Softening and Salts Movement in the Ripening Process of Camembert Cheese

Experimental Camembert cheese softened from the surface to the center portion after 3-4 weeks of ripening.As ripening progressed,pH value rose from 4.5 to 7.8,lactic acid content decreased from 1.0% to 0.1%,ammonia content increased from 0.04g to 0.063g/100g,calcium content decreased from 0.3g to 0.048g/100g and phosphorus content decreased from 0.25g to 0.12g/100g in the center portion of cheese. The changes in these values were considered as criteria leading to softening of mold surface-ripened cheeses.Mold starter Penicillium candidum AM used the cheese manufacture possesses the abilities lactic acid,producing ammonia and lowering pH when supplemented with lactic acid and peptone Czapek Dox solution.However,normal softening was not observed by incubation of green cheese under ammonia atomsphere conditions.Also,lactic acid free cheese did not soften in spite of mold growth.It is proposed that the primary factor of softening in mold surface-ripened cheese is a rise of casein solubility caused by lowering of calcium crosslinking due to a decrease of calcium level in the cheese texture.The results suggested that the lactic acid metabolism and pH rise play a main part in inducement,and that insolble calcium phosphate accumulates in the cheese surface.本研究は、カマンベールチーズの熟成における軟化の主因と考えられているチーズ内でのpHや塩類の動態を追跡したものである。熟成開始前のグリーンチーズに比べて熟成が完了した4週目のチーズ中心部では、pHは4.5から7.8に上昇、乳酸は1.0% から0.1% で約1/10に低下、アンモニアは100g当たり0.04gから0.063gで約1.5倍に上昇、カルシウムは100g当たり0.3gから0.04gで約1/10のに減少、リンは100g当たり0.25gから0.12gで約1/2に減少した。これらの変化が本チーズの熟成軟化の要件と推察される。培養試験から、本チーズに使用したかびスターター　Pen. candidumに乳酸の代謝能とアンモニアの生成能を有すること、その結果pHが上昇することが確認された。しかし、未成熟のグリーンチーズをアンモニア蒸気にさらした場合も、乳酸を含まないチーズを熟成させた場合も正常な軟化は生じなかった。最も顕著な変化は、pH、乳酸、カルシウムに認められたが、これらのチーズ内での動態が主導的な役割を果たすものと推察された

Quantum chemical study on the oxidation process of a hydrogen terminated Si surface

科研費報告書収録論文(課題番号:09450296・基盤研究(B)(2)・H9～H10/研究代表者:宮本, 明/新しい高速化第一原理分子動力学計算プログラムの開発と金属超微粒子触媒への応用

18F-fluorodeoxyglucose positron emission tomography and magnetic resonance imaging evaluation of chorea

Chorea is thought to be caused by deactivation of the indirect pathway in the basal ganglia circuit. However, few imaging studies have evaluated the basal ganglia circuit in actual patients with chorea. We investigated the lesions and mechanisms underlying chorea using brain magnetic resonance imaging (MRI) and 18F-fluorodeoxyglucose positron emission tomography (FDG-PET). This retrospective case series included three patients with chorea caused by different diseases: hyperglycemic chorea, Huntington’s disease, and subarachnoid hemorrhage. All the patients showed dysfunction in the striatum detected by both MRI and FDG-PET. These neuroimaging findings confirm the theory that chorea is related to an impairment of the indirect pathway of basal ganglia circuit

Role of cyclooxygenase-2-mediated prostaglandin E2-prostaglandin E receptor 4 signaling in cardiac reprogramming

Direct cardiac reprogramming from fibroblasts can be a promising approach for disease modeling, drug screening, and cardiac regeneration in pediatric and adult patients. However, postnatal and adult fibroblasts are less efficient for reprogramming compared with embryonic fibroblasts, and barriers to cardiac reprogramming associated with aging remain undetermined. In this study, we screened 8400 chemical compounds and found that diclofenac sodium (diclofenac), a non-steroidal anti-inflammatory drug, greatly enhanced cardiac reprogramming in combination with Gata4, Mef2c, and Tbx5 (GMT) or GMT plus Hand2. Intriguingly, diclofenac promoted cardiac reprogramming in mouse postnatal and adult tail-tip fibroblasts (TTFs), but not in mouse embryonic fibroblasts (MEFs). Mechanistically, diclofenac enhanced cardiac reprogramming by inhibiting cyclooxygenase-2, prostaglandin E2/prostaglandin E receptor 4, cyclic AMP/protein kinase A, and interleukin 1β signaling and by silencing inflammatory and fibroblast programs, which were activated in postnatal and adult TTFs. Thus, anti-inflammation represents a new target for cardiac reprogramming associated with aging

Implementing action for acute stroke based on Japanese National Plan for Promotion of Measures Against Cerebrovascular and Cardiovascular Disease in Tokushima

Cerebrovascular and cardiovascular disease are the main causes of death in Japan. The leading causes of the need for long-term care in Japan are also cerebrovascular and cardiovascular disease, which together account for more than one-fourth of the total. The Cerebrovascular and Cardiovascular Disease Control Act, of Japanese national law, was promulgated by a legislative act in 2018. On the basis of the Cerebrovascular and Cardiovascular Disease Control Act, the Ministry of Health, Labour and Welfare, Japan, published the Japanese National Plan for Promotion of Measures Against Cerebrovascular and Cardiovascular Disease （Japanese National Plan） in 2020. By the example of the Japanese National Plan, Tokushima prefecture established a cerebrovascular and cardiovascular disease countermeasure promotion plan to progress cerebrovascular and cardiovascular disease measures according to their own circumstances. One of the important measures of the plan is improving emergency transportation systems. Patients with intracranial large vessel occlusion strokes should be served by direct transfer to endovascular capable centers avoiding delays by misguided transfer to primary stroke centers. Considering the limited availability of endovascular capable centers, accurate identification of patients with high probability of having large vessel occlusion strokes in the prehospital setting is importance. To address this problem, we introduced prehospital scale called Field Assessment Stroke Triage for Emergency Destination （FAST-ED） on emergency transportation systems in Tokushima city

Changing trends in prognostic factors for patients with multiple myeloma after autologous stem cell transplantation during the immunomodulator drug/proteasome inhibitor era

We evaluated the clinical significance of prognostic factors including the International Staging System (ISS) and modified European Group for Blood and Marrow Transplantation response criteria in 1650 Japanese patients with multiple myeloma (MM) who underwent upfront single autologous stem cell transplantation (ASCT). We categorized patients into two treatment cohorts: pre-novel agent era (1995-2006) and novel agent era (2008-2011). The combined percentage of pre-ASCT complete response and very good partial response cases (463 of 988, 47%) significantly increased during the novel agent era compared with the pre-novel agent era (164 of 527, 31%; P < 0.0001). The 2-year overall survival (OS) rate of 87% during the novel agent era was a significant improvement relative to that of 82% during the pre-novel agent era (P = 0.019). Although significant differences in OS were found among ISS stages during the pre-novel agent era, no significant difference was observed between ISS I and II (P = 0.107) during the novel agent era. The factors independently associated with a superior OS were female gender (P = 0.002), a good performance status (P = 0.024), lower ISS (P < 0.001), pre-ASCT response at least partial response (P < 0.001) and ASCT during the novel agent era (P = 0.017). These results indicate that the response rate and OS were significantly improved, and the ISS could not clearly stratify the prognoses of Japanese patients with MM who underwent upfront single ASCT during the novel agent era. © 2014 The Authors. Cancer Science published by Wiley Publishing Asia Pty Ltd on behalf of Japanese Cancer Association

Overexpression of transmembrane protein 168 in the mouse nucleus accumbens induces anxiety and sensorimotor gating deficit

Transmembrane protein 168 (TMEM168) comprises 697 amino acid residues, including some putative transmembrane domains. It is reported that TMEM168 controls methamphetamine (METH) dependence in the nucleus accumbens (NAc) of mice. Moreover, a strong link between METH dependence-induced adaptive changes in the brain and mood disorders has been evaluated. In the present study, we investigated the effects of accumbal TMEM168 in a battery of behavioral paradigms. The adeno-associated virus (AAV) Tmem168 vector was injected into the NAc of C57BL/6J mice (NAc-TMEM mice). Subsequently, the accumbal TMEM168 mRNA was increased approximately by seven-fold when compared with the NAc-Mock mice (controls). The NAc-TMEM mice reported no change in the locomotor activity, cognitive ability, social interaction, and depression-like behaviors; however, TMEM168 overexpression enhanced anxiety in the elevated-plus maze and light/dark box test. The increased anxiety was reversed by pretreatment with the antianxiety drug diazepam (0.3 mg/kg i.p.). Moreover, the NAc-TMEM mice exhibited decreased prepulse inhibition (PPI) in the startle response test, and the induced schizophrenia-like behavior was reversed by pretreatment with the antipsychotic drug risperidone (0.01 mg/kg i.p.). Furthermore, accumbal TMEM168 overexpression decreased the basal levels of extracellular GABA in the NAc and the high K+ (100 mM)-stimulated GABA elevation; however, the total contents of GABA in the NAc remained unaffected. These results suggest that the TMEM168-regulated GABAergic neuronal system in the NAc might become a novel target while studying the etiology of anxiety and sensorimotor gating deficits