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| 1 | Metabolically based liver damage pathophysiology in patients with urea cycle disorders-A new hypothesis显示文摘The underlying pathophysiology of liver dysfunction in urea cycle disorders(UCDs) is still largely elusive. There is some evidence that the accumulation of urea cycle(UC) intermediates are toxic for hepatocyte mitochondria. It is possible that liver injury is directly caused by the toxicity of ammonia. The rarity of UCDs, the lack of checking of iron level in these patients, superficial knowledge of UC and an underestimation of the metabolic role of fumaric acid, are the main reasons that are responsible for the incomprehension of the mechanism of liver injury in patients suffering from UCDs. Owing to our routine clinical practice to screen for iron overload in severely ill neonates, with the focus on the newborns suffering from acute liver failure, we report a case of citrullinemia with neonatal liver failure and high blood parameters of iron overload. We hypothesize that the key is in the decreased-deficient fumaric acid production in the course of UC in UCDs that causes several sequentially intertwined metabolic disturbances with final result of liver iron overload. The presented hypothesis could be easily tested by examining the patients suffering from UCDs, for liver iron overload. This could be easily performed in countries with a high population and comprehensive national register for inborn errors of metabolism. Conclusion: Providing the hypothesis is correct, neonatal liver damage in patients having UCD can be prevented by the supplementation of pregnant women with fumaric or succinic acid, prepared in the form of iron supplementation pills. After birth, liverdamage in patients having UCDs can be prevented by supplementation of these patients with zinc fumarate or zinc succinylate, as well. | Ivan Ivanovski Milos Jesic Ana Ivanovski Livia Garavelli Petar Ivanovski | 2017 | World Journal of Gastroenterology2017，23，44： | 4 |
| 2 | Mitotic crossover- an evolutionary rudiment which promotes carcinogenesis of colorectal carcinoma显示文摘Mitotic crossover is a natural mechanism that is a main source of the genetic variability of primitive organisms.In complex organisms such as mammals,it represents an evolutionary rudiment which persisted as one of the numerous DNA repair mechanisms,and results in the production of homozygous allele combinations in all heterozygous genes located on the chromosome arm distal to the crossover.This event is familiar as loss of heterozygosity,which is one of the key mechanisms responsible for the development and progression of almost all cancers.We propose the hypothesis in which mitotic crossover is a principal source of the increased loss of heterozygosity that leads to the initiation and progression of colorectal carcinoma.The hypothesis could be tested by in vitro inhibition of Rad51 protein,orthotopic grafting of human colon cancer tissue into the gut of mice,and treatment with potential inhibitors.After these procedures,the frequency of mitotic crossover would be estimated.The development of selective inhibitors of mitotic crossover could stop further carcinogenesis of colorectal carcinoma,as well as many other neoplastic events.Loss of heterozygosity is an event responsible for carcinogenesis,its reduction by selective inhibitors of mitotic crossover could have a positive effect on cancer chemoprevention,as well as on growth reduction and a cessation in the progression of earlier developed tumors. | Branislav Rovcanin Ivan Ivanovski Olivera Djuric Dimitrije Nikolic Jelena Petrovic Petar Ivanovski | 2014 | World Journal of Gastroenterology2014，20，35： | 2 |
| 3 | Erythrocytic transglutaminase inhibition hemolysis at presentation of celiac disease显示文摘Celiac disease (CD) is a common autoimmune condition.Previously it was considered to be a rare childhood disorder,but is actually considered a relatively common condition,present at any age,which may have multiple complications and manifestations.Hematological disorders of the disease are not uncommon.Among these disorders,the most frequently reported are anemias as a result of iron deficiency,often associated with folate and/or B12 deficiency.Anemias caused by hemolysis are very rarely reported in celiac patients.An 11-year-old girl with a previous uneventful medical history presented with severe hemolytic anemia.Hemolysis was Coombs negative,accompanied by inappropriate low reticulocyte count,despite exaggerated bone marrow hyperplasia of the erythroid precursors which showed normal maturation.Serology for recent infections,including EpsteinBarr virus,parvovirus B19,cytomegalovirus and mycoplasma,were all negative.Levels of serum IgA,IgG and IgM,were all within normal ranges for age.Screeningfor anti-DNA,antinuclear,antineutrophil cytoplasmic,antimicrosomal,antithyroglobulin,and antimitochondrial antibodies and lupus anticoagulants,was negative.She was also negative for human immunodeficiency virus.Conventional therapy with corticosteroids and intravenous immunoglobulin failed.CD was serendipitously discovered upon screening for anti-tissue transglutaminase autoantibodies.The disease was confirmed by biopsy of the small intestine mucosa.The patient recovered with gluten-free diet.A unique case of CD is presented.CD should be serologically screened in each patient with Coombs negative 'immune'hemolytic anemia,particularly if accompanied by 'reticulocytopenia'.A new hemolytic mechanism and very speculative explanation for 'reticulocytopenia'are discussed. | Petar Ivanovski Dimitrije Nikoli Nikola Dimitrijevi Ivan Ivanovski Vojislav Perii | 2010 | World Journal of Gastroenterology2010，16，44： | 1 |
| 4 | Childhood leukemia genetic bottleneck phenomenon related to TEL-AMLI: the postulation by a mathematical model显示文摘 | Petar Ivanovski Ivan Ivanovski Dimitrije Nikolic Ivana Jovanovic | 2012 | Chinese Medical Journal2012，，6： | 1 |
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