RESUMO
OBJECTIVES: Johrei is a type of biofield therapy that is said to bring physical and mental well-being to the recipient. This study sought to measure changes in body temperature and circulation resulting from Johrei treatment, for generally healthy subjects and for individuals with a tendency toward hypothermia. PARTICIPANTS: A total of 199 qualified Johrei practitioners and 144 non-qualified operators provided Johrei and placebo treatments, respectively. Volunteer subjects -186 in general health and 39 with a hypothermia tendency - participated in this study to receive either or both of these treatments. METHODS: Each subject was given a 10 min treatment daily by either a qualified practitioner or a non-qualified operator. The effects on subjects of receiving each treatment were compared by observing quantitative changes in blood flow and surface body temperature after a course of treatment. RESULTS: A total of 107 healthy subjects were randomly assigned to the qualified-practitioner group or the non-qualified operator group. Treatment by qualified practitioners significantly enhanced blood flow and surface body temperature in the subjects' designated neck area compared to that in treatment by non-qualified operators. This finding was further corroborated by a comparative experiment in which each healthy subject was treated by both a qualified practitioner and a non-qualified operator. These results indicate that only the qualified-practitioner treatment increased the subject's-blood flow and surface body temperature. Similarly, in a comparative study of qualified-practitioner treatment against non-qualified-operator treatment, subjects tending toward hypothermia showed increased blood flow and elevated body temperature with only the authentic Johrei treatment.
Assuntos
Hipotermia , Humanos , Hipotermia/terapia , Terapias Mente-CorpoRESUMO
Euglena gracilis is widely utilized as food or supplement to promote human and animal health, as it contains rich nutrients. In this study, we administered spray-dried powder of E. gracilis and paramylon, ß-glucan stored in E. gracilis cells, to A4gnt knockout (KO) mice. A4gnt KO mice are a mutant mouse model that spontaneously develops gastric cancer through hyperplasia-dysplasia-adenocarcinoma sequence in the antrum of the stomach, and we observed the effects of E. gracilis and paramylon on the early involvements of A4gnt KO mice. Male and female 10-week-old A4gnt KO mice and their age-matched wildtype C57BL/6J mice were orally administered with 50 mg of E. gracilis or paramylon suspended in saline or saline as a control. After 3-week administration, animals were euthanatized and the stomach was examined histopathologically and immunohistochemically. Gene expression patterns of the stomach, which have been reported to be altered with A4gnt KO, and IgA concentration in small intestine were also analyzed with real-time PCR and ELISA, respectively. Administration of Euglena significantly reduced the number of stimulated CD3-positive T-lymphocytes in pyloric mucosa of A4gnt KO mice and tend to reduce polymorphonuclear leukocytes infiltration. Euglena administration further downregulated the expression of Il11 and Cxcl1 of A4gnt KO mice. Euglena administration also affected IgA concentration in small intestinal contents of A4gnt KO mice. Paramylon administration reduced the number of CD3-positive lymphocytes in pyloric mucosa of A4gnt KO mice, and downregulated the expressions of Il11 and Ccl2 of A4gnt KO mice. Although we found no significant effects on gross and microscopic signs of gastric dysplasia and cell proliferation, the present study suggests that the administration of Euglena and paramylon may ameliorate the early involvements of A4gnt mice through the effects on inflammatory reactions in the gastric mucosa. The cancer-preventing effects should be studied with long-term experiments until actual gastric cancer formation.
Assuntos
Anticarcinógenos/uso terapêutico , Euglena gracilis , Glucanos/uso terapêutico , N-Acetilglucosaminiltransferases/genética , Neoplasias Gástricas/prevenção & controle , Administração Oral , Animais , Anticarcinógenos/administração & dosagem , Anticarcinógenos/análise , Suplementos Nutricionais/análise , Euglena gracilis/química , Feminino , Mucosa Gástrica/efeitos dos fármacos , Mucosa Gástrica/patologia , Glucanos/administração & dosagem , Glucanos/análise , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Neoplasias Gástricas/genética , Neoplasias Gástricas/patologiaRESUMO
Metabolic changes in sulfatides and other sulfated glycans have been related to various diseases, including Alzheimer's disease (AD). However, the importance of polyunsaturated fatty acids (PUFA) in sulfated lysosomal substrate metabolism and its related disorders is currently unknown. We investigated the effects of deficiency or supplementation of PUFA on the metabolism of sulfatides and sulfated glycosaminoglycans (sGAGs) in sulfatide-rich organs (brain and kidney) of mice. A PUFA-deficient diet for over 5 weeks significantly reduced the sulfatide expression by increasing the sulfatide degradative enzymes arylsulfatase A and galactosylceramidase in brain and kidney. This sulfatide degradation was clearly associated with the activation of autophagy and lysosomal hyperfunction, the former of which was induced by suppression of the Erk/mTOR pathway. A PUFA-deficient diet also activated the degradation of sGAGs in the brain and kidney and that of amyloid precursor proteins in the brain, indicating an involvement in general lysosomal function and the early developmental process of AD. PUFA supplementation prevented all of the above abnormalities. Taken together, a PUFA deficiency might lead to sulfatide and sGAG degradation associated with autophagy activation and general lysosomal hyperfunction and play a role in many types of disease development, suggesting a possible benefit of prophylactic PUFA supplementation.
Assuntos
Autofagia , Encéfalo/patologia , Dieta com Restrição de Gorduras/efeitos adversos , Ácidos Graxos Insaturados/deficiência , Lisossomos/metabolismo , Polissacarídeos/metabolismo , Sulfatos/metabolismo , Sulfoglicoesfingolipídeos/metabolismo , Animais , Encéfalo/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BLRESUMO
ß-Glucan refers to a heterogeneous group of chemically defined storage polysaccharides containing ß-(1,3)-d-linked glucose polymers with branches connected by either ß-(1,4) or ß-(1,6) glycosidic linkage. To date, an extensive amount of scientific evidence supports their multifunctional biological activities, but their potential involvement in the progression of premalignant lesions remains to be clarified. A4gnt KO mice that lack α1,4-N-acetylglucosamine-capped O-glycans in gastric gland mucin are a unique animal model for gastric cancer because the mutant mice spontaneously develop gastric cancer through hyperplasia-dysplasia-adenocarcinoma sequence. In particular, A4gnt KO mice show gastric dysplasia during 10-20â¯weeks of age. Here we investigated the putative gastro-protective activity of brown seaweed-derived ß-glucan (Laminaran) against development of gastric dysplasia, precancerous lesion for gastric cancer in A4gnt KO mice. The mutant mice at 12â¯weeks of age were randomly assigned into three treatment groups namely, wildtype controlâ¯+â¯distilled water (normal control), A4gnt KO miceâ¯+â¯distilled water (untreated control), and A4gnt KO miceâ¯+â¯100â¯mg/kg Laminaran. After 3â¯weeks, the stomach was removed and examined for morphology and gene expression patterns. In contrast to the untreated control group, administration of Laminaran substantially attenuated gastric dysplasia development and counterbalanced the increased induction in cell proliferation and angiogenesis. Furthermore, Laminaran treatment effectively overcame the A4gnt KO-induced alteration in the gene expression profile of selected cytokines as revealed by real-time PCR analysis. Collectively, our present findings indicate that ß-glucan can potentially restrain the development of gastric dysplasia to mediate their tissue-preserving activity.
Assuntos
Adenocarcinoma/prevenção & controle , Anticarcinógenos/uso terapêutico , Glucanos/uso terapêutico , Phaeophyceae , Alga Marinha , Neoplasias Gástricas/prevenção & controle , Animais , Anticarcinógenos/farmacologia , Citocinas/genética , Feminino , Mucosa Gástrica/efeitos dos fármacos , Mucosa Gástrica/imunologia , Mucosa Gástrica/patologia , Regulação da Expressão Gênica/efeitos dos fármacos , Glucanos/farmacologia , Masculino , Camundongos Knockout , FitoterapiaAssuntos
Artrite/genética , Dermatite/genética , Interleucina-1beta/genética , Dermatopatias Genéticas/genética , Artrite/metabolismo , Células Cultivadas , Dermatite/metabolismo , Expressão Gênica , Humanos , Proteína Antagonista do Receptor de Interleucina 1/uso terapêutico , Interleucina-1beta/biossíntese , Leucócitos Mononucleares/efeitos dos fármacos , Leucócitos Mononucleares/metabolismo , Proteína Adaptadora de Sinalização NOD2/genética , Proteína Adaptadora de Sinalização NOD2/metabolismo , Mutação Puntual , Dermatopatias Genéticas/metabolismoRESUMO
OTT/RBM15-BSAC/MAL/MKL1/MRTF-A was identified as a fusion transcript generated by t(1;22)(p13;q13) in acute megakaryoblastic leukemia. Previous studies have shown that BSAC (basic, SAP, and coiled-coil domain) activates the promoters containing CArG boxes via interaction with serum response factor, and OTT (one twenty-two) negatively regulates the development of megakaryocytes and myeloid cells. However, the mechanism by which OTT-BSAC promotes leukemia is largely unknown. Here we show that OTT-BSAC, but not BSAC or OTT strongly activates several promoters containing a transcription factor Yin Yang 1-binding sequence. In addition, although BSAC predominantly localizes in the cytoplasm and its nuclear translocation is considered to be regulated by the Rho-actin signaling pathway, OTT-BSAC exclusively localizes in the nucleus. Moreover, OTT interacts with histone deacetylase 3, but this interaction is abolished in OTT-BSAC. Collectively, these functional and spatial changes of OTT and BSAC caused by the fusion might perturb their functions, culminating in the development of acute megakaryoblastic leukemia.
Assuntos
Núcleo Celular/metabolismo , Proteínas de Ligação a DNA/metabolismo , Leucemia Megacarioblástica Aguda/metabolismo , Proteínas de Fusão Oncogênica/metabolismo , Proteínas de Ligação a RNA/metabolismo , Elementos de Resposta , Transcrição Gênica , Transporte Ativo do Núcleo Celular/genética , Linhagem Celular Tumoral , Núcleo Celular/genética , Proteínas de Ligação a DNA/genética , Histona Desacetilases/genética , Histona Desacetilases/metabolismo , Humanos , Leucemia Megacarioblástica Aguda/genética , Megacariócitos/metabolismo , Proteínas de Fusão Oncogênica/genética , Estrutura Terciária de Proteína/genética , Proteínas de Ligação a RNA/genética , Elementos de Resposta/genética , Transativadores , Transcrição Gênica/genética , Regulação para Cima/genética , Fator de Transcrição YY1/genética , Fator de Transcrição YY1/metabolismoRESUMO
The mouse homeobox gene Otx2 plays essential roles at each step and in every tissue during head development. We have previously identified a series of enhancers that are responsible for driving the Otx2 expression in these contexts. Among them the AN enhancer, existing 92 kb 5' upstream, directs Otx2 expression in anterior neuroectoderm (AN) at the headfold stage. Analysis of the enhancer mutant Otx2(DeltaAN/-) indicated that Otx2 expression under the control of this enhancer is essential to the development of AN. This study demonstrates that the AN enhancer is promoter-dependent and regulated by acetylated YY1. YY1 binds to both the AN enhancer and promoter region. YY1 is acetylated in the anterior head, and only acetylated YY1 can bind to the sequence in the enhancer. Moreover, YY1 binding to both of these two sites is essential to Otx2 expression in AN. These YY1 binding sites are highly conserved in AN enhancers in tetrapods, coelacanth and skate, suggesting that establishment of the YY1 regulation coincides with that of OTX2 function in AN development in an ancestral gnathostome.