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Anti-tumor necrosis factor-alpha monoclonal antibody treatment in a case with persistent juvenile ankylosing spondylitis and inflammatory bowel disease [Jüvenil ankilozan spondilit ve enflamatuvar bagirsak hastaligi olan bir hastada anti-tümör nekrozis faktör-alfa monoklonal antikor tedavisi]
(2003) Öztürk C.; Genel F.; Aksu G.; Bakiler A.R.; Kütükçüler N.
Juvenile ankylosing spondylitis and inflammatory bowel disease rarely develop simultaneously, and the treatment of the disease with disease-modifying antirheumatic drugs might be difficult. In this report we present an eight-year old boy with juvenile ankylosing spondylitis and inflammatory bowel disease resistant to combined therapy of antirheumatismal drugs because of its rarity in childhood. Anti-tumor necrosis factor-? monoclonal antibody administration, a new biological treatment, is discussed in view of the literature.
Association between anti-endomysial antibody and total intestinal villous atrophy in children with coeliac disease
(D.K. Publishing House, 2003) Ozgenc F.; Aksu G.; Aydogdu S.; Akman S.; Genel F.; Kutukculer N.; Alkanat M.B.; Vural Yagci R.
Background: There is growing evidence to suggest that detection of anti-gliadin antibody (AGA) and anti-endomysial antibody (EmA) can serve as sensitive markers of the degree of histological abnormalities in patients with coeliac disease. Aim: To evaluate the association between the presence of AGA and EmA and villous atrophy in intestinal biopsies of children with suspected coeliac disease. Settings and design: Intestinal samples of 46 children with failure to thrive, chronic diarrhoea, malabsorption and short stature with either AGA and/or EmA positivity were evaluated, retrospectively. The diagnosis of coeliac disease was based on ESPGHAN criteria. Methods and material: Patients with total villous atrophy who fulfilled the ESPGHAN criteria for the diagnosis of coeliac disease were diagnosed to have coeliac disease. Nine patients without villous atrophy were taken as negative controls for this study. AGA-IgA was measured both by immunoflourescence (IF) and ELISA and EmA-IgA by IF while patients were on normal diet. Relationship between autoantibody positivity and intestinal total villous atrophy was evaluated. Results: Overall positivity for AGA IgA was 85% (39/46) by IF+EUSA and EmA positivity was 85% (39/46) by IF within the study group. Histological examination revealed total villous atrophy with lymphocyte infiltration and crypt hyperplasia in 37 (80%) patients. AGA IgA was positive in 14 (38%) and 31 (84%) of these children by ELISA and IF, respectively. EmA positivity was detected in 35/37 (95%) cases with atrophy and 4/9 (44%) without atrophy (p=0.002). Thirty out of 37 (81%) patients with villous atrophy had both AGA IgA (IF) and EmA positivity (p=0.186). All of the sixteen patients that had both positive AGA IgA (ELISA+IF) and EmA had total villous atrophy (p=0.037). Conclusion: A significant association between total villous atrophy and EmA positivity has been documented in this study.
Cutaneous leukocytoclastic vasculitis in a child with interleukin-12 receptor beta-1 deficiency
(2006) Kutukculer N.; Genel F.; Aksu G.; Karapinar B.; Ozturk C.; Cavusoglu C.; Casanova J.-L.; Fieschi C.
We report a patient with complete interleukin-12 receptor beta-1 deficiency associated with cutaneous leukocytoclastic vasculitis. The patient experienced Bacille Calmette Guérin, Mycobacterium chelonae, and Salmonella enteritidis infection. Vasculitis affecting both small arteries and postcapillary venules due to deposition of immune complexes was probably caused by S. enteritidis and/or M. chelonae infection. © 2006 Elsevier Inc. All rights reserved.
Dedicator of cytokinesis 8 regulates signal transducer and activator of transcription 3 activation and promotes TH17 cell differentiation
(Mosby Inc., 2016) Keles S.; Charbonnier L.M.; Kabaleeswaran V.; Reisli I.; Genel F.; Gulez N.; Al-Herz W.; Ramesh N.; Perez-Atayde A.; Karaca N.E.; Kutukculer N.; Wu H.; Geha R.S.; Chatila T.A.
Background The autosomal recessive hyper-IgE syndrome (HIES) caused by dedicator of cytokinesis 8 (DOCK8) deficiency shares clinical features with autosomal dominant HIES because of signal transducer and activator of transcription 3 (STAT3) mutations, including recurrent infections and mucocutaneous candidiasis, which are suggestive of TH17 cell dysfunction. The mechanisms underlying this phenotypic overlap are unclear. Objective We sought to elucidate common mechanisms operating in the different forms of HIES. Methods We analyzed the differentiation of CD4+ TH cell subsets in control and DOCK8-deficient subjects. We also examined the role of DOCK8 in regulating STAT3 activation in T cells. TH cell differentiation was analyzed by ELISA, flow cytometry, and real-time PCR measurements of cytokines and TH cell transcription factors. The interaction of DOCK8 and STAT3 signaling pathways was examined by using flow cytometry, immunofluorescence, coimmunoprecipitation, and gene expression analysis. Results There was a profound block in the differentiation of DOCK8-deficient naive CD4+ T cells into TH17 cells. A missense mutation that disrupts DOCK8 guanine nucleotide exchange factor (GEF) activity while sparing protein expression also impaired TH17 cell differentiation. DOCK8 constitutively associated with STAT3 independent of GEF activity, whereas it regulated STAT3 phosphorylation in a GEF activity–dependent manner. DOCK8 also promoted STAT3 translocation to the nucleus and induction of STAT3-dependent gene expression. Conclusion DOCK8 interacts with STAT3 and regulates its activation and the outcome of STAT3-dependent TH17 differentiation. These findings might explain the phenotypic overlap between DOCK8 deficiency and autosomal dominant HIES. © 2016 American Academy of Allergy, Asthma & Immunology
Defects along the TH17 differentiation pathway underlie genetically distinct forms of the hyper IgE syndrome
(Mosby Inc., 2009) Al Khatib S.; Keles S.; Garcia-Lloret M.; Karakoc-Aydiner E.; Reisli I.; Artac H.; Camcioglu Y.; Cokugras H.; Somer A.; Kutukculer N.; Yilmaz M.; Ikinciogullari A.; Yegin O.; Yüksek M.; Genel F.; Kucukosmanoglu E.; Baki A.; Bahceciler N.N.; Rambhatla A.; Nickerson D.W.; McGhee S.; Barlan I.B.; Chatila T.
Background: The hyper IgE syndrome (HIES) is characterized by abscesses, eczema, recurrent infections, skeletal and connective tissue abnormalities, elevated serum IgE, and diminished inflammatory responses. It exists as autosomal-dominant and autosomal-recessive forms that manifest common and distinguishing clinical features. A majority of those with autosomal-dominant HIES have heterozygous mutations in signal transducer and activator of transcription (STAT)-3 and impaired TH17 differentiation. Objective: To elucidate mechanisms underlying different forms of HIES. Methods: A cohort of 25 Turkish children diagnosed with HIES were examined for STAT3 mutations by DNA sequencing. Activation of STAT3 by IL-6 and IL-21 and STAT1 by IFN-? was assessed by intracellular staining with anti-phospho (p)STAT3 and -pSTAT1 antibodies. TH17 and TH1 cell differentiation was assessed by measuring the production of IL-17 and IFN-?, respectively. Results: Six subjects had STAT3 mutations affecting the DNA binding, Src homology 2, and transactivation domains, including 3 novel ones. Mutation-positive but not mutation-negative subjects with HIES exhibited reduced phosphorylation of STAT3 in response to cytokine stimulation, whereas pSTAT1 activation was unaffected. Both patient groups exhibited impaired TH17 responses, but whereas STAT3 mutations abrogated early steps in TH17 differentiation, the defects in patients with HIES with normal STAT3 affected more distal steps. Conclusion: In this cohort of Turkish children with HIES, a majority had normal STAT3, implicating other targets in disease pathogenesis. Impaired TH17 responses were evident irrespective of the STAT3 mutation status, indicating that different genetic forms of HIES share a common functional outcome. © 2009 American Academy of Allergy, Asthma & Immunology.
Do elevated serum IgM levels have to be included in probable diagnosis criteria of patients with ataxia-telangiectasia?
(Biolife s.a.s., 2014) Azarsiz E.; Karaca N.E.; Gunaydin N.C.; Gulez N.; Ozturk C.; Aksu G.; Genel F.; Kutukculer N.
Ataxia-telangiectasia (AT) is a rare multisystem, neurodegenerative genetic disorder that is characterised by progressive neurological abnormalities, oculocutaneous telangiectasias and immunodeficiency. Delay in diagnosis or misdiagnosis is probable due to its wide clinical heterogeneity in infancy. Recurrent sinopulmonary infections are often the only presenting symptom and usually patients have decreased immunoglobulins. A total 10% of patients who present with decreased serum immunoglobulin G and A and with normal or elevated immunoglobulin M levels are often misdiagnosed as hyperimmunoglobulin M syndrome. Definitive diagnosis is made if a patient with progressive cerebellar ataxia has a disease causing mutation on the ATM gene. Ataxia-telangiectasia guideline of the European Society for Immunodeficiencies defines the probable diagnosis criteria. We evaluated twenty ataxia-telangiectasia patients (mean age 13.8±4.1 years) retrospectively who were followed-up for a mean of 38.6±27.0 months. Twelve patients had a family history of consanguinity. A total of 80% patients suffered from various infections. Neoplasms occurred in three of them. Patients showed immunological abnormalities as low IgG (45%), low IgA (65%) and elevated IgM (60%) levels. CD3+CD4+ T lymphocyte frequency was low in 45% patients. The mean AFP concentration at the diagnosis was 191.9±140.1 ng/ mL and the raised IgM values did not show any statistically significant relationship with high AFP concentrations. Frequency of the elevated IgM concentrations in (60%) patients raises the concerns about thinking this finding has to be accepted as a probable diagnosis criterium.
DOCK8 Deficiency: Clinical and Immunological Phenotype and Treatment Options - a Review of 136 Patients
(Springer New York LLC, 2015) Aydin S.E.; Kilic S.S.; Aytekin C.; Kumar A.; Porras O.; Kainulainen L.; Kostyuchenko L.; Genel F.; Kütükcüler N.; Karaca N.; Gonzalez-Granado L.; Abbott J.; Al-Zahrani D.; Rezaei N.; Baz Z.; Thiel J.; Ehl S.; Marodi L.; Orange J.S.; Sawalle-Belohradsky J.; Keles S.; Holland S.M.; Sanal Ö.; Ayvaz D.C.; Tezcan I.; Al-Mousa H.; Alsum Z.; Hawwari A.; Metin A.; Matthes-Martin S.; Hönig M.; Schulz A.; Picard C.; Barlogis V.; Gennery A.; Ifversen M.; van Montfrans J.; Kuijpers T.; Bredius R.; Dückers G.; Al-Herz W.; Pai S.-Y.; Geha R.; Notheis G.; Schwarze C.-P.; Tavil B.; Azik F.; Bienemann K.; Grimbacher B.; Heinz V.; Gaspar H.B.; Aydin R.; Hagl B.; Gathmann B.; Belohradsky B.H.; Ochs H.D.; Chatila T.; Renner E.D.; Su H.; Freeman A.F.; Engelhardt K.; Albert M.H.
Mutations in DOCK8 result in autosomal recessive Hyper-IgE syndrome with combined immunodeficiency (CID). However, the natural course of disease, long-term prognosis, and optimal therapeutic management have not yet been clearly defined. In an international retrospective survey of patients with DOCK8 mutations, focused on clinical presentation and therapeutic measures, a total of 136 patients with a median follow-up of 11.3 years (1.3–47.7) spanning 1693 patient years, were enrolled. Eczema, recurrent respiratory tract infections, allergies, abscesses, viral infections and mucocutaneous candidiasis were the most frequent clinical manifestations. Overall survival probability in this cohort [censored for hematopoietic stem cell transplantation (HSCT)] was 87 % at 10, 47 % at 20, and 33 % at 30 years of age, respectively. Event free survival was 44, 18 and 4 % at the same time points if events were defined as death, life-threatening infections, malignancy or cerebral complications such as CNS vasculitis or stroke. Malignancy was diagnosed in 23/136 (17 %) patients (11 hematological and 9 epithelial cancers, 5 other malignancies) at a median age of 12 years. Eight of these patients died from cancer. Severe, life-threatening infections were observed in 79/136 (58 %); severe non-infectious cerebral events occurred in 14/136 (10 %). Therapeutic measures included antiviral and antibacterial prophylaxis, immunoglobulin replacement and HSCT. This study provides a comprehensive evaluation of the clinical phenotype of DOCK8 deficiency in the largest cohort reported so far and demonstrates the severity of the disease with relatively poor prognosis. Early HSCT should be strongly considered as a potential curative measure. © 2015, Springer Science+Business Media New York.
Evaluation of p53, bcl-2, and interleukin- 15 levels in gingival crevicular fluid of cyclosporin A-treated patients
(2003) Buduneli E.; Genel F.; Atilla G.; Kütükçüler N.
Background: Apoptosis plays an important role in the maintenance of tissue homeostasis. Considering that apoptosis mediators may play a role in the pathogenesis of drug-induced gingival overgrowth, this study was conducted to evaluate p53, bcl-2, and interleukin-15 (IL-15) levels in gingival crevicular fluid (GCF) of cyclosporin A (CsA)-treated patients. Methods: Twenty renal transplant patients exhibiting CsA-induced gingival overgrowth and 15 systemically healthy gingivitis patients were included in the study; 15 systemically and periodontally healthy volunteer subjects served as the healthy control group. GCF samples were obtained from one interdental site with gingival overgrowth (GO+) and one site without (GO-) from each CsA-treated patient; hyperplasia index, probing depth, papilla bleeding index, and plaque presence were recorded. One site from each gingivitis patient and healthy control was selected, GCF samples were obtained, and the same clinical parameters were recorded. GCF p53, bcl-2, and IL-15 levels were analyzed by enzyme-linked immunosorbent assay. The results were tested statistically. Results: p53 and bcl-2 levels were below the minimum detectable level in all GCF samples analyzed. CsA GO+ and CsA GO- sites, as well as gingivitis sites, exhibited significantly higher GCF levels of IL-15 compared to healthy controls (P <0.05). The difference between CsA GO+ sites and gingivitis sites was not statistically significant, although the total amount of IL-15 in CsA GO+ sites was lower than gingivitis sites (P >0.05). The total amount of IL-15 in CsA GO- sites was significantly lower than gingivitis sites (P <0.05). No significant correlation was found between the clinical parameters and GCF IL-15 levels (P >0.05). Conclusions: The pathogenesis of CsA-induced gingival overgrowth is multifactorial. The findings of the present study indicate that IL-15 may play a role in the pathogenesis of CsA-induced gingival overgrowth due to its interactions with CsA and its role in apoptosis and inflammation.
The extended clinical phenotype of 64 patients with dedicator of cytokinesis 8 deficiency
(Mosby Inc., 2015) Engelhardt K.R.; Gertz M.E.; Keles S.; Schäffer A.A.; Sigmund E.C.; Glocker C.; Saghafi S.; Pourpak Z.; Ceja R.; Sassi A.; Graham L.E.; Massaad M.J.; Mellouli F.; Ben-Mustapha I.; Khemiri M.; Kilic S.S.; Etzioni A.; Freeman A.F.; Thiel J.; Schulze I.; Al-Herz W.; Metin A.; Sanal Ö.; Tezcan I.; Yeganeh M.; Niehues T.; Dueckers G.; Weinspach S.; Patiroglu T.; Unal E.; Dasouki M.; Yilmaz M.; Genel F.; Aytekin C.; Kutukculer N.; Somer A.; Kilic M.; Reisli I.; Camcioglu Y.; Gennery A.R.; Cant A.J.; Jones A.; Gaspar B.H.; Arkwright P.D.; Pietrogrande M.C.; Baz Z.; Al-Tamemi S.; Lougaris V.; Lefranc G.; Megarbane A.; Boutros J.; Galal N.; Bejaoui M.; Barbouche M.-R.; Geha R.S.; Chatila T.A.; Grimbacher B.
Background Mutations in dedicator of cytokinesis 8 (DOCK8) cause a combined immunodeficiency (CID) also classified as autosomal recessive (AR) hyper-IgE syndrome (HIES). Recognizing patients with CID/HIES is of clinical importance because of the difference in prognosis and management. Objectives We sought to define the clinical features that distinguish DOCK8 deficiency from other forms of HIES and CIDs, study the mutational spectrum of DOCK8 deficiency, and report on the frequency of specific clinical findings. Methods Eighty-two patients from 60 families with CID and the phenotype of AR-HIES with (64 patients) and without (18 patients) DOCK8 mutations were studied. Support vector machines were used to compare clinical data from 35 patients with DOCK8 deficiency with those from 10 patients with AR-HIES without a DOCK8 mutation and 64 patients with signal transducer and activator of transcription 3 (STAT3) mutations. Results DOCK8-deficient patients had median IgE levels of 5201 IU, high eosinophil levels of usually at least 800/µL (92% of patients), and low IgM levels (62%). About 20% of patients were lymphopenic, mainly because of low CD4+ and CD8+ T-cell counts. Fewer than half of the patients tested produced normal specific antibody responses to recall antigens. Bacterial (84%), viral (78%), and fungal (70%) infections were frequently observed. Skin abscesses (60%) and allergies (73%) were common clinical problems. In contrast to STAT3 deficiency, there were few pneumatoceles, bone fractures, and teething problems. Mortality was high (34%). A combination of 5 clinical features was helpful in distinguishing patients with DOCK8 mutations from those with STAT3 mutations. Conclusions DOCK8 deficiency is likely in patients with severe viral infections, allergies, and/or low IgM levels who have a diagnosis of HIES plus hypereosinophilia and upper respiratory tract infections in the absence of parenchymal lung abnormalities, retained primary teeth, and minimal trauma fractures. © 2015 American Academy of Allergy, Asthma & Immunology.
Hypercoagulability: Interaction between inflammation and coagulation in familial Mediterranean fever
(2007) Aksu G.; Ozturk C.; Kavakli K.; Genel F.; Kutukculer N.
Familial Mediterranean fever (FMF) patients in clinical remission are reported to have increased baseline inflammation. Normal function of the natural anticoagulant pathways is particularly needed in diminishing inflammatory responses. In the presence of subclinical inflammation, natural anticoagulant response may be exaggerated. We aimed to observe the anticoagulant-procoagulant status in attack-free FMF patients. Twenty-seven FMF patients diagnosed in accordance with Tel-Hashomer criteria, and 26 healthy controls were included. All patients were attack-free under regular colchicine treatment. Amyloidosis, autoimmunity, accompanying liver and renal disease, and vasculitis were excluded. Predisposing factors for thrombosis were not present. Acute phase reactants (APRs), anticardiolipin antibody positivity, prothrombin time (PT), activated prothrombin time, thrombin time (TT) and d-dimer, protein C activity, activated protein C resistance, free protein S, antithrombin, lupus anticoagulant, human prothrombin fragment F 1 + 2, and human thrombin/antithrombin III complex were analyzed for all subjects. APRs were comparable with controls. Autoimmune markers were negative in all. Anti-streptolysin titers were significantly different than the control group. PT, TT, protein C activity, and F 1 + 2 levels were significantly different from those of healthy controls. Shortened PT and TT, decreased protein C activity vs increased levels of F 1 + 2 suggested a hypercoagulable state in our patients. The hypercoagulable state detected in FMF patients suggests that screening with abnormal coagulation tests may be beneficial for tracing the future consequences of subclinical inflammation in these patients. Studies covering larger groups of patients are needed to verify the currently observed hypercoagulable status in FMF. © Clinical Rheumatology 2006.
Idiopathic CD4+ T cell lymphocytopenia with the absence of B cells and CD8+28+ cells in peripheral blood
(2002) Kutukculer N.; Aksu G.; Genel F.; Ozturk C.
The absence of B cells and a severe decrease in CD8+28+ cells were observed in two female children with CD4+ T cell lymphocytopenia. Idiopathic (primary) CD4+ lymphocytopenia is a rare entity and its pathogenesis and genetics are not yet known. The literature was reviewed, in particular for severe alterations in B and CD8+28+ cells and for the role of NF-kappa B and p56lck in the immunopathogenesis. Whether the underlying mechanism in idiopathic CD4+ lymphocytopenia is found or not, these patients who present with severe symptoms of a combined immunodeficiency must be treated with intravenous immunoglobin regularly until they have a compatible donor for bone marrow transplantation.
Maternally acquired varicella-zoster virus antibodies disappear at 6 months of age in prematurely born children [1]
(2003) Akisu M.; Yalaz M.; Aksu G.; Arslanoglu S.; Genel F.; Kutukculer N.; Kultursay N.
[No abstract available]
Mechanisms of action of intravenous immunoglobulins [İntravenöz i·mmünglobulinlerin etki mekanizmalari]
(2002) Genel F.; Kütükçüler N.
Intravenous immunoglobulin was originally developed for the treatment of primary immunodeficiencies and subsequently it has been used increasingly in the treatment of patients with autoimmune and inflammatory diseases with beneficial effects. The mode of action of intravenous immunoglobulin is probably multiple distinct mechanisms involving Fc receptor blockade, inhibition of complement binding, modulation of cytokine production, restoration of the idiotypic network and neutralization of pathogenic autoantibodies, modulation of T and B cell activation and differentiation. This article discusses the proposed mechanisms of action of intravenous immunoglobulin in various disorders.
Prospective, Randomized Comparison of OM-85 BV and a Prophylactic Antibiotic in Children with Recurrent Infections and Immunoglobulin A and/or G Subclass Deficiency
(Excerpta Medica Inc., 2003) Genel F.; Kutukculer N.
Background: Patients with immunoglobulin (Ig)A and/or IgG subclass deficiency may be asymptomatic or may have recurrent, mainly respiratory infections. Objective: This study compared the clinical efficacy and tolerability of prophylactic therapy with either the oral immunomodulator bacterial extract OM-85 BV or benzathine penicillin G (BPG) in the prevention of recurrent infections in symptomatic patients. Methods: In this 26-month, prospective, randomized study conducted at the Department of Pediatric Immunology, Ege University (Izmir, Turkey), children aged 1 to 12 years with recurrent infections and IgA and/or IgG subclass deficiency were enrolled. After an initial 12-month control period, patients were randomized to receive OM-85 BV or BPG. OM-85 BV (3.5-mg capsule) was given once daily for the first 10 days of each month for the first 3 months of the study. IM injections of BPG were given at a dose of 1.2 million units (for patients with body weight > 27 kg) or at a half-dose (for patients with body weight ?27 kg) every 3 weeks for 12 months. In nonresponders (ie, those who continued to have recurrent infections at 12-month follow-up), IV immunoglobulin (IVIG) replacement therapy at 400 mg/kg body weight was given every 4 weeks for an additional 12 months. The results of IVIG therapy were assessed by the authors using clinical observation. Adverse effects and adverse drug reactions were documented by the authors for each vaccine, prophylactic therapy, and IVIG. Results: A total of 91 children (56 boys, 35 girls; mean [SD] age at the start of the control period, 46.4 [31.0] months) were enrolled. Of these, 44 were randomized to the OM-85 BV group and 47 to the BPG group. The year before prophylactic therapy, the mean (SD) number of reported infections was 10.7 (3.6) and the mean (SD) number of antibiotic courses was 9.7 (3.6) (OM-85 BV group: mean [SD] number of reported infections, 10.5 [3.3]; mean (SD) number of antibiotic courses, 9.3 [3.3]; BPG group: mean [SD] number of reported infections, 10.8 [3.9], mean (SD) number of antibiotic courses, 10.1 [3.9]). At 12 months, the number of infections and antibiotic courses decreased significantly in the entire study population, but the between-group difference was not significant. Five patients in each group (OM-85 BV group, 11.4%; BPG group, 10.6%) were considered nonresponders and received IVIG treatment. Compared with responders, nonresponders were significantly younger (mean [SD] age, 34.40 [21.70] months vs 52.65 [30.52] months; P = 0.036) and had lower serum IgG (P < 0.001), IgG1 (P = 0.006), IgG2 (P = 0.003), IgG3 (P = 0.035), and IgM (P = 0.008) levels and antibody responses to tetanus toxoid and Haemophilus influenzae type b (Hib) vaccines (P = 0.036 and 0.013, respectively). At 12-month follow-up, a protective effect of the prophylactic IVIG therapy was seen, with a statistically significant reduction in the number of infections to 3.3 (2.4) and in the number of antibiotic courses to 2.7 (2.5) (both P = 0.005). Conclusions: In this study population of children with recurrent infections and IgA and/or IgG subclass deficiency, prophylactic therapy with either OM-85 BV or an antibiotic significantly decreased the number of infections per year. In addition, nonresponders benefited from IVIG replacement therapy. Copyright © 2003 Excerpta Medica, Inc.

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