The Experts below are selected from a list of 2382 Experts worldwide ranked by ideXlab platform

Hiroshi Nose - One of the best experts on this subject based on the ideXlab platform.

  • effects of dried tofu supplementation during interval walking training on the methylation of the NFKB2 gene in the whole blood of older women
    Journal of Physiological Sciences, 2018
    Co-Authors: Mayuko Morikawa, Shizue Masuki, Sakura Nakano, Nobuo Mitsui, Hisashi Murasawa, Hiroshi Nose
    Abstract:

    Muscle atrophy with aging is closely associated with chronic systemic inflammation and lifestyle-related diseases. Here, we assessed whether dried tofu intake during 5-month interval walking training (IWT) enhanced increases in thigh muscle mass and strength and ameliorated susceptibility to inflammation in older women. Subjects (n = 32, ~ 65 years) who performed IWT for > 6 months participated in this study. They were randomly divided into 2 groups: IWT + placebo intake (PLG, n = 16; 108 kcal, 0.2 g protein, 5.5 g fat, and 14.4 g carbohydrate) and IWT + dried tofu intake (DTG, n = 16; 111 kcal, 9.6 g protein, 6.0 g fat, and 4.6 g carbohydrate). They were instructed to repeat ≥ 5 sets of fast and slow walking for 3 min each at ≥ 70 and 40% peak aerobic capacity for walking, respectively, per day for ≥ 4 days/week. Immediately after daily exercise, subjects were instructed to consume the supplements assigned to each group. In the DTG, after IWT, the methylation increased at 4/6 sites in the promoter region of the NFKB2 gene in the whole blood (all, P 0.2). Altogether, dried tofu supplementation during IWT likely enhanced the methylation of the NFKB2 gene more than IWT alone, without detectably enhanced increases in thigh muscle strength or cross-sectional area.

  • effects of milk product intake on thigh muscle strength and nfkb gene methylation during home based interval walking training in older women a randomized controlled pilot study
    PLOS ONE, 2017
    Co-Authors: Shizue Masuki, Kensei Nishida, Shigenari Hashimoto, Mayuko Morikawa, Satoshi Takasugi, Shunichiro Taniguchi, Kazuhito Rokutan, Masashi Nagata, Hiroshi Nose
    Abstract:

    Background Muscle atrophy with aging is closely associated with chronic systemic inflammation and lifestyle-related diseases. In the present study, we assessed whether post-exercise milk product intake during 5-month interval walking training (IWT) enhanced the increase in thigh muscle strength and ameliorated susceptibility to inflammation in older women. Methods Subjects [n = 37, 66±5 (standard deviation) yrs] who had been performing IWT for >6 months participated in this study. They were randomly divided into the following 3 groups: IWT alone (CNT, n = 12), IWT + low-dose post-exercise milk product intake (LD, n = 12; 4 g protein and 3 g carbohydrate) or IWT + a 3-times higher dose of milk product intake than the LD group (HD, n = 13). They were instructed to repeat ≥5 sets of fast and slow walking for 3 min each at ≥70% and 40% peak aerobic capacity for walking, respectively, per day for ≥4 days/week. Results After IWT, thigh muscle strength increased in the HD group (8±2%) more than in the CNT group (-2±3%, P = 0.022), despite similar IWT achievements between the groups (P>0.15). Pyrosequencing analysis using whole blood showed that methylation of NFKB1 and NFKB2, master genes of inflammation, was enhanced in the HD group (29±7% and 44±11%, respectively) more than in the CNT group (-20±6% and -10±6%, respectively; P<0.001). Moreover, the genome-wide DNA methylation analysis showed that several inflammation-related genes were hyper-methylated in the HD group compared with that in the CNT group, suggesting greater pro-inflammatory cytokine gene suppression in the HD group. Conclusion HD milk product intake after exercise produced a greater percent increase in thigh muscle strength and NFKB1 and NFKB2 gene methylation during IWT in physically active older women. Trial registration UMIN-CTR No. UMIN000024544 and No. UMIN000024912

  • Effects of milk product intake on thigh muscle strength and NFKB gene methylation during home-based interval walking training in older women: A randomized, controlled pilot study.
    PLOS ONE, 2017
    Co-Authors: Shizue Masuki, Kensei Nishida, Shigenari Hashimoto, Mayuko Morikawa, Satoshi Takasugi, Shunichiro Taniguchi, Kazuhito Rokutan, Masashi Nagata, Hiroshi Nose
    Abstract:

    Background Muscle atrophy with aging is closely associated with chronic systemic inflammation and lifestyle-related diseases. In the present study, we assessed whether post-exercise milk product intake during 5-month interval walking training (IWT) enhanced the increase in thigh muscle strength and ameliorated susceptibility to inflammation in older women. Methods Subjects [n = 37, 66±5 (standard deviation) yrs] who had been performing IWT for >6 months participated in this study. They were randomly divided into the following 3 groups: IWT alone (CNT, n = 12), IWT + low-dose post-exercise milk product intake (LD, n = 12; 4 g protein and 3 g carbohydrate) or IWT + a 3-times higher dose of milk product intake than the LD group (HD, n = 13). They were instructed to repeat ≥5 sets of fast and slow walking for 3 min each at ≥70% and 40% peak aerobic capacity for walking, respectively, per day for ≥4 days/week. Results After IWT, thigh muscle strength increased in the HD group (8±2%) more than in the CNT group (-2±3%, P = 0.022), despite similar IWT achievements between the groups (P>0.15). Pyrosequencing analysis using whole blood showed that methylation of NFKB1 and NFKB2, master genes of inflammation, was enhanced in the HD group (29±7% and 44±11%, respectively) more than in the CNT group (-20±6% and -10±6%, respectively; P

Ulrich Keller - One of the best experts on this subject based on the ideXlab platform.

  • myc suppression of NFKB2 accelerates lymphomagenesis
    BMC Cancer, 2010
    Co-Authors: Ulrich Keller, Juergen Huber, Jonas A Nilsson, Mark A Hall, Christian Peschel, Mohammad Fallahi, John L Cleveland
    Abstract:

    Deregulated c-Myc expression is a hallmark of several human cancers where it promotes proliferation and an aggressive tumour phenotype. Myc overexpression is associated with reduced activity of Rel/NF-κB, transcription factors that control the immune response, cell survival, and transformation, and that are frequently altered in cancer. The Rel/NF-κB family member NFKB2 is altered by chromosomal translocations or deletions in lymphoid malignancies and deletion of the C-terminal ankyrin domain of NF-κB2 augments lymphocyte proliferation. Precancerous Eμ-Myc-transgenic B cells, Eμ-Myc lymphomas and human Burkitt lymphoma samples were assessed for NFKB2 expression. The contribution of NFKB2 to Myc-driven apoptosis, proliferation, and lymphomagenesis was tested genetically in vivo. Here we report that the Myc oncoprotein suppresses NFKB2 expression in vitro in primary mouse fibroblasts and B cells, and in vivo in the Eμ-Myc transgenic mouse model of human Burkitt lymphoma (BL). NFKB2 suppression by Myc was also confirmed in primary human BL. Promoter-reporter assays indicate that Myc-mediated suppression of NFKB2 occurs at the level of transcription. The contribution of NFKB2 to Myc-driven lymphomagenesis was tested in vivo, where NFKB2 loss was shown to accelerate lymphoma development in Eμ-Myc transgenic mice, by impairing Myc's apoptotic response. NFKB2 is suppressed by c-Myc and harnesses Myc-driven lymphomagenesis. These data thus link Myc-driven lymphomagenesis to the non-canonical NF-κB pathway.

  • myc promotes tumorigenesis by supressing NFKB2
    Blood, 2006
    Co-Authors: Ulrich Keller, Juergen Huber, Jonas A Nilsson, Mark A Hall, Christian Peschel, John L Cleveland
    Abstract:

    Rel/NF-kappaB transcription factors are mediators of immune responses, cell survival, and transformation, and are frequently deregulated in cancer. The NF-kappaB2 subunit is associated with chromosomal translocations or deletions in lymphoid malignancies, and deletion of the COOH-terminal ankyrin domain of NF-kappaB2 results in increased lymphocyte proliferation. Here, we report that activation of the Myc oncogene leads to suppression of NFKB2 expression in early passage mouse embryonic fibroblasts and primary bone marrow-derived B cells. Accordingly, transgenic expression of c-Myc in the Eμ-Myc model of human Burkitt lymphoma results in reduced NFKB2 transcript and NF-kappaB2 p100 and p52 protein levels in pre-cancerous B cells. NFKB2 expression is further reduced in the majority of Eμ-Myc lymphomas and in human Burkitt lymphoma. NFKB2 suppression by Myc occurs at least in part by transcriptional repression as shown by promoter studies. To evaluate the relevance of Myc-mediated suppression of NFKB2 for tumorigenesis, consequences of complete NFKB2 loss were evaluated in vivo. In pre-cancerous B cells of Myc-transgenic mice, loss of NFKB2 affects Myc-induced apoptosis while B cell proliferation is unaffected. Deletion of NFKB2 results in an acceleration of lymphoma development in Eμ-Myc transgenic mice. Therefore, Myc-induced NFKB2 suppression promotes lymphomagenesis.

John L Cleveland - One of the best experts on this subject based on the ideXlab platform.

  • myc suppression of NFKB2 accelerates lymphomagenesis
    BMC Cancer, 2010
    Co-Authors: Ulrich Keller, Juergen Huber, Jonas A Nilsson, Mark A Hall, Christian Peschel, Mohammad Fallahi, John L Cleveland
    Abstract:

    Deregulated c-Myc expression is a hallmark of several human cancers where it promotes proliferation and an aggressive tumour phenotype. Myc overexpression is associated with reduced activity of Rel/NF-κB, transcription factors that control the immune response, cell survival, and transformation, and that are frequently altered in cancer. The Rel/NF-κB family member NFKB2 is altered by chromosomal translocations or deletions in lymphoid malignancies and deletion of the C-terminal ankyrin domain of NF-κB2 augments lymphocyte proliferation. Precancerous Eμ-Myc-transgenic B cells, Eμ-Myc lymphomas and human Burkitt lymphoma samples were assessed for NFKB2 expression. The contribution of NFKB2 to Myc-driven apoptosis, proliferation, and lymphomagenesis was tested genetically in vivo. Here we report that the Myc oncoprotein suppresses NFKB2 expression in vitro in primary mouse fibroblasts and B cells, and in vivo in the Eμ-Myc transgenic mouse model of human Burkitt lymphoma (BL). NFKB2 suppression by Myc was also confirmed in primary human BL. Promoter-reporter assays indicate that Myc-mediated suppression of NFKB2 occurs at the level of transcription. The contribution of NFKB2 to Myc-driven lymphomagenesis was tested in vivo, where NFKB2 loss was shown to accelerate lymphoma development in Eμ-Myc transgenic mice, by impairing Myc's apoptotic response. NFKB2 is suppressed by c-Myc and harnesses Myc-driven lymphomagenesis. These data thus link Myc-driven lymphomagenesis to the non-canonical NF-κB pathway.

  • myc promotes tumorigenesis by supressing NFKB2
    Blood, 2006
    Co-Authors: Ulrich Keller, Juergen Huber, Jonas A Nilsson, Mark A Hall, Christian Peschel, John L Cleveland
    Abstract:

    Rel/NF-kappaB transcription factors are mediators of immune responses, cell survival, and transformation, and are frequently deregulated in cancer. The NF-kappaB2 subunit is associated with chromosomal translocations or deletions in lymphoid malignancies, and deletion of the COOH-terminal ankyrin domain of NF-kappaB2 results in increased lymphocyte proliferation. Here, we report that activation of the Myc oncogene leads to suppression of NFKB2 expression in early passage mouse embryonic fibroblasts and primary bone marrow-derived B cells. Accordingly, transgenic expression of c-Myc in the Eμ-Myc model of human Burkitt lymphoma results in reduced NFKB2 transcript and NF-kappaB2 p100 and p52 protein levels in pre-cancerous B cells. NFKB2 expression is further reduced in the majority of Eμ-Myc lymphomas and in human Burkitt lymphoma. NFKB2 suppression by Myc occurs at least in part by transcriptional repression as shown by promoter studies. To evaluate the relevance of Myc-mediated suppression of NFKB2 for tumorigenesis, consequences of complete NFKB2 loss were evaluated in vivo. In pre-cancerous B cells of Myc-transgenic mice, loss of NFKB2 affects Myc-induced apoptosis while B cell proliferation is unaffected. Deletion of NFKB2 results in an acceleration of lymphoma development in Eμ-Myc transgenic mice. Therefore, Myc-induced NFKB2 suppression promotes lymphomagenesis.

Leon Bernalmizrachi - One of the best experts on this subject based on the ideXlab platform.

  • phase ii trial of ixazomib and dexamethasone versus ixazomib dexamethasone and lenalidomide randomized with NFKB2 rearrangement proteasome inhibitor NFKB2 rearrangement driven trial pinr
    Blood, 2018
    Co-Authors: Leon Bernalmizrachi, Munevver Cinar, Zhengjia Chen, Ajay K Nooka, Leonard Heffner, Craig E. Cole, Zhao Chang, Nyaya Kelkar, Akshata Sridhar, Sagar Lonial
    Abstract:

    Introduction: Proteasome inhibitors (PI) and immunomodulatory drugs have become the backbone of therapy for multiple myeloma (MM). The oral boron-containing selective and reversible proteasome inhibitor ixazomib has shown to induce deep and durable responses (Kumar RK et la, Blood 2016. 128(20):2415-2422). Triplets containing ixazomib, has shown to be more efficacious than doublet regimens in the relapse setting (Moreau P, et al. N Engl J Med 2016. 374:1621-1634).However, to date there is not companion diagnostics capable of predicting PI response. We have recently discovered that MM patients resistant to PI lack of the ankyrin (ANK) and death domain (DD) present in the 39-end of NFKB2. Loss of NFKB2 39end frequently resulted from a structural rearrangements. We found that NFKB2-ANK and -DD are crucial at initiating bortezomib9s apoptotic signal by facilitating caspase-8 activation. Activation of this caspase resulted from NFKB2 interaction with FADD/caspase-8/p62 (unpublished data). Based on this findings, we design this study to examine the efficacy of NFKB2 break apart FISH to predict the response to the duplet ixazomib and dexamethasone (Id) vs ixazomib, lenalidomide and dexamethasone (IRd) in early relapse MM patients (1-3 lines of therapy). Methods: In this phase 2 biomarker driven open label trial, relapse patients with Results: At the moment of interim analysis, 26 patients have achieved 4 cycles of treatment. All treatment groups (NFKB2 FISH [-] Id, n=16, NFKB2 FISH [+] Id, n=6 and IRd, n=4) received a median of 2 prior lines of therapy. A higher ORR was observed in NFKB2 FISH negative treated with Id compared with NFKB2 FISH positive (56.3% CI:29.9%-80.3% vs. 16.7% CI:0.4%-64.1%, P=0.16), including significantly higher rates of ≥very good partial response, ≥ partial response, ≥ minimal response (12%, 37.5%, 6% vs. 0%, 0%, 16%, respectively). ORR for IRd arm is for now 25% CI:0.6%-80.6%. Patients that continue treatment after cycle 4 that achieve minimal response or better improved their depth of response in 6% in Id treated NFKB2 FISH negative patients and 25% of IRd treated NFKB2 FISH negative patients. The most common (≥10%) grade 2/4 include pneumonia 20% (Id treated NFKB2 FISH negative), thrombocytopenia 16% (Id NFKB2 FISH positive), neutropenia 60% (IRd NFKB2 FISH positive. Treatment discontinuations only occurred in 1 Id treated patient (5%). Conclusion: Interim analysis demonstrate a trend higher efficacy of ixazomib with dexamethasone in MM patients with negative NFKB2 break-apart FISH compared to those with a positive test. Efficacy and toxicity of the triplet regimen are comparable to what is seen in Tourmaline 1 trial. This study was registered at www.clinicaltrials.gov as # NCT02765854. Disclosures Bernal-Mizrachi:Takeda Pharmaceutical Company: Research Funding; Kodikaz Therapeutic Solutions: Consultancy, Equity Ownership. Cole:Cancer Support Community myeloma advisory board: Membership on an entity9s Board of Directors or advisory committees; University of Michigan: Employment. Heffner:ADC Therapeutics: Research Funding; Kite Pharmaceuticals: Research Funding; Pharmacyclics: Research Funding; Genentech: Research Funding. Nooka:GSK: Consultancy, Membership on an entity9s Board of Directors or advisory committees; Takeda: Consultancy, Membership on an entity9s Board of Directors or advisory committees; Spectrum Pharmaceuticals: Consultancy, Membership on an entity9s Board of Directors or advisory committees; Amgen: Consultancy, Membership on an entity9s Board of Directors or advisory committees; BMS: Consultancy, Membership on an entity9s Board of Directors or advisory committees; Janssen pharmaceuticals: Consultancy, Membership on an entity9s Board of Directors or advisory committees; Celgene: Consultancy, Membership on an entity9s Board of Directors or advisory committees; Adaptive technologies: Consultancy, Membership on an entity9s Board of Directors or advisory committees. Vij:Celgene: Honoraria, Membership on an entity9s Board of Directors or advisory committees, Research Funding; Amgen: Honoraria, Membership on an entity9s Board of Directors or advisory committees; Takeda: Honoraria, Membership on an entity9s Board of Directors or advisory committees, Research Funding; Jazz Pharmaceuticals: Honoraria, Membership on an entity9s Board of Directors or advisory committees; Jansson: Honoraria, Membership on an entity9s Board of Directors or advisory committees; Karyopharma: Honoraria, Membership on an entity9s Board of Directors or advisory committees; Bristol-Myers Squibb: Honoraria, Membership on an entity9s Board of Directors or advisory committees, Research Funding. Kelkar:Empire Genomics: Employment. Lonial:Amgen: Research Funding. Kaufman:Karyopharm: Other: data monitoring committee; Abbvie: Consultancy; Roche: Consultancy; BMS: Consultancy; Janssen: Consultancy.

  • novel sirna expressing lymphoma model identify distinct molecular mechanisms regulating nfkb1 and NFKB2 induced cell proliferation
    Blood, 2006
    Co-Authors: Leon Bernalmizrachi, John C S Harding
    Abstract:

    The NF k B pathway has been implicated in tumorigenesis of several lymphoid malignancies. Most aggressive lymphomas have a constitutively active NF k B. Activation of NF k B results in processing of p105 and p100 to produce p50 and p52, respectively, and degradation of I k B. As a result, heterodimers of p65 and p50 or p52 and REL-B are formed and translocated to the nucleus where they induce transcription. Previously, it has been suggested that NF k B regulation of cyclin D and Myc expression is important for cell proliferation. However, these studies fail to explain all the NF k B regulatory effects, as well as the role of each individual pathway. To address these questions we tested the effect of NF k B on proliferation in two virally mediated murine lymphoma cell lines over-expressing Tax/HTLV-1 oncoprotein (SC and BLA) after knocking down (KD) p105 or p100, using a lentivirus expressing siRNAs. After synchronization, cells were released for 24 hrs and the rate of proliferation and cell cycle analysis were measured by thymidine incorporation and PI staining (4,8,16,24 hrs), respectively. As it is seen below, KD p100 or p105 cell lines had a reduced rate of thymidine incorporation compare to controls (Luciferase-siRNA). However, minimal changes were observed between cell lines in cell cycle analysis. To confirm these findings, xenograft experiments with siRNA expressing cell lines were developed. These experiments demonstrated that KD p100 or p105 in xenografts, prevented (in some) or delayed tumor formation, reduced tumor size and prolonged disease free survival. We then investigated NF k B regulation of cell proliferation by assessing gene expression in each cell line. Our results revealed a distinct proliferation-related gene profile between pathways: KD p105 dependent genes include: Cell cycle: Cyclin D2, B2 and G, CDK-8, P27, RB6, Transcription factor Dp2 and AKT-substrate-1, Growth factors: Platelet derived growth factor and RhoG, RNA synthesis: RNA Pol III. On the other hand KD p100 dependent genes include: Cell cycle: Cyclin D1,B2, retinoblastoma-like 1 (p107), p16, ring box-1 and histone deacetylase 2, Growth factors: HRAS and RhoG, RNA/DNA synthesis: RNA pol III and DNA pol (p17), histone 1 and 2, and thymidine kinases. Interestingly, both KD cell lines share many over-expressed genes such as TGFB, p21, p53, RB7 and BRCA1. In conclusion, our novel experimental model demonstrates: the main effect of both NF k B pathways involves DNA replication and early S phase. KD of either p100 or p105 reduces tumor development. The mechanism of cell proliferation regulated by each NF k B pathway is more complex than what was previously suspected; we suggest that RNA, DNA synthesis and regulation of p21, BRCA-1 and other cell cycle regulatory proteins also play an important role.

  • accumulation of nfkb1 p105 and NFKB2 p100 is essential for apoptosis induced by proteasome inhibition in a lymphoma model
    Blood, 2005
    Co-Authors: Leon Bernalmizrachi, Sarah K Edwards, Lee Ratner
    Abstract:

    The proteasome is a novel target in the therapeutic approach against different subtypes of lymphomas due to its role in the degradation of many proteins involved in cell cycle progression and apoptosis. This multi-enzyme complex controls gene expression by degrading transcription factors such as NF- k B, p53, c-Jun, c-Myc, HIFla, and MATa2. Among these, the best characterized is the NF k B family of transcription factors. Mammals express five NF k B proteins including REL-A (p65), c-REL, REL-B, p50 and p52. All NF k B proteins contain a highly conserved REL-homology domain (RHD), which is responsible for DNA binding, dimerization, nuclear translocation, and interaction with the I k B proteins. Active NF k B is present in the nucleus as heterodimers of p65 and p50 or p52 and REL-B subunits. In contrast, inactive NF k B dimers are sequestered in the cytoplasm due to their interaction with inhibitory proteins such as the I k B’s or the large NF k B subunits p105 and p100. Activation of the NF k B pathway is mediated by proteasome processing of p105 and p100 to produce p50 and p52, respectively, and proteasome degradation of the I k B proteins. Therefore, the proteasome plays a central role in the equilibrium between anti-apoptotic signals derived from p50 and p52, and the NF k B inhibitory signals of p105 and p100. However, it is still undetermined whether modulation of the inhibitory signals or the anti-apoptotic signals by proteasome inhibition is more important for the induction of apoptosis in lymphomas. To address this question we tested the apoptotic effect of the proteasome inhibitor PS341 in two lymphoma cell lines (Daudi and SC) after knocking down p105 and/or p100, using lentivirus expressing siRNA’s. After 24 hours of treatment with titration doses of PS341 (5, 10, 50, and 100nM), we measured apoptosis and NF k B inhibition by Annexin V-Alexa fluorescence and an NF k B luciferase reporter assay, respectively. Interestingly, co-expression of siRNA against both p100 and p105 rendered cells resistant to the induction of apoptosis at clinical doses of PS341 (5 and 10nM) compared to the controls (see table). Similar results were obtained after selective knock down of either p105 or p100. Western Blot analysis showed much lower accumulation of p105 and p100 in siRNA expressing cells than in control cells. However, I k B levels remain stable or increase during treatment in the p105 and/or p100 siRNA expressing cells, despite the observed reduction in apoptosis. These results suggest that the accumulation of p105 and p100, rather than I k B, contributes to the induction of apoptosis. In addition, the expression of NF k B anti-apoptotic signals, such as BCL-xL, increased in all cell lines, including controls. Therefore, the presence of anti-apoptotic signals has no impact on the apoptotic effect produced by PS341. In conclusion, the current study in our lymphoma model demonstrates that the accumulation of p105 and p100 is essential for the induction of apoptosis produced by proteasome inhibition.

Mayuko Morikawa - One of the best experts on this subject based on the ideXlab platform.

  • effects of dried tofu supplementation during interval walking training on the methylation of the NFKB2 gene in the whole blood of older women
    Journal of Physiological Sciences, 2018
    Co-Authors: Mayuko Morikawa, Shizue Masuki, Sakura Nakano, Nobuo Mitsui, Hisashi Murasawa, Hiroshi Nose
    Abstract:

    Muscle atrophy with aging is closely associated with chronic systemic inflammation and lifestyle-related diseases. Here, we assessed whether dried tofu intake during 5-month interval walking training (IWT) enhanced increases in thigh muscle mass and strength and ameliorated susceptibility to inflammation in older women. Subjects (n = 32, ~ 65 years) who performed IWT for > 6 months participated in this study. They were randomly divided into 2 groups: IWT + placebo intake (PLG, n = 16; 108 kcal, 0.2 g protein, 5.5 g fat, and 14.4 g carbohydrate) and IWT + dried tofu intake (DTG, n = 16; 111 kcal, 9.6 g protein, 6.0 g fat, and 4.6 g carbohydrate). They were instructed to repeat ≥ 5 sets of fast and slow walking for 3 min each at ≥ 70 and 40% peak aerobic capacity for walking, respectively, per day for ≥ 4 days/week. Immediately after daily exercise, subjects were instructed to consume the supplements assigned to each group. In the DTG, after IWT, the methylation increased at 4/6 sites in the promoter region of the NFKB2 gene in the whole blood (all, P 0.2). Altogether, dried tofu supplementation during IWT likely enhanced the methylation of the NFKB2 gene more than IWT alone, without detectably enhanced increases in thigh muscle strength or cross-sectional area.

  • effects of milk product intake on thigh muscle strength and nfkb gene methylation during home based interval walking training in older women a randomized controlled pilot study
    PLOS ONE, 2017
    Co-Authors: Shizue Masuki, Kensei Nishida, Shigenari Hashimoto, Mayuko Morikawa, Satoshi Takasugi, Shunichiro Taniguchi, Kazuhito Rokutan, Masashi Nagata, Hiroshi Nose
    Abstract:

    Background Muscle atrophy with aging is closely associated with chronic systemic inflammation and lifestyle-related diseases. In the present study, we assessed whether post-exercise milk product intake during 5-month interval walking training (IWT) enhanced the increase in thigh muscle strength and ameliorated susceptibility to inflammation in older women. Methods Subjects [n = 37, 66±5 (standard deviation) yrs] who had been performing IWT for >6 months participated in this study. They were randomly divided into the following 3 groups: IWT alone (CNT, n = 12), IWT + low-dose post-exercise milk product intake (LD, n = 12; 4 g protein and 3 g carbohydrate) or IWT + a 3-times higher dose of milk product intake than the LD group (HD, n = 13). They were instructed to repeat ≥5 sets of fast and slow walking for 3 min each at ≥70% and 40% peak aerobic capacity for walking, respectively, per day for ≥4 days/week. Results After IWT, thigh muscle strength increased in the HD group (8±2%) more than in the CNT group (-2±3%, P = 0.022), despite similar IWT achievements between the groups (P>0.15). Pyrosequencing analysis using whole blood showed that methylation of NFKB1 and NFKB2, master genes of inflammation, was enhanced in the HD group (29±7% and 44±11%, respectively) more than in the CNT group (-20±6% and -10±6%, respectively; P<0.001). Moreover, the genome-wide DNA methylation analysis showed that several inflammation-related genes were hyper-methylated in the HD group compared with that in the CNT group, suggesting greater pro-inflammatory cytokine gene suppression in the HD group. Conclusion HD milk product intake after exercise produced a greater percent increase in thigh muscle strength and NFKB1 and NFKB2 gene methylation during IWT in physically active older women. Trial registration UMIN-CTR No. UMIN000024544 and No. UMIN000024912

  • Effects of milk product intake on thigh muscle strength and NFKB gene methylation during home-based interval walking training in older women: A randomized, controlled pilot study.
    PLOS ONE, 2017
    Co-Authors: Shizue Masuki, Kensei Nishida, Shigenari Hashimoto, Mayuko Morikawa, Satoshi Takasugi, Shunichiro Taniguchi, Kazuhito Rokutan, Masashi Nagata, Hiroshi Nose
    Abstract:

    Background Muscle atrophy with aging is closely associated with chronic systemic inflammation and lifestyle-related diseases. In the present study, we assessed whether post-exercise milk product intake during 5-month interval walking training (IWT) enhanced the increase in thigh muscle strength and ameliorated susceptibility to inflammation in older women. Methods Subjects [n = 37, 66±5 (standard deviation) yrs] who had been performing IWT for >6 months participated in this study. They were randomly divided into the following 3 groups: IWT alone (CNT, n = 12), IWT + low-dose post-exercise milk product intake (LD, n = 12; 4 g protein and 3 g carbohydrate) or IWT + a 3-times higher dose of milk product intake than the LD group (HD, n = 13). They were instructed to repeat ≥5 sets of fast and slow walking for 3 min each at ≥70% and 40% peak aerobic capacity for walking, respectively, per day for ≥4 days/week. Results After IWT, thigh muscle strength increased in the HD group (8±2%) more than in the CNT group (-2±3%, P = 0.022), despite similar IWT achievements between the groups (P>0.15). Pyrosequencing analysis using whole blood showed that methylation of NFKB1 and NFKB2, master genes of inflammation, was enhanced in the HD group (29±7% and 44±11%, respectively) more than in the CNT group (-20±6% and -10±6%, respectively; P