Relationship between granulomatous lobular mastitis and methylene tetrahydrofolate reductase gene polymorphism

BACKGROUND Variations in the methylene tetrahydrofolate reductase(MTHFR)gene have been reported as risk factors for numerous conditions,including cardiovascular disease,thrombophilia,stroke,hypertension and pregnancy-related complications.Moreover,it was reported there is an association between breast cancer and mutations in MTHFR-C677T.However,whether there is an association between MTHFR gene polymorphism and granulomatous lobular mastitis or not has been rarely investigated.AIM To analyze the association between MTHFR gene polymorphism and granulomatous lobular mastitis.METHODS Fifty-one patients with granulomatous lobular mastitis admitted to The First Hospital of Kunming were selected as study samples.Their hospitalization time ranged from February 2018 to February 2019.The 51 patients were included in the experimental group,and another 51 women who underwent physical examination at The First Hospital of Kunming in the same period were included in the control group.Deoxyribonucleic acid and MTFR genetic polymorphism testing were performed in each group.The association between MTHFR gene polymorphism and granulomatous lobular mastitis was observed.RESULTS There were significant differences in genotype frequency and allele frequency of C/C and C/T between the experimental group and the control group(all P<0.05).However,there was no significant difference in frequency of T/T genotype between the two groups(P>0.05).In addition,there was no significant difference in genotype frequency and allele frequency of A/A,A/C and C/C between the two groups(P>0.05).CONCLUSION MTHFR gene C677T locus polymorphism is closely related to granulomatous lobular mastitis.

Rearrangement of Hydrolysis Products of Tetrahydrofolate model compound

The hydrolysis products of tetrahydrofolate model compound 4 were a mixture of 6 and 7 and the rearrangement reaction between 6 and 7 via 5 was in a state of equilibrium, confirmed by (HNMR)-H-1 and IR spectra.

Homocysteinemia and methylene tetrahydrofolate reductase gene’s relation to increased risk of coronary artery disease

Objective To review the association of methylene tetrahydrofolate reductase (MTHFR) C677T mutant with coronary artery disease, as well as to highlight the results of some of these studies and to emphasize the need to focus on the genetic architecture of CAD. Data SourcesData used in this article is mainly from relevant articles obtained through Pubmed, OVID and Google Scholar published from 1980 to 2008. Major studies and trials in this period were taken into account to draw accurate conclusion on the relation of those mutations in MTHFR with homocysteinemia and CAD. ResultOur analysis shows that hyperhomocysteinemia, a risk factor for occlusive arterial diseases, can be caused by disruptions of homocysteine metabolism catalyzed by MFTHR. A common alanine to valine mutation in MTHFR may contribute to mild heperhomocysteinemia in CAD. Individuals with the homozygous mutant genotype had higher plasma homocysteine, particularly when plasma folate was below the median value. ConclusionThis MTHFR mutant in the setting of insufficient folate may be a risk factor of CAD and can be regarded as a model of genetic-environmental interaction in the development of CAD.

Formyl tetrahydrofolate deformylase affects hydrogen peroxide accumulation and leaf senescence by regulating the folate status and redox homeostasis in rice

It is well established that an abnormal tetrahydrofolate(THF)cycle causes the accumulation of hydrogen peroxide(H_(2)O_(2))and leaf senescence,however,the molecular mechanism underlying this relationship remains largely unknown.Here,we reported a novel rice tetrahydrofolate cycle mutant,which exhibited H_(2)O_(2)accumulation and early leaf senescence phenotypes.Map-based cloning revealed that HPA1 encodes a tetrahydrofolate deformylase,and its deficiency led to the accumulation of tetrahydrofolate,5-formyl tetrahydrofolate and 10-formyl tetrahydrofolate,in contrast,a decrease in 5,10-methenyl-tetrahydrofolate.The expression of tetrahydrofolate cycle-associated genes encoding serine hydroxymethyl transferase,glycine decarboxylase and 5-formyl tetrahydrofolate cycloligase was significantly down-regulated.In addition,the accumulation of H_(2)O_(2)in hpa1 was not caused by elevated glycolate oxidation.Proteomics and enzyme activity analyses further revealed that mitochondria oxidative phosphorylation complex I and complex V were differentially expressed in hpa1,which was consistent with the H_(2)O_(2)accumulation in hpa1.In a further feeding assay with exogenous glutathione(GSH),a non-enzymatic antioxidant that consumes H_(2)O_(2),the H_(2)O_(2)accumulation and leaf senescence phenotypes of hpa1 were obviously compensated.Taken together,our findings suggest that the accumulation of H_(2)O_(2)in hpa1 may be mediated by an altered folate status and redox homeostasis,subsequently triggering leaf senescence.

Synthesis of tetrahydrofolate coenzyme models 1,2-dimethyl-3-m(p)-nitrophenylsulfonyl imidazolinium iodide and their methyl-substituted one carbon unit transfer reactions

Tetrahydrofolate (THF) coenzymes are involved in biochemical transfer of aone-carbon fragment at different oxidation levels. The study of THF models may providea valuable class of reagents for group transfer reactions with practical significance. Onlya few researches about 5, 10-methenyl-THF models have been reported in literature.

Tetrahydrofolate coenzyme models I·Synthesis of l-methyl-2-phenyl-3-aryl imidazoliniumiodide and benzylildyne(phenyl-substitutef one carbon unit)transfer reactions

Four 1, 2, 3-trisubstituted imidazolinium iodides which were used as 5,10-^+CPh-THF model (7-10) at formic acid oxidation level were synthesized. The benzylidyne group (phenyl- substituted one carbon unit)transfer reactions from these compounds to Grignard reagent were in- vestigated, and the reactions of these compounds with KBH_4 and NaOH were also studied.

Epidemiological aspects of Budd-Chiari in Egyptian patients:A single-center study

AIM： TO describe the socio-demographic features, etiology, and risk factors for Budd-Chiari syndrome （BCS） in Egyptian patients. METHODS： Ninety-four Egyptian patients with confirmed primary Budd-Chiari syndrome were presented to the Budd-Chiari Study Group （BCSG） and admitted to the Tropical Medicine Department of Ain Shams University Hospital （Cairo, Egypt）. Complete clinical evaluation and laboratory investigations, including a thrombophilia workup and full radiological assessment, were performed to determine underlying disease etiologies.RESULTS： BCS was chronic in 79.8% of patients, acute or subacute in 19.1%, and fulminant in 1.1%. Factor V Leiden mutation （FVLM） was the most common etiological cause of disease （53.1%）, followed by mutation of the gene encoding methylene tetrahydrofolate reductase （MTHFR） （51.6%）. Current or recent hormonal treatment was documented in 15.5% of females, and BCS associated with pregnancy was present in 17.2% of females. Etiology could not be determined in 8.5% of patients. Males had significantly higher rates of MTHFR gene mutation and Behcet＇ s disease, and females had significantly higher rates of secondary antiphospholipid antibody syndrome. A highly significant positive relationship was evident between the presence of Behcet＇s disease and inferior vena caval occlusion, either alone or combined with occlusion of the hepatic veins （,0 〈 0.0001）. CONCLUSION： FVLM is the most common disease etiology and MTHFR the second most common in Egyptian BCS patients. BCS etiology tends to vary with geographic region.

Study on the Reaction of Benzimidazolium Salt with Amine Compounds

The addition-hydrolysis reaction of benzimidazolium salt with some mono- and bifunctional amine nucleophiles is reported, and a novel method of biomimetic synthesis for formamides and heterocycle compounds is provided.

A Novel Method for Biomimetic Synthesis of Mannich Bases

Since the early studies of Mannich, Mannich reaction has become an important tool for the synthesis of new compounds. Mannich bases can be either directly employed or used as intermediates. In this work, the one-carbon unit transfer reaction of tetrahydrofolate coenzyme was initiated. 1,3-Dimethylimidazolidine as a new tetrahydrofolate coenzyme model at formaldehyde oxidation level was used to react with ketone having active hydrogen atoms and amine to give the corresponding Mannich base in good yield by a covert Mannich reaction. A novel method for biomimetic synthesis of various Mannich bases is provided.