• Contact Us
  • Indexing
  • Submit Manuscript
  • Open Access
  • Journals
  • Home
  • ISSN: 2333-6706
    Volume 5, Issue 2
    Review Article
    Shing Yan Robert Lee*
    Metabolic bone disease (MBD) of prematurity is mainly caused by inadequate amount of calcium and phosphate in parenteral nutrition admixtures given to premature infants in early days of life before full enteral feeding is established. According to published guidelines/ survey of parenteral nutrition for premature infants in Australia, USA and Europe, it is still a common practice to prepare parenteral nutrition admixtures with calcium and phosphate concentration not high enough to achieve the fetal accretion rate. Therefore, as these bones of premature infants grow without adequate supply of calcium and phosphorus, they are under-mineralized. MBD of prematurity is still prevalent worldwide. Solubility of calcium and phosphate has been a limiting factor for provision of adequate amounts of calcium and phosphate in parenteral nutrition. However, this is no longer true because for more than a decade there have already been studies on the use of organic phosphate and organic calcium in parenteral nutrition showing their compatibility at high concentration, which if provided could achieve the fetal accretion rates. In addition, several studies have shown that these organic forms of calcium and phosphate at such high concentrations are mostly retained. The retention rates vary from 80% to 97% across these studies. Therefore we advocate the use of organic phosphate and organic calcium in preparing parenteral nutrition for premature infants. We recommend: for infants less than 1.2 kg administer calcium and phosphate at 2.2 and 1.7 mmol/kg/day when they are growing. At this rate MBD of prematurity could be minimized.
    Research Article
    Marlene Nunez Aldin, Diana Gabriela Estevez Fernandez, Sayuri Miyamoto, Antonio Martins Figueiredo Neto, and Nagila Raquel Teixeira Damasceno*
    Background: Omega-3 fatty acids (ω-3 FA) have multiple potential mechanisms able to prevent cardiovascular diseases (CVD), however, some clinical trials had failed to confirm changes total and cardiovascular fatal and non-fatal events. Regarding that, our goal was investigated the effect of omega-3 in simultaneous changes in electronegative low-density lipoprotein [LDL(-)] and size of lipoproteins.
    Method: Based in a clinical trial design, subjects of the both sexes, aged 30-74 years old and without previous CVD received 3 g/d of ω-3 FA (37% EPA and 23% DHA) during 8 weeks. At baseline, and after four (T4) and eight (T8) weeks of intervention lipid biomarkers (total cholesterol/TC, LDL-c, HDL-c, Apo AI, Apo B, and NEFA), LDL(-) and physicochemical aspects of LDL and HDL (phenotype, size and concentration) were analyzed.
    Results: ω-3 FA promoted an increase of 4% in plasma DHA, and this change was associated with significant decreasing in TG (P<0.001), TC (P = 0.002), LDL-c (P = 0.003), non-HDL-c (P < 0.001) and their ratios with apolipo proteins. LDL(-) showed significant decrease (∆ T8-T0 = 1.5 U/L; 22.7%). The similar way, HDLLARGE and HDLINTERMEDIATE showed increase, while HDLSMALL decreased. Physical parameters related with LDL not change during fallow-up time. Regression models adjusted for age, sex and smoking showed that individuals with higher incorporation of EPA+DHA in plasma had a higher content of HDLLARGE (P = 0.041) and decreasing in LDL(-) levels (P = 0.004).
    Conclusion: ω-3 supplementation rich in EPA+DHA contributes to improve the size of HDL and decreasing of LDL (-) levels in Brazilian adults with multiple risk factors and previous cardiovascular events.
    Andreza Linhares Floripes, Alanne Ysla Souza de Moura, Fabiana Maria Coimbra de Carvalho, Daliana Caldas Pessoa da Silva, Raphael Paschoal Serquiz, Hugo Alexandre Oliveira Rocha, and Alexandre Coelho Serquiz
    Atemoya is a hybrid fruit containing phenolic substances, mainly flavonoids, which can provide antioxidant, and antimicrobial properties, among others. The phenolic compounds inhibit the action of free radicals, protecting organic molecules, thus being able to prevent carcinogenic processes. Thereby, the present paper aims to evaluate the phytochemical compounds and the cellular viability of atemoya extracts in human renal carcinogenic lineages. For such, the cytotoxicity capacity of three extracts of the fruit (seed, pulp and peel) was tested for tumor (786-0) and normal (HEK-273) lineages. Cytotoxicity was evaluated indirectly by the enzymatic reduction of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) for formazan crystals and the mitochondrial activity was evaluated by coenzyme Q10 (HPLC) and creatine kinase (chemical kinetics) dosages. The results show that there is an increase in normal cell mitochondrial activity, and inhibition of mitochondrial activity in tumor cells in specific concentration tests. Therefore, it is suggested that atemoya extracts alter the metabolism of normal and tumor cells, thus being a potential biomarker for tumor cells, allowing several benefits to emerge, such as the reduction of side effects from innovative treatments.
    Jean-Claude Lavoie*, Julie Rebeuh, Denise Herzog, Christophe Faure, Therese Rouleau
    Background: The immaturity of glutathione metabolism is believed to explain the oxidative stress observed in premature neonates on total parenteral nutrition [TPN]. Animal studies report that peroxides contaminating TPN induce the low glutathione levels as a consequence of the inhibition of the generation of substrates for its synthesis. We hypothesize that older children receiving long-term TPN have low levels of glutathione with the consequence to have an increased oxidative stress.
    Methods: Total glutathione and oxidative stress markers [hydroperoxides and isoprostane-F2α] were measured in urine, plasma or erythrocytes from 6 children aged 77 ± 24 months treated with TPN for a mean duration of 28 ± 7 months and from 7 control children aged of 87 ± 21 months.
    Results: In the TPN group, glutathione was lower [p<0.01] whereas hydroperoxide and isoprostane-F2α were higher [p<0.01] than in control group. Plasma isoprostane-F2α was negatively correlated with erythrocytes glutathione [r2 = 0.60, p<0.01]. Ascorbate levels were similar in erythrocyte, but higher [p<0.05] in urine of the TPN group.
    Conclusion: Similar to premature infants, oxidative stress is increased in children on long-term TPN. The oxidative stress is associated with low glutathione.
    Short communication
    Sara Schwab, Timothy Xu, Kathleen Ryan, and Nanette Steinle*
    Background: Eating behavior is influenced by genetics and environment, and is associated with many obesity related conditions.
    Objective: We assessed the relationship between self-reported disinhibition scores and insulin resistance assessed during an oral glucose tolerance test (OGTT).
    Design: The study included 779 volunteers from the Amish Family Diabetes Study; 77 with Type 2 Diabetes Mellitus, 133 with Impaired Glucose Tolerance [IGT] and 569 with Normal Glucose Tolerance [NGT]. All patients with IGT and NGT completed oral glucose tolerance tests [OGTT], and had insulin levels measured during the OGTT. Volunteers completed the Three-Factor Eating Questionnaire to quantify self-perceived disinhibition.
    Conclusions: Higher disinhibition scores are associated with higher fasting insulin levels and insulin area under the curve during an OGTT. These results suggest a highly significant, positive correlation between the eating behavior disinhibition and insulin insensitivity. Treatments aimed at modifying eating behavior may be helpful in mitigating insulin resistance.
  • Highlights
  • JSciMed Central welcomes back astronaut Scott Kelly and cosmonaut Mikhail Kornienko.

    Wonder Women Tech not only disrupted the traditional conference model but innovatively changed the way conferences should be held.

    JSciMed Central Peer-reviewed Open Access Journals
    10120 S Eastern Ave, Henderson,
    Nevada 89052, USA
    Tel: (702)-751-7806
    Toll free number: 1-800-762-9856
    Fax: (844)-572-4633 (844-JSCIMED)
    E-mail: JHNFS@jscimedcentral.com
    1455 Frazee Road, Suite 570
    San Diego, California 92108, USA
    Tel: (619)-373-8720
    Toll free number: 1-800-762-9856
    Fax: (844)-572-4633 (844-JSCIMED)
    E-mail: JHNFS@jscimedcentral.com
    About      |      Journals      |      Open Access      |      Special Issue Proposals      |      Guidelines      |      Submit Manuscript      |      Contacts
    Copyright © 2016 JSciMed Central All Rights Reserved
    Creative Commons Licence Open Access Publication by JSciMed Central is licensed under a Creative Commons Attribution 4.0 International License.
    Based on a work at https://jscimedcentral.com/. Permissions beyond the scope of this license may be available at https://creativecommons.org/.