Expansion of Antibacterial Spectrum of Muraymycins toward Pseudomonas aeruginosa

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Null allele alpha-1 antitrypsin deficiency: case report of the total pleural covering technique for disease-associated pneumothorax

A 44-year-old woman, who had been diagnosed as having null type alpha-1 antitrypsin (AAT) deficiency, was admitted with right recurrent pneumothorax. She had undergone right visceral pleural strengthening and pleural adhesion-preventing surgery, the total pleural covering technique (TPC), with oxidized regenerative cellulose (ORC). Three years after the operation, she developed left recurrent pneumothorax and underwent left TPC. AAT deficiency is a rare inherited disease in Japan that causes early-onset emphysema and secondary pneumothorax. In addition, null/null phenotype has the highest risk of emphysema and may require lung transplantation. For future lung transplantation, pleural adhesion should be prevented. However, pleurodesis and surgery for pneumothorax generally cause adhesion. TPC with ORC is a surgical treatment for pneumothorax that is done to strengthen visceral pleura and prevent pleural adhesions. The patient has had no recurrence of pneumothorax 3.5 years after right TPC and 6 months after left TPC.     

Auraptene attenuates gastritis via reduction of Helicobacter pylori colonization and pro-inflammatory mediator production in C57BL/6 mice

Helicobacter pylori is a major human pathogen that plays central roles in chronic gastritis and gastric cancer. Recently, we reported that auraptene suppressed H. pylori adhesion via expression of CD74, which has been identified as a new receptor for H. pylori urease. In this study, we attempted to clarify the effects of oral feeding of auraptene on H. pylori infection and resultant inflammatory responses in C57BL/6 mice and found that it remarkably attenuated H. pylori colonization and gastritis. Biochemical analyses revealed that auraptene inhibited H. pylori-induced expression and/or production of CD74, macrophage migration inhibitory factor, interleukin-1β, and tumor necrosis factor-α in gastric mucosa, together with serum macrophage inhibitory protein-2. It is notable that treatment with this coumarin during the pretreatment period was more effective than that during posttreatment. Our results suggest that auraptene is a promising phytochemical for reducing the risk of H. pylori-induced gastritis and carcinogenesis.     

Linear ubiquitination signals in adaptive immune responses

Ubiquitin can form eight different linkage types of chains using the intrinsic Met 1 residue or one of the seven intrinsic Lys residues. Each linkage type of ubiquitin chain has a distinct three-dimensional topology, functioning as a tag to attract specific signaling molecules, which are so-called ubiquitin readers, and regulates various biological functions. Ubiquitin chains linked via Met 1 in a head-to-tail manner are called linear ubiquitin chains. Linear ubiquitination plays an important role in the regulation of cellular signaling, including the best-characterized tumor necrosis factor (TNF)-induced canonical nuclear factor-κB (NF-κB) pathway. Linear ubiquitin chains are specifically generated by an E3 ligase complex called the linear ubiquitin chain assembly complex (LUBAC) and hydrolyzed by a deubiquitinase (DUB) called ovarian tumor (OTU) DUB with linear linkage specificity (OTULIN). LUBAC linearly ubiquitinates critical molecules in the TNF pathway, such as NEMO and RIPK1. The linear ubiquitin chains are then recognized by the ubiquitin readers, including NEMO, which control the TNF pathway. Accumulating evidence indicates an importance of the LUBAC complex in the regulation of apoptosis, development, and inflammation in mice. In this article, I focus on the role of linear ubiquitin chains in adaptive immune responses with an emphasis on the TNF-induced signaling pathways.     

Relationship between tongue strength and 1-year life expectancy in elderly people needing nursing care

Tongue strength is a useful indicator of oral function and has been found to decrease with aging and reduced physical functioning. The present study aimed to assess the relationships of tongue strength with physical function, mental function, and nutritional status, and also between these factors and 1-year outcomes, to determine whether tongue strength is related to life expectancy in elderly people needing nursing care. The subjects were 140 elderly individuals requiring needing nursing care (49 men and 91 women; ≥65 years). The investigated items included sex, age, activities of daily living (ADL), comorbidity, cognitive function, nutritional status, eating function, occlusal support, and tongue strength. Furthermore, a follow-up study was conducted 1 year later, and factors related to death were identified. The mean tongue strength of the total 140 subjects was 20.3 ± 8.6 kPa. Tongue strength was assessed relative to each of the investigated items, using the t test and one-way analysis of variance. Tongue strength was significantly related to ADL, comorbidity, cognitive function, calf circumference, food intake, and occlusal support. Fifteen subjects were found to have died at the 1-year follow-up study. We assessed the relationships of 1-year outcomes with each of the factors examined, and 1-year outcomes were found to be significantly related to ADL and tongue strength.     

JNK/c‐Jun Signaling Mediates an Anti‐Apoptotic Effect of RANKL in Osteoclasts

Introduction: RANKL is known to be important not only for differentiation and activation of osteoclasts but also for their survival. Experimentally, apoptosis of osteoclasts is rapidly induced by the deprivation of RANKL. RANKL activates Elk‐related tyrosine kinase (ERK), p38, c‐Jun N‐terminal kinase (JNK), and NF‐κB pathways through TRAF6 in osteoclasts and the precursor cells. It has been shown that ERK is critical for regulation of osteoclast survival. However, an involvement of other RANKL signaling pathways such as JNK signaling in survival of osteoclasts has not been fully understood yet. Materials and Methods: Osteoclasts derived from primary mouse bone marrow cells by soluble RANKL (sRANKL) were treated with a JNK inhibitor, SP600125, or infected with adenovirus carrying dominant‐negative (DN)‐c‐jun, DN‐c‐fos, mitogen‐activated protein kinase kinase 1 (MEKK1), I‐κBα mutant, or NF‐κB components, p50 and p65. Osteoclasts were cultured with or without sRANKL, and apoptotic phenotype was determined by TUNEL assay, DAPI staining, and expression of cleaved caspase 3 followed by TRACP staining. Results: Overexpression of TRAF6 activated JNK and NF‐κB signaling pathways and clearly prevented osteoclasts from apoptosis caused by abrogation of sRANKL. An anti‐apoptotic effect of RANKL/RANK/TRAF6 signaling on osteoclast was inhibited by JNK‐specific inhibitor SP600125 and by overexpression of dominant‐negative JNK1, c‐jun, and c‐fos. Also, overexpression of MEKK1 inhibited apoptosis of osteoclasts even in the absence of sRANKL along with activation of JNK/c‐jun signaling. On the other hand, blockade of NF‐κB signaling by I‐κBα mutant or overexpression of NF‐κB components showed a marginal effect on apoptosis of osteoclasts. Conclusions: An important role of RANKL‐induced activation of MEKK1/JNK/c‐jun signaling in the regulation of apoptosis in osteoclasts was shown. Our study suggests that c‐fos plays a role as a partner of activator protein‐1 factor, c‐jun, during the regulation of apoptosis in osteoclasts.     

Oxidation Potentials of Flavonoids Determined by Flow-through Column Electrolysis

1　ＩｎｔｒｏｄｕｃｔｉｏｎＦｌａｖｏｎｏｉｄｓａｒｅｎａｔｕｒａｌｃｏｍｐｏｕｎｄｓ ,ｗｉｄｅｌｙｄｉｓｔｒｉｂｕｔｅｄｉｎｆｒｕｉｔｓ,ｖｅｇｅｔａｂｌｅｓ,ａｎｄｔｅａｓ.Ｔｈｅｒｅｉｓａｎｉｎｃｒｅａｓｉｎｇｉｎｔｅｒｅｓｔｉｎｔｈｅｓｅｃｏｍｐｏｕｎｄｓｂｅｃａｕｓｅｏｆｔｈｅｉｒｂｒｏａｄ ｐｈａｒｍａｃｏｌｏｇｉｃａｌａｃｔｉｖｉ ｔｉｅｓ ,[1,2 ] ｅｓｐｅｃｉａｌｌｙｔｈｅｉｒａｎｔｉｏｘｉｄａｎｔａｃｔｉｖｉｔｙ .[3～ 5 ] Ａｓａｎｔｉｏｘｉｄａｎｔｓ ,ｆｌａｖｏｎｏｉｄｓｈａｖｅｔｈｅａｂｉｌｉｔｙｔｏｓｃａｖｅｎｇｅｆｒｅｅｒａｄｉｃａｌｓｂｙｐｒｏｔｅｉｎａｎｄｅｌｅｃｔｒｏｎｔｒａｎｓｆｅｒｐｒｏｃｅｓｓｅｓ.Ｏｎｔｈｅｏｔｈｅｒｈａｎｄ ,ａｓｍｅｔａｌ ｃｈｅｌａｔｉｎｇａｇｅｎｔｓ ,ｆｌａｖｏｎｏｉｄｓｃａｎｄｅｐｒｅｓｓｔｈｅｓｕｐｅｒｏｘｉｄｅ ｄｒｉｖｅｎＦｅｎｔｏｎｒｅａｃｔｉｏｎ .[6 ] Ｔｈｅｒｅａｒｅａｌｓｏｒｅｐｏｒｔｓｏｆｆｌａｖｏｎｏｉｄｓｉｎｈｉｂｉｔｉｎｇｔｈｅａｃｔｉｖｉｔｉｅｓｏｆａｎａｒｒａｙｏｆｅｎｚｙｍｅｓ.[1,7,...