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For the prevalence of lung cancer and its poor diagnosis, the seeking of the efficient biomarkers for this disease is an urgent requirement, especially from non-invasive samples such as plasma. The mitochondria DNA (mtDNA) copy number change has been evaluated as a potential indicator of cancer risk, however, there have been few studies regarding mtDNA in plasma derived exosomes. In this study, the mtDNA copy number was measured on 29 plasma exosome samples of patients with non-small cell lung cancer (NSCLC) and 29 plasma exosome samples of cancer-free controls by real-time PCR assay, then being statistically analyzed to evaluate the relationship between these figures and several pathological features of NSCLC patients. As the results, the existence of mtDNA in exosomes isolated from plasma was detected through PCR assay using primers covering most of the mtDNA length. The relative mtDNA copy numbers determined in the exosomes of the disease and control groups were 1619.1 ± 2589.0 and 1207.0 ± 1550.0, respectively, whereas these values in two disease stages were 783.6 ± 759.3 (stage I-II) and 2647.0 ± 3584.0 (stage III-IV). Comparing among these groups, the difference was only statistically significant between the disease groups of stage I-II and stage III-IV (p

Soil salinity may damage crop production. Besides proper management of irrigation water, salinity reduction can be achieved through soil amendment. The objectives of this study were to evaluate the effects of rice husk biochar and compost amendments on alleviation of salinity and rice growth. Field experiments were conducted at two salt-affected paddy rice fields located in distinct sites for five continuous crops. Treatments, with four replicates, consisted of continuous three rice crops per year (RRR), two rice crops rotated with fallow in spring&ndash, summer crop (FRR), FRR plus compost at 3 Mg ha&minus, 1 crop&minus, 1 (FRR + Comp), and biochar at 10 Mg ha&minus, 1 (FRR + BC). Salt contents and hydraulic properties of soils, plant biomass, and plant uptake of cations were investigated. Soil bulk density (BD), exchangeable sodium (Na+), and exchangeable sodium percentage (ESP) were reduced remarkably by biochar application. Biochar application significantly increased other soil properties including total porosity, saturated hydraulic conductivity (Ksat), soluble and exchangeable potassium (K+), K+/Na+ ratio, available P, and total C. Compost application also improved BD, total porosity, and available P, but not exchangeable Na+ and ESP. Total aboveground biomass of rice showed a trend of FRR + BC &gt, FRR + Comp &gt, FRR &gt, RRR. Relatively higher K+ uptake and lower Na+ uptake in rice straw in FRR + BC resulted in a significant two times higher K+/Na+ ratio over other treatments. Our results highlight that biochar amendment is a beneficial option for reducing ESP and providing available K+ and P under salinity-affected P-deficient conditions, hence improving straw biomass.

The MT-ATP8 gene encodes for A6L protein subunit belonging to the proton channel of the ATP synthase. MT-ATP8 gene’s mutations can affect the structure and function of the ATP synthase, which may cause diseases. In this study, alterations of MT-ATP8 gene were investigated in tumor tissues of patients with breast cancer and control blood samples using PCR combined with direct sequencing and PCR-RFLP methods, data were analyzed using bioinformatics tools and statistical methods. Sequencing results revealed 5 variants of MT-ATP8 gene on 35 breast tumor tissues and 26 blood samples of controls, of which two mutations C8414T and C8417T altered the amino acid sequence of the resulting protein. The C8417T was further screened by PCR-RFLP and was found in 0,98% (1/102) of breast tumor samples. This change lead to substitution of lecine to phenylalanine (L18F) in a highly conserved position of A6L and was predicted as probably damaging to the structure and function of the protein. Additionally, a 9 bp deletion was also observed in a non-coding region of mtDNA in 26,5% (27/102) of breast cancer patients and 27% (7/26) of controls. Thus, these results showed that C8417T variant in the conserved position of MT-ATP8 gene was rare and first identified in a group of breast cancer patients in Vietnam. Keywords Breast cancer, mitochondrial DNA, MT-ATP8 References [1] Petros JA, Baumann AK, Ruiz-Pesini E, Amin MB, Sun CQ, Hall J, Lim S, Issa MM, Flanders WD, Hosseini SH, Marshall FF, Wallace DC, mtDNA mutations increase tumorigenicity in prostate cancer, Proc Natl Acad Sci U S A (2005), 102(3):719-24.[2] Wang X, The expanding role of mitochondria in apoptosis, Genes Dev (2001), 15(22):2922-33.[3] Jonckheere AI, Smeitink JA, Rodenburg RJ, Mitochondrial ATP synthase: architecture, function and pathology, J Inherit Metab Dis (2012), 35(2):211-25.[4] Grzybowska-Szatkowska L, Slaska B, Rzymowska J, Brzozowska A, Florianczyk B, Novel mitochondrial mutations in the ATP6 and ATP8 genes in patients with breast cancer, Mol Med Rep (2014), 10(4):1772-8.[5] Adzhubei IA, Schmidt S, Peshkin L, Ramensky VE, Gerasimova A, Bork P, Kondrashov AS, Sunyaev SR, A method and server for predicting damaging missense mutations, Nat Methods (2010), 7(4):248-9.[6] Thapa S, Lalrohlui F, Ghatak S, Zohmingthanga J, Lallawmzuali D, Pautu JL, Senthil Kumar N, Mitochondrial complex I and V gene polymorphisms associated with breast cancer in mizo-mongloid population, Breast Cancer (2016), 23(4):607-16.[7] Warburg O, On the origin of cancer cells, Science (1956), 123:309-14.[8] Dumas JF, Rousse D, Servais S, Mitochondria and cancer, Cellular Bioenergetics in Health and Diseases: New Perspectives in Mitochondrial Biology (2012), 115-47.[9] Mkaouar-Rebai E, Kammoun F, Chamkha I, Kammoun N, Hsairi I, Triki C, Fakhfakh F, A de novo mutation in the adenosine triphosphatase (ATPase) 8 gene in a patient with mitochondrial disorder, J Child Neurol (2010), 25(6):770-5.[10] Jonckheere AI, Hogeveen M, Nijtmans LG et al., A novel mitochondrial ATP8 gene mutation in a patient with apical hypertrophic cardiomyopathy and neuropathy, J Med Genet (2008), 45:129-33.[11] Ware SM, El-Hassan N, Kahler SG et al., Infantile cardiomyopathy caused by a mutation in the overlapping region of mitochondrial ATPase 6 and 8 genes, J Med Genet (2009), 46:308-14.[12] Liu VW, Shi HH, Cheung AN, Chiu PM, Leung TW, Nagley P, Wong LC, Ngan HY, High incidence of somatic mitochondrial DNA mutations in human ovarian carcinomas, Cancer Res (2001), 61(16):5998-6001.[13] Zhuo G, Feng G, Leng J, et al., A 9-bp deletion homoplasmy in women with polycystic ovary syndrome revealed by mitochondrial genome-mutation screen, Biochem Genet (2010), 48:157-163.[14] Abu-Amero KK, Alzahrani AS, Zou M, Shi Y, Association of mitochondrial DNA transversion mutations with familial medullary thyroid carcinoma/multiple endocrine neoplasia type 2 syndrome, Oncogene (2006), 25:677-84.[15] Bonora E, Porcelli AM, Gasparre G, et al., Defective oxidative phosphorylation in thyroid oncocytic carcinoma is associated with pathogenic mitochondrial DNA mutations affecting complexes I and III, Cancer Res (2006), 66:6087-96.[16] Costa-Guda J, Tokura T, Roth SI, Arnold A, Mitochondrial DNA mutations in oxyphilic and chief cell parathyroid adenomas, BMC Endocr Disord (2007); 7:8.[17] Chintha R, Kaipa PR, Sekhar N, Hasan Q, Mitochondria and tumors: A new perspective, Indian J Cancer (2013), 50(3).[18] Tan DJ, Bai RK, Wong LJ, Comprehensive scanning of somatic mitochondrial DNA mutations in breast cancer, Cancer Res (2002), 62(4):972-6.[19] Tipirisetti NR, Lakshmi RK, Govatati S, Govatati S, Vuree S, Singh L, Raghunadha Rao D, Bhanoori M, Vishnupriya S, Mitochondrial genome variations in advanced stage breast cancer: a case-control study, Mitochondrion (2013), 13(4):372-8. 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The MT-ATP6 gene encodes for a protein subunit which is central to the proton channel of the ATP synthase. Mutations of MT-ATP6 gene can affect the ATP synthesis and may play an important role in the process of tumorigenesis. The purpose of this study was to identify potential changes of MT-ATP6 gene in pair of tumor and adjacent tissues of 102 patients with breast cancer and in blood samples of 65 controls by using direct DNA sequencing and PCR-RFLP method. Then, statistical analysis was used to analyze the association between some typical changes and pathological features of breast cancer. As a result, 20 changes in the MT-ATP6 gene in 35 examined breast cancer tissues and 13 changes in 26 blood control samples were reported, of which 12 alterations altered the amino acid and a variant, 9183insC, had not been described in the literature so far. Most of the variants had low frequencies from 2.86% to 5.71%. Two variants, G9053A and G8584A, which changed the amino acid sequence and had high frequency, were screened in all samples. Our results indicated that the frequencies of G9053A and G8584A were 21,6% (22/102 cases) and 24,5% (25/102 cases) respectively in tissues of breast cancer patients and 18,5% (12/65 cases) in normal blood controls. However, there was no statistically significant difference in G9053A and G8485A rates between breast cancer patients and controls as well as between mtDNA alterations and the pathological features of breast cancer such as age, size of tumors, number of lymph nodes, size of lymph nodes, T stage, N stage, tumor differentiation and stages of disease. This study showed that the variations of MT-ATP6 gene differed from patient groups. In Vietnamese patients with breast cancer, the rates of G9053A and G8485A were relatively high but these changes were not statistically related to breast cancer.