We have investigated the effect on blood pressure of treatment with vitamin C (an antioxidant and free radical scavenger) in patients with both systolic and essential hypertension. Following a 2-week run-in phase, two age- and sex-matched groups of untreated hypertensive subjects were randomised in a double-blind study to receive 6 weeks’ oral treatment with either vitamin C, 250 mg twice daily (n = 22; 8M/14F, mean age 73.7 ± 4.9 years) or placebo, one capsule twice daily (n = 26; 10M/16F, mean age 73.8 ± 5.3 years). Blood pressure was measured in the sitting position using a random zero sphygmomanometer on three occasions during the run-in phase, and again at 2, 4 and 6 weeks after commencing treatment. Venous blood samples for measurement of plasma ascorbic acid (AA) and lipid peroxides (LP) were measured in all subjects at baseline and at 4 and 6 weeks after the start of vitamin C or placebo treatment. During the study period, significant falls in both systolic (vitamin C group, mean change -10.3 (95% CI 0.7-20.0) mm Hg, p = 0.05) and diastolic (vitamin C group, mean change -5.9 (95% CI 0.2-11.5) mm Hg, p = 0.03; placebo group, mean change -4.7 (95% CI 0.3-9.1) mm Hg, p = 0.05) blood pressure occurred. However, no statistical difference between the effects of either treatment on blood pressure was observed. At baseline, AA concentrations were lower in the vitamin C-treated group compared with the placebo group (44.6 ± 2.4 vs. 57.7 ± 4.2 μmol/l, p < 0.05). At 6 weeks, AA concentrations were similar to baseline in the placebo group (50.8 ± 4.6 μmol/l) but were significantly higher than at baseline in the vitamin C-treated group (80.7 ± 7.5 μmol/lp < 0.001). At baseline, LP concentrations were similar in the vitamin C and placebo-treated groups (5.0 ± 1.0 vs. 3.6 ± 0.8 nmol/l, respectively). After 6 weeks’ treatment with vitamin C, LP concentrations fell significantly to 1.6 ± 0.4 nmol/l, but no significant change after placebo was observed (4.4 ± nmol/l). We conclude: (1) No significant fall in blood pressure occurred after 6 weeks’ treatment with vitamin C in comparison with placebo; (2) vitamin C treatment is associated with a marked antioxidant action but further studies are required to relate whether this action is relevant to any hypotensive action of this vitamin; (3) the small fall in systolic blood pressure after vitamin C may have wider implications in population-based studies in reducing stroke incidence in elderly patients and suggests the need for large long-term studies to be established.

No abstract

No abstract

No abstract

Table of contents O1 Regulation of genes by telomere length over long distances Jerry W. Shay O2 The microtubule destabilizer KIF2A regulates the postnatal establishment of neuronal circuits in addition to prenatal cell survival, cell migration, and axon elongation, and its loss leading to malformation of cortical development and severe epilepsy Noriko Homma, Ruyun Zhou, Muhammad Imran Naseer, Adeel G. Chaudhary, Mohammed Al-Qahtani, Nobutaka Hirokawa O3 Integration of metagenomics and metabolomics in gut microbiome research Maryam Goudarzi, Albert J. Fornace Jr. O4 A unique integrated system to discern pathogenesis of central nervous system tumors Saleh Baeesa, Deema Hussain, Mohammed Bangash, Fahad Alghamdi, Hans-Juergen Schulten, Angel Carracedo, Ishaq Khan, Hanadi Qashqari, Nawal Madkhali, Mohamad Saka, Kulvinder S. Saini, Awatif Jamal, Jaudah Al-Maghrabi, Adel Abuzenadah, Adeel Chaudhary, Mohammed Al Qahtani, Ghazi Damanhouri O5 RPL27A is a target of miR-595 and deficiency contributes to ribosomal dysgenesis Heba Alkhatabi O6 Next generation DNA sequencing panels for haemostatic and platelet disorders and for Fanconi anaemia in routine diagnostic service Anne Goodeve, Laura Crookes, Nikolas Niksic, Nicholas Beauchamp O7 Targeted sequencing panels and their utilization in personalized medicine Adel M. Abuzenadah O8 International biobanking in the era of precision medicine Jim Vaught O9 Biobank and biodata for clinical and forensic applications Bruce Budowle, Mourad Assidi, Abdelbaset Buhmeida O10 Tissue microarray technique: a powerful adjunct tool for molecular profiling of solid tumors Jaudah Al-Maghrabi O11 The CEGMR biobanking unit: achievements, challenges and future plans Abdelbaset Buhmeida, Mourad Assidi, Leena Merdad O12 Phylomedicine of tumors Sudhir Kumar, Sayaka Miura, Karen Gomez O13 Clinical implementation of pharmacogenomics for colorectal cancer treatment Angel Carracedo, Mahmood Rasool O14 From association to causality: translation of GWAS findings for genomic medicine Ahmed Rebai O15 E-GRASP: an interactive database and web application for efficient analysis of disease-associated genetic information Sajjad Karim, Hend F Nour Eldin, Heba Abusamra, Elham M Alhathli, Nada Salem, Mohammed H Al-Qahtani, Sudhir Kumar O16 The supercomputer facility “AZIZ” at KAU: utility and future prospects Hossam Faheem O17 New research into the causes of male infertility Ashok Agarwa O18 The Klinefelter syndrome: recent progress in pathophysiology and management Eberhard Nieschlag, Joachim Wistuba, Oliver S. Damm, Mohd A. Beg, Taha A. Abdel-Meguid, Hisham A. Mosli, Osama S. Bajouh, Adel M. Abuzenadah, Mohammed H. Al-Q...

No abstract

No abstract

Background: Occult dissemination of tumor cellular and nuclear material into the bloodstream is well-recognized and has been reported for a variety of tumor types, including pancreatic ductal adenocarcinoma (PDAC). These cells and nuclear material can be detected in the blood as circulating tumor cells (CTCs) or cell-free DNA (cfDNA) as a means of "liquid biopsy" and their presence is referred to as "tumoremia." Limited data suggest that various biopsy procedures and surgery can also precipitate tumoremia. There are no published data indicating the risk of hematogenous tumor seeding following EUS FNA and no data clarifying whether any factors may be associated with its occurrence. In PDAC patients, we aimed to prospectively evaluate peripheral blood to determine the risk of EUS FNA-induced tumoremia and to identify the associated clinical, laboratory, and tumor demographic features. Methods: Peripheral blood from 35 patients with PDAC was collected before and following primary tumor EUS FNA. Plasma cfDNA concentrations and KRAS 12/13 mutation status were evaluated. Tumor seeding was defined by a !2fold increase in cfDNA and/or conversion from circulating tumor deoxyribonucleic acid (ctDNA) KRAS mutant non-detectable to detectable. Factors that were evaluated to determine their correlation with tumoremia included age, gender, BMI, ECOG status, serum glucose level, CA 19-9 concentration, tumor location, tumor diameter, tumor stage, resectability status, number of FNA passes, infiltration of major arteries and veins, presence of IPMN, mortality, survival duration, pre-FNA cfDNA level, and the tumor allelic ratio. Results: Based on our pre-defined metrics, either a !2-fold increase in the total cfDNA concentration (nZ7; 20.6%), and/or conversion in ctDNA mutant detection status (nZ3; 8.8%) primary tumor EUS FNA-induced hematogenous tumor seeding occurred in 10/35 (28.6%) patients. A broad spectrum of clinical, laboratory, and tumor demographic features were evaluated, none of which statistically correlated with a !2-fold increase in cfDNA, other than the number of major arteries and/or veins infiltrated by the primary tumor. (Table ) The only feature that correlated with the conversion in KRAS mutation status was the CA 19-9 level. For the combined group (nZ10), who met either metric for FNA-induced tumoremia, there were no characteristics that correlated with these endpoints. Conclusions: Our data indicate that the occurrence of hematogenous tumor seeding associated with EUS FNA at the present time, cannot be predicted based upon an evaluation of an extensive array of clinical, laboratory, and tumor related characteristics. Additional studies are needed to determine the clinical impact of EUS FNAinduced tumor seeding as well as to verify whether any predictive features can be identified to help predict its occurrence.