American Medical Holdings Inc.

Staten Island, NY, United States

American Medical Holdings Inc.

Staten Island, NY, United States
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Stohs S.J.,Creighton University | Badmaev V.,American Medical Holdings Inc.
Phytotherapy Research | Year: 2016

Obesity and overweight are major health issues. Exercise and calorie intake control are recognized as the primary mechanisms for addressing excess body weight. Naturally occurring thermogenic plant constituents offer adjunct means for assisting in weight management. The controlling mechanisms for thermogenesis offer many intervention points. Thermogenic agents can act through stimulation of the central nervous system with associated adverse cardiovascular effects and through metabolic mechanisms that are non-stimulatory or a combination thereof. Examples of stimulatory thermogenic agents that will be discussed include ephedrine and caffeine. Examples of non-stimulatory thermogenic agents include p-synephrine (bitter orange extract), capsaicin, forskolin (Coleus root extract), and chlorogenic acid (green coffee bean extract). Green tea is an example of a thermogenic with the potential to produce mild but clinically insignificant undesirable stimulatory effects. The use of the aforementioned thermogenic agents in combination with other extracts such as those derived from Salacia reticulata, Sesamum indicum, Lagerstroemia speciosa, Cissus quadrangularis, and Moringa olifera, as well as the use of the carotenoids as lutein and fucoxanthin, and flavonoids as naringin and hesperidin can further facilitate energy metabolism and weight management as well as sports performance without adverse side effects. © 2016 The Authors Phytotherapy Research published by John Wiley & Sons Ltd.


Karpinski M.,Medical University of Bialystok | Popko J.,The College of Computer Science | Maresz K.,International Science & Health Foundation | Badmaev V.,American Medical Holdings Inc | Stohs S.J.,Creighton University
Journal of the American College of Nutrition | Year: 2017

The research on skeletal system health in children and young adults, while recognizing the important role of calcium and vitamin D, goes beyond these nutritional standards. This review focuses on the role of vitamin K in combination with vitamin D and other factors in bone health. The current understanding is that maintaining bone health and prevention of low-energy fractures in any pediatric population includes nutritional factors combined with an active lifestyle. Calcium, vitamin D, and vitamin K supplementation contribute independently and collectively to bone health. The beneficial role of vitamin K, particularly vitamin K2 as menaquinone-7 (MK-7), in bone and cardiovascular health is reasonably well supported scientifically, with several preclinical, epidemiological, and clinical studies published over the last decade. Osteocalcin and matrix-Gla (glutamate-containing) protein (MGP) exemplify vitamin K–dependent proteins involved in building bone matrix and keeping calcium from accumulating in the arterial walls, respectively. An important part of the mechanism of vitamin K involves carboxylation and posttranslational activation of the family of vitamin K–dependent proteins, which prevent expression of pro-inflammatory factors and support improvement in bone mineral concentration, bone mineral density, and the quality of bone matrix. Understanding the combined approach to a healthy skeletal system in children and young adults, including the roles of vitamins D and K, calcium, healthy diet, and exercise, is particularly important in view of reports of subclinical insufficiency of vitamins D and K in otherwise healthy pediatric populations with low-energy bone fractures. © 2017 American College of Nutrition.


Wu J.-C.,National Cheng Kung University | Wang F.-Z.,National Kaohsiung Marine University | Tsai M.-L.,National Kaohsiung Marine University | Lo C.-Y.,National Chiayi University | And 8 more authors.
Molecular Nutrition and Food Research | Year: 2015

Scope: Selenium (Se)-conjugated compounds have been established as anti-carcinogenic compounds. The use of chemicals as cancer chemotherapeutic agents to induce programmed cell death (PCD) involves genetic and epigenetic modifications. In this study, we investigated the underlying molecular mechanisms of Se-allylselenocysteine (ASC)-induced PCD and protocadherin 17 (PCDH17) expression in HT-29 cells. Methods and results: Cell viability analysis indicated that the ability of ASC to induce cancer cell death was greater than that of Se-methylselenocysteine in colorectal cancer cells. ASC also decreased global DNA methylation levels via downregulation of DNA methyltransferase 1 expression. The autophagic cell death is the cause in ASC-induced cytotoxicity that was inhibited by pretreatment with autophagy inhibitor. At the molecular level, ASC induced PCDH17 expression through decreased PCDH17 promoter hypermethylation. PCDH17 is also an important role in ASC-induced autophagy by HT-29 transfected with PCDH17 shRNA or expression plasmid. Our western blot analysis showed that ASC significantly induced autophagy via the AMPK/mTOR pathway that was also regulated PCDH17 expression. Additionally, we used the HT-29 tumor xenograft models to confirm the ability of ASC inhibited tumor growth. Conclusion: These results reveal that ASC is an effective inducer of autophagy through regulating the AMPK/mTOR and PCDH17 expression via epigenetic modification. © 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.


Arthur S.T.,Laboratory of Systems Physiology | Zwetsloot K.A.,Appalachian State University | Lawrence M.M.,Laboratory of Systems Physiology | Nieman D.C.,Appalachian State University | And 13 more authors.
European Review for Medical and Pharmacological Sciences | Year: 2014

BACKGROUND: The declining myogenic potential of aged skeletal muscle is multifactorial. Insufficient satellite cell activity is one factor in this process. Notch and Wnt signaling are involved in various biological processes including orchestrating satellite cell activity within skeletal muscle. These pathways become dysfunctional during the aging process and may contribute to the poor skeletal muscle competency. Phytoecdysteroids are natural adapto-genic compounds with demonstrated benefit on skeletal muscle. AIM: To determine the extent to which a phy-toecdysteroid enriched extract from Ajuga turkestanica (ATE) affects Notch and Wnt signaling in aged skeletal muscle. MATERIALS AND METHODS: Male C57BL/6 mice (20 months) were randomly assigned to Control (CT) or ATE treatment groups. Chow was supplemented with either vehicle (CT) or ATE (50 mg/kg/day) for 28 days. Following supplementation, the triceps brachii muscles were harvested and immunohistochemical analyses performed. Components of Notch or Wnt signaling were co-labelled with Pax7, a quiescent satellite cell marker. RESULTS: ATE supplementation significantly increased the percent of active Notch/Pax7+ nuclei (p = 0.005), Hes1/Pax7+ nuclei (p = 0.038), active B-catenin/Pax7+ nuclei (p = 0.011), and Lef1/Pax7+ nuclei (p = 0.022), compared to CT. ATE supplementation did not change the resting satellite cell number. CONCLUSIONS: ATE supplementation in aged mice increases Notch and Wnt signaling in triceps brachii muscle. If Notch and Wnt benefit skeletal muscle, then phytoecdysteroids may provide a protective effect and maintain the integrity of aged skeletal muscle.


PubMed | National Chiayi University, American Medical Holdings Inc, National Kaohsiung Marine University, National Cheng Kung University and 2 more.
Type: Journal Article | Journal: Molecular nutrition & food research | Year: 2016

Selenium (Se)-conjugated compounds have been established as anti-carcinogenic compounds. The use of chemicals as cancer chemotherapeutic agents to induce programmed cell death (PCD) involves genetic and epigenetic modifications. In this study, we investigated the underlying molecular mechanisms of Se-allylselenocysteine (ASC)-induced PCD and protocadherin 17 (PCDH17) expression in HT-29 cells.Cell viability analysis indicated that the ability of ASC to induce cancer cell death was greater than that of Se-methylselenocysteine in colorectal cancer cells. ASC also decreased global DNA methylation levels via downregulation of DNA methyltransferase 1 expression. The autophagic cell death is the cause in ASC-induced cytotoxicity that was inhibited by pretreatment with autophagy inhibitor. At the molecular level, ASC induced PCDH17 expression through decreased PCDH17 promoter hypermethylation. PCDH17 is also an important role in ASC-induced autophagy by HT-29 transfected with PCDH17 shRNA or expression plasmid. Our western blot analysis showed that ASC significantly induced autophagy via the AMPK/mTOR pathway that was also regulated PCDH17 expression. Additionally, we used the HT-29 tumor xenograft models to confirm the ability of ASC inhibited tumor growth.These results reveal that ASC is an effective inducer of autophagy through regulating the AMPK/mTOR and PCDH17 expression via epigenetic modification.


Weerawatanakorn M.,Naresuan University | Hsieh S.-C.,National Taiwan University of Science and Technology | Tsai M.-L.,National Kaohsiung Marine University | Lai C.-S.,National Taiwan University of Science and Technology | And 5 more authors.
Journal of Functional Foods | Year: 2014

Chronic liver disease is characterized by an exacerbated accumulation of deposition of collagen, causing progressive fibrosis, which may lead to cirrhosis. We evaluated the inhibitory effect of tetrahydrocurcumin (THC), a major metabolite of curcumin, on liver fibrogenesis both in vitro, HSC-T6 cell, and in vivo, dimethylnitrosamine (DMN)-induced liver fibrosis in rat. The liver inflammation in HSC-T6 cell was initiated by transforming growth factor-β1 (TGF-β1), and fibrosis in Sprague-Dawley rats was induced by intraperitoneal ( i.p.) injection of DMN (10. mg/kg) 3. days per week for four consecutive weeks. THC (10. mg/kg) was administered in rats by oral gavage daily. DMN caused hepatic injury as indicated by analysis of liver function, morphology, histochemistry, and fibrotic parameters. Once-daily dosing with THC alleviated liver damage as signified by histopathological examination of the α-smooth muscle actin (α-SMA) and collagen I, accompanied by the reduction TGF-β1 and serum levels of transaminase ( P<. 0.05). These data revealed that the THC exerts hepatoprotective activity in experimental fibrosis, potentially by inhibiting the TGF-β1/Smad signaling. © 2014 Elsevier Ltd.


Lee M.-F.,Chang Jung Christian University | Lai C.-S.,National Taiwan University of Science and Technology | Cheng A.-C.,Chang Jung Christian University | Hou J.-S.,National Kaohsiung Marine University | And 4 more authors.
Journal of Functional Foods | Year: 2015

Krill oil (KO) is rich in omega-3 long-chain polyunsaturated fatty acids, eicosapentaenoic acid and docosahexaenoic acid. Previous studies have shown that KO supplementation alleviated hepatic steatosis in rodents. Xanthigen (brown marine algae fucoxanthin + pomegranate seed oil) is an important source of fucoxanthin and punicic acid. Our recent work indicated that xanthigen (Xan) significantly suppressed 3T3-L1 preadipocyte differentiation and lipid accumulation. Here we investigated the effect of KO and Xan on lipid accumulation in HepG2 liver cancer cells and on high fat diet (HFD)-induced obesity in C57BL/6J mice. KO potently inhibited triacylglycerol accumulation in Hep G2 cells. Supplementation with 2.5% KO or Xan effectively reduced HFD-induced body weight gain and adipose mass increase without affecting food intake, and improved diet-induced hepatic steatosis. In summary, KO and Xan may act as novel agents for the treatment of diet-induced obesity and steatosis. © 2014 Elsevier Ltd.


PubMed | Creighton University and American Medical Holdings Inc.
Type: Journal Article | Journal: Phytotherapy research : PTR | Year: 2016

Obesity and overweight are major health issues. Exercise and calorie intake control are recognized as the primary mechanisms for addressing excess body weight. Naturally occurring thermogenic plant constituents offer adjunct means for assisting in weight management. The controlling mechanisms for thermogenesis offer many intervention points. Thermogenic agents can act through stimulation of the central nervous system with associated adverse cardiovascular effects and through metabolic mechanisms that are non-stimulatory or a combination thereof. Examples of stimulatory thermogenic agents that will be discussed include ephedrine and caffeine. Examples of non-stimulatory thermogenic agents include p-synephrine (bitter orange extract), capsaicin, forskolin (Coleus root extract), and chlorogenic acid (green coffee bean extract). Green tea is an example of a thermogenic with the potential to produce mild but clinically insignificant undesirable stimulatory effects. The use of the aforementioned thermogenic agents in combination with other extracts such as those derived from Salacia reticulata, Sesamum indicum, Lagerstroemia speciosa, Cissus quadrangularis, and Moringa olifera, as well as the use of the carotenoids as lutein and fucoxanthin, and flavonoids as naringin and hesperidin can further facilitate energy metabolism and weight management as well as sports performance without adverse side effects. 2016 The Authors Phytotherapy Research published by John Wiley & Sons Ltd.

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