obesity/hyperphagia, developmental delay/intellectual disability and short stature. Scoliosis and growth hormone insufficiency are also prevalent in PWS.There is extensive documentation of the endocrine and metabolic phenotypes for PWS, but not for SYS. This study served to investigate the hormonal, metabolic and body composition phenotype of SYS and its potential overlap with PWS. METHODS: In nine individuals with SYS (5 female/4 male; aged 5-17 years), we measured serum ghrelin, glucose, insulin-like growth factor 1 (IGF-1), insulin-like growth factor binding protein 3, follicle-stimulating hormone, luteinising hormone, thyroid-stimulating hormone, free T4, uric acid and testosterone, and performed a comprehensive lipid panel. Patients also underwent X-ray and dual-energy X-ray absorptiometry analyses to assess for scoliosis and bone mineral density. RESULTS: Low IGF-1 levels despite normal weight/adequate nutrition were observed in six patients, suggesting growth hormone deficiency similar to PWS. Fasting ghrelin levels were elevated, as seen in individuals with PWS. X-rays revealed scoliosis >10° in three patients, and abnormal bone mineral density in six patients, indicated by Z-scores of below -2 SDs. CONCLUSION: This is the first analysis of the hormonal, metabolic and body composition phenotype of SYS. Our findings suggest that there is marked, but not complete overlap between PWS and SYS.

The complex behavioral phenotype of 15q13.3 microdeletion syndrome.

BACKGROUND: Chromosome 15q13.3 represents a hotspot for genomic rearrangements due to repetitive sequences mediating nonallelic homologous recombination. Deletions of 15q13.3 have been identified in the context of multiple neurological and psychiatric disorders, but a prospective clinical and behavioral assessment of affected individuals has not yet been reported. METHODS: Eighteen subjects with 15q13.3 microdeletion underwent a series of behavioral assessments, along with clinical history and physical examination, to comprehensively define their behavioral phenotypes. RESULTS: Cognitive deficits are the most prevalent feature in 15q13.3 deletion syndrome, with an average nonverbal IQ of 60 among the patients studied. Autism spectrum disorder was highly penetrant, with 31% of patients meeting clinical criteria and exceeding cutoff scores on both ADOS-2 and ADI-R. Affected individuals exhibited a complex pattern of behavioral abnormalities, most notably hyperactivity, attention problems, withdrawal, and externalizing symptoms, as well as impairments in functional communication, leadership, adaptive skills, and activities of daily living. CONCLUSIONS: The 15q13.3 deletion syndrome encompasses a heterogeneous behavioral phenotype that poses a major challenge to parents, caregivers, and treating providers. Further work to more clearly delineate genotype-phenotype relationships in 15q13.3 deletions will be important for anticipatory guidance and development of targeted therapies.Genet Med 18 11, 1111-1118.

Assessment of Cognitive Outcome Measures in Teenagers with 15q13.3 Microdeletion Syndrome.

15q13.3 microdeletion syndrome causes a spectrum of cognitive disorders, including intellectual disability and autism. We aimed to determine if any or all of three cognitive testing systems (the KiTAP, CogState, and Stanford-Binet) are suitable for assessment of cognitive function in affected individuals. These three tests were administered to ten individuals with 15q13.3 microdeletion syndrome (14-18 years of age), and the results were analyzed to determine feasibility of use, potential for improvement, and internal consistency. It was determined that the KiTAP, CogState, and Stanford-Binet are valid tests of cognitive function in 15q13.3 microdeletion patients. Therefore, these tests may be considered for use as objective outcome measures in future clinical trials, assessing change in cognitive function over a period of pharmacological treatment.

Presymptomatic differences in Toll-like receptor function in infants who have allergy.

BACKGROUND: Microbial exposure might play a key role in allergy development, but little is known about the role of Toll-like receptors (TLRs). OBJECTIVE: This study explored the association between neonatal TLR microbial recognition/function, allergy risk (maternal allergy), and prospective allergy development. METHODS: Cord blood mononuclear cells (n = 111) were cultured either alone or with optimal concentrations of TLR ligands: lipoteichoic acid (TLR2), polyinosinicpolycytidylic acid (TLR3), LPS with IFN-gamma (TLR4), flagellin (TLR5), imiquimod R837 (TLR7), or CpG (TLR9). Cytokine responses were assessed in relation to allergy risk (maternal allergy) and allergy outcomes (sensitization, food allergy, and atopic dermatitis) at 12 months of age. RESULTS: Maternal allergy (n = 59) was associated with significantly higher neonatal IL-12 and IFN-gamma responses to TLR2, TLR3, and TLR4 activation, whereas TNF-alpha and IL-6 responses to TLR2, TLR4, and TLR5 activation were significantly higher in newborns who subsequently had allergic disease (n = 32). Notably, consistent with previous reports, newborns who had disease had lower T(H)1 IFN-gamma response to mitogens (PHA). CONCLUSION: Allergic disease was associated with increased (rather than decreased) perinatal TLR responses. Further studies are needed to determine how these responses track in the postnatal period and whether this relative hyperresponsiveness is a product of intrauterine influences, including maternal atopy, functional genetic polymorphisms, or both.

NOS1 polymorphism is associated with atopy but not exhaled nitric oxide levels in healthy children.

Exhaled nitric oxide (FENO) is raised in atopy. The mechanism for this is unclear. The aim of this study was to investigate whether the number of AAT repeats in intron 20 of the NOS1 gene, recently associated with variations in FENO in adults with asthma and cystic fibrosis, was associated with the raised FENO in healthy atopic children. Eighty-seven healthy children (44 girls, 42 atopic, age range 6-18 years) underwent measurements of FENO, spirometry, airway responsiveness and skin prick testing. Genotyping was carried out to determine the number of AAT repeats. There was no association between the number of AAT repeats and FENO in either the whole sample of healthy children (n = 87) or in the subsample of healthy atopics (n = 42). However, a greater number of atopic children had two high repeat alleles compared with non-atopic children (33.3% vs. 13.6%, respectively, p = 0.03). This suggests that variations in the NOS1 gene may contribute to atopy without this relationship being reflected by FENO.