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PubMed2004

Recessively inherited coagulation disorders.

Deficiencies of coagulation factors other than factor VIII and factor IX that cause bleeding disorders are inherited as autosomal recessive traits and are rare, with prevalences in the general population varying between 1 in 500 000 and 1 in 2 million for the homozygous forms. As a consequence of the rarity of these deficiencies, the type and severity of bleeding symptoms, the underlying molecular defects, and the actual management of bleeding episodes are not as well established as for hemophilia A and B. We investigated more than 1000 patients with recessively inherited coagulation disorders from Italy and Iran, a country with a high rate of recessive diseases due to the custom of consanguineous marriages. Based upon this experience, this article reviews the genetic basis, prevalent clinical manifestations, and management of these disorders. The steps and actions necessary to improve the condition of these often neglected patients are outlined.

Blood Coagulation Disorders, Inherited↗
PubMed2006

Autosomal recessive cerebellar ataxias.

Autosomal recessive cerebellar ataxias (ARCA) are a heterogeneous group of rare neurological disorders involving both central and peripheral nervous system, and in some case other systems and organs, and characterized by degeneration or abnormal development of cerebellum and spinal cord, autosomal recessive inheritance and, in most cases, early onset occurring before the age of 20 years. This group encompasses a large number of rare diseases, the most frequent in Caucasian population being Friedreich ataxia (estimated prevalence 2-4/100,000), ataxia-telangiectasia (1-2.5/100,000) and early onset cerebellar ataxia with retained tendon reflexes (1/100,000). Other forms ARCA are much less common. Based on clinicogenetic criteria, five main types ARCA can be distinguished: congenital ataxias (developmental disorder), ataxias associated with metabolic disorders, ataxias with a DNA repair defect, degenerative ataxias, and ataxia associated with other features. These diseases are due to mutations in specific genes, some of which have been identified, such as frataxin in Friedreich ataxia, alpha-tocopherol transfer protein in ataxia with vitamin E deficiency (AVED), aprataxin in ataxia with oculomotor apraxia (AOA1), and senataxin in ataxia with oculomotor apraxia (AOA2). Clinical diagnosis is confirmed by ancillary tests such as neuroimaging (magnetic resonance imaging, scanning), electrophysiological examination, and mutation analysis when the causative gene is identified. Correct clinical and genetic diagnosis is important for appropriate genetic counseling and prognosis and, in some instances, pharmacological treatment. Due to autosomal recessive inheritance, previous familial history of affected individuals is unlikely. For most ARCA there is no specific drug treatment except for coenzyme Q10 deficiency and abetalipoproteinemia.

Abetalipoproteinemia↗
PubMed2002

A novel form of autosomal recessive pure hereditary spastic paraplegia maps to chromosome 13q14.

BACKGROUND: Hereditary spastic paraplegia (HSP) is a clinically and genetically heterogeneous disorder characterized by a progressive weakening and spasticity of the lower limbs. HSP is classified according to the presence or absence of accompanying neurologic problems and by the mode of inheritance. Currently, 17 loci have been linked to the various forms of HSP. OBJECTIVE: To determine the chromosomal location of a gene causing pure autosomal recessive spastic paraplegia. METHODS: Genotyping using fluorescently labeled microsatellite markers was performed on three affected individuals and three unaffected individuals from a family displaying pure autosomal recessive HSP (ARHSP) and sensorineural deafness. All family members were then included in the analysis to narrow the genetic interval. Candidate genes were screened for the presence of mutations by heteroduplex analysis. RESULTS: The paraplegic trait linked to a 1.8-Mb region of chromosome 13q14 flanked by the FLJ11712 gene and the microsatellite marker D13S270. The deafness did not link to this region and did not cosegregate with the paraplegic trait. CONCLUSION: The HSP that this family had represents a novel genetic form of pure ARHSP as no other form of HSP (autosomal dominant or recessive) has been linked to chromosome 13.

Abnormalities, Multiple↗
PubMed1997

A clinical, electrophysiologic, neuropathologic, and genetic study of two large Algerian families with an autosomal recessive demyelinating form of Charcot-Marie-Tooth disease.

The hereditary sensory and motor neuropathies form a clinically heterogenous group of disorders, the most frequent of which is Charcot-Marie-Tooth disease (CMT). The autosomal dominant forms of CMT are well characterized, but the nosology of autosomal recessive CMT is still controversial. We report two large consanguineous Algerian families with an autosomal recessive demyelinating CMT and similar clinical manifestations. The clinical, electrophysiologic, and neuropathologic features resemble those of autosomal dominant CMT1, but the early onset and rapid progression of deformities are specific. We excluded by linkage analysis the three loci CMT1A (17p11.2), CMT1B (1q22-23), and CMT4A (8q11-21.1) responsible for demyelinating forms of CMT. These findings suggest a subtype of autosomal recessive neuropathy, the locus of which is undetermined.

Adolescent↗
PubMed1998

Multiple mtDNA deletions features in autosomal dominant and recessive diseases suggest distinct pathogeneses.

Multiple mitochondrial DNA (mtDNA) deletions have been described in patients with autosomal dominant progressive external ophthalmoplegia (AD-PEO) and in autosomal recessive disorders including mitochondrial neurogastrointestinal encephalomyopathy (MNGIE) and autosomal recessive cardiomyopathy ophthalmoplegia (ARCO). The pathogenic bases of these disorders are unknown. We studied three patients with AD-PEO and three patients with autosomal recessive (AR)-PEO (two patients with MNGIE and one patient with ARCO). Histochemistry and Southern blot analyses of DNA were performed in skeletal muscle from the patients. Muscle mtDNA was used to characterize the pattern and amounts of the multiple mtDNA rearrangements; PCR analysis was performed to obtain finer maps of the deleted regions in both conditions. The patients with AD-PEO had myopathic features; the patients with AR-PEO had multisystem disorders. The percentage of ragged-red and cytochrome c oxidase-negative fibers tended to be higher in muscle from the patients with AD-PEO (19% +/- 13.9, 29.7 +/- 26.3) than in muscle from the patients with AR-PEO (1.4% +/- 1.4, 3.3% +/- 3.2; p < 0.10). The sizes of the multiple mtDNA deletions ranged from approximately 4.0 to 10.0 kilobases in muscle from both groups of patients, and in both groups, we identified only deleted and no duplicated mtDNA molecules. Patients with AD-PEO harbored a greater proportion of deleted mtDNA species in muscle (31% +/- 5.3) than did patients with AR-PEO (9.7% +/- 9.1; p < 0.05). In the patients with AD-PEO, we identified a deletion that included the mtDNA heavy strand promoter (HSP) region, which had been previously described as the HSP deletion. The HSP deletion was not present in the patients with AR-PEO. Our findings show the clinical, histologic, and molecular genetic heterogeneity of these complex disorders. In particular, the proportions of multiple mtDNA deletions were higher in muscle samples from patients with AD-PEO than in those from patients with AR-PEO.

Adult↗
PubMed2000

Linkage to chromosome 13q11-12 of an autosomal recessive cerebellar ataxia in a Tunisian family.

OBJECTIVE: To report the clinical findings and the genetic linkage mapping of an autosomal recessive cerebellar ataxia associated to peripheral neuropathy, showing an early onset cerebellar ataxia with retained tendon reflexes (EOCA) phenotype. BACKGROUND: EOCA is a clinical syndrome delimited by Harding distinguished from Friedreich's ataxia (FA) mainly by the preservation of tendon reflexes. Molecular genetic study of patients with EOCA has demonstrated genetic heterogeneity. A form of autosomal recessive spastic ataxia has been described in Charlevoix Saguenay area in Quebec (ARSACS); the gene responsible has been mapped to chromosome 13q. METHODS: Genetic linkage analysis was performed on 18 members of a large family including 8 of 9 members with EOCA. After exclusion of FA and ataxia with vitamin E deficiency loci as well as loci of autosomal dominant cerebellar ataxias, we performed a linkage analysis to markers of 13q11-12 region. RESULTS: The 9 affected members of this family showed stereotyped clinical features with cerebellar ataxia, pyramidal syndrome, and a variable degree of axonal peripheral neuropathy. Linkage was detected between the disease locus and the microsatellite marker D13S232. Surrounding markers to D13S232 confirmed the linkage and showed the homozygosity of the affected members. CONCLUSION: The family reported here showed the same locus as autosomal recessive spastic ataxia Charlevoix Saguenay disease.

Adolescent↗
PubMed2001

A somatic and germline mosaic mutation in MPZ/P(0) mimics recessive inheritance of CMT1B.

OBJECTIVE: To identify the molecular basis of a demyelinating Charcot-Marie-Tooth disease type 1 (CMT1) with presumed autosomal recessive inheritance. BACKGROUND: CMT1, an inherited motor and sensory neuropathy with low nerve conduction velocities, is caused by dominantly inherited mutations in the genes of the peripheral myelin protein 22 (PMP22), myelin protein zero (MPZ/P(0)), and early growth response 2 transcription factor (EGR2/Krox-20). PATIENTS AND METHODS: Two young sisters born of clinically and electrophysiologically healthy parents had a severe CMT1 neuropathy of presumed autosomal recessive inheritance. The older sister underwent a nerve biopsy. The authors analyzed PMP22, MPZ/P(0), and EGR2/Krox-20 by automated direct nucleotide sequencing. For rapid mutation detection, they determined the restriction-fragment-length polymorphisms for TaqI in the fluorescein-labeled target DNA sequence amplified by PCR. RESULTS: Nerve biopsy disclosed a demyelinating and remyelinating neuropathy with onion bulb formations. Both sisters had a novel heterozygous G308-->A transition of MPZ/P(0) without any mutation of PMP22 or EGR2/Krox-20. The G308-->A transition was a nonconservative mutation that changed a glycine into a glutamate at the amino acid residue 74 in the extracellular domain of the mature MPZ/P(0). None of 50 healthy controls had the mutation. The healthy mother had a low amount of the mutation in blood (congruent with 20%) as well as in skin, buccal epithelium, and hairs (30%). Because the healthy mother carried clones of somatic mutant cells and had transmitted the G308-->A transition to the affected daughters, she also harbored germline mutant cells. CONCLUSION: In hereditary demyelinating neuropathies, somatic and germline mosaicism of dominant mutations in the myelin protein genes may mimic autosomal recessive inheritance.

Adolescent↗
PubMed2001

Adult-onset autosomal recessive ataxia with thalamic lesions in a Finnish family.

OBJECTIVE: To describe an unusual kindred with adult-onset ataxia and thalamic lesions detected by brain MRI. METHODS: The authors characterized clinical, laboratory, and pathologic features of the disease and sought linkage to previously recognized ataxia loci. RESULTS: Two sisters and a brother developed progressive ataxia, dysarthria, mild cognitive impairment, and sensorimotor neuropathy at age 30, combined with epilepsy in one sibling. MRI showed symmetric thalamic lesions, changes in brainstem gray matter, and white matter changes in the cerebellum. Autopsy in one of the patients revealed neuronal degeneration with a peculiar vacuolar change in thalamus, probably representing transsynaptic degeneration in response to deafferentation. Neuronal and secondary tract degeneration was observed in the spinal cord, cerebellum, and brainstem suggesting a spinocerebellar degeneration. The disorder appears to be transmitted as an autosomal recessive trait. Genetic and sequence analysis of the FRDA gene and comprehensive laboratory examinations excluded Friedreich's ataxia and other similar recessive diseases. CONCLUSION: Adult-onset recessive ataxia with bilateral thalamic lesions in this family may represent a distinct hereditary spinocerebellar ataxia.

Adult↗
PubMed2006

Molecular genetics of autosomal-recessive axonal Charcot-Marie-Tooth neuropathies.

Autosomal-recessive forms of Charcot-Marie-Tooth (ARCMT) account for less than 10% of the families with CMT. On the other hand, in countries with a high prevalence of consanguinity this mode of inheritance accounts, likely, for the vast majority of CMT phenotypes. Like dominant forms, autosomal-recessive forms are generally subdivided into demyelinating forms (autosomal-recessive CMT1: ARCMT1 or CMT4) and axonal forms (ARCMT2). Until now, demyelinating ARCMT were more extensively studied at the genetic level than the axonal forms. Although the latter are undoubtedly the rarest forms among the heterogeneous group of CMT, three distinct forms have been genetically mapped and recent studies in the past 4 yr provided evidence that their respective causing genes have been characterized. Indeed, gene defects in encoding A-type lamins (LMNA), encoding Ganglioside-induced Differentiation-Associated Protein-1 (GDAP1) and encoding the mediator of RNA polymerase II transcription, subunit 25 homolog (MED25) have been identified in ARCMT2 subtypes. Given the clinical, electrophysiological and histological heterogeneity of CMT2, it is likely that unreported forms of ARCMT2, related to novel genes, remain to be discovered, leading to an even more complex classification. However, our goal in this review is to provide the reader with a clear view on the known genes and mechanisms involved in ARCMT2 and their associated phenotypes.

Animals↗
PubMed1992

Identification of the homozygous recessive genotype for the deficiency of uridine monophosphate synthase in 35-day bovine embryos.

Holstein-Friesian cattle heterozygous for the deficiency of uridine monophosphate (UMP) synthase have half-normal activity of UMP synthase. The homozygous recessive genotype would result in little or no activity, has not been observed among live animals and apparently leads to embryonic mortality at approximately Day 40 of gestation. Activity of UMP synthase averaged 2.74 +/- 0.61 units/mg protein for 19 obligatory normal embryos (from normal x normal matings). Activity for 18 embryos from heterozygote x heterozygote matings yielded three non-overlapping groups as follows: (i) five presumed normals with greater than two-thirds normal activity, (ii) ten apparent heterozygotes with one-third to two-thirds normal activity and (iii) three putative homozygous recessive embryos with less than one-third normal activity. The distribution among these groups was consistent with the 1:2:1 ratio expected for autosomal inheritance. Conception of embryos homozygous recessive for this disorder was demonstrated.

Animals↗
PubMed2001

Resistance to Bacillus sphaericus in Culex pipiens (Diptera: Culicidae): interaction between recessive mutants and evolution in southern France.

In southern France, failure to control Culex pipiens L. with Bacillus sphaericus Neide toxin (Bs) was first detected in 1994, at the extreme east of the Languedoc-Roussillon coast. This failure was due to a single recessive mutant, sp-1R. Two complementary strategies were used to test whether sp-1R had invaded the Bs-controlled area by 1998. First, a strain (BP) was selected from resistant larvae sampled in the western part of the Bs-controlled area. In BP strain, resistance involved a single recessive gene, sp-2R, distinct from sp-1R, that conferred a similarly high resistance in the homozygous state (approximately 6,000-fold). Combining one copy of sp-1R and one of sp-2R conferred a > 100-fold resistance. Second, Bs-resistance was monitored among the offspring of field females crossed to sp-1RR homozygous males. Females were sampled in 20 localities of southern France and three localities of the Llobregat delta (Barcelona, Spain) where C. pipiens control is also intensive. The 537 females in the study produced enough larvae to infer their genotype: 462 progenies were susceptible and the survival rate of 51 others was explained by the presence of sp-1R and/or sp-2R. The remaining 24 cases indicated that other factors could confer resistance when combined with sp-1R. The current data showed that, even when recessive, resistant mutants can rapidly increase in frequency, providing some interactions that protect them from disappearance. We discuss the consequences of this finding on the current strategies aimed to avoid or delay resistance in the pests controlled with B. sphaericus or B. thuringiensis Berliner toxins.

Animals↗
PubMed2006

Genetic investigation of autosomal recessive distal renal tubular acidosis: evidence for early sensorineural hearing loss associated with mutations in the ATP6V0A4 gene.

Mutations in the ATP6V1B1 and ATP6V0A4 genes, encoding subunits B1 and 4 of apical H(+) ATPase, cause recessive forms of distal renal tubular acidosis (dRTA). ATP6V1B mutations have been associated with early sensorineural hearing loss (SNHL), whereas ATP6V0A4 mutations are classically associated with either late-onset SNHL or normal hearing. The phenotype and genotype of 39 new kindreds with recessive dRTA, 18 of whom were consanguineous, were assessed. Novel and known loss-of-function mutations were identified in 31 kindreds. Fourteen new and five recurrent mutations of the ATP6V0A4 gene were identified in 21 families. For the ATP6V1B1 gene, two new and two previously described mutations were identified in 10 families. Surprisingly, seven probands with ATP6V0A4 gene mutations developed severe early SNHL between the ages of 2 mo and 10 yr. No mutation was detected in eight families. These data extend the spectrum of disease-causing mutations and provide evidence for genetic heterogeneity in SNHL. The data also demonstrate that mutations in either of these genes may cause early deafness, and they highlight the importance of genetic screening for recessive forms of dRTA independent of hearing status.

Acidosis, Renal Tubular↗
PubMed2003

Surgical therapies for the treatment of gingival recession. A systematic review.

BACKGROUND: A variety of soft tissue augmentation procedures directed at root coverage have been documented in the literature utilizing autogenous or allogenic soft tissue grafting or guided tissue regeneration (GTR). RATIONALE: The purpose of this systematic review was to assess the literature regarding the efficacies of various surgical gingival augmentation procedures relative to clinical and patient-oriented outcomes. FOCUSED QUESTION: What is the effect of surgical therapy for root coverage in patients with gingival recession compared with other treatment modalities or baseline values? SEARCH PROTOCOL: PubMed and the Cochrane Oral Health Group Trials Register were searched to identify human studies in English investigating the therapeutic use of a soft tissue surgical procedure to treat gingival recession. Searches were performed for articles published by April 2002. SELECTION CRITERIA: Initial screening of identified abstracts accepted all studies evaluating surgical intervention of gingival recession. Independent review by 2 reviewers evaluated full-text reports regarding study characteristics. Only those studies determined to be randomized clinical trials (RCTs) were included in the final analysis. DATA ANALYSIS AND COLLECTION: Outcome measures included changes in root coverage, clinical attachment levels (CAL), probing depth (PD), and width of keratinized tissue (KT). The only data suitable for meta-analysis were comparisons of the efficacy of connective tissue grafts with GTR. MAIN RESULTS: 1. Thirty-two articles (total study population: 687) met the criteria for RCTs: 11 (population: 286) related to various autogenous soft tissue augmentation procedures; 18 (population: 360) to GTR; and 3 (population: 41) to allogenic soft tissue augmentation. 2. Meta-analysis identified greater gains in both root coverage and keratinized tissue width for connective tissue graft procedures compared to GTR. 3. No other data were compatible with meta-analysis. REVIEWERS' CONCLUSIONS: 1. Soft tissue augmentation procedures are effective means of obtaining root coverage. 2. Connective grafting techniques appear to have an advantage over GTR. 3. There is a need for further efficacy studies and for investigation of these procedures relative to patient-oriented outcomes such as esthetics, root sensitivity, and postoperative morbidities.

Connective Tissue↗
PubMed1993

Histologic assessment of new attachment following the treatment of a human buccal recession by means of a guided tissue regeneration procedure.

A deep, long-standing recession on a mandibular incisor was treated in a 56-year-old female patient. The tooth was tilted buccally and was scheduled for extraction. The recession was 8 mm deep, with a pocket depth of 1 mm and no keratinized tissue. The recession was treated by guided tissue regeneration; the membrane was left in place for 4 weeks. The tooth was extracted along with marginal tissues 5 months after the removal of the membrane. At the time of extraction, 4 mm of root coverage had been achieved and 3 mm of keratinized tissue were measured buccally. Histologic measurements showed that 3.66 mm of new connective tissue attachment had been obtained associated with newly formed cementum (2.48 mm) and bone growth (1.84 mm). The crestal bone level after treatment was located coronal to the preoperative location of the gingival margin.

Alveolar Process↗
PubMed1994

Combined guided tissue regeneration, root conditioning, and fibrin-fibronectin system application in the treatment of gingival recession. A 15-case report.

This paper describes a surgical technique to achieve root coverage in deep, wide gingival recessions using a root isolation procedure with ePTFE membrane, combined with tetracycline conditioning of the root surface and fibrin-fibronectin sealing system application. The technique was used on 15 patients with isolated mucogingival defects 4 to 6 mm deep. A large trapezium-shaped flap was raised 3 to 4 mm apical to the margin of the bone dehiscence. The root surface was thoroughly scaled by hand and rotating instruments. Tetracycline HCl solution (100 mg/ml) was topically applied for 4 minutes. Expanded polytetrafluoroethylene (ePTFE) membrane was adapted at least 1 mm coronal to the CEJ and retained in position by sling sutures. A film of fibrin-fibronectin sealing system was injected between the membrane and the root surface. The flap was sutured coronally and the membrane removed 6 weeks later. The patients were reevaluated 6 months after the reentry procedure. The mean recession depth decreased from 4.7 mm initially to 1.1 mm at the final postoperative appointment. This represents a mean root coverage of 77.4%. Mean probing depth reduction was 0.9 mm and the mean width of keratinized tissue increased from 1.8 mm preoperatively to 2.9 mm 6 months after surgery. These findings show that the treatment of buccal gingival recession using guided tissue regeneration procedure plus tetracycline root demineralization and fibrin-fibronectin glue application results in a consistent and predictable improvement of mucogingival defects.

Adult↗
PubMed1998

Histologic evaluation of new attachment utilizing a titanium-reinforced barrier membrane in a mucogingival recession defect. A case report.

Guided tissue regeneration was USED to treat a localized, deep, buccal recession on a mandibular left central incisor. This tooth was labially displaced and scheduled for extraction for orthodontic reasons. The mucogingival defect had 7 mm of facial gingival recession, and 4 mm mid-buccal probing depths. The attachment loss was 11 mm. There was no attached gingiva. At surgery the root was notched as landmarks for assessing the histological examination. A titanium reinforced barrier membrane was left in place for 4 weeks. At the time of extraction, 9 months post-initial treatment, there was a gain of 3 mm of root coverage and 1 mm of gingiva. The tooth and facial tissues were removed by block section for histologic evaluation. The root surface exhibited a total amount of a histologic new connective tissue attachment of 5.6 mm and regeneration of a new bone growth of 6.7 mm of bone. The histologic findings demonstrated that the coronal extent of the new attachment and new facial bone, 9 months after guided tissue regeneration treatment, were located coronal to the preoperative location, in a root surface previously exposed by a deep, long-standing recession.

Bone Regeneration↗
PubMed1999

Adverse effects associated with a bioabsorbable guided tissue regeneration device in the treatment of human gingival recession defects. A clinicopathologic case report.

This clinicopathologic case report documents an adverse effect associated with the use of a polylactic acid-based barrier in the treatment of human gingival recession defects. A total of 27 consecutively treated patients, in whom guided tissue regeneration with a polylactic acid barrier was used to correct gingival recession defects, were evaluated. This adverse effect consisted of a midradicular-apical swelling, generally asymptomatic, with no apparent predilection for gender, age, tooth type or location (maxilla/mandible), or surgical procedure. It was observed in 14 of 27 (52%) patients and 22 of 41 (54%) defects. The swelling decreased in size over time and in most cases, it completely resolved within 12 months postsurgery. Histopathologic evaluation of a 14-week specimen indicated characteristics (multinucleated giant cells, foamy macrophages) consistent with a foreign body reaction. These findings suggest that patients undergoing GTR procedures with synthetic absorbable devices for the treatment of gingival recession defects should be advised of the possible occurrence of such an adverse effect.

Absorbable Implants↗
PubMed2001

Clinical evaluation of acellular allograft dermis for the treatment of human gingival recession.

BACKGROUND: Periodontal root coverage procedures to treat recession areas are indicated for unesthetic, exposed, and/or painful root surfaces. Many methods, most using autogenous soft tissue grafts, have been utilized, but with associated morbidity at the donor sites. An alternative donor material would reduce the morbidity and provide for sufficient available donor tissue. METHODS: An acellular allogeneic dermal connective tissue matrix (AD) and autogenous palatal connective tissue (CT) were compared as subepithelial grafts for the treatment of gingival recession. Twenty-two patients with similar isolated gingival recession of > or = 2 mm on 2 separate teeth were treated with the subepithelial graft technique. Exposed roots were hand root planed only and, by random allocation, either a fitted AD or fitted CT graft was secured in place and covered by coronally positioned flaps. RESULTS: Mann Whitney U test analysis found the following changes at 6 months for AD and CT, respectively, compared to presurgical conditions: root coverage of 1.7 +/- 1.2 (65.9%) and 2.2 +/- 1.1 mm (74.1%) (both P<0.01), increase in keratinized tissue (KT) of 1.2 +/- 1.3 and 1.6 +/- 1.9 (both P<0.01), and an increase in gingival thickness with both; 83.2% of expected root coverage was obtained with AD and 88.6% with CT (P= 0.43). There were no significant differences between treatments for any parameter. Global assessments by clinicians and patients suggested a more esthetic clinical result with AD. CONCLUSIONS: These results suggest that acellular allogeneic dermal matrix may be a useful substitute for autogenous connective tissue grafts in root coverage procedures.

Adult↗