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While there have been numerous reports about colovesical fistulas and ruptured intestinal diverticula, there have been far fewer reports about vesicointestinal fistulas caused by Meckel’s diverticula. Most Meckel’s diverticula are asymptomatic. Furthermore, they seldom cause vesicointestinal fistulas, and the associated complications are non-specific. Thus, their preoperative diagnosis is difficult. We experienced a case in which a vesicointestinal fistula was caused by a Meckel’s diverticulum and was treated with laparoscopic surgery. A 46-year-old male was referred to our hospital after exhibiting hematuria. Cystoscopy revealed a fistula between the small intestine and bladder. Contrast-enhanced computed tomography and magnetic resonance imaging showed a diverticulum in the ileum and a fistula between the ileum and bladder, which passed through the diverticulum. A Meckel’s diverticulum was suspected. We conducted a laparoscopic operation. We dissected the Meckel’s diverticulum with an automatic suturing device and removed it together with part of the ileum. The patient’s postoperative course was good. We experienced a case in which a vesicointestinal fistula was caused by a Meckel’s diverticulum and was successfully treated with laparoscopic surgery. In selected cases of Meckel’s diverticulum, the dissection of the diverticulum with an automatic suturing device is appropriate.

Aim Sphingosine 1-phosphate (S1P) is a bioactive sphingolipid metabolite released from erythrocytes and platelets, and is a potent stimulus for endothelial cell proliferation. However, the role of S1P on human liver sinusoidal endothelial cells (LSEC) remains unclear. The proliferation and inhibition of apoptosis in LSEC are involved in the promotion of liver regeneration and the suppression of liver injury after liver resection and transplantation. The aim of this study is to investigate the role of S1P on human LSEC and the interaction between S1P and LSEC in hepatocyte proliferation in vitro. Methods Immortalized human LSEC were used. LSEC were cultured with S1P, and the cell proliferation, anti-apoptosis, signal transductions and production of cytokines and growth factors were subsequently examined. To investigate the interaction between S1P and LSEC in hepatocyte proliferation, primary human hepatocytes were cultured with the supernatants of LSEC with and without S1P. DNA synthesis and signal transductions in hepatocytes were examined. Results S1P induced LSEC proliferation through activation of Akt and extracellular signal-related kinase pathways and suppressed LSEC apoptosis by affecting the expression levels of Bcl-2, Bax and cleaved caspase-3. S1P promoted interleukin-6 (IL-6) and vascular endothelial growth factor (VEGF) production in LSEC. The supernatants of LSEC cultured with S1P enhanced hepatocyte DNA synthesis more strongly than the supernatants of LSEC cultured without S1P through activation of the signal transducer and activator of transcription-3 pathway. Conclusion S1P has proliferative and anti-apoptotic effects and promotes the production of IL-6 and VEGF in human LSEC, thereby promoting hepatocyte proliferation.

Platelets contain three types of granules: alpha granules, dense granules, and lysosomal granules. Each granule contains various growth factors, cytokines, and other physiological substances. Platelets trigger many kinds of biological responses, such as hemostasis, wound healing, and tissue regeneration. This review presents experimental evidence of platelets in accelerating liver regeneration and improving liver fibrosis. The regenerative effect of liver by platelets consists of three mechanisms; i.e., the direct effect on hepatocytes, the cooperative effect with liver sinusoidal endothelial cells, and the collaborative effect with Kupffer cells. Many signal transduction pathways are involved in hepatocyte proliferation. One is activation of Akt and extracellular signal-regulated kinase (ERK)1/2, which are derived from direct stimulation from growth factors in platelets. The other is signal transducer and activator of transcription-3 (STAT3) activation by interleukin (IL)-6 derived from liver sinusoidal endothelial cells and Kupffer cells, which are stimulated by contact with platelets during liver regeneration. Platelets also improve liver fibrosis in rodent models by inactivating hepatic stellate cells to decrease collagen production. The level of intracellular cyclic adenosine monophosphate (cyclic AMP) is increased by adenosine through its receptors on hepatic stellate cells, resulting in inactivation of these cells. Adenosine is produced by the degradation of adenine nucleotides such as adenosine diphosphate (ADP) and adenosine tri-phosphate (ATP), which are stored in abundance within the dense granules of platelets.

(-)-Epigallocatechin-3-gallate (EGCG), the major constituent of green tea, has been shown to inhibit cell proliferation and induce apoptosis in several types of human tumors. The most common site of distant metastases in colorectal cancer is the liver. However, no previous studies have reported the ability of EGCG to suppress liver metastases of human colorectal cancer. The aim of the present study was to elucidate the potential use of EGCG as chemotherapy targeting liver metastases of human colorectal cancer. To assess the effect of EGCG on human colorectal cancer cell lines, RKO and HCT116, cell viability, cell proliferation and apoptosis were measured by cell counting kit-8, BrdU assay and TUNEL staining, respectively. Protein and gene expression were measured by western blot analysis and RT-PCR analysis, respectively. EGCG inhibited cell proliferation and induced apoptosis. EGCG dephosphorylated constitutively activated Akt and increased the activation of p38. EGCG also decreased the expression of vascular endothelial growth factor receptor 2. Additionally, the ability of EGCG to prevent the development of liver metastases of RKO tumors was evaluated in SCID mice. EGCG suppressed angiogenesis and induced apoptosis in liver metastases without associated body weight loss or hepatotoxicity. Furthermore, the liver metastatic area was significantly reduced by EGCG administration. Our findings indicate that EGCG may be useful in the treatment of liver metastases of human colorectal cancer.

Chronic liver disease (CLD), such as hepatitis C, is a progressive disease consisting of the destruction and regeneration of the liver parenchyma, leading to fibrosis and cirrhosis. Platelets contain various growth factors and may play important roles in liver regeneration. Thus, to investigate whether platelet transfusion improves liver function in patients with CLD and cirrhosis, we conducted an exploratory clinical trial. The study included 10 patients with CLD and cirrhosis (Child-Pugh class A or B), who all presented thrombocytopenia (platelet counts between 50,000 and 100,000 /µl). The subjects received 10 units of platelet concentrate once a week for 12 weeks. They were followed up for 9 months after the last transfusion. One patient discontinued platelet transfusion because of pruritus, and 2 patients discontinued because of platelet transfusion refractoriness. One patient was excluded from the analysis for receiving a procedural treatment after 12 platelet transfusions. Thus, the remaining 6 patients were analyzed. The platelet count did not increase significantly after the last transfusion. Significant improvement of serum albumin was observed at 1 month and 3 months after the last transfusion. Serum cholinesterase improved significantly at 1 week, 3 months, and 9 months after the last transfusion. Serum hyaluronic acid showed a tendency toward improvement after the last transfusion. In conclusion, platelet transfusion improved some of the indicators of liver function in patients with CLD and cirrhosis, though adverse events related to platelet transfusion were observed in some patients. Platelet increment therapy could be a new strategy for treating CLD and cirrhosis.

Aim Liver cirrhosis (LC) is the end stage of chronic liver disease. No definitive pharmacological treatment is currently available. We previously reported that thrombopoietin (TPO) promoted liver regeneration and improved liver cirrhosis by increasing platelet count. TPO is therefore considered to be a therapeutic agent for LC; however, it is unclear whether TPO has proliferative effects on hepatocellular carcinoma (HCC), which arises frequently in cirrhotic livers. In this study, we examined the effects of TPO on growth of HCC. Methods Expression of the TPO receptor, myeloproliferative leukemia virus oncogene (MPL) was examined in various liver tumor cell lines and liver cell types. In an in vitro study, the effects of TPO on signal transduction, cell proliferation, migration and invasion were examined in Huh7 cells, in which MPL is highly expressed. In an in vivo study, we subcutaneously transplanted Huh7 cells into nude mice that were divided into a TPO-treated group and a control group, and the tumor volume of each group was measured. Results MPL was expressed strongly in hepatocytes but not in other cell types. Among liver tumor cell lines, Huh7 showed the highest expression of MPL. In Huh7, the addition of TPO activated Akt phosphorylation but not cell proliferation, migration or invasion. In the mouse experiment, there was no significant difference in tumor volume between the two groups. Conclusion TPO had no proliferative effect on HCC in vitro or in vivo, and could therefore be useful in the treatment of liver cirrhosis.

Aim: Activated hepatic stellate cells (HSC) play a critical role in liver fibrosis. Suppressing abnormal function of HSC or reversion from activated to quiescent form is a hopeful treatment for liver cirrhosis. The interaction between platelets and HSC remains unknown although platelets go through hepatic sinusoids surrounded by HSC. This study aimed at clarifying the hypothesis that platelets control activation of HSC. Methods: We used human platelets, platelet extracts, and primary or immortalized human HSC. We examined the effect of platelets on the activation, DNA synthesis, type I collagen production, and fibrosis-relating gene expressions of HSC. We investigated what suppressed activation of HSC within platelets and examined the mechanism of controlling activation in vitro. Results: Platelets and platelet extracts suppressed activation of HSC. Platelets decreased type I collagen production without affecting DNA synthesis. Platelets increased the expression of matrix metallopeptidase 1. As platelet extracts co-cultured with an enzyme of degrading adenosine 5′-triphosphate (ATP) suppressed activation, we detected adenine nucleotides within platelets or on their surfaces and confirmed the degradation of adenine nucleotides by HSC and the production of adenosine. Adenosine and platelets increased the intracellular cyclic adenosine 5′-monophosphate (cAMP), which is important in quiescent HSC. A great amount of adenosine and ATP also suppressed activation of HSC. Conclusion: Activation of human HSC is suppressed by human platelets or platelet-derived ATP via adenosine-cAMP signaling pathway in vitro. Therefore, platelets have the possibility to be used in the treatment of liver cirrhosis.

Sphingosine 1-phosphate (S1P) is a bioactive sphingolipid metabolite released from erythrocytes and platelets, and is a potent stimulus for endothelial cell proliferation. However, the role of S1P on human liver sinusoidal endothelial cells (LSEC) remains unclear. The proliferation and inhibition of apoptosis in LSEC are involved in the promotion of liver regeneration and the suppression of liver injury after liver resection and transplantation. The aim of this study is to investigate the role of S1P on human LSEC and the interaction between S1P and LSEC in hepatocyte proliferation in vitro.Immortalized human LSEC were used. LSEC were cultured with S1P, and the cell proliferation, anti-apoptosis, signal transductions and production of cytokines and growth factors were subsequently examined. To investigate the interaction between S1P and LSEC in hepatocyte proliferation, primary human hepatocytes were cultured with the supernatants of LSEC with and without S1P. DNA synthesis and signal transductions in hepatocytes were examined.S1P induced LSEC proliferation through activation of Akt and extracellular signal-related kinase pathways and suppressed LSEC apoptosis by affecting the expression levels of Bcl-2, Bax and cleaved caspase-3. S1P promoted interleukin-6 (IL-6) and vascular endothelial growth factor (VEGF) production in LSEC. The supernatants of LSEC cultured with S1P enhanced hepatocyte DNA synthesis more strongly than the supernatants of LSEC cultured without S1P through activation of the signal transducer and activator of transcription-3 pathway.S1P has proliferative and anti-apoptotic effects and promotes the production of IL-6 and VEGF in human LSEC, thereby promoting hepatocyte proliferation.

Liver cirrhosis (LC) is the end stage of chronic liver disease. No definitive pharmacological treatment is currently available. We previously reported that thrombopoietin (TPO) promoted liver regeneration and improved liver cirrhosis by increasing platelet count. TPO is therefore considered to be a therapeutic agent for LC; however, it is unclear whether TPO has proliferative effects on hepatocellular carcinoma (HCC), which arises frequently in cirrhotic livers. In this study, we examined the effects of TPO on growth of HCC.Expression of the TPO receptor, myeloproliferative leukemia virus oncogene (MPL) was examined in various liver tumor cell lines and liver cell types. In an in vitro study, the effects of TPO on signal transduction, cell proliferation, migration and invasion were examined in Huh7 cells, in which MPL is highly expressed. In an in vivo study, we subcutaneously transplanted Huh7 cells into nude mice that were divided into a TPO-treated group and a control group, and the tumor volume of each group was measured.MPL was expressed strongly in hepatocytes but not in other cell types. Among liver tumor cell lines, Huh7 showed the highest expression of MPL. In Huh7, the addition of TPO activated Akt phosphorylation but not cell proliferation, migration or invasion. In the mouse experiment, there was no significant difference in tumor volume between the two groups.TPO had no proliferative effect on HCC in vitro or in vivo, and could therefore be useful in the treatment of liver cirrhosis.

Activated hepatic stellate cells (HSC) play a critical role in liver fibrosis. Suppressing abnormal function of HSC or reversion from activated to quiescent form is a hopeful treatment for liver cirrhosis. The interaction between platelets and HSC remains unknown although platelets go through hepatic sinusoids surrounded by HSC. This study aimed at clarifying the hypothesis that platelets control activation of HSC. We used human platelets, platelet extracts, and primary or immortalized human HSC. We examined the effect of platelets on the activation, DNA synthesis, type I collagen production, and fibrosis-relating gene expressions of HSC. We investigated what suppressed activation of HSC within platelets and examined the mechanism of controlling activation in vitro. Platelets and platelet extracts suppressed activation of HSC. Platelets decreased type I collagen production without affecting DNA synthesis. Platelets increased the expression of matrix metallopeptidase 1. As platelet extracts co-cultured with an enzyme of degrading adenosine 5'-triphosphate (ATP) suppressed activation, we detected adenine nucleotides within platelets or on their surfaces and confirmed the degradation of adenine nucleotides by HSC and the production of adenosine. Adenosine and platelets increased the intracellular cyclic adenosine 5'-monophosphate (cAMP), which is important in quiescent HSC. A great amount of adenosine and ATP also suppressed activation of HSC. Activation of human HSC is suppressed by human platelets or platelet-derived ATP via adenosine-cAMP signaling pathway in vitro. Therefore, platelets have the possibility to be used in the treatment of liver cirrhosis.

合成繊維,特にポリアクリロニトリル系繊維に対する良好なケイ光増白染料をうるための一つの試みとして,イソニコチン酸-,α,α'-ジピコリン酸-またはα,β'-ジピコリン酸-クロリドとo-アミノフェノール誘導体を縮合したのち脱水閉環することにより,ピリジン環を有するオキサゾール化合物,すなわちγ-ベンズオキサゾリル-(2)-(I),α,α'-ビス(ベンズオキサゾリル-(2))-(III),α,β'-ビス(ベンズオキサゾリル-(2))-ピリジン(V),およびそれぞれ相当する5-メチル誘導体(II),(IV),(VI)を合成した。さらにIおよびIIをベンゼン中,ジメチル硫酸で処理してピリジニウム塩型の(VII)および(VIII)を得た。これらの化合物を用いてポリアクリロニトリル系繊維(カシミロン-F,ボンネル-W,エクスラン-L),アセテート,ビニロンおよびアミラン(ナイロン6)を増白した。III,IVを除いてすべて可視部にケイ光を有するがII,II,VIIおよびVIIIで処理したアクリル系繊維が最も良好に増白された。この場合IおよびIIはカチオン型のVIIおよびVIIIと同様に,アクリル系繊維に対して繊維中の酸性基と,イオン交換的に染着するが,他の繊維に対する染着挙動は分散染料の場合と同様である。このような染着挙動の相異は,吸着等温線の決定,増白布のケイ光スペクトルの測定および溶液に酢酸,硫酸およびベンゼンスルホン酸を添加した際の吸収およびケイ光スペクトルの変化からも認められた。増白布の日光堅ろう度は,総体的に十分ではないが,アクリル系繊維上におけるI,II,VII,VIIIが比較的良好であった。

ピリジン環に活性メチル基を有する2-メチル-5-(5-メチルベンズオキサゾリル-(2))-ピリジン(MBP)と種々の置換基を持ったべンズアルデヒドおよびヘテロ環アルデヒドを無水酢酸中で縮合せしめ1 1 種の4 - ( 5 - メチルベンズオキサゾリル-(2))-スチルベン(A)のアザ同構体を合成した。また上記MBPを二酸化セレンで酸化し5-(5-メチルベンズオキサリゾリル-(2))-2-ピリジンアルデヒドとし, これを活性メチル基を有する2-メチル-5-エチルピリジンと縮合し同型の誘導体(12)を得た。これら誘導体のジオキサン溶液における吸収およびケイ光スペクトルの極大波長はAに比べて,一般に長波長側に移り, そのケイ光相対強度は吸光度が同程度であるにもかかわらず小さい。とくにサリチルアルデヒド, フルフラール,チオフェンアルデヒドからの誘導体のようにオキサゾール環の2-位に結合したピリジン環に対して電子供給性基を有する誘導体は深色移動ならびに強度の減少がいちじるしい。これらの化合物で各種合成繊維を染色した結果, カシミロンF上では黄色に着色しその増白効果は劣るが,一般にピリジン環に対して電子吸引的に働く置換基を有するものが良好であった。増白布をカーボンアーク灯退色試験機中で照射して布のケイ光強度の減少を測定することにより耐光堅ロウ性を試験した。増白結果とあわせてアミランに対しベンズアルデヒドおよび4-カルボキシベンズアルデヒドとの誘導体が, またテトロンに対してベンズアルデヒドおよび4-シアノベンズアルデヒドとの誘導体ならびに12がすぐれた結果を示す。

塩基性基を有するナフタル酸イミド型ケイ光増白染料として,4-位にジエチルアミノおよびN-ピペリジル-アセチルアミノ基を有する誘導体,および4-アセチルアミノナフタル酸イミドのイミド成分に塩基性置換基を有するアミノ化合物を用いた誘導体を合成した。これらの化合物は溶液中で可視部に吸収を示さず460mμ 付近にケイ光の極大を示す。これら誘導体はカシミロンFに対して主としてイオン交換的に染着する。また4-位のアセチルアミノ基をジェチルアミノアセチルアミノ基に代えることによって加水分解に対する安定性の増すことを確かめた。種々の合成繊維(ビェロンアセテート, アミランおよびカシミロンF)に対する増白効果および耐光堅ロウ性を試験した。4-ジエチルアミノアセチルアミノナフタル酸-n-ブチルイミドおよびシクロヘキシルイミドをジメチル硫酸によって四級化した誘導体はカシミロンFに対してすぐれた増白効果を示し,その耐光性は良好であった。

α,β-ビス(5-メチルベンズオキサゾリル-(2)-)エチレン(A)において二つのオキサゾール環を連結するエチレン基をピリジン環を含む共役鎖で代えた5 種の誘導体を合成し, A およびベンゼン環を含む共役鎖によって連結された類似誘導体と溶液中における吸収およびケイ光スペクトルを比較するとともに, テトロンおよびポリプロピレンに対する増白効果ならびに耐光堅ロウ性を試験した。ジメチルホルムアミド中での吸収スペクトルは連結基がピリジン, ビニルピリジン, ジピリジルエチレン,ピリジルーフェニルエチレン,ジビニルーピリジルフェニレンの順に共役が長くなるに従って極大は長波長側に移り吸光度は大となる。ケイ光スペクトルの極大および相対強度も同様な関係がある。これらにそれぞれ対応するベンゼン誘導体は上記アザ同構体に比べ吸収およびケイ光の極大ともやや短波長側にあり,ケイ光強度はやや大きい値を示す。テトロン上では既知のようにAが最も増白効果はすぐれており,一般に比較的共役系の短いものが良好な結果を与える。ポリプロピレン上ではスチレンで連結された誘導体とビニルピリジン誘導体がすぐれた増白効果を示す。前者の耐光性は良好であったが後者はやや劣る。

ポリアクリロニトリル系繊維に良好な親和性を有するカチオン型ケイ光増白染料をうる試みの一つとして,ポリエステル系繊維用のケイ光増白染料Unitex ER類の主成分であるα,β-ビス(5-メチルベンズオキサゾリル-(2))-エチレン(A)を過剰のクロルスルホン酸とともに120～130℃に加熱することによってクロルスルホン化し,これをエチレンイミンと低温で縮合し,ついで各種第二アミンと反応させてN-置換アミノエチルスルファモイル誘導体を合成した。これらは固体状あるいはジメチルホルムアミド中でケイ光を示さないが,酢酸酸性で水に可溶となりケイ光を示す。さらにこれらの誘導体を硫酸ジメチルで4級化した誘導体は水に易溶で,ケイ光を有する。これらの化合物のビニロン,アセテート,アミランおよびカシミロンFに対する増白効果ならびに布上における耐光堅ロウ性を試験した。アクリル系繊維(カシミロンF)に対して,とくに4級塩は亜塩素酸ナトリウムを併用して処理することによって,増白効果および耐光性ともすぐれた結果を与えた。

Ciba社からUnitexER類として市販されている,ポリエステル繊維用のすぐれたケイ光増白染料の主成分であるα,β-ビス(5-メチルベンズオキサゾリル-(2))-エチレン(A)に置換基を導入し,それらの化合物の性質および各種合成繊維に対する適用性等を検討した。すなわち(A)を過剰のクロルスルホン酸とともに120～130℃に加熱して,クロルスルホン化し,これをアンモニアおよびn-ブチルアミン,β-シアノエチルアミン,シクロヘキシルアミン,アニリンなどの第一アミンおよびジエチルアミン,ジβ-オキシエチルアミン,ジβ-シアノエチルアミン,ピペリジン,モルホリンなどの第ニアミンと反応させて種々のスルホンアミド化合物を合成した。置換基の位置は赤外スペクトルの結果などからみて,4-位置であると考えられる。これらの化合物のジオキサンおよびジメチルホルムアミド溶液の吸収,およびケイ光ス,およびケイ光スペクトルの極大波長は一般に(A)に比べ5～10mμ程度長波長側に移動する。吸収強度は同程度であるが,ケイ光強度は減少する。これらの化合物でテトロン,アセテート,アミラン,ビニロンおよびカシミロンFなどの平織布を染色し,その増白効果ならびに増白布をフェードテスター中で照射し,布のケイ光強度の減少を測定することによって,日光堅ロウ性を試験した。一般に増白効果の特にすぐれたものは得られなかったが,第一アミンからの誘導体の方が第二アミンからの誘導体に比べて良好な結果を与えることを知った。

1,3,5-トリフェニル-2-ピラゾリン誘導体の構造とケイ光スペクトルの関係を考察し,1-フェニル基のp-位に親核性基を,また3-フェニル基のp-位に親電子性基を有する場合ケイ光極大は長波長側に移り,反対に1-フェニル基に親電子,3-フェニル基に親核性基を導入することによってケイ光は短波長側に移され,前者はとくにその傾向がいちじるしいルという事実を見いだした。このことが,ピリジン環を有するカルコンとアリールヒドラジンとから合成された3-(2-メチ-5-ピリジル)-1,5-ジフェニル-2-ピラゾリン誘導体においても成立することを確認した。これらピリジン環を有するピラゾリン類はテトロンおよびポリプロピレンに対しては染着性が低く,カシミロンF上では黄色に着色して増白効果を示さない。アセテートおよびアミランに対しては増白効果を有するが,ケイ光極大が一般に長波長側にある。しかしながら1-フェニル基のp - 位にカルボキシル, メトキシカルボニル, スルファモイルなどの親電子性基を導入することによってケイ光は短波長側に移り良好な増白効果を示すようになった。カーボンアーク灯退色試験機で照射して耐光堅ロウ性を比較したところ,メトキシカルボニル基を持った誘導体はアミラン上で耐光性は劣るが他のものは比較的良好な結果を示した。

繊維と共有結合により染色するいわゆる反応性染料の反応基としてフッ化スルホニル基を有する染料のうち,本報では分散染料,および新しい方法によって二,三の水溶性染料を合成し,種々の繊維に対する反応性染料としての適用性,色調,堅ロウ度などを調べた。分散染料はフッ化スルホニル基を有するアミン類,およびp-ニトロアニリンをジアゾ化し,N,N-ジエチル-,N,N-ジオキシエチル-アニリンおよび3-フッ化スルホニル-N,N-ジエチルアニリンとカップリングして得た。これらの染料を用いて絹, ナイロン, ビニロン, アセテートを分散状で染色し, 希アルカリで処理して繊維と反応させた。また, テトラ-塩化スルホニル化した銅,コバルトフタロシアニンおよびアミノ基を有する水溶性染料を,前者はフッ化カリにより置換するか,またはp-フッ化スルホニルアニリンと,後者はp-フッ化スルホニル塩化ベンゾイルと縮合させてそれぞれフッ化スルホニル基を有する染料を合成し,絹,ナイロンを酢酸酸性でビスコースレーヨン,モメンを中性で染色した後,前と同様に希アルカリで処理して繊維と反応させた。繊維と反応しなかった染料はフッ化スルホニル基が加水分解を受けてスルホン酸基となっているため,水溶性を増し,ソーピングによって簡単に除去され堅ロウな染色物を得た。一般にこれらの染料は含窒素繊維,とくに絹には非常によく反応固着されたが,セルロース繊維では少し劣った。これはその結合が不安定なエステル結合であり,固着やソーピング処理中において希アルカリによって徐々に分解されるためであろう。染料-繊維間の共有結合生成に対する証拠は既報と同様な方法で確かめた。

先にフッ化スルホニル基を有するナフトール染料が繊維の官能基と共有結合し,堅ロウ度良好な染色物をうることを知ったが,この際未結合染料を容易に繊維上から除去するため,また染色方法の簡略化のために,スルホン酸基を有する酸性染料型の反応性染料を合成した。すなはちフッ化スルホニル基を有する数種のアミンをジアゾ成分とし,スルホフェニルメチルピラゾロン, γ-酸, H-誘導体に酸性またはアルカリ性でそれぞれカップリングさせ, 黄, 赤および青色の染料を合成した。これらの染料を用い絹,アミランには酢酸酸性で,またモメン,ビニロンには中性で染色後,炭酸ナトリウム希水溶液で処理して繊維に反応,固着させた。この場合繊維と反応しなかった染料の-SO2F基は加水分解されて-SO3Na基となり,そのためより水に可溶性となりソーピングによってこれら分解染料の除去が非常に簡単に行なうことが出来た。しかしモメン,ビニロンの場合はその結合様式が不安定なエステル結合であるため,ソーピング中においてもアルカリによって徐々に加水分解され淡色となった。絹,アミラン上においては濃色,かつ鮮明な染色物を得,これらは非常に堅ロウであった。30%ピリジン水溶液による抽出や,ハイドロサルファイトによる還元後繊維と結合したアミンのジアゾ化,再カップリングによって共有結合の生成したことを確かめた。また繊維に染着した染料と反応した染料の割合を分光光電法によって測定した。