フジスタッフホールディングス株式会社
FujiStaff Holdings, Inc.
| 種類 |
株式会社 |
| 市場情報 |
| 東証JQ |
2147 |
2007年4月2日 - 2011年1月13日 |
|
| 略称 |
フジスタッフH、FSHD |
| 本社所在地 |
日本
〒102-8578
東京都千代田区紀尾井町4番1号
ニューオータニガーデンコート 8階 |
| 本店所在地 |
〒100-0005
東京都千代田区丸の内一丁目8番3号
丸の内トラストタワー本館 21階 |
| 設立 |
2007年（平成19年）4月2日 |
| 業種 |
サービス業 |
| 事業内容 |
グループ全体の戦略的意思決定および事業会社の経営指導管理 |
| 代表者 |
マルセル・ウィガース（代表取締役会長）
井上守（代表取締役社長） |
| 資本金 |
20億円 |
| 売上高 |
連結603億円（2010年3月期） |
| 決算期 |
12月31日 |
| 主要株主 |
ランスタッド日本合同会社 |
| 主要子会社 |
株式会社フジスタッフ（完全子会社）
株式会社アイライン（完全子会社）
株式会社マルチメディアスクール・ウェーヴ |
| 関係する人物 |
増山律子（名誉副会長。元・フジスタッフ代表取締役会長） |
| 外部リンク |
http://www.fujistaff-holdings.jp/ |
| テンプレートを表示 |
フジスタッフホールディングス株式会社(英:FujiStaff Holdings, Inc.)は、かつて東京都千代田区に本社を置いていた人材派遣・業務請負の持株会社。2007年4月2日に株式移転によってフジスタッフ(現・ランスタッド)、アイラインを完全子会社とする形で設立された。
目次
- 1 概要
- 2 沿革
- 3 傘下企業の偽装請負
- 4 傘下企業の「協力会費」の天引き
- 5 脚注
- 6 関連項目
- 7 外部リンク
概要
人材派遣・業務請負等を中心とした総合人材サービスを展開する、いずれも東京都と宇都宮市の2本社制を敷くフジスタッフ（ホワイトカラー系、登記上の本店・東京都中央区[1]）とアイライン（ブルーカラー系、登記上の本店・宇都宮市）の経営統合により設立。この際の株式は、フジスタッフ株1株およびアイライン株430株に対し、それぞれHD株を1株割当となった。
当社発足当初、孫会社を含めたグループ企業をフジスタッフホールディングスグループと称していたが、2010年4月よりフジスタッフグループに改めている。HPドメインもこのときから、fshd.co.jpからfujistaff-holdings.jpに変更されている。
2011年1月、TOBにより、ランスタッド・ホールディングの日本における投資事業を手がける子会社(中間持株会社)であるランスタッド日本合同会社（事業会社たる日本法人であるランスタッド株式会社とは別法人）の完全子会社となる（すなわち、中間持株会社化）。同年7月1日付で、ランスタッドブランドの浸透を目的とした経営統合の名目により、ランスタッド日本を吸収合併し、ランスタッドグループジャパン株式会社へ改称。さらに、子会社のフジスタッフにアイラインとランスタッド日本法人を吸収させ、ランスタッド株式会社に改称した[2]。
これにより、当社はランスタッドグループにおけるアジア地域の統括を手がける中間持株会社であるランスタッド・アジア・パシフィック・ビー・ヴィー（本社・オランダ王国）の子会社に、新ランスタッド社は当社の完全子会社となった。
沿革
- 2007年（平成19年）4月2日 - フジスタッフとアイラインによる株式移転方式での経営統合により、フジスタッフホールディングス株式会社として設立。
- 2009年（平成21年）
- 1月 - 就職支援向けパソコンスクールなどを手がけるマルチメディアスクール・ウェーヴと資本提携し、同社を子会社化。
- 11月30日 - 本社を千代田区丸の内のパシフィックセンチュリープレイス丸の内より、同丸の内トラストタワー本館へ移転。
- 2010年（平成22年）4月1日 - グループ呼称を「フジスタッフグループ」に改称。
- 2011年（平成23年）
- 1月 - 蘭・ランスタッド・ホールディングの日本法人・ランスタッド日本合同会社によるTOBに伴い、ランスタッド日本の完全子会社化。大阪証券取引所・ジャスダックの上場廃止がなされた。
- 7月 - ランスタッド日本を吸収合併し、ランスタッドグループジャパン株式会社へ社名を変更。同時に、子会社のフジスタッフがアイライン・ランスタッド日本法人の2社を吸収合併し、ランスタッド株式会社に社名変更[2]。同時に、1億円への減資を実施。
2011年7月1日以降の沿革については「ランスタッドグループジャパン#沿革」を参照
傘下企業の偽装請負
フジスタッフホールディングスの完全子会社である業務請負会社のアイラインは、キヤノン宇都宮工場にて偽装請負を行っている。雇用主はアイラインであるにも関わらず労働者はキヤノンの正社員より教育を受けていた。当初は請負契約であったものが、2005年5月に労働者派遣契約に変更し、2006年5月に請負契約に変更するといった、雇用形態の変更が複数回行われた。2006年秋には本偽装請負に対して労働局が指導を行った。
2007年2月にはキヤノンユニオン宇都宮支部長が衆議院予算委員会の公聴会に招かれ、本偽装請負について意見を述べている[3] [4] [5] [6]。
傘下企業の「協力会費」の天引き
フジスタッフホールディングス完全子会社の業務請負会社アイラインの労働者は「協力会費」名目で不透明な天引きを受けていると主張し、同社への指導を求め労働基準監督署に申告を行なっている。労働者側は「協力会費」は強制的に徴収されていたと主張している。
一方アイライン側は、「協力会費」の支払いは任意と主張し、廃止や返金を否定している。「協力会費」の天引きは請負・派遣労働者から月額300円、日雇い労働者から派遣1回ごとに120円となっており、その総額は2007年時点で年間約8000万円となっている。同様の天引きはグッドウィルやフルキャストの日雇い派遣で明らかになっており、厚生労働省が一斉指導を行なっている[7]。
脚注
- ^ 経営統合当時の東京本社は、千代田区に所在していたが、2009年12月1日に移転。
- ^ a b フジスタッフホールディングスとは コトバンク
- ^ 『偽装請負労働が製造業で横行』朝日新聞 2006年7月31日
- ^ 『偽装請負への思い、国会で訴えへ キヤノン工場の男性』朝日新聞 2007年2月21日
- ^ 『キヤノン請負労働者 生身の人間。正社員と同じ賃金を』朝日新聞 2007年2月22日
- ^ 『抜け殻正社員:派遣・請負依存経営のツケ』日経ビジネス 2007年4月2日号
- ^ 『「偽装請負」でも天引き 労働者が申告「協力会費」名目で』朝日新聞夕刊14面 2007年7月13日
関連項目
外部リンク
"FSHD" redirects here. For other uses, see FSHD (disambiguation).
| Facioscapulohumeral muscular dystrophy |
| Classification and external resources |
| ICD-10 |
G71.0 |
| ICD-9 |
359.1 |
| OMIM |
158900 158901 |
| DiseasesDB |
7247 |
| MedlinePlus |
000707 |
| eMedicine |
neuro/133 |
| MeSH |
D020391 |
| GeneReviews |
- Facioscapulohumeral muscular dystrophy
|
Facioscapulohumeral muscular dystrophy (sometimes switched as faciohumeroscapular) (FSHMD, FSHD or FSH), which is also known as Landouzy-Dejerine,[1] is a usually autosomal dominant inherited form of muscular dystrophy (MD)[2] that initially affects the skeletal muscles of the face (facio), scapula (scapulo) and upper arms (humeral). While it is widely stated to be the third most common genetic disease of skeletal muscle, a 2008 analysis of rare diseases listed FSHD as the most prevalent form of MD at 7/100,000.[3]
Symptoms may develop in early childhood and are usually noticeable in the teenage years with 95% of affected individuals manifesting disease by age 20 years. A progressive skeletal muscle weakness usually develops in other areas of the body as well; often the weakness is asymmetrical. Life expectancy is normal, but up to 20% of affected individuals become severely disabled and eventually must use a wheel chair. In a Dutch study approximately 1% of patients required (nocturnal of diurnal) ventilatory support.[4] Non-muscular symptoms frequently associated with FSHD include subclinical sensorineural hearing loss and retinal telangiectasia.
In more than 95% of known cases, the disease is associated with deletions of the D4Z4 repeat in the 4q35 subtelomeric region of Chromosome 4. Seminal research published in August 2010 now shows that a second mechanism is needed for FSHD, which for the first time provides a unifying theory for the underlying genetics of FSHD. The second mechanism was found to be a "toxic gain of function" of the DUX4 gene which is the first time in the history of genetic research that a "dead gene" has been found to "wake up" and cause disease.[5][6]
Contents
- 1 History
- 2 Pathophysiology
- 3 Genetics
- 3.1 FSHMD1A (4q35 deletion)
- 3.2 FSHMD1B (unknown locus)
- 3.3 A Unifying Theory
- 4 Testing
- 5 Symptoms and prevalence
- 6 Treatment and research
- 6.1 Compounds of interest
- 6.2 Procedures used to improve quality of life
- 6.3 FSHD Foundation
- 6.4 FSHD-EUROPE
- 7 References
- 8 External links
History
Number of FSHD Papers[7]
| 1900–1950 |
0 |
| 1951–1975 |
30 |
| 1976–1990 |
133 |
| 1991–1996 |
148 |
| 1997–2006 |
294 |
| data from the Entrez-Pubmed database[7] |
FSHD was first described in 1884 by French physicians Louis Landouzy and Joseph Dejerine. In their paper of 1886, Landouzy and Dejerine drew attention to the familial nature of the disorder and mentioned that four generations were affected in the kindred that they had investigated.[8] Formal definition of FSHD's clinical features didn't occur until 1952 when a large Utah family with FSHD was studied. Beginning about 1980 an increasing interest in FSHD led to increased understanding of the great variability in the disease and a growing understanding of the genetic and pathophysiological complexities. By the late 1990s, researchers were finally beginning to understand the regions of Chromosome 4 associated with FSHD.[9]
FSHD is also known by the following names:
- Landouzy-Dejerine[1]
- Landouzy-Dejerine syndrome[8]
- Erb-Landouzy-Dejerine syndrome[8]
- Landouzy-Dejerine dystrophy or atrophy[8]
Pathophysiology
The exact pathophysiology of FSHD remains unknown as of March 2007. Muscle histologic changes are nonspecific for the muscle wasting. There is evidence of early inflammatory changes in the muscle, but reported responses to high dose open labeled corticosteroid treatment have been negative. Animal studies of anabolic effects of beta adrenergic agonists on models of muscle wasting led to an open trial of salbutamol (a beta adrenergic agonist) in which limited preliminary results support an improvement of muscle mass and strength in FSHD. Preliminary studies of muscle cultures suggest an increased sensitivity to oxidative stress, but require further exploration.
Genetics
FSHMD1A (4q35 deletion)
More than 95% of cases of FSHD are associated with the deletion of integral copies of a tandemly repeated 3.2kb unit (D4Z4 repeat) at the subtelomeric region 4q35 on Chromosome 4 of the human genome of which a normal chromosome will include between 11-150 repetitions of D4Z4.[9] There are both heterochromatin and euchromatin structures within D4Z4 and one putative gene called DUX4.[9][10] Inheritance is autosomal dominant, though up to one-third of the cases appear to be the result of de novo (new) mutations. The heterochromatin is specifically lost in the deletions of FSHD while the euchromatin structures remain.[9] If the entire region is removed, there are birth defects, but no specific defects on skeletal muscle. Individuals appear to require the existence of 11 or fewer repeat units to be at risk for FSHD.
In addition, a few cases of FSHD are the result of rearrangements between subtelomeric chromosome 4q and a subtelomeric region of 10q. This location contains a tandem repeat structure highly homologous to 4q35.[11] Disease occurs when the translocation results in a critical loss of tandem repeats to the 4q site.
FSHMD1B (unknown locus)
Finally, there is a large family with a phenotype indistinguishable from FSHD in which no pathological changes at the 4q site or translocation of 4q-10q are found.[12][13]
It has been suggested that this may be due to limitations in the available tests.[14]
A Unifying Theory
On 19 August 2010, a paper entitled A Unifying Genetic Model for Facioscapulohumeral Muscular Dystrophy was published in Science showing that the candidate gene DUX4 undergoes a "toxic gain of function" as a result of single nucleotide polymorphisms in the region distal to the last D4Z4 repeat. According to the research, this leads to a "canonical polyadenylation signal for transcripts derived from DUX4".[6] This is the first time in the history of genetics in which "junk" DNA has been shown to reanimate and cause disease. The documentation of the conditions under which the DUX4 gene became reanimated answered the question of why no one whose dead gene was repeated more than 10 times ever got FSHD but only some people with fewer than 10 copies did get the disease[5] Several organizations including the New York Times highlighted this research (See MDA, FSH Society, University of Rochester, NYT).
Dr. Francis Collins, who oversaw the first sequencing of the Human Genome with the National Institutes of Health stated:[5]
“If we were thinking of a collection of the genome’s greatest hits, this would go on the list,”
Daniel Perez, co-founder, President and CEO of the FSH Society hailed the new findings saying:
"This is a long-sought explanation of the exact biological workings of a disease that affects an estimated one in 14,000 or 22,100 Americans and 490,000 worldwide,” he said, adding that this discovery “creates an enormous opportunity for research to develop ways to prevent or treat FSHD.”
The MDA stated that:
"The new findings will make it easier to diagnose FSHD in someone with symptoms and predict who will develop the disease in someone without symptoms. Now, the hunt is on for which proteins or genetic instructions (RNA) are causing the problem for muscle tissue in FSHD."
Quoted in the University of Rochester press release, one of the report's co-authors, Silvère van der Maarel of the University of Leiden, stated that
“It is amazing to realize that a long and frustrating journey of almost two decades now culminates in the identification of a single small DNA variant that differs between patients and people without the disease. We finally have a target that we can go after.”
The original identification of the D4Z4 deletions was found in 1992. This research now shows that a second mechanism is needed for FSHD to be present and that the remaining versions of the DUX4 become more active (open for transcription) because the DNA at the tip of chromosome 4 is less tightly coiled as a result of the deletions.
Testing
Since the early 2000s genetic testing that measures the size of the D4Z4 deletions on 4q35 has become the preferred mechanism for confirming the presence of FSHD. As of 2007, this test is considered highly accurate but is still performed by a limited set of labs in the US, such as Athena diagnostics under test code 405. However, because the test is expensive, patients and doctors may still rely on one or more of the following tests, all of which are far less accurate and specific than the genetic test:[15]
- Creatine kinase (CK) level: This test measures the Creatine kinase enzyme in the blood. Elevated levels of CK are related to muscle atrophy.
- electromyogram (EMG): This test measures the electrical activity in the muscle
- nerve conduction velocity (NCV): This test measures the how fast signals travel from one part of a nerve to another. The nerve signals are measured with surface electrodes (similar to those used for an electrocardiogram), and the test is only slightly uncomfortable.
- muscle biopsy: Through outpatient surgery a small piece of muscle is removed (usually from the arm or leg) and evaluated with a variety of biochemical tests. Researchers are attempting to match results of muscle biopsies with DNA tests to better understand how variations in the genome present themselves in tissue anomalies.
Symptoms and prevalence
Because of the extreme variability of the disease, an authoritative and scientifically confirmed set of symptoms does not yet exist. The prevalence is widely quoted to be 1/20,000, but the exact prevalence is not known. A November 2008 report from Orpha.net, an organization backed by the Institut National de la Santé et de la Recherche Médicale (INSERM), lists a prevalence of 7/100,000 which would make FSHD the most prevalent form of Muscular Dystrophy (Duchenne and Becker are listed at 5/100,000).[3]
Symptoms:
- Facial muscle weakness (eyelid drooping, inability to whistle, decreased facial expression, depressed or angry facial expression, difficulty pronouncing the letters M, B, and P)
- Shoulder weakness (difficulty working with the arms raised, sloping shoulder)
- Hearing loss
- Abnormal heart rhythm
- Unequal weakening of the biceps, triceps, deltoids, and lower arm muscles
- Loss of strength in abdominal muscles (causing a protuberant abdomen and lumbar lordosis) and eventual progression to the legs
- Foot drop
Treatment and research
- No Food and Drug Administration approved therapies exist specifically for FSHD.
- Physiotherapy could improve patients' functional status by providing therapeutic exercise and ADL training.
- Occupational therapy can sometimes be used to help cope with new devices to make things easier.
Compounds of interest
ACVR2B is a compound identified in 2005/2006 by Johns Hopkins[1]. It increased muscle mass in a non-Muscular Dystrophy Mouse by up to 60% in two weeks.
MY0-029
Main article: Stamulumab
MYO-029 is an experimental myostatin inhibiting drug developed by Wyeth Pharmaceuticals for the treatment of muscular dystrophy. Myostatin is a protein that inhibits the growth of muscle tissue, MYO-029 is a recombinant human antibody designed to bind and inhibit the activity of myostatin.[16] A 2005/2006 study was completed by Wyeth in Collegeville, PA and included participants afflicted with FSHD. The study could not prove its efficacy.
Procedures used to improve quality of life
- Scapular fusion: surgical fusion of the scapula to the thorax.
- Scapular bracing: a scapular brace helps stabilize the shoulder and correct glenohumeral positioning.
FSHD Foundation
In 2007 the FSHD Global Research Foundation was established to increase the amount of funding available to research bodies. The Foundation has identified 13 priority areas of interest for FSHD research.[17]
FSHD-EUROPE
In 2009 the FSHD-EUROPE was founded by European associations.[18]
References
- ^ a b disease overview, MDA, date accessed 6 March 2007
- ^ Lemmers RJ, Wohlgemuth M, van der Gaag KJ, et al. (November 2007). "Specific sequence variations within the 4q35 region are associated with facioscapulohumeral muscular dystrophy". Am. J. Hum. Genet. 81 (5): 884–94. doi:10.1086/521986. PMC 2265642. PMID 17924332.
- ^ a b Prevalence of rare diseases: Bibliographic data, www.orpha.net, November 2008 Number 1, Orphanet Report Series
- ^ Wohlgemuth M, van der Kooi EL, van Kesteren RG, van der Maarel SM, Padberg GW Ventilatory support in facioscapulohumeral muscular dystrophy Neurology. 2004 Jul 13;63(1):176-8 PMID 15249635
- ^ a b c Kolata, Gina (19 August 2010). "Reanimated 'Junk' DNA Is Found to Cause Disease". New York Times. Retrieved 29 August 2010.
- ^ a b Lemmers, Richard; Patrick J. van der Vliet, Rinse Klooster, Sabrina Sacconi, Pilar Camaño, Johannes G. Dauwerse, Lauren Snider, Kirsten R. Straasheijm, Gert Jan van Ommen, George W. Padberg, Daniel G. Miller, Stephen J. Tapscott, Rabi Tawil, Rune R. Frants, and Silvère M. van der Maarel (19 August 2010). "A Unifying Genetic Model for Facioscapulohumeral Muscular Dystrophy". Science 329 (5999): 1650–3. doi:10.1126/science.1189044. PMID 20724583.
- ^ a b "FSHSociety Update: 2006 Year in Review - Your Dollars at Work", FSH Society, Fall 2006
- ^ a b c d Landouzy-Dejerine syndrome, whonamedit.com, date accessed March 11, 2007
- ^ a b c d Impossible Things: Through the looking glass with FSH Dystrophy Researchers, Margaret Wahl, MDA, Quest magazine, Vol 14, No 2, March–April 2007
- ^ Dixit M, Ansseau E, Tassin A, et al. (November 2007). "DUX4, a candidate gene of facioscapulohumeral muscular dystrophy, encodes a transcriptional activator of PITX1". Proc. Natl. Acad. Sci. U.S.A. 104 (46): 18157–62. doi:10.1073/pnas.0708659104. PMC 2084313. PMID 17984056.
- ^ Rossi M, Ricci E, Colantoni L, et al. (2007). "The Facioscapulohumeral muscular dystrophy region on 4qter and the homologous locus on 10qter evolved independently under different evolutionary pressure". BMC Med. Genet. 8: 8. doi:10.1186/1471-2350-8-8. PMC 1821008. PMID 17335567.
- ^ Gilbert JR, Stajich JM, Wall S, et al. (August 1993). "Evidence for heterogeneity in facioscapulohumeral muscular dystrophy (FSHD)". Am. J. Hum. Genet. 53 (2): 401–8. PMC 1682358. PMID 8328457.
- ^ Speer MC, Pericak-Vance MA, Stajich JM, et al. (September 1997). "Further exclusion of FSHD1B from the telomeric region of 10q". Neurogenetics 1 (2): 151–2. doi:10.1007/s100480050023. PMID 10732819.
- ^ Deak KL, Lemmers RJ, Stajich JM, et al. (February 2007). "Genotype-phenotype study in an FSHD family with a proximal deletion encompassing p13E-11 and D4Z4". Neurology 68 (8): 578–82. doi:10.1212/01.wnl.0000254991.21818.f3. PMID 17229919.
- ^ FSHD Fact Sheet, MDA, 11/1/2001
- ^ Wyeth Initiates Clinical Trial with Investigational Muscular Dystrophy Therapy MYO-029
- ^ http://www.fshdglobal.org/
- ^ http://www.fshd-europe.org/
External links
- list of clinical trials for FSHD, Clinicaltrials.gov.
- FSHD Global Research Foundation
- Photo and additional links at Washington University
- Richard Fields Center for FSHD and Neuromuscular Research
- National Registry of Myotonic Dystrophy and Facioscapulohumeral Muscular Dystrophy Patients and Family Members, University of Rochester Medical Center
- The FSH Society was organized in 1991 and addresses issues and needs related to FacioScapuloHumeral muscular Dystrophy (FSHD).
- Pacific Northwest Friends of FSH Research
- European FSH patients Group & FSH-EUROPE
- The MDA addresses the gamut of issues related to Muscular Dystrophy.
- Muscular Dystrophy Association's website in Greece
- 1980104746 at GPnotebook
- Fascioscapulohumeral_muscular_dystrophy at the Duke University Health System's Orthopedics program
- fsh at NIH/UW GeneTests
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Muscular dystrophy
|
|
| The Nine Primary Muscular Dystrophies |
- Congenital
- dystrophin
- Distal
- Emery-Dreifuss
- Facioscapulohumeral
- Limb-girdle muscular dystrophy
- Myotonic
- Oculopharyngeal
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| National/International Organizations |
- Muscular Dystrophy Association (USA)
- Muscular Dystrophy Canada
- Myotonic Dystrophy Foundation
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| National/International Events |
- MDA Muscle Walk (USA)
- MDA Show of Strength (USA)
- Décrypthon (France)
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| Recent or Ongoing Clinical Trials |
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anat (h/n, u, t/d, a/p, l)/phys/devp/hist
|
noco (m, s, c)/cong (d)/tumr, sysi/epon, injr
|
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|
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Diseases of myoneural junction and muscle / neuromuscular disease (G70–G73, 358–359)
|
|
Neuromuscular-
junction disease |
- autoimmune
- Myasthenia gravis
- Lambert–Eaton myasthenic syndrome
|
|
Myopathy/
congenital myopathy |
Muscular dystrophy
(DAPC) |
| AD |
- Limb-girdle muscular dystrophy 1
- Oculopharyngeal
- Facioscapulohumeral
- Myotonic
- Distal (most)
|
|
| AR |
- Limb-girdle muscular dystrophy 2
- Congenital
- Fukuyama
- Ullrich
- Walker–Warburg
|
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| XR |
- dystrophin
- Emery–Dreifuss
|
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| Other structural |
- collagen disease
- PTP disease
- adaptor protein disease
- BIN1-linked centronuclear myopathy
- cytoskeleton disease
- Nemaline myopathy
- Zaspopathy
|
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| Channelopathy |
| Myotonia |
- Myotonia congenita
- Thomsen disease
- Neuromyotonia/Isaacs syndrome
- Paramyotonia congenita
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| Periodic paralysis |
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| Other |
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| Mitochondrial myopathy |
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| Other |
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anat (h/n, u, t/d, a/p, l)/phys/devp/hist
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noco (m, s, c)/cong (d)/tumr, sysi/epon, injr
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