{"title":"Iodine deficiency diseases in children and adolescents (plenary lecture)","authors":"E. Kasatkina, Э П Касаткина","doi":"10.14341/probl10385","DOIUrl":"https://doi.org/10.14341/probl10385","url":null,"abstract":"The main consequence of iodine deficiency in the environment is the development of goiter in people living in iodine-deficient regions (endemic goiter). In this regard, for a long time it was considered that goiter is the only manifestation of this condition. It has now been proven that, in addition to goiter, iodine deficiency also has other adverse effects on human health. In 1983, the term \"endemic goiter\" was replaced by the term \"iodine deficiency diseases\" (IDD). These diseases are caused by a decrease in the functional activity of the thyroid gland in response to iodine deficiency.","PeriodicalId":342539,"journal":{"name":"Problems of Endocrinology","volume":"100 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132018952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
N. P. Mikaelyan, Y. Knyazev, A. G. Maxina, B. A. Dainyak, A. Y. Gurina, E. P. Mikaelyan, F. S. Dzugkoyeva
{"title":"Insulinreceptor interactions and EPR spectroscopy in experimental diabetes mellitus","authors":"N. P. Mikaelyan, Y. Knyazev, A. G. Maxina, B. A. Dainyak, A. Y. Gurina, E. P. Mikaelyan, F. S. Dzugkoyeva","doi":"10.14341/probl10396","DOIUrl":"https://doi.org/10.14341/probl10396","url":null,"abstract":"Insulin concentration in the blood and the level of its binding in tissues inversely correlate in experimental diabetes mellitus. Insulin-binding activity in cells and the microviscosity and hydrophilism of plasma membranes are in inverse correlation. ATP modifies insulin reception.","PeriodicalId":342539,"journal":{"name":"Problems of Endocrinology","volume":"28 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"133174012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Diabetic involvement of the organ of vision","authors":"A. P. Nesterov","doi":"10.14341/probl10388","DOIUrl":"https://doi.org/10.14341/probl10388","url":null,"abstract":"Diabetic involvements of the organ of vision may be divided into extraocular and ocular. The first group includes xanthelasma and eczemas of the eyelids, hordeolum, chalasion, blepharitis, acute and chronic conjunctivitis, conjunctival angiopathies, and pareses of the extraocular muscles. The second group in- cludes*iridal dystrophy, anterior uveitis, cataract, glaucoma, asteroid hyalosis, lipemia rctinalis, and diabetic retinopathy with its complications (hemophthalmia, detachment of the retina, and neovascu- lar glaucoma). Diabetic retinopathy is a late complication of diabetes mellitus. The author discusses the epidemiology of this condition, its pathophysiological and clinical features, classification, contribution of local factors to its pathogenesis, and possibilities of treatment and prevention of the disease. He emphasizes the leading role of optimal correction of carbohydrate metabolism as a means preventing diabetic retinopathy and of timely laser photocoagulation of the retina in its treatment.","PeriodicalId":342539,"journal":{"name":"Problems of Endocrinology","volume":"18 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126018592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. Shestakova, A. Vorontsov, S. G. Vykhristyuk, I. Dedov
{"title":"Prospects in the treatment of diabetic nephropathy","authors":"M. Shestakova, A. Vorontsov, S. G. Vykhristyuk, I. Dedov","doi":"10.14341/probl10389","DOIUrl":"https://doi.org/10.14341/probl10389","url":null,"abstract":"The authors discuss new approaches to the treatment and prevention of diabetic nephropathy based on elimination of the pathogenetic factors of its development. Hyperglycemia, the main triggering factor of vascular complications of diabetes mellitus. induces a cascade of other pathological reactions, such as renal dysfunction, biochemical and structural changes in the basal membranes of renal capillaries, and stimulates the secretion of vasoactive factors of vascular endothelium and platelets. Blocking of these reactions by specific agents inhibits the progress of diabetic nephropathy. The authors share their experience gained in the treatment of diabetic nephropathy with inhibitors of angiotensin-converting enzyme, glycosaminoglycanes, and thromboxane synthesis inhibitors. These drugs are more effective if prescribed at the early stages of diabetic involvement of the kidneys.","PeriodicalId":342539,"journal":{"name":"Problems of Endocrinology","volume":"88 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132651894","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The macroprolactinemia phenomenon: origin and clinical diagnostic significance","authors":"A. Bulatov","doi":"10.14341/probl10397","DOIUrl":"https://doi.org/10.14341/probl10397","url":null,"abstract":"The authors discuss the experimental and clinical data on the origin, properties, and diagnostic value of serum immunoreactive prolactin (irPRL) with a high molecular mass (macroprolactin, 100K-PRL). This form predominates in the blood of about 25% of women of a reproductive age with hyperprolactinemia. Comparison of the biochemical, immunochemical, and functional characteristics of the blood serum 100K-PRL and the monomeric fraction irPRL (23K-PRL) showed them to differ in principle. A low biological activity of 100K-PRL explains the absence of typical clinical signs of hyperprolactinemia in many women with macroprolactinemia. In contrast to 23K-PRL, 100K.-PRL weakly reacts to stimulants and inhibitors of PRL secretion by the pituitary. PRL-binding protein, apparently an immunoglobulin, is the basis of fraction 100K-PRL. The authors consider that analysis of not only total irPRL in the blood, but of its high and low-molecular forms be included in the algorithm of diagnostic search in some forms of hyperprolactinemia. This will help determine the treatment policy, because moderate hyperprolactinemia with predominating 100K- PRL as a rule cannot be corrected by dopamine agonists.","PeriodicalId":342539,"journal":{"name":"Problems of Endocrinology","volume":"43 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132777096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
V. Kandror, I. Kryukova, S. Krainova, N. Mkrtumova, Y. Keda, N. Sviridenko, E. N. Bazarova, N. Latkina
{"title":"Antithyroid antibodies and autoimmune diseases of the thyroid","authors":"V. Kandror, I. Kryukova, S. Krainova, N. Mkrtumova, Y. Keda, N. Sviridenko, E. N. Bazarova, N. Latkina","doi":"10.14341/probl10392","DOIUrl":"https://doi.org/10.14341/probl10392","url":null,"abstract":"The significance and mechanisms of action of different antithyroid antibodies in diffuse toxic goiter (Graves' disease) and chronic lymphocytic thyroiditis (Hashimoto’s disease) arc analyzed. Antibodies immediately decreasing the level of cAMP in isolated thyrocytes were revealed in the sera of adolescents with juvenile struma, often resulting from lymphocytic thyroiditis. Complement-fixing cytotoxic antibodies are heterogeneous in patients with Graves' diseases and Hashimoto's thyroiditis. Thyrocytes from the tissue of diffuse toxic goiter are resistant to the cytolytic effect of such antibodies from patients with Graves' diseases but not from patients with Hashimoto's thyroiditis. The causes and mechanisms of development of resistance of thyrocytes from diffuse toxic goiter to antibody-dependent complement-mediated cytotoxicity of sera from patients with Graves' disease and the possibility of using this phenomenon as a differential diagnostic test are discussed.","PeriodicalId":342539,"journal":{"name":"Problems of Endocrinology","volume":"89 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126217997","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
N. V. Trusov, S. Apryatin, A. Gorbachev, V. Naumov, K. V. Mzhelskaya, I. Gmoshinski
{"title":"The effect of hypercaloric diet and Quercetin on the full-transcriptome liver tissue profile of Zucker-LEPRfa rats","authors":"N. V. Trusov, S. Apryatin, A. Gorbachev, V. Naumov, K. V. Mzhelskaya, I. Gmoshinski","doi":"10.14341/PROBL9936","DOIUrl":"https://doi.org/10.14341/PROBL9936","url":null,"abstract":"BACKGROUND: The peptidic hormone leptin (Lep) occupies a central place in the control of energy homeostasis and body weight in mammals. A convenient model for studying the role of impaired Lep reception is the Zucker-LEPRfa rats, which carry a mutation in the homozygote of the LEPR gene. Quercetin (Q; 3.3 ‘, 4’, 5.7-pentahydroxyflavone) is currently being considered as one of the promising biologically active substances, which allows to correct metabolic disorders in obesity and metabolic syndrome. \u0000AIM: to study changes in the expression of genes in liver tissue of rats with impaired receptivity of Lep under the influence of high-fat and high-carbohydrate diet (HFCR) or/and Q supplementation. \u0000MATERIAL AND METHODS: 4 groups of six male Zucker-LEPRfa male rats were used in experiment. Within 61 days the animals of the 1st group (control) received a balanced semi-synthetic diet, the second group received the same diet with the addition of quercetin in a dose of 50 mg/kg of body weight, the third group — the HFCR (30% fat by dry weight and 20% fructose instead of water), the 4th group is the same diet and supplement of quercetin. Full transcriptional profiling of liver tissue was performed on microchips from the Gene Expression Hybridization Kit (Agilent Technologies), a real-time polymerase chain reaction combined with reverse transcription (RT-PCR) was performed for liver transcripts of Crot, FTO, NpY, Prdx1, Prom1, Ugt2b37 and GAPDH genes contained in liver tissue. \u0000RESULTS: It was shown that feeding of Zucker-LEPRfa rats with Q and/or HFCR led to significant changes in the level of transcription of 1604 genes in liver tissue, from which the effect of quercetin proper was manifested for 1396 genes. Changes were more pronounced in the transcriptome of liver tissue caused by HFCR, than caused by the addition of Q against the background of a standard diet. Q influenced the expression of genes responsible for xenobiotic detoxification processes (UGT2b37), redox homeostasis (Prdx1), beta-oxidation of fatty acids (Crot), and central mechanisms affecting hunger and satiety (NpY), and potentiated, or abolished the effects of HFCR against a number of other functionally important genes. Bioinformatic analysis revealed the influence of HFCR and/or Q on 23 metabolic pathways (KEGGS), of which 7 (the metabolism of steroids, arachidonic and linoleic acids, retinoids, drugs and xenobiotics (due to cytochrome P-450), bile secretion) were affected in all experimental groups. \u0000CONCLUSIONS: Changes in the transcriptome of the liver of Zucker-LEPRfa rats, caused by consumption of HFCR and/or Q, were consistent with experimental data on changes in short-term memory, anxiety and mineral metabolism in these animals.","PeriodicalId":342539,"journal":{"name":"Problems of Endocrinology","volume":"83 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115765222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
E. Nagaeva, Нагаева Елена Витальевна, T. Shiryaeva, Ширяева Татьяна Юрьевна, V. Peterkova, Петеркова Валентина Александровна, O. Bezlepkina, Безлепкина Ольга Борисовна, A. Tiulpakov, Тюльпаков Анатолий Николаевич, N. Strebkova, Н А Стребкова, A. V. Kiiaev, Кияев Алексей Васильевич, E. E. Petryaykina, Петряйкина Елена Ефимовна, E. Bashnina, Башнина Елена Борисовна, Oleg A. Мalievsky, Малиевский Олег Артурович, Т. Е. Тaranushenko, Таранушенко Татьяна Евгеньевна, Irina B. Коstrova, Кострова Ирина Борисовна, Lyubov A. Shapkina, Шапкина Любовь Александровна, I. Dedov, Дедов Иван Иванович
{"title":"Russian national consensus. Diagnostics and treatment of hypopituitarism in children and adolescences","authors":"E. Nagaeva, Нагаева Елена Витальевна, T. Shiryaeva, Ширяева Татьяна Юрьевна, V. Peterkova, Петеркова Валентина Александровна, O. Bezlepkina, Безлепкина Ольга Борисовна, A. Tiulpakov, Тюльпаков Анатолий Николаевич, N. Strebkova, Н А Стребкова, A. V. Kiiaev, Кияев Алексей Васильевич, E. E. Petryaykina, Петряйкина Елена Ефимовна, E. Bashnina, Башнина Елена Борисовна, Oleg A. Мalievsky, Малиевский Олег Артурович, Т. Е. Тaranushenko, Таранушенко Татьяна Евгеньевна, Irina B. Коstrova, Кострова Ирина Борисовна, Lyubov A. Shapkina, Шапкина Любовь Александровна, I. Dedov, Дедов Иван Иванович","doi":"10.14341/PROBL10091","DOIUrl":"https://doi.org/10.14341/PROBL10091","url":null,"abstract":"The materials of the National Consensus reflect the modern domestic and international experience on this issue. \u0000Before conducting a specialized endocrinological examination of a short child, all other causes of short stature should be excluded: severe somatic diseases in a state of decompensation that can affect growth velocity, congenital systemic skeletal diseases, syndromic short stature (all girls with growth retardation require a mandatory study of karyotype, depending on the presence or absence of phenotypic signs of Turner syndrome), endocrine diseases in decompensation. \u0000A specialized examination of the state of GH-IGF-I axis is carried out when the proportionally folded child has pronounced short stature: if the child’s height is < –2.0 SDS, if the difference between the child’s height SDS and child’s midparental height SDS exceeds 1.5 SDS and/or a low growth velocity. \u0000The consensus reflects clear criteria for the diagnosis of GH-deficiency, central hypothyroidism, central hypocorticosolism, central hypogonadism, diabetes insipidus, hypoprolactinemia, and also the criteria for their compensation. \u0000The dose of somatropin with GH-deficiency in children and adolescents is 0.025–0.033 mg/kg/day. With total somatotropic insufficiency, especially in young children, it is advisable to start therapy with somatropin from lower doses: 25–50% of the substitution, gradually increasing it within 3–6 months to optimal. In children with a growth deficit when entering puberty, the dose may be increased to 0.045–0.05 mg/kg/day. \u0000With the development of side effects, the dose of somatropin can be reduced (by 30–50%), or temporarily canceled (depending on the severity of the clinical picture) until the complete disappearance of undesirable symptoms. With swelling of the optic nerve, treatment is temporarily stopped until the picture of the fundus of the eye fully normalizes. If therapy has been temporarily discontinued, treatment is resumed in smaller doses (50% of the initial) with a gradual (within 1–3 months) return to the optimum. \u0000GH treatment at pediatric doses not continue beyond attainment of a growth velocity below 2–2.5 cm/year, closure of the epiphyseal growth zones, or earlier, when: the achievement of genetically predicted height, but not more than 170 cm in girls, 180 cm in boys, the patient’s desire and his parents / legal representatives satisfied with the achieved result of the final height. \u0000Re-evaluation of the somatotropic axis is carried out after reaching the adult height, after 1–3 months GH therapy will be discontinued. Patients with isolated GH-deficiency or patients with 1 (besides GH) pituitary hormone deficiencies in the presence of a normal IGF-1 level (against the background of somatropin withdrawal) and not having molecular genetic confirmation of the diagnosis need re- evaluation. Patients with two or more (besides GH) pituitary hormone deficiencies, acquired hypothalamic-pituitary lesions due to operations on the pituitar","PeriodicalId":342539,"journal":{"name":"Problems of Endocrinology","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123886867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
E. Choynzonov, L. Balatskaya, S. Chizhevskaya, O. Cheremisina, E. Krasavina, L. Zhuikova
{"title":"Voice rehabilitation of patients with unilateral laryngeal paresis after thyroid cancer surgery","authors":"E. Choynzonov, L. Balatskaya, S. Chizhevskaya, O. Cheremisina, E. Krasavina, L. Zhuikova","doi":"10.14341/PROBL9648","DOIUrl":"https://doi.org/10.14341/PROBL9648","url":null,"abstract":"BACKGROUND: Recurrent laryngeal nerve injury is one of the most frequent complications of surgery for thyroid cancer. This injury may result in vocal cord paresis and respiratory failure. Repeat surgery for recurrent tumors involves increased risk of recurrent nerves paresis. \u0000AIM: to evaluate the efficacy of voice rehabilitation in patients with unilateral laryngeal paresis after surgery for thyroid cancer. \u0000MATERIAL AND METHODS: Between 2008 and 2017, a total of 54 patients with unilateral laryngeal nerve paralysis after surgery for thyroid cancer were treated at the Cancer Research Institute. All patients had histologically verified advanced stage (T3–4N0–2M0–1) of thyroid cancer. Papillary thyroid cancer was diagnosed in 87% cases. Endoscopic or laryngoscopic examination and acoustic voice analysis were the criteria for assessing voice rehabilitation efficacy. \u0000RESULTS: Positive outcomes of voice rehabilitation were obtained in 54 patients. The vocal fold mobility was completely restored in 36 (67%) patients. The voice function was recovered due to the compensation provided by the healthy half of the larynx in 11 (21%) patients. In 7 (12%) patients, the vocal sound improved, patients no longer complained of . speech fatigue, but hoarseness persisted. By the time of discharge, the patients were able to go back to work. The effectiveness of voice restoration in patients with unilateral laryngeal paresis was directly dependent on the early start of rehabilitation measures (5–7 days after surgery) subject to interdisciplinary approach. The voice rehabilitation course ranged from 3 to 6 weeks. \u0000CONCLUSIONS: Our technique of voice rehabilitation in patients with unilateral laryngeal paresis after surgery for thyroid cancer shortened the rehabilitation time, reduced disability in oncological patients practicing voice and speech professions and improved the quality of life and social adaptation of these patients.","PeriodicalId":342539,"journal":{"name":"Problems of Endocrinology","volume":"14 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116285752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
I. Belovalova, N. Sviridenko, E. Bessmertnaya, A. A. Chepurina, M. S. Sheremeta, A. Mikheenkov
{"title":"Phenotypes of endocrine ophthalmopathy: clinical manifestation and tomographic characteristics","authors":"I. Belovalova, N. Sviridenko, E. Bessmertnaya, A. A. Chepurina, M. S. Sheremeta, A. Mikheenkov","doi":"10.14341/PROBL9618","DOIUrl":"https://doi.org/10.14341/PROBL9618","url":null,"abstract":"The clinical manifetstations of endocrine orbitopathy (EOP) significantly because autoimmune process may involve various anatomical structures of the eye. Choosing an effective method for EOP treatment requires to determine the selectivity of orbital tissue damage, which is difficult when only clinical criteria are applied. 102 patients with EOP and Graves’ disease were examined. All patients underwent the standard ophthalmological examination and multispiral computed tomography of orbits. The analysis of clinical and tomographic parameters allowed us to distinguish 3 variants of EOP flow: classical, lipogenic, and myogenic. The prevailing symptoms of patients with the lipogenic variant were distinct exophthalmos without a disturbance of the function of extraocular muscles (EOM) and visual disturbances. Oculomotor disorders, diplopia, strabismus, and decreased vision were prevalent in patients with the myogenic variant. Patients with the classical variant suffered from exophthalmos, periorbital edema, and oculomotor disorders. The identification of independent clinical variants of EOP with specific clinical symptoms and different tomographic characteristics testifies different pathogenetic mechanisms of EOP development is to determine personalized approaches to treatment.","PeriodicalId":342539,"journal":{"name":"Problems of Endocrinology","volume":"18 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"133104848","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}