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Eyal Banin

Publications and source records attributed to Eyal Banin.

At least 19 recordsLinked to original sources
PubMed2025

Founder Homozygous Nonsense CREB3 Variant and Variable-Onset Retinal Degeneration.

IMPORTANCE: Uncovering the genetic basis of inherited retinal diseases (IRDs) can enhance both diagnostic accuracy and the development of targeted treatment strategies. OBJECTIVE: To evaluate the association between a homozygous nonsense variant in CREB3 with IRDs. DESIGN, SETTING, AND PARTICIPANTS: Thirteen patients with a clinical diagnosis of retinitis pigmentosa or cone-rod degeneration were analyzed by whole-genome sequencing (WGS) and whole-exome sequencing (WES). Clinically, patients presented with 2 main phenotypes, rod-cone and cone-rod dystrophies, demonstrating variable electrophysiological and fundoscopic findings. Expression analysis was performed on patient-derived skin fibroblasts using the reverse transcription-polymerase chain reaction and Western blot analysis, and by interrogating previously published retinal single-cell RNA sequence data. Immunohistochemistry staining was performed on wild-type mouse retinal sections using an anti-CREB3 antibody. Patients with variable phenotypes of IRDs were recruited from 3 medical centers in Israel and Italy. Ophthalmologists clinically diagnosed patients at the relevant medical centers and referred them for genetic screening. WES and WGS were performed at different national and international centers, and the findings of the previously unreported gene were shared between investigators. EXPOSURES: CREB3 and IRDs. MAIN OUTCOMES AND MEASURES: The main outcome was evidence supporting an association between CREB3 and IRD. Measures included WES, WGS, and immunohistochemistry staining. RESULTS: A founder homozygous nonsense variant in CREB3 (c.881G>A, p.Trp294*) was identified in 13 patients from 4 unrelated families; 12 descendent from North-African Jewish origins and 1 from Italian origins. All patients manifested retinal degeneration with varying ages at onset. In patient-derived fibroblasts, the variant mRNA transcript generated a truncated CREB3 protein. Expression analysis and immunohistochemistry staining revealed CREB3 RNA and protein expression in various retinal cell types, indicating its vital role in photoreceptor function. CONCLUSIONS AND RELEVANCE: This study found an association between CREB3 and IRDs. CREB3 was previously shown to be upregulated following ultraviolet radiation. This might contribute to the extensive clinical variability observed in this relatively large cohort of homozygous patients with the same truncated variant.

Humans↗
PubMed2025

Non-coding single-nucleotide and structural variants affecting the EYS putative promoter cause autosomal recessive retinitis pigmentosa.

PURPOSE: Variants in untranslated genomic regions are difficult to identify as pathogenic but are capable of causing disease by interfering with gene expression. This study aimed to characterize the effect of variants identified in the 5'-untranslated region of EYS in patients with autosomal recessive retinitis pigmentosa (RP). METHODS: Variant screening included gene panels, Sanger, exome, and genome sequencing. Functional validation included an electrophoretic mobility shift assay and various luciferase assays. RESULTS: Patients with RP from 6 EYS biallelic Arab-Muslim families harbored a 5' noncoding EYS variant, c.-453G>T, and 4 harbored a structural variant affecting the 5' noncoding exons. Electrophoretic mobility shift assay analysis revealed an effect on binding of transcription factors for c.-453G>T and a neighboring variant c.-454G>T. Dual luciferase assays using overexpression of various transcription factors showed distinct effects on expression. c.-453G>T was associated with higher luciferase expression with CRX overexpression and c.-454G>C with OTX2 overexpression. In addition, the 2 variants were found to influence translation by affecting upstream initiation codons. Interestingly, visual function of EYS RP patients who harbor c.-453G>T are better than those with biallelic null EYS variants. CONCLUSION: Our analysis revealed both single-nucleotide and structural variants in the EYS promoter as the cause of autosomal recessive RP. These variants may affect EYS expression via a dual mechanism by altering transcription factor binding affinity at the EYS promoter and by affecting upstream open reading frames.

Humans↗
PubMed2025

Biallelic null variants in C19orf44 cause a unique late-onset retinal dystrophy phenotype characterized by patchy perifoveal chorioretinal atrophy.

PURPOSE: To identify the genetic cause for disease in individuals affected with inherited retinal disease and to characterize their retinal phenotype and the properties of the underlying gene. METHODS: Participants underwent a comprehensive ophthalmological evaluation, including best-corrected visual acuity, visual field testing, fundus autofluorescence, optical coherence tomography, and electroretinography. Genetic analyses included exome, genome, and Sanger sequencing. Gene expression pattern was analyzed by reverse transcription-polymerase chain reaction. Localization of the encoded protein in cells and in the human retina was examined by immunofluorescence staining. RESULTS: Four different pathogenic variants in C19orf44 were identified in 15 biallelic individuals from 11 unrelated families. The most common variant was c.549_550del p.(Ser185ProfsTer2). Most individuals were affected with a unique clinical phenotype characterized by late-onset patchy perifoveal chorioretinal atrophy and electroretinographic features of rod-cone degeneration. C19orf44 is expressed in various human tissues, including the retina, where it was found in the outer nuclear layer and in the outer plexiform layer. In cultured cells (hTERT RPE-1 and HeLa) and in human primary fibroblasts, C19orf44 is found in the nucleus, and it is downregulated during mitosis. CONCLUSION: Based on our results, C19orf44 is crucial for normal human retinal function, and pathogenic variants in this gene are associated with autosomal recessive inherited retinal disease.

Humans↗
PubMed2006

Myeloid progenitors differentiate into microglia and promote vascular repair in a model of ischemic retinopathy.

Vision loss associated with ischemic diseases such as retinopathy of prematurity and diabetic retinopathy are often due to retinal neovascularization. While significant progress has been made in the development of compounds useful for the treatment of abnormal vascular permeability and proliferation, such therapies do not address the underlying hypoxia that stimulates the observed vascular growth. Using a model of oxygen-induced retinopathy, we demonstrate that a population of adult BM-derived myeloid progenitor cells migrated to avascular regions of the retina, differentiated into microglia, and facilitated normalization of the vasculature. Myeloid-specific hypoxia-inducible factor 1alpha (HIF-1alpha) expression was required for this function, and we also demonstrate that endogenous microglia participated in retinal vascularization. These findings suggest what we believe to be a novel therapeutic approach for the treatment of ischemic retinopathies that promotes vascular repair rather than destruction.

Animals↗
PubMed2006

Autozygosity mapping of Bardet-Biedl syndrome to 12q21.2 and confirmation of FLJ23560 as BBS10.

Bardet-Biedl syndrome (BBS) is a genetically heterogeneous autosomal recessive disorder characterized by variable obesity, pigmentary retinopathy, polydactyly, mental retardation, hypogonadism and renal failure. In order to identify novel BBS loci we undertook autozygosity mapping studies using high-density SNP microarrays in consanguineous kindreds. We mapped a BBS locus to a 10.1 Mb region at 12q15-q21.2 in a large Omani BBS family (peak lod score 8.3 at theta = 0.0 for marker D12S1722) that contained the recently described BBS10 locus. Mutation analysis of candidate genes within the target interval, including the BBS10 gene, revealed a homozygous frameshift mutation in FLJ23560 and mutations were also detected in four smaller consanguineous families with regions of autozygosity at 12q21.2. These findings (a) confirm a previous report that FLJ23560 (BBS10) mutations are a significant cause of BBS, and (b) further demonstrate the utility of high-density SNP array mapping in consanguineous families for the mapping and identification of recessive disease genes.

Adult↗
PubMed2006

Phenotypic variability among adult siblings with Sjögren-Larsson syndrome.

BACKGROUND: Sjögren-Larsson syndrome (SLS) is an early childhood-onset disorder with ichthyosis, mental retardation, spastic paraparesis, macular dystrophy, and leukoencephalopathy caused by the deficiency of fatty aldehyde dehydrogenase due to mutations in the ALDH3A2 gene (the gene that encodes microsomal fatty aldehyde dehydrogenase). Cerebral proton magnetic resonance spectroscopy in those with SLS demonstrates an abnormal white matter peak at 1.3 ppm, consistent with long-chain fatty alcohol accumulation. OBJECTIVE: To define the clinical course and proton magnetic resonance spectroscopic findings of SLS in adults. DESIGN AND SETTING: Case series in a tertiary care center. PATIENTS: Six siblings of a consanguineous Arab family with early childhood-onset SLS who carry the 682C-->T mutation in the ALDH3A2 gene were reinvestigated in adulthood. RESULTS: The 6 affected siblings ranged in age from 16 to 36 years. All exhibited the typical clinical and imaging manifestations of SLS, but their severity markedly varied. Neurological involvement was apparently nonprogressive, and its severity showed no correlation with age. Cerebral proton magnetic resonance spectroscopy showed a lipid peak at 1.3 ppm, with decreasing intensity in the older siblings. CONCLUSION: These observations document significant clinical variability and the nonprogressive neurological course of SLS in adult siblings with the same ALDH3A2 genotype, and demonstrate possible correlation of proton magnetic resonance spectroscopic changes with age, suggesting unknown pathogenic mechanisms to compensate for the responsible biochemical defect in this disease.

Adolescent↗
PubMed2006

Application of the standard photodynamic treatment protocol for symptomatic circumscribed choroidal hemangioma.

PURPOSE: To describe the results of photodynamic therapy (PDT) using a standard protocol, developed for treating choroidal neovascularization (CNV), for the treatment of circumscribed choroidal hemangioma (CCH). METHODS: A prospective, uncontrolled, consecutive case series of patients with symptomatic CCH that were treated using the standard PDT protocol was evaluated periodically with ophthalmic exams and echography. RESULTS: Nine CCH patients were included in the study. Mean tumor height decreased from 2.7 mm before treatment to 0.8 mm at the end of the follow-up period. Mean visual acuity improved from 6/15 to 6/12. Six patients required one PDT session, two patients two sessions, and one patient three sessions. Side effects included transient visual disturbances in two patients. One patient, who concomitantly presented with age-related macular degeneration, developed CNV. CONCLUSIONS: The standard PDT protocol is effective for the treatment of CCH. Complications are uncommon. Further studies should assess the optimal PDT protocol for the treatment of CCH.

Adult↗
PubMed2006

T2-TrpRS inhibits preretinal neovascularization and enhances physiological vascular regrowth in OIR as assessed by a new method of quantification.

PURPOSE: A carboxyl-terminal fragment of tryptophan tRNA synthetase (T2-TrpRS) has demonstrated potent angiostatic activity during retinal developmental neovascularization in vivo. The effects of T2-TrpRS on pathologic neovascularization were tested and compared with a potent VEGF antagonist using the mouse model of oxygen-induced retinopathy (OIR). METHODS: C57BL/6J mice were transiently exposed to hyperoxic conditions (75% O2) between postnatal day 7 (P7) and P12 and then returned to room air. Retinas were isolated, blood vessels stained with isolectin Griffonia simplicifolia, images of retinal whole-mounts acquired, and the area of vascular obliteration and extent of preretinal neovascularization quantified. This method was compared to the commonly used method of OIR quantification in which the number of pre-inner limiting membrane (ILM) nuclei is counted in serial sections of whole eyes. To assess the angiostatic activity of T2-TrpRS, mice were injected intravitreally at P12 with either T2-TrpRS, a VEGF aptamer, or vehicle (PBS) alone, and the effects on area of obliteration and on preretinal neovascular tuft formation were assessed. RESULTS: Using a modified method of quantification in the mouse OIR model based on images of isolectin-stained retinal wholemounts, we were able to assess reliably and consistently both vascular obliteration and preretinal neovascular tuft formation in the same specimen. T2-TrpRS demonstrated potent angiostatic activity, reducing the appearance of pathologic neovascular tufts by up to 90%. Surprisingly, T2-TrpRS also enhanced physiological revascularization of the obliterated retinal vasculature, reducing these areas by up to 60% compared with PBS-injected eyes. In contrast, the VEGF antagonist, while similarly reducing preretinal neovascular tuft formation, did not enhance revascularization of the obliterated areas. CONCLUSIONS: Use of a rapid, quantifiable method to assess the effect of T2-TrpRS on retinal angiogenesis in the OIR model demonstrates the importance of a quantification system that permits simultaneous analysis of a drug's effect on vascular obliteration as well as on preretinal neovascularization. The results obtained using this method suggest enhanced clinical value for compounds such as T2-TrpRS that not only inhibit pathologic neovascularization, but also facilitate physiological revascularization of ischemic tissue.

Angiostatic Proteins↗
PubMed2005

Retinal incorporation and differentiation of neural precursors derived from human embryonic stem cells.

Retinal and macular degenerations are a major cause of blindness. Cell transplantation is a possible therapeutic approach for the replacement of degenerating retinal cells. Here, we studied the potential of human embryonic stem cells (hESCs) to survive, integrate, and differentiate into retinal cells after intraocular transplantation. Highly enriched cultures of neural precursors (NPs) expressing transcripts of key regulatory genes of retinal development were developed from the hESCs. After spontaneous differentiation in vitro, the NPs gave rise to progeny expressing markers of retinal progenitors and photoreceptor development, though this was uncommon and cells expressing markers of mature photoreceptors were not observed. After transplantation into rat eyes, the NPs survived for 16 weeks, migrated large distances, and integrated in the host retina. Teratoma tumors were not observed. Human cells expressing rhodopsin, blue cone opsin, and neural retina leucine zipper transcription factor were observed in subretinal grafts, but not within vitreal and inner retinal grafts. The results suggest that hESCs have the potential to differentiate into retinal cells and that the subretinal microenvironment supports their differentiation toward a photoreceptor fate. This may be the first step toward further developments that eventually may allow the use of hESCs for transplantation in retinal degenerations.

Animals↗
PubMed2005

Does postmenopausal hormone replacement therapy affect intraocular pressure?

PURPOSE: To assess the effects of postmenopausal hormone replacement therapy (HRT) on intraocular pressure (IOP). PATIENTS AND METHODS: This was a cross-sectional controlled study, including 107 women aged 60 to 80 years receiving HRT and 107 controls who have never received HRT. All subjects underwent IOP assessment and funduscopic photography for cup-to-disc (C/D) ratios, and completed questionnaires regarding personal and family history of glaucoma, hormone replacement therapy, lifetime estrogen and progesterone exposure, and cardiovascular risk factors. Main Outcome Measures included IOP, prevalence of increased IOP, and C/D ratios. RESULTS: The groups did not differ in mean IOP (15.3 versus 15.3 mm Hg), mean vertical (0.18 versus 0.21) and horizontal (0.17 versus 0.14) C/D ratios, and in prevalence of increased IOP (15% versus 14%), C/D ratio (7% versus 7%), or glaucoma (9% versus 11%). A personal history of ischemic heart disease was the only risk factor associated with increased IOP (O.R. = 4.63, P = 0.003). Lifetime estrogen and progesterone exposure, including pregnancies, deliveries, menstruation years, and the use of oral contraceptives did not significantly affect the risk for increased IOP. CONCLUSION: Hormone replacement therapy and lifetime estrogen and progesterone exposure do not seem to affect IOP or the risk for increased IOP. A personal history of ischemic heart disease may be associated with a higher risk for this disorder.

Aged↗
PubMed2005

Treatment of ocular tissues exposed to nitrogen mustard: beneficial effect of zinc desferrioxamine combined with steroids.

PURPOSE: Exposure of the ocular surface to mustard gas chemical warfare leads to a destructive inflammatory reaction. Both steroids and a novel metalocomplex free radical scavenger, zinc desferrioxamine (Zn/DFO), have been shown to be effective separately in reducing ocular damage. The purpose of the present study was to investigate whether the effectiveness of both medications applied simultaneously is superior to the effectiveness of either one applied alone. METHODS: One eye in each of 52 rabbits was exposed to 2% nitrogen mustard (NM). Topical treatment with eye drops of a metal complex-zinc desferrioxamine (Zn/DFO)-combined with dexamethasone phosphate (0.1%), was compared with the administration of saline or treatment with Zn/DFO or dexamethasone alone. Eight eyes (four animals) that were not exposed to NM served as the control. Examiners masked to the treatment groups assessed the extent of ocular injury and the response to treatment using clinical, histologic, and biochemical criteria. RESULTS: Treatment with the combination of Zn/DFO and dexamethasone was significantly more effective than was dexamethasone or Zn/DFO alone in reducing NM injury to ocular anterior segment structures. In combination-treated eyes, corneal re-epithelization was faster, corneal neovascularization was less severe, and intraocular pressure was not as severely elevated as in the saline or the Zn/DFO- or dexamethasone-alone groups. In addition, systemic antioxidant status was better conserved in the combination-treated animals. CONCLUSIONS: The findings suggest that the combination of topically applied Zn/DFO and dexamethasone, by virtue of their additive inhibitory effects on free radical formation and inflammation, should be considered as a basis for the treatment of ocular mustard gas injuries.

Animals↗
PubMed2005

Three-dimensional in vivo imaging of the mouse intraocular vasculature during development and disease.

PURPOSE: Aberrant growth of blood vessels in the eye is a major cause of vision loss, occurring as a complication of diabetic retinopathy, age-related macular degeneration, and retinal vascular occlusions, among others. Whereas in humans, in vivo angiography is routinely used to image such diseases, many animal models of ocular vascular disease and development rely on dissected tissues that may not accurately represent in vivo conditions and require enucleation of the eye, the death of the animal, or both. METHODS: A method of three-dimensional imaging of blood vessels was used in the living mouse eye that involved scanning laser confocal microscopy and computer-aided image reconstruction. RESULTS: This minimally invasive technique was used to collect three-dimensional images of intraocular vessels in vivo during development. The retinal and choroidal vasculature was studied during development and disease, in models of retinal degeneration, central retinal vein occlusion, and oxygen-induced retinopathy. To aid in investigations into cell-based therapies for retinal disease, two-color imaging was used to localize transplanted cells in relation to the vasculature. This technique was used to perform serial imaging of the ocular vasculature over time, when developmental regression of vessels was observed. CONCLUSIONS: This in vivo vascular imaging approach is valuable in monitoring normal development, disease progression, and efficacy of experimental treatments in mouse models of ocular vascular disease and may have broader applications to the field of angiogenesis by using the readily visualized ocular vascular bed as a surrogate to test pro- and antiangiogenic compounds.

Animals↗
PubMed2004

A two-compartment model of the human retina.

PURPOSE: In this article we question a basic concept in retinal pathology, which views the retina as composed primarily of neural elements, in a single compartment. METHODS: We suggest an alternative approach, centering on the epithelial-glial elements of the retina, dividing the retina into two distinct compartments. The framework of these two compartments is composed of two epithelial-like monostratified cell layers facing each other by their apical surfaces. This model is in agreement with the embryological development of the retina. RESULTS: Each compartment is composed of a monostratified cell layer in which neural elements are embedded and each is supplied by a different blood supply. The inner compartment, also referred to as the Muller cell compartment, extends between the inner and outer limiting membranes. The outer, or RPE, compartment extends between the outer limiting and Bruch's membranes. The border between the two compartments is formed by the outer limiting membrane (OLM). One simplified example utilizing the two-compartment concept is as follows: inner compartment edema (inner blood-retinal barrier breakdown) may manifest as cystoid edema, but not as serous retinal detachment, while outer compartment edema (outer blood-retinal barrier breakdown) may manifest as serous retinal detachment but not as cystoid edema, as long as the integrity of the OLM is maintained. CONCLUSION: A two-compartment approach to the structure of the retina, centering on non-neural elements, may enhance our understanding of some retinal pathologies. Various retinal diseases, mainly of vascular origin, are limited to one of the two compartments.

Animals↗
PubMed2004

Susac syndrome.

OBJECTIVE: The objective of this study was to describe the clinical manifestations; radiographic, audiometric, and retinal fluorescein angiography findings; pathogenesis and treatment of Susac syndrome with review of the literature. STUDY DESIGN: We conducted a retrospective case review. SETTING: This study was conducted at a tertiary referral center. PATIENT: A 50-year-old woman presented with recurrent episodes of neurologic symptoms, bilateral sensorineural hearing loss, and silent retinal artery occlusion. INTERVENTIONS: The patient underwent complete evaluation, including magnetic resonance image studies, audiometric tests, and retinal fluorescein angiography. She was treated initially with corticosteroids and later with other immunosuppressive agents. RESULTS: The patient was initially diagnosed with left sudden sensorineural hearing loss. Despite comprehensive clinical and laboratory studies that did not reveal systemic disease, 3 weeks later, the patient developed vertigo, sensorineural hearing loss, and tinnitus in the opposite ear. The neurologic involvement and the bilateral audiologic manifestations raised the possibility of Susac syndrome. CONCLUSION: Susac syndrome is a rare disorder of unknown origin characterized by the triad of encephalopathy, fluctuating hearing loss, and visual loss resulting from microangiopathy of the brain, cochlea, and retina. The multiple organ involvement seen in Susac syndrome raises a differential diagnosis ranging from autoimmune disease, through systemic vasculitis, to multiple sclerosis. Otolaryngologists should be aware of this syndrome as a result of the vestibulocochlear manifestations and the multidisciplinary evaluation that is required.

Audiometry, Pure-Tone↗
PubMed2004

Rescue of retinal degeneration by intravitreally injected adult bone marrow-derived lineage-negative hematopoietic stem cells.

Inherited retinal degenerations afflict 1 in 3,500 individuals and are a heterogeneous group of diseases that result in profound vision loss, usually the result of retinal neuronal apoptosis. Atrophic changes in the retinal vasculature are also observed in many of these degenerations. While it is thought that this atrophy is secondary to diminished metabolic demand in the face of retinal degeneration, the precise relationship between the retinal neuronal and vascular degeneration is not clear. In this study we demonstrate that whenever a fraction of mouse or human adult bone marrow-derived stem cells (lineage-negative hematopoietic stem cells [Lin- HSCs]) containing endothelial precursors stabilizes and rescues retinal blood vessels that would ordinarily completely degenerate, a dramatic neurotrophic rescue effect is also observed. Retinal nuclear layers are preserved in 2 mouse models of retinal degeneration, rd1 and rd10, and detectable, albeit severely abnormal, electroretinogram recordings are observed in rescued mice at times when they are never observed in control-treated or untreated eyes. The normal mouse retina consists predominantly of rods, but the rescued cells after treatment with Lin- HSCs are nearly all cones. Microarray analysis of rescued retinas demonstrates significant upregulation of many antiapoptotic genes, including small heat shock proteins and transcription factors. These results suggest a new paradigm for thinking about the relationship between vasculature and associated retinal neuronal tissue as well as a potential treatment for delaying the progression of vision loss associated with retinal degeneration regardless of the underlying genetic defect.

Adult↗
PubMed2004

[Experimental therapeutic modalities for retinitis pigmentosa].

Retinitis Pigmentosa (RP) is a heterogeneous group of inherited diseases that cause retinal degeneration, often leading to blindness. Over the last decade, significant insights have been obtained into the mechanisms underlying retinal degeneration in RP. This improved understanding of the pathogenesis of RP, combined with advances in molecular and cellular biology methods as well as electro-optical technologies, have contributed to renewed interest and increasing efforts to design novel therapeutic approaches for RP. In the first part of this review (Harefuah, April 2003), we summarized recent developments in the fields of gene therapy for RP, the use of neurotrophic growth factors, and attempts to alter disease progression by vitamins and nutritional modifications. In this second part of the review, retinal and retinal pigment epithelium transplantation, the potential use of stem cells to replace degenerating retinal cells and attempts to develop a retinal prosthesis using electro-optical devices are described. The exciting progress made in these various experimental directions raises hope that slowing or preventing the progression of retinal degeneration in RP patients, and perhaps even partial restoration of visual function in RP, is within reach.

Disease Progression↗
PubMed2003

Retinal function abnormalities in patients treated with vigabatrin.

OBJECTIVE: To evaluate central and peripheral retinal function in patients treated with vigabatrin, an antiepileptic drug associated with peripheral visual field constriction (VFC). METHODS: Six patients with epilepsy treated with vigabatrin as add-on therapy for at least 3 years were included in this observational case series. All patients underwent a clinical ophthalmologic examination, color vision testing, standard perimetry, and full-field and focal foveal cone electroretinography. Four patients, 3 of whom had VFC, completed specialized computerized static light- and dark-adapted perimetry. RESULTS: In 9 of 11 eyes tested, foveal cone electroretinographic amplitudes were at or below the lower limit of normal. Dark-adapted perimetry demonstrated abnormal rod-derived visual fields in the 3 patients with vigabatrin-attributed VFC, whereas rod-derived thresholds were within normal limits throughout the visual field in the patient who did not have VFC. CONCLUSIONS: Our results suggest that vigabatrin not only impairs peripheral cone-derived function as manifested by VFC but also affects foveal cone electroretinographic amplitudes and rod-derived visual fields. The clinical dilemma regarding the use of vigabatrin therapy is further complicated since central as well as peripheral visual function seems to be adversely affected.

Adolescent↗