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Implication of granulocyte-macrophage colony-stimulating factor induced neutrophil gelatinase-associated lipocalin in pathogenesis of rheumatoid arthritis revealed by proteome analysis
Masayoshi Katano, Kazuki Okamoto, Mitsumi Arito, Yuki Kawakami, Manae S Kurokawa, Naoya Suematsu, Sonoko Shimada, Hiroshi Nakamura, Yang Xiang, Kayo Masuko, Kusuki Nishioka, Kazuo Yudoh, Tomohiro Kato
Arthritis Research & Therapy , 2009, DOI: 10.1186/ar2587
Abstract: Neutrophils stimulated by GM-CSF were divided into four subcellular fractions: cytosol, membrane/organelle, nuclei, and cytoskeleton. Then, proteins were extracted from each fraction and digested by trypsin. The produced peptides were detected using matrix-assisted laser desorption ionisation-time-of-flight mass spectrometry (MALDI-TOF MS).We detected 33 peptide peaks whose expression was upregulated by more than 2.5-fold in GM-CSF stimulated neutrophils and identified 11 proteins out of the 33 peptides using MALDI-TOF/TOF MS analysis and protein database searches. One of the identified proteins was neutrophil gelatinase-associated lipocalin (NGAL). We confirmed that the level of NGAL in SF was significantly higher in patients with RA than in those with osteoarthritis. We next addressed possible roles of the increased NGAL in RA. We analysed proteome alteration of synoviocytes from patients with RA by treatment with NGAL in vitro. We found that, out of the detected protein spots (approximately 3,600 protein spots), the intensity of 21 protein spots increased by more than 1.5-fold and the intensity of 10 protein spots decreased by less than 1 to 1.5-fold as a result of the NGAL treatment. Among the 21 increased protein spots, we identified 9 proteins including transitional endoplasmic reticulum ATPase (TERA), cathepsin D, and transglutaminase 2 (TG2), which increased to 4.8-fold, 1.5-fold and 1.6-fold, respectively. Two-dimensional electrophoresis followed by western blot analysis confirmed the upregulation of TERA by the NGAL treatment and, moreover, the western blot analysis showed that the NGAL treatment changed the protein spots caused by post-translational modification of TERA. Furthermore, NGAL cancelled out the proliferative effects of fibroblast growth factor (FGF)-2 and epidermal growth factor (EGF) on chondrocytes from a patient with RA and proliferative effect of FGF-2 on chondrosarcoma cells.Our results indicate that GM-CSF contributes to the pathogenesis
Characteristics of Geriatric Health Service Facilities Designated as Sites of Death  [PDF]
Mitsumi Ono, Hideyuki Kanda, Yuko Takeda, Sachiko Hara
Health (Health) , 2015, DOI: 10.4236/health.2015.710142
Abstract: There are many deaths occurring among the aged population in Japan. Geriatric Health Service Facilities (GHSFs) are highlighted as some of the chosen facilities designated as sites of death. The aim of our study was to clarify the characteristics and related factors, including physical signs first noticed by staff at the end-of-life period, in GHSFs designated as sites of death, using a nationwide survey in Japan. We administered a questionnaire to 3971 GHSFs in Japan. Eligible responses for the study were obtained from 854 GHSFs. We found that GHSFs designated as sites of death were more likely to have basic policies and documented preferences regarding end-of-life care. We also found that staff members in GHSFs designated as sites of death were less likely to first notice physical signs of pain. We found that GHSFs designated as sites of death tended to identify earlier symptoms, such as reduced oral intake and less vigor. Our results would enable elderly persons, their families, and staff in GHSFs to prepare for the elderly’s death more efficiently though earlier identification of the end-of-life period. We hope that GHSFs have an important role to play in end-of-life care provision to elderly persons in Japan, through the strengthening of these intermediate facilities.
Developing a Scale for Measuring Uncertainty in Patients with Unruptured Intracranial Aneurysms Undergoing Endovascular Coiling  [PDF]
Mitsumi Masuda, Hidenori Ohishi, Noriko Terunuma, Ikuko Tojima
Open Journal of Nursing (OJN) , 2015, DOI: 10.4236/ojn.2015.510097
Abstract: A measure called the Uncertainty in Unruptured Intracranial Aneurysm Patients Undergoing Endovascular Coiling Scale (UUIACS) was developed and its validity and reliability were examined. The 49 questions that comprised the original draft of the UUIACS were created based on interview data. Based on data from 172 participants, exploratory and confirmatory factor analyses were conducted. As a result of exploratory factor analysis, the UUIACS e retained 17 items and extracted four factors (“Lack of decision-making cues”, “Lack of information and complexity of information interpretation”, “The ambiguous nature of the disease”, and “The unpredictable living with UIA”). All of the UUIACS items showed adequate internal consistency. Between the UUIAC scale and the Universal Uncertainty in Illness Scale (UUIS), the Health Locus of Control (HLC) scale, and the SF-36v2® (Japanese version), positive correlations were found between the UUIACS and UUIS, and the HLC scale at a 1% significance level indicating concurrent validity. According to confirmatory factor analysis, the UUIACS had an acceptable goodness of fit. Given these findings, the UUIACS was judged to have satisfied the criteria for use in a clinical setting, although further investigation was required.
Factors Related to Nocturia in Elderly People Living in Local Remote Area in Japan  [PDF]
Yuko Takeda, Mitsumi Ono, Hideyuki Kanda, Sachiko Hara, Keiko Takeda
Health (Health) , 2017, DOI: 10.4236/health.2017.94047
The elderly people are prone to be affected by quality of life (QOL) by nocturia becoming the multiple times. A purpose of this study was to determine it about a factor associated with the night urination. This survey was conducted in 2015 as a cross-sectional study. Anonymous, self-administered questionnaires were used to prevent individuals from being identified. The analysis subjects were 699 elderly people with the nocturia which belonged to club of the aged 65 years or older. Those with nocturia were placed in the Nocturia-1 group if they reported experiencing nocturia once per night or in the Nocturia- ≥ 2 group if they reported experiencing nocturia two or more times per night. We analyzed the relationships between the characteristics, lower urinary tract symptoms, and opportunities to go outdoors in the Nocturia-1 and Nocturia- ≥ 2 groups based on sex using the χ2 test. In addition, to investigate the factors that influence the change from nocturia once per night to two or more times per night, we performed logistic regression analysis using the χ2 test on the characteristics and lower urinary tract symptoms that showed significant differences separately for men and women. Among the men, factors with a significant positive relation-ship were age, diabetes mellitus, lower back pain, daytime frequency, and urinary urgency. Among the women, factors with a significant positive relationship were age, requiring support 1-requiring long-term care 2, urinary urgency, and feeling of incomplete emptying. It was suggested that the life of elderly people improved by nocturia not increasing.
Proteomic Analysis of Celecoxib on Chondrocytes from Patients with Osteoarthritis  [PDF]
Kenji Takenouchi, Mitusmi Arito, Toshiyuki Sato, Kenji Takahashi, Manae S. Kurokawa, Kazuo Yudoh, Shinro Takai, Tomohiro Kato, Hiroshi Nakamura
Modern Research in Inflammation (MRI) , 2014, DOI: 10.4236/mri.2014.33011

Objective: To study a comprehensive proteomic analysis of celecoxib in oseteoarthritis (OA) chondrocytes. Methods: OA chondrocytes were stimulated with celecoxib, IL-1β and IL-1β together with celecoxib. Proteins were extracted from the cells and subjected to 2-dimensional differential image gel electrophoresis (2D-DIGE). Proteins of interest were identified by mass spectrometry. Results: Eighty-six protein spots showed significantly different intensities with each reagent or reagent combination. AAA+ protein, HSP47/Serpin, cAMP-dependent protein kinase type II-beta regulatory subunit, alpha-actin-4 and tubulin decreased with the addition of celecoxib, while apolipoprotein A-V, glutamate carboxipeptide 2, mitochondrial stress-70 protein, sorting nexin-9 and GRP78 increased with the addition of celecoxib. GRP78 is a stress protein and may be chondroprotective. Celecoxib modulated IL-1β stimulated chondrocytes, and CD200R and moesin were identified as such resulting proteins. Conclusion: Protein profiles of OA chondrocytes changed after administration of celecoxib. Further investigation is needed to elucidate the function of each protein in OA chondrocytes.

Complex Regional Pain Syndrome Revived by Epileptic Seizure Then Disappeared Soon during Treatment with Regional Intravenous Nerve Blockade: A Case Report
Masahiko Sumitani,Arito Yozu,Toshiya Tomioka,Satoru Miyauchi,Yoshitsugu Yamada
Anesthesiology Research and Practice , 2011, DOI: 10.1155/2011/494975
Abstract: We present a case of complex regional pain syndrome (CRPS), in which symptoms, including burning pain and severe allodynia, were alleviated by using a regional intravenous nerve blockade (Bier block) combined with physiotherapy, but reappeared following an epileptic seizure. Symptoms disappeared again following control of epileptic discharges, as revealed by single-photon emission computed tomography (SPECT) and electroencephalography (EEG) results. Although systemic toxicity of a local anesthetic applied by Bier block was suspected as a cause of the first seizure, the patient did not present any other toxic symptoms, and seizures repeatedly occurred after Bier block cessation; the patient was then diagnosed as having temporal symptomatic epilepsy. This case suggests that symptoms of CRPS may be sustained by abnormal brain conditions, and our findings contribute to the understanding of how the central nervous system participates in maintaining pain and allodynia associated with CRPS. 1. Introduction Complex regional pain syndrome (CRPS) causes extreme pain. Dysfunctions of the peripheral nervous system, including the sensory and sympathetic nervous systems, are typically considered to sustain CRPS. The central nervous system (CNS) has also been reported to play an important role in CRPS emergence and maintenance [1]. Although many clinical studies on CRPS and studies using animal models have been conducted, the pathophysiological mechanism of CRPS is not yet clear [2–5]. Here, we report a case of a CRPS patient whose pain was improved by a regional intravenous nerve blockade combined with physiotherapy; however, CRPS relapsed into intolerable pain and severe allodynia following an epileptic seizure. Recurrent CRPS then rapidly improved through the control of epileptic discharges. During epileptic episodes, we investigated the CRPS patient using single-photon emission computed tomography (SPECT) and electroencephalography (EEG). Our findings may contribute to the understanding of how the CNS participates in maintaining CRPS-related pain and allodynia. 2. Case Report A 65-year-old woman with aortic regurgitation following infectious endocarditis had undergone twice aortic valve replacement procedures within 2 months. After the second operation, more than 3 weeks were required before she could be weaned from intensive treatment, including artificial ventilation and sedative drug administration. Following recovery from heart failure, sedative drug administration was discontinued. The patient’s clouded consciousness persisted for several days, but she did
Oral Local Anesthesia Successfully Ameliorated Neuropathic Pain in an Upper Limb Suggesting Pain Alleviation through Neural Plasticity within the Central Nervous System: A Case Report
Jun Hozumi,Masahiko Sumitani,Arito Yozu,Toshiya Tomioka,Hiroshi Sekiyama,Satoru Miyauchi,Yoshitsugu Yamada
Anesthesiology Research and Practice , 2011, DOI: 10.1155/2011/984281
Abstract: Neural blockades are considered an alternative to pharmacotherapy for neuropathic pain although these blockades elicit limited effects. We encountered a patient with postbrachial plexus avulsion injury pain, which was refractory to conventional treatments but disappeared temporarily with the administration of the local anesthetic lidocaine around the left mandibular molar tooth during dental treatments. This analgesic effect on neuropathic pain by oral local anesthesia was reproducible. Under conditions of neuropathic pain, cerebral somatotopic reorganization in the sensorimotor cortices of the brain has been observed. Either expansion or shrinkage of the somatotopic representation of a deafferentated body part correlates with the degree of neuropathic pain. In our case, administration of an oral local anesthetic shrank the somatotopic representation of the mouth, which is next to the upper limb representation and thereby expanded the upper limb representation in a normal manner. Consequently, oral local anesthesia improved the pain in the upper limb. This case suggests that pain alleviation through neural plasticity within the brain is related to neural blockade. 1. Introduction Neuropathic pain typically appears following peripheral nerve injury due to neuropathies, plexopathies, and trauma to selected sites within the central nervous system (CNS). Recently, evidence-based recommendations of pharmacological treatments for neuropathic pain have been proposed based on both positive and negative results from multiple randomized controlled trials. However, approximately 10–15% of all neuropathic pain patients are refractory to pharmacotherapy. For these cases, more invasive pain-management interventions, such as intrathecal drug delivery, neurostimulation, or neural blockade, may be used. Ideally, blocking neural transmission, either temporarily by using local anesthetics or permanently by surgical nerve ablation, can reduce neuropathic pain; however, no neural blockades have been found to be consistently successful [1]. Here, we report on a case of a patient with postbrachial plexus avulsion injury pain whose neuropathic pain had been refractory to several evidence-based pharmacotherapies and interventions, such as spinal cord stimulation, cervical epidural blockade, and brachial plexus blockade. His pain could be well controlled by oral local anesthesia, suggesting pain alleviation through neural plasticity within the CNS. 2. Case Report A 49-year-old man, who had a left brachial plexus avulsion injury 10 years before, experienced severe neuropathic
Hemorrhagic shock and encephalopathy syndrome – the markers for an early HSES diagnosis
Hiroshi Rinka, Takeshi Yoshida, Tetsushi Kubota, Miho Tsuruwa, Akihiro Fuke, Akira Yoshimoto, Masanori Kan, Dai Miyazaki, Hideki Arimoto, Toshinori Miyaichi, Arito Kaji, Satoru Miyamoto, Ichiro Kuki, Masashi Shiomi
BMC Pediatrics , 2008, DOI: 10.1186/1471-2431-8-43
Abstract: We examined the clinical, biological and radiological findings of 8 patients (4 months to 9 years old) who met the HSES criteria.Although cerebral edema, disseminated intravascular coagulopathy (DIC), and multiple organ failure were seen in all 8 cases during their clinical courses, brain computed tomography (CT) scans showed normal or only slight edema in 5 patients upon admission. All 8 patients had normal platelet counts, and none were in shock. However, they all had severe metabolic acidosis, which persisted even after 3 hours (median base excess (BE), -7.6 mmol/L). And at 6 hours after admission (BE, -5.7 mmol/L) they required mechanical ventilation. Within 12 hours after admission, fluid resuscitation and vasopressor infusion for hypotension was required. Seven of the patients had elevated liver enzymes and creatine kinase (CK) upon admission. Twenty-four hours after admission, all 8 patients needed vasopressor infusion to maintain blood pressure.CT scan, platelet count, hemoglobin level and renal function upon admission are not useful for an early diagnosis of HSES. However, the elevated liver enzymes and CK upon admission, hypotension in the early stage after admission with refractory acid-base disturbance to fluid resuscitation and vasopressor infusion are useful markers for an early HSES diagnosis and helpful to indicate starting intensive neurological treatment.Since the original description of the hemorrhagic shock and encephalopathy syndrome (HSES) by Levin et al. [1], numerous cases have been reported in the literature. Although the etiology of HSES remains unknown, this syndrome is associated with acute onset of encephalopathy, shock, watery diarrhea, severe disseminated intravascular coagulopathy (DIC), and renal and hepatic dysfunction.As some authors have defined the HSES criteria [2-4], patients meeting them will usually have very poor prognoses with a fatal course or severe neurological sequelae. Our experience suggests that early detection of HS
Cis Association of Galectin-9 with Tim-3 Differentially Regulates IL-12/IL-23 Expressions in Monocytes via TLR Signaling
Cheng J. Ma, Guang Y. Li, Yong Q. Cheng, Jia M. Wang, Ruo S. Ying, Lei Shi, Xiao Y. Wu, Toshiro Niki, Mitsumi Hirashima, Chuan F. Li, Jonathan P. Moorman, Zhi Q. Yao
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0072488
Abstract: Human monocytes/macrophages (M/MФ) of the innate immunity sense and respond to microbial products via specific receptor coupling with stimulatory (such as TLR) and inhibitory (such as Tim-3) receptors. Current models imply that Tim-3 expression on M/M? can deliver negative signaling to TLR-mediated IL-12 expression through trans association with its ligand Galectin-9 (Gal-9) presented by other cells. However, Gal-9 is also expressed within M/M?, and the effect of intracellular Gal-9 on Tim-3 activities and inflammatory responses in the same M/M? remains unknown. In this study, our data suggest that Tim-3 and IL-12/IL-23 gene transcriptions are regulated by enhanced or silenced Gal-9 expression within monocytes through synergizing with TLR signaling. Additionally, TLR activation facilitates Gal-9/Tim-3 cis association within the same M/M? to differentially regulate IL-12/IL-23 expressions through STAT-3 phosphorylation. These results reveal a ligand (Gal-9) compartment-dependent regulatory effect on receptor (Tim-3) activities and inflammatory responses via TLR pathways—a novel mechanism underlying cellular responses to external or internal cues.
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