予防接種法

http://elaws.e-gov.go.jp/search/elawsSearch/elaws_search/lsg0500/detail?lawId=323AC0000000068&openerCode=1

第二条 この法律において「予防接種」とは、疾病に対して免疫の効果を得させるため、疾病の予防に有効であることが確認されているワクチンを、人体に注射し、又は接種することをいう。

  1. この法律において「A類疾病」とは、次に掲げる疾病をいう。
    1. ジフテリア
    2. 百日せき
    3. 急性灰白髄炎
    4. 麻しん
    5. 風しん
    6. 日本脳炎
    7. 破傷風
    8. 結核
    9. Hib感染症
    10. 肺炎球菌感染症(小児がかかるものに限る。)
    11. ヒトパピローマウイルス感染症
    12. 前各号に掲げる疾病のほか、人から人に伝染することによるその発生及びまん延を予防するため、又はかかった場合の病状の程度が重篤になり、若しくは重篤になるおそれがあることからその発生及びまん延を予防するため特に予防接種を行う必要があると認められる疾病として政令で定める疾病
  2. この法律において「B類疾病」とは、次に掲げる疾病をいう。
    1. インフルエンザ
    2. 前号に掲げる疾病のほか、個人の発病又はその重症化を防止し、併せてこれによりそのまん延の予防に資するため特に予防接種を行う必要があると認められる疾病として政令で定める疾病
  3. この法律において「定期の予防接種」とは、次に掲げる予防接種をいう。
    1. 第五条第一項の規定による予防接種
    2. 前号に掲げる予防接種に相当する予防接種として厚生労働大臣が定める基準に該当する予防接種であって、市町村長以外の者により行われるもの
  4. この法律において「臨時の予防接種」とは、次に掲げる予防接種をいう。
    1. 第六条第一項又は第三項の規定による予防接種
    2. 前号に掲げる予防接種に相当する予防接種として厚生労働大臣が定める基準に該当する予防接種であって、第六条第一項又は第三項の規定による指定があった日以後当該指定に係る期日又は期間の満了の日までの間に都道府県知事及び市町村長以外の者により行われるもの
  5. この法律において「定期の予防接種等」とは、定期の予防接種又は臨時の予防接種をいう。
  6. この法律において「保護者」とは、親権を行う者又は後見人をいう。

法律に基づく予防接種

  • 予防接種法及び結核予防法による定期の予防接種は市町村長が行うこととされており,予防接種法に基づく一類疾病及び結核予防法に基づく結核の予防接種の対象者は予防接種を受けるよう努めなければならないこととされている。予防接種法に基づく二類疾病の予防接種の対象者については努力義務が課されていない。
  • また,予防接種法に基づく臨時の予防接種は,都道府県知事が行い,又は市町村長に行うよう指示することができることとなっており,当該予防接種の対象者は予防接種を受けるよう努めなければならない

一類疾病(定期予防接種)

−ポリオ(弱毒生ワクチン、3種類のウイルス型を含む、経口)
−麻疹(生後3ヶ月から90ヶ月の間)(弱毒生ワクチン)
−風疹(弱毒生ワクチン)
日本脳炎(不活化ワクチン)

二類(定期予防接種)

インフルエンザ(65歳以上)(不活化)

結核予防法

BCG(6ヶ月未満)(弱毒生)

任意接種

  • インフルエンザ

おたふく風邪(弱毒生)
−水痘(弱毒生)
B型肝炎
−肺炎球菌
−A型肝炎
狂犬病

麻疹ウイルス

パラミクソウイルス科(麻疹のほか、ムンプス、牛疫、RSウイルス、パラインフルエンザウイルスなど)
エンベロープをもち非分節一本鎖マイナス鎖RNAをゲノムにもつ
かつてはすべての子供が罹患する病気だったが、生ワクチンが導入されて激減した。
一過性の免疫抑制を起こすこと、稀に中枢神経系の持続感染を起こす。
Hタンパク質とFタンパク質に対する抗体のいずれもが感染防御効果があり、抗原性の変化も起こりにくい。

症状

不顕性感染は見られない。
京畿道的感染。10-14日の潜伏期間をおく。
発熱を伴う結膜炎、上気道炎で発症する。(カタル期)涙や、唾液中に大量のウイルスが排出されている。
今日粘膜にコプリック斑を認める。
二峰性の発熱ののち、発疹(顔、頸部二始まり下行性に広がる。
合併症(10−20%):中耳炎、肺炎、喉頭炎、細菌の二次感染による。麻疹後脳炎(交差免疫反応による)
死亡の原因は細菌性肺炎の合併
亜急性硬化性全脳炎
数年の潜伏の後に発症する
二次リンパ組織に多核巨細胞を生じさせる。(一過性の免疫能低下によるツ反が陰転する)合併症と関連する。
予防
弱毒生ワクチン。
終生免疫では無いと考えられ、成人麻疹例が増加している。

SI基本単位

基本単位に該当する物理量は、

  • 長さ(メートル)
  • 質量(キログラム)
  • 時間(秒)
  • 電流(アンペア)
  • 熱力学温度(ケルビン
  • 物質量(モル)
  • 光度(カンデラ

誘導単位

AKT1

  • AKT1 is one of 3 closely related serine/threonine-protein kinases (AKT1, AKT2 and AKT3) called the AKT kinase, and which regulate many processes including metabolism, proliferation, cell survival, growth and angiogenesis.
  • This is mediated through serine and/or threonine phosphorylation of a range of downstream substrates.
  • Over 100 substrate candidates have been reported so far, but for most of them, no isoform specificity has been reported.
  • AKT is responsible of the regulation of glucose uptake by mediating insulin-induced translocation of the SLC2A4/GLUT4 glucose transporter to the cell surface.
  • Phosphorylation of PTPN1 (Tyrosine-protein phosphatase non-receptor type 1) at 'Ser-50' negatively modulates its phosphatase activity preventing dephosphorylation of the insulin receptor and the attenuation of insulin signaling. プロテインチロシンホスファターゼをリン酸化し活性を低下させることで、インスリン刺激を増強する。
  • Phosphorylation of TBC1D4 triggers the binding of this effector to inhibitory 14-3-3 proteins, which is required for insulin-stimulated glucose transport. リン酸化を受けたTBC1D4はGLUT4の細胞膜への移動に必要である。
  • AKT regulates also the storage of glucose in the form of glycogen by phosphorylating GSK3A at 'Ser-21' and GSK3B at 'Ser-9', resulting in inhibition of its kinase activity. グリコーゲンシンターゼキナーゼをリン酸化して阻害することで、グリコーゲン合成を促進する。
  • Phosphorylation of GSK3 isoforms by AKT is also thought to be one mechanism by which cell proliferation is driven. AKT regulates also cell survival via the phosphorylation of MAP3K5 (apoptosis signal-related kinase).
  • Phosphorylation of 'Ser-83' decreases MAP3K5 kinase activity stimulated by oxidative stress and thereby prevents apoptosis.
  • AKT mediates insulin-stimulated protein synthesis by phosphorylating TSC2 at 'Ser-939' and 'Thr-1462', thereby activating mTORC1 signaling and leading to both phosphorylation of 4E-BP1 and in activation of RPS6KB1.
  • AKT is involved in the phosphorylation of members of the FOXO factors (Forkhead family of transcription factors), leading to binding of 14-3-3 proteins and cytoplasmic localization. In particular, FOXO1 is phosphorylated at 'Thr-24', 'Ser-256' and 'Ser-319'. FOXO3 and FOXO4 are phosphorylated on equivalent sites.
  • AKT has an important role in the regulation of NF-kappa-B-dependent gene transcription and positively regulates the activity of CREB1 (cyclic AMP (cAMP)-response element binding protein).
  • The phosphorylation of CREB1 induces the binding of accessory proteins that are necessary for the transcription of pro-survival genes such as BCL2 and MCL1. AKT phosphorylates 'Ser-454' on ATP citrate lyase (ACLY), thereby potentially regulating ACLY activity and fatty acid synthesis. Activates the 3B isoform of cyclic nucleotide phosphodiesterase (PDE3B) via phosphorylation of 'Ser-273', resulting in reduced cyclic AMP levels and inhibition of lipolysis. CREB(cAMP-response element binding protein)をリン酸化しBCL2などの生存に必要な遺伝子の転写を促す。
  • Phosphorylates PIKFYVE on 'Ser-318', which results in increased PI3P-5 activity.
  • The Rho GTPase-activating protein DLC1 is another substrate and its phosphorylation is implicated in the regulation cell proliferation and cell growth.
  • AKT plays a role as key modulator of the AKT-mTOR signaling pathway controlling the tempo of the process of newborn neurons integration during adult neurogenesis, including correct neuron positioning, dendritic development and synapse formation.
  • Signals downstream of phosphatidylinositol 3-kinase (PI3K) to mediate the effects of various growth factors such as platelet-derived growth factor (PDGF), epidermal growth factor (EGF), insulin and insulin-like growth factor I (IGF-I).
  • AKT mediates the antiapoptotic effects of IGF-I. Essential for the SPATA13-mediated regulation of cell migration and adhesion assembly and disassembly.
  • May be involved in the regulation of the placental development. Phosphorylates STK4/MST1 at 'Thr-120' and 'Thr-387' leading to inhibition of its: kinase activity, nuclear translocation, autophosphorylation and ability to phosphorylate FOXO3.
  • Phosphorylates STK3/MST2 at 'Thr-117' and 'Thr-384' leading to inhibition of its: cleavage, kinase activity, autophosphorylation at Thr-180, binding to RASSF1 and nuclear translocation.
  • Phosphorylates SRPK2 and enhances its kinase activity towards SRSF2 and ACIN1 and promotes its nuclear translocation. Phosphorylates RAF1 at 'Ser-259' and negatively regulates its activity.
  • Phosphorylation of BAD stimulates its pro-apoptotic activity. Phosphorylates KAT6A at 'Thr-369' and this phosphorylation inhibits the interaction of KAT6A with PML and negatively regulates its acetylation activity towards p53/TP53.
  • AKT1-specific substrates have been recently identified, including palladin (PALLD), which phosphorylation modulates cytoskeletal organization and cell motility; prohibitin (PHB), playing an important role in cell metabolism and proliferation; and CDKN1A, for which phosphorylation at 'Thr-145' induces its release from CDK2 and cytoplasmic relocalization. These recent findings indicate that the AKT1 isoform has a more specific role in cell motility and proliferation. Phosphorylates CLK2 thereby controlling cell survival to ionizing radiation.

Glycogen synthase kinase-3 beta

Function

Constitutively active protein kinase that acts as a negative regulator in the hormonal control of glucose homeostasis,

  • Want signaling and regulation of transcription factors and microtubules, by phosphorylating and inactivating glycogen synthase (GYS1 or GYS2), EIF2B, CTNNB1/beta-catenin, APC, AXIN1, DPYSL2/CRMP2, JUN, NFATC1/NFATC, MAPT/TAU and MACF1.
  • Requires primed phosphorylation of the majority of its substrates. In skeletal muscle, contributes to insulin regulation of glycogen synthesis by phosphorylating and inhibiting GYS1 activity and hence glycogen synthesis.
  • May also mediate the development of insulin resistance by regulating activation of transcription factors. Regulates protein synthesis by controlling the activity of initiation factor 2B (EIF2BE/EIF2B5) in the same manner as glycogen synthase.
  • In Wnt signaling, GSK3B forms a multimeric complex with APC, AXIN1 and CTNNB1/beta-catenin and phosphorylates the N-terminus of CTNNB1 leading to its degradation mediated by ubiquitin/proteasomes.
  • Phosphorylates JUN at sites proximal to its DNA-binding domain, thereby reducing its affinity for DNA. Phosphorylates NFATC1/NFATC on conserved serine residues promoting NFATC1/NFATC nuclear export, shutting off NFATC1/NFATC gene regulation, and thereby opposing the action of calcineurin.
  • Phosphorylates MAPT/TAU on 'Thr-548', decreasing significantly MAPT/TAU ability to bind and stabilize microtubules. MAPT/TAU is the principal component of neurofibrillary tangles in Alzheimer disease. Plays an important role in ERBB2-dependent stabilization of microtubules at the cell cortex.
  • Phosphorylates MACF1, inhibiting its binding to microtubules which is critical for its role in bulge stem cell migration and skin wound repair.
  • Probably regulates NF-kappa-B (NFKB1) at the transcriptional level and is required for the NF-kappa-B-mediated anti-apoptotic response to TNF-alpha (TNF/TNFA). Negatively regulates replication in pancreatic beta-cells, resulting in apoptosis, loss of beta-cells and diabetes.
  • Through phosphorylation of the anti-apoptotic protein MCL1, may control cell apoptosis in response to growth factors deprivation.
  • Phosphorylates MUC1 in breast cancer cells, decreasing the interaction of MUC1 with CTNNB1/beta-catenin. Is necessary for the establishment of neuronal polarity and axon outgrowth.
  • Phosphorylates MARK2, leading to inhibit its activity. Phosphorylates SIK1 at 'Thr-182', leading to sustain its activity.
  • Phosphorylates ZC3HAV1 which enhances its antiviral activity. Phosphorylates SNAI1, leading to its BTRC-triggered ubiquitination and proteasomal degradation.
  • Phosphorylates SFPQ at 'Thr-687' upon T-cell activation. Phosphorylates NR1D1 st 'Ser-55' and 'Ser-59' and stabilizes it by protecting it from proteasomal degradation.
  • Regulates the circadian clock via phosphorylation of the major clock components including ARNTL/BMAL1, CLOCK and PER2. Phosphorylates CLOCK AT 'Ser-427' and targets it for proteasomal degradation.
  • Phosphorylates ARNTL/BMAL1 at 'Ser-17' and 'Ser-21' and primes it for ubiquitination and proteasomal degradation.
  • Phosphorylates OGT at 'Ser-3' or 'Ser-4' which positively regulates its activity. Phosphorylates MYCN in neuroblastoma cells which may promote its degradation (PubMed:24391509).

Miscellaneous

Higher expression and activity of GSK3B are found in the skeletal muscle (vastus lateralis) of patients with type 2 diabetes (PubMed:10868943). Several potent GSK3 (GSK3A and GSK3B) inhibitors have been identified and characterized in preclinical models for treatments of type 2 diabetes (PubMed:19366350).

Enzyme regulation

  • Activated by phosphorylation at Tyr-216.
  • In response to insulin, inhibited by phosphorylation at Ser-9 by PKB/AKT1 and RPS6KA3; phosphorylation at this site causes a conformational change, preventing access of substrates to the active site. Inhibited by lithium.