The removal process of fatty acid in aqueous systems was investigated using well-defined model detergent systems consisting of polymer, carbon, silica, and gold as substrates, and stearic acid as soil. The detergency was evaluated by the quartz crystal microbalance (QCM) technique. The experimental results were discussed based on detergent solution, soil deposited state and surface properties of the substrate. From the QCM frequency change during the soil removal, it was found that in the alkali solution the stearic acid deposited by the Langmuir–Blodgett (LB) method was rapidly removed due to the neutralization, whereas in the anionic surfactant solutions the LB films was removed by the liquid penetration. By comparing the removal efficiencies obtained from the area (evaluated using microscopic image analysis) and the mass (evaluated using QCM method) of soil deposited on the substrate, it was suggested that the nonionic surfactant micelles contributed to the removal of stearic acid.

Tumor growth and metastasis are dependent on angiogenesis, which is the formation of new blood vessels. The newly formed blood vessels around the tumor supply oxygen and nutrients to the tumor, supporting its progression. Moreover, these blood vessels also serve as channels through which tumor cells metastasize to distant organs. The balance between angiogenic stimulators and inhibitors regulates angiogenesis in the tumor microenvironment. Tumor blood vessels, and especially the endothelial cells lining tumor blood vessels(tumor endothelial cells [TECs]), are important targets in cancer therapy. Since newly formed tumor blood vessels originate from pre-existing normal vessels, tumor blood vessels and TECs have traditionally been considered to be the same as normal ones.

However, tumor blood vessels have a distinctively abnormal phenotype, including morphological alterations. Recently it has been revealed that TECs constitute a heterogeneous population, exhibiting characteristics induced largely by tumor microenvironmental factors. Furthermore, TECs induce cancer progression through metastasis. In this review, we describe recent studies on TEC abnormalities related to cancer progression and consider their therapeutic implications.

Eukaryotic cells are equipped with coordinated systems to contend with DNA damage, such as those which are used in cell cycle arrest, DNA repair, apoptosis and premature senescence to maintain genomic integrity. These systems are regulated at least in part by transcriptional activation or repression. Although processes to activate transcription of specific genes have been characterized in the context of sequence-specific DNA binding factors, mechanisms of transcriptional repression have been largely unexplored. Recently, we identified phosphorylation of histone H3-threonine 11 (H3-T11), a novel chromatin modification for transcriptional activation, that was rapidly reduced after DNA damage. We have begun to unravel the biological significance of H3-T11 phosphorylation in transcriptional regulation and uncovered a novel mechanism underlying DNA damage induced transcriptional repression. Namely, Chk1-release from chromatin and PP1 activation upon DNA damage cooperatively dephosphorylate H3-pT11 in response to DNA damage. We propose that the Chk1-dependent repression of cell cycle related genes may serve as a long term checkpoint arrest for DNA damage, leading cells with severe or unrepairable DNA damage to permanently exit from cell cycle.

Fibromyalgia (FM) is a disease of uncertain cause that is associated with chronic widespread pain and tenderness. Because the cause of FM is unclear, there is currently no curative treatment. Guidelines recommend pharmacotherapy such as pregabalin, duloxetine, amitriptyline and milnacipran hydrochloride and non-pharamacotherapy such as aerobic strengthening exercise, resistance exercise, water exercise and recognitive behavioral therapy as evidence-based therapies. However, some patients remain unable to manage their symptoms with these therapies and seek other effective treatments. Such treatments include nerve block therapy and trigger point injection (TPI) therapy. TPI is not strictly defined as nerve block therapy, but it is sometimes included in the nerve block therapy group. To date, no randomized controlled trials have been conducted to evaluate nerve block therapy for fibromyalgia alone., although many case reports have been published in Japanese. In this mini-review, we summarize and review nerve block therapy and trigger point injection therapy in English.