Physiological Activities of Perilla Frutescens Var. Frutescens Leaf Extracts and Storage Stability in Kneaded Noodles

Perilla (Perilla frutescens var. frutescens) leaves were fractionated based on their chemical properties, and the physiological activities of the fractions were evaluated. The acidic fraction had high radical scavenging ability, whereas the superoxide dismutase-like activities of all fractions were low. A positive correlation was observed between scavenging activity and polyphenol content. The inhibitory effects of the extracts on a-amylase and on a-glucosidase activities were low, indicating a weak suppressive effect of the leaf extracts on diabetes. The acidic and phenolic fractions suppressed pancreatic lipase activity and accelerated lipid hydrolysis in adipocytes differentiated from 3T3-L1 cells. Flour noodles kneaded with leaf powder were prepared, and storage stability was examined. The functional compounds in the leaves were heat-sensitive in the flour noodles. We fractionated perilla leaves to isolate and identify valuable components to provide functionality to processed food and determined that some conditions, such as storage temperature, must be considered to effectively use the compounds

Гомосексуальный субъект в пространстве публичного: нарративное измерение камин-аута

<div><p>Background</p><p>Although <i>Helicobacter pylori</i> (<i>H</i>. <i>pylori</i>) infection is closely associated with the development of peptic ulcer, its involvement in pathophysiology in the lower intestinal tract and gastrointestinal (GI) motility remains unclear. Glucagon-like peptide-1 (GLP-1) is a gut hormone produced in the lower intestinal tract and involved in GI motility. Here, we investigated the effect of <i>H</i>. <i>pylori</i> infection on the link between GLP-1 expression and motility of the GI tract.</p><p>Methods</p><p>C57BL/6 mice were inoculated with a <i>H</i>. <i>pylori</i> strain. Twelve weeks later, the <i>H</i>. <i>pylori</i>-infected mice underwent <i>H</i>. <i>pylori</i> eradication treatment. GI tissues were obtained from the mice at various time intervals, and evaluated for the severity of gastric inflammatory cell infiltration and immunohistochemical expression of GLP-1 and PAX6 in the colonic mucosa. Gastrointestinal transit time (GITT) was measured by administration of carmine-red solution.</p><p>Results</p><p>GLP-1 was expressed in the endocrine cells of the colonic mucosa, and PAX6 immunoreactivity was co-localized in such cells. The numbers of GLP-1- and PAX6-positive cells in the colon were significantly increased at 12 weeks after <i>H</i>. <i>pylori</i> infection and showed a positive correlation with each other. The GITT was significantly longer in <i>H</i>. <i>pylori</i>-infected mice than in non-infected controls and showed a positive correlation with GLP-1 expression. When <i>H</i>. <i>pylori</i>-infected mice underwent <i>H</i>. <i>pylori</i> eradication, GITT and PAX6/GLP-1 expression did not differ significantly from those in untreated <i>H</i>. <i>pylori</i>-infected mice.</p><p>Conclusions</p><p><i>H</i>. <i>pylori</i> infection may impair GI motility by enhancing the colonic GLP-1/PAX6 expression.</p></div

Significance of serum palmitoleic acid levels in inflammatory bowel disease

Inflammatory bowel diseases (IBDs), including ulcerative colitis (UC) and Crohn’s disease (CD), are chronic intestinal diseases of unknown etiology that present with variable disease extents and outcomes. The use of biomarkers for the diagnosis and management of IBDs is considered beneficial. Palmitoleic acid (PO) is an adipose tissue-derived mono-unsaturated free fatty acid that potentially serves as a lipokine in metabolic and inflammatory diseases. The aim of this study was to investigate the significance of PO levels in the serum of patients with UC and CD. The study included patients with UC (n = 22), patients with CD (n = 35), and controls (n = 22). The levels of serum PO were analyzed using gas chromatography. The association of serum PO levels with the clinical features and disease outcomes in IBD was examined. Serum PO levels were significantly higher in patients with CD than in controls, whereas no difference in these levels was observed between patients with UC and controls. Serum PO levels were significantly associated with the CD activity index. Additionally, high serum PO levels were associated with an increased risk of surgical intervention requirement during follow-up. In a pilot study with a few patients, high PO levels were observed in the mesenteric tissue in the active disease site of patients with CD (n = 7) compared with those with colon cancer (n = 6). Elevated serum PO levels might serve as a marker for local inflammation and prognosis in patients with CD

Phenotypic Plasticity of Mouse Spermatogonial Stem Cells

BACKGROUND:Spermatogonial stem cells (SSCs) continuously undergo self-renewal division to support spermatogenesis. SSCs are thought to have a fixed phenotype, and development of a germ cell transplantation technique facilitated their characterization and prospective isolation in a deterministic manner; however, our in vitro SSC culture experiments indicated heterogeneity of cultured cells and suggested that they might not follow deterministic fate commitment in vitro. METHODOLOGY AND PRINCIPAL FINDINGS:In this study, we report phenotypic plasticity of SSCs. Although c-kit tyrosine kinase receptor (Kit) is not expressed in SSCs in vivo, it was upregulated when SSCs were cultured on laminin in vitro. Both Kit(-) and Kit(+) cells in culture showed comparable levels of SSC activity after germ cell transplantation. Unlike differentiating spermatogonia that depend on Kit for survival and proliferation, Kit expressed on SSCs did not play any role in SSC self-renewal. Moreover, Kit expression on SSCs changed dynamically once proliferation began after germ cell transplantation in vivo. CONCLUSIONS/SIGNIFICANCE:These results indicate that SSCs can change their phenotype according to their microenvironment and stochastically express Kit. Our results also suggest that activated and non-activated SSCs show distinct phenotypes

低蛋白血症で発見された骨髄腫関連疾患の一症例

広義の骨髄腫関連疾患には,古典的なmyelomaを始めとして,plasmacytic leukemia,plasmacytomaさらにmacroglobulinemia,lymphoplasmacytic lymphomaなどが含まれる.一般的には特徴的検査所見の一つに,血清総蛋白の高値がある.ところが,今回我々は血清総蛋白がむしろ低値であった骨髄腫関連疾患を経験した.症例は85歳女性.貧血軽度,黄疸(-),肝脾腫(-),リンパ節腫大(-),骨病変は軽微であった.検査所見:末梢血WBC4370/μl,RBC242万/μl,Hgb8.1g/dl,Hct25.6%,PLT6.2万/μl,Neut70.7%,Lym23.6%,Mono5.0%,Eos0.2%,Bas0.5%.生化学:TP5.3g/dl,Alb2.0g/dl,Glob3.3g/dlそのうちIgG532mg/dl,IgA79mg/dl,IgM2,035mg/dlで,免疫電気泳動にて明らかなM-bowを認め,IgM-_K型と判明した.骨髄:採取した標本では低形成で,Mgk10/μl,赤芽球15.6%,顆粒球系60.3%,リンパ球系23.8%,そのうち形質細胞1.9%であった.形態学的には,マクログロブリン血症の際にみられるリンパ・形質細胞様の所見であった.細胞表面マーカーの検索では,リンパ球全体ではCD7 33.5%,CD138 0.7%,CD19 7.0%,CD20 32.8%,形質細胞ではCD7 21.8%,CD138 57.7%,CD19 21.1%,CD20 39.7%であった.病理検査では,N/C比が高く異型性のある核を持つ細胞のシート状の集簇が認められた.腫瘍細胞の透過型電顕所見では,核は偏在し,大型のゴルジ野を有し,粗面小胞体はよく発達し,蛋白合成の盛んなことが推測された.細胞によっては,分化度が低く核クロマチンは繊細で明らかに芽球様の細胞も認められた.染色体分析:46,XX.末梢血生化学所見では総蛋白量の明らかな減少が認められたが,その病因は腫瘍細胞によるIgMの過剰産生にあり,その腫瘍性性質のため正常免疫グロブリン特にIgGおよびIgAの著しい産生抑制を生じたものと考えられる.細胞学的にはマクログロブリン血症と多発性骨髄腫とにまたがる境界領域に位置付けられるBリンパ球系悪性疾患と推定される.It is known that myeloma-related disorders include classical myeloma, plasmacytic leukemia, plasmacytoma, macroglobulinemia, lymphoplasmacytic lymphoma and others. Increased serum protein is one of the characteristic features in these disorders. We have recently experienced a case of myeloma-related disorder with hypoproteinemia. The patient (a 85 year-old female) demonstrated hypoproteinemia (total protein 5.3g/dl, Alb2.0g/dl, Glob3.3g/dl) with increased IgM 2,035mg/dl contrary to decreased IgG(532mg/dl) and IgA(79mg/dl). The presence of IgM-_K monoclonality was detected by immunoelectrophoresis. Peripheral blood showed slight anemia(RBC 2.42×10^6/μl) and thrombocytopenia(62×10^3/μl). Peripheral lymphocytes were 23.6% with lymphoplasmacytic appearance. Bone marrow examination revealed that lymphocytes were 23.8% with 1.9% of plasma cells: CD79a(+), CD138(+/-), CD20(+/-), CD5(-), cyclin D1(-), IgM(+), IgA(-), IgG(+-), and IgM_K -monoclonality(+) by immune staining method. Surface makers of all lymphoid cells indicated CD138 57.7%, CD19 21.1%, and CD20 39.7%. Clusters of malignant lymphoid cells were present in bone marrow specimen. Transmission electron microscopy (TEM) on the lymphoid cells indicated the dislocated nucleus and profound rough-surfaced ribosomes with large Golgi apparatus suggesting the markedly enhanced protein production. In some cells, the blastic appearance with fine nuclear chromatin structure was observed. The pathogenesis of hypoproteinemia appears to be due to suppression of IgG and IgA by increased IgM monoclonality, in addition to decreased level of serum albumin. The disorder is considered to be localized at the border area between classical myeloma and macroglobulinemia

ヒト メンエキ フゼン ウイルス 1ガタ Vpr ワ ミトコンドリア キノウ ショウガイ オ カイシテ シンケイ サイボウ ノ ジクサク シンチョウ オ ヨクセイスル

京都大学0048新制・課程博士博士(医学)甲第13709号医博第3224号新制||医||967(附属図書館)UT51-2008-C626京都大学大学院医学研究科病理系専攻(主査)教授 生田 宏一, 教授 秋山 芳展, 教授 横出 正之学位規則第4条第1項該当Doctor of Medical ScienceKyoto UniversityDA

Human Immunodeficiency Virus Type 1 Vpr Inhibits Axonal Outgrowth through Induction of Mitochondrial Dysfunction▿

Human immunodeficiency virus type 1 (HIV-1)-infected macrophages damage mature neurons in the brain, although their effect on neuronal development has not been clarified. In this study, we show that HIV-1-infected macrophages produce factors that impair the development of neuronal precursor cells and that soluble viral protein R (Vpr) is one of the factors that has the ability to suppress axonal growth. Cell biological analysis revealed that extracellularly administered recombinant Vpr (rVpr) clearly accumulated in mitochondria where a Vpr-binding protein adenine nucleotide translocator localizes and also decreased the mitochondrial membrane potential, which led to ATP synthesis. The depletion of ATP synthesis reduced the transportation of mitochondria within neurites. This mitochondrial dysfunction inhibited axonal growth even when the frequency of apoptosis was not significant. We also found that point mutations of arginine (R) residues to alanine (A) residues at positions 73, 77, and 80 rendered rVpr incapable of causing mitochondrial membrane depolarization and axonal growth inhibition. Moreover, the Vpr-induced inhibition was suppressed after treatment with a ubiquinone analogue (ubiquinone-10). Our results suggest that soluble Vpr is a major viral factor that causes a disturbance in neuronal development through the induction of mitochondrial dysfunction. Since ubiquinone-10 protects the neuronal plasticity in vitro, it may be a therapeutic agent that can offer defense against HIV-1-associated neurological disease

APOBEC1-Mediated Editing and Attenuation of Herpes Simplex Virus 1 DNA Indicate That Neurons Have an Antiviral Role during Herpes Simplex Encephalitis ▿ †

APOBEC1 (A1) is a cytidine deaminase involved in the regulation of lipids in the small intestine. Herpes simplex virus 1 (HSV-1) is a ubiquitous pathogen that is capable of infecting neurons in the brain, causing encephalitis. Here, we show that A1 is induced during encephalitis in neurons of rats infected with HSV-1. In cells stably expressing A1, HSV-1 infection resulted in significantly reduced virus replication compared to that in control cells. Infectivity could be restored to levels comparable to those observed for control cells if A1 expression was silenced by specific A1 short hairpin RNAs (shRNA). Moreover, cytidine deaminase activity appeared to be essential for this inhibition and led to an impaired accumulation of viral mRNA transcripts and DNA copy numbers. The sequencing of viral gene UL54 DNA, extracted from infected A1-expressing cells, revealed G-to-A and C-to-T transitions, indicating that A1 associates with HSV-1 DNA. Taken together, our results demonstrate a model in which A1 induction during encephalitis in neurons may aid in thwarting HSV-1 infection