The chemical groups were identified by characteristic colour changes using standard procedures.5 and 6 The acetic acid-induced writhing response was evaluated according to procedure reported previously.5 and 7 The experimental animals were arbitrarily divided into control, positive control and test groups

with five mice in each group. The animals of test groups were treated with plant extract at the doses of 250 and 500 mg/kg body weight, positive control group received diclofenac sodium at the dose of 25 mg/kg body weight and control group was treated with 1% Tween-80 in water at the dose of Selleckchem Entinostat 10 ml/kg body weight orally. After 30 min, 0.7% acetic acid was administered intra-peritoneally. With an interval of 5 min, the mice were observed for specific tightening (squirms) of body referred as ‘writhing’ Veliparib order for 15 min. A significant reduction of writhes in experimental animals compared to those

in the control group was considered as an antinociceptive response. Student’s t-test was used to determine a significant difference between the control group and experimental groups. The criterion for statistical significance was considered as P values of 0.05 or less. The results of phytochemical study of the ethanol extracts of P. acuminata are summarized in Table 1. It reveals the presence of alkaloid, flavonoid, tannin, reducing sugar and saponin in both extracts. However, steroid is present only in stem extract. In acetic acid-induced writhing test, both extracts showed considerable dose-dependent decrease in the number of writhing. The leaf extract produced 25.00% and 53.57% writhing inhibition at the doses of 250 and 500 mg/kg of body weight respectively. Similarly, same doses of stem extract produced 26.79% and 50% writhing inhibition respectively. The results are comparable to the

standard drug diclofenac sodium where the inhibition was 57.15% at the dose of 25 mg/kg of body weight (Table 2). The acetic acid induced writhing response is the widely used, primary and sensitive procedure to evaluate Lonafarnib in vivo peripherally acting antinociceptive agents. Increased levels of PGE2 & PGF2α in the peritoneal fluid have been reported to be responsible for pain sensation caused by intraperitoneal administration of acetic acid.8 The significant antinociceptive activity of the plant extracts might be due to the presence of pain-relieving principles acting through the prostaglandin pathways. Moreover, several flavonoids and tannins isolated from medicinal plants have been reported for their considerable antinociceptive activity.

Compound (R)-5; Rf = 0.44 (20:80 ethyl acetate/hexane); off white semi-solid; [α]D25 = −25.33 (c = 0.03 g/100 mL); 1H NMR (400 MHz, MeOD) δ: 2.63 (1H, dd, J = 10.7, 13.3 Hz, H-9a), 2.70-2.72 (1H, m, H-3), 3.15 (1H, dd, J = 4.0, 13.5 Hz, Sunitinib nmr H-9b), 3.82 (3H, s, Ar–OCH3-7), 3.87 (3H, s, Ar–OCH3-5), 4.10 (1H, dd, J = 6.9, 11.2 Hz, H-2b), 4.27 (1H, dd, J = 3.9, 11.2 Hz, H-2a), 6.06 (1H,

s, H-6), 6.07 (1H, s, H-8), 6.80 (2H, d, J = 8.4 Hz, H-2′,6′), 7.07 (2H, d, J = 8.4 Hz, H-3′,5′); 13C NMR (100 MHz, MeOD) 32.1 (CH2, C-9), 48.5 (CH, C-3), 55.0 (OCH3, C-7), 55.9 (OCH3, C-5), 68.9 (CH2, C-2), 92.9 (CH, C-8), 93.2 (CH, C-6), 105.3 (C, C-4a), 115.5 (CH, C-3′,5′), 130.2 (C, C-1′), 130.3 (CH, C-2′,6′), 154.5 (C, C-4′), 162.6 (C, C-7), 165.0 (C, C-8a), 165.9 (C,

C-5), 191.7 (C, C-4); HRMS (EI) calcd for C18H19O5 315.1154, found 315.1226. Compound (S)-5; Rf = 0.44 (20:80 http://www.selleckchem.com/products/AZD2281(Olaparib).html ethyl acetate/hexane); off white semi-solid; [α]D25 = +25.66 (c = 0.03 g/100 mL); 1H NMR (400 MHz, MeOD) δ: 2.64 (1H, dd, J = 10.4, 13.5, H-9a), 2.69-2.70 (1H, m, H-3), 3.14 (1H, dd, J = 4.1, 13.4 Hz, H-9b), 3.82 (3H, s, Ar–OMe-7), 3.86 (3H, s, Ar–OMe-5), 4.11 (1H, dd, J = 4.2, 7.0 Hz, H-2b), 4.27 (1H, dd, J = 3.9, 11.2 Hz, H-2a), 6.06 (1H, s, H-6), 6.07 (1H, s, H-8), 6.80 (2H, d, J = 8.4 Hz, H-2′,6′), 7.07 (2H, d, J = 8.4 Hz, H-3′,5′); 13C NMR (100 MHz, MeOD) 32.1 (CH2, C-9), 48.5 (CH, C-3), 55.0 (OCH3, C-7), 55.9 (OCH3, C-5), 68.9 (CH2, C-2), 92.8 (CH, C-8), 93.2 (CH, C-6), 105.3 (C, C-4a), 115.5 (CH, C-3′,5′), 130.1 (C, C-1′), 130.2 (CH, C-2′,6′), 154.7 (C, C-4′), 162.6 (C, C-7), 165.0 (C, C-8a), 165.9 (C, C-5), 191.9 (C, C-4); HRMS (EI) calcd for C18H19O5 315.1154, found 315.1220. Compound (R)-5, (S)-5 and the racemate were assessed for their potential anti-inflammatory activity. Ethical approval (003/09/Animal)

from the University of KwaZulu-Natal Celastrol Animal Ethics subcommittee was obtained prior to the investigation of acute croton oil-induced auricular dermatitis in a mouse model. Guidelines by the University of KwaZulu-Natal Animal Ethics Subcommittee and Biomedical Resources Unit for the maintenance and treatment of laboratory animals were followed. Eight-week old male Balb/c mice of approximately 30 g each were used. Equal volumes of croton oil (25 μl) were mixed with acetone (25 μl) as vehicle and applied (50 μl total volume; 1 h) onto the inner surface of the right auricle of each mouse to induce oedema. 9 Acetone has not been documented to have an anti-inflammatory effect by itself. 10 Thereafter, (R)-5, (S)-5 or the racemate were dissolved in acetone and 0.1 mg applied for 3 or 6 h treatment onto the right auricle to assess the reduction in oedema. The non-steroidal anti-inflammatory drug diclofenac was included as a positive control. Mice were euthanized after treatment for 3 and 6 h.

Our findings show

synergistic increases in the expression of GFAP and AQP4 in some regions depending on the time course Adriamycin mouse after envenomation. It was found that GFAP and AQP4 increased in parallel in the WM of P14 animals and in the ML of 8-week-old animals 24 h after envenoming (see Figs. 2 and 3) and in the GL of 8-week-old PNV-treated animals after 2 h (Fig. 4). At other time points there was a nonparallel upregulation of either AQP4 or GFAP. PNV induced upregulation of GFAP in protoplasmic astrocytes of ML (named Bergmann glia) at all time-points and in the velate protoplasmic astrocytes of GL at 2 and 5 h and in astrocytes of PL of P14 rats at 24 h. As per AQP4, the increase in GFAP expression was confined to protoplasmic astrocytes of the gray matter, except within the PL, in adults. Considering that PNV effects are transient, do not cause neuronal death and demyelination (Le Sueur et al., 2003, 2004), we suggest that increases in GFAP expression here observed is a mechanism for neuroprotection (Li et al., 2008). In this particular, the increased expression of AQP4 in neonate rats without a concomitant increase in that of GFAP could be a compensatory mechanism for protection

against PNV transient toxicity. Nevertheless, it remains unclear why upregulation of GFAP paralleled with upregulation of AQP4 in the WM of neonates (24 h), in the ML of adults (24 h) and in the GL all of adults (2 h). However, such findings are interesting, because http://www.selleckchem.com/products/LBH-589.html it is known that while only one or two processes of protoplasmic astrocytes have contact with microvessels or pia, the vast majority of

them are peri-synaptic, both in pre- and post-synaptic compartments, and hence in close contact with neuronal communication in the gray matter. Recent reviews report that vascular and synaptic endfeet of astrocytes exhibit segregation of intramembranous proteins, creating autonomous loci which contain different transporters, channels, receptors, or different densities of them (see Wang and Bordey, 2008; Kimelberg, 2010; Kimelberg and Nedergaard, 2010 for review). This type of domain organization of the glia membrane allows differential dynamics in neural signal transduction, blood flow and fluid homeostasis ( Reichenbach et al., 2010). Whether the differential modulation undergone by AQP4 and GFAP throughout the cerebellar parenchyma here seen would be associated with the compartment’s functional specificity in relation to astrocyte:neural interactions and heterogeneity of the types of neurons and astrocytes ( Matyash and Kettenmann, 2010) is unknown.

While consideration should be given to the individual capabilities of diagnostic laboratories, the testing selleck inhibitor of these additional samples may lead to an increase in the number of successful mutation results, enabling a greater number of patients to be accurately diagnosed, and receive the most effective and personalized therapy. This work was supported by AstraZeneca, UK. J.C.-H. Yang has received advisory fees from AstraZeneca, Roche, Genentech, Pfizer, and Clovis, and has been an uncompensated advisor to Boehringer Ingelheim and Eli Lilly. Y.-L. Wu and K. Nakagawa have received speaker fees from

AstraZeneca. G. McWalter and R. McCormack are employees of AstraZeneca and hold shares in AstraZeneca. T.S. Mok has received research funding from AstraZeneca and advisory fees from AstraZeneca, Roche, Eli Lilly, Boehringer Ingelheim, Merck Serono, and Pfizer. M. Fukuoka, N. Saijo, V. Chan, and J. Kurnianda have no conflicts of Dasatinib in vitro interest to disclose. The authors would like to thank the patients and investigators for their participation in the IPASS study. Sample analysis

was performed by Dr Guanshan Zhu, Dr Li Zheng, and Dr Peter Lu at Innovation Center China (China cohort) and Genzyme genetics (non-China samples). Statistical analysis was performed by Dr Rosie Taylor from AstraZeneca, UK. Editing support funded by AstraZeneca was provided by Sarah Lewis, from Complete Medical Communications. “
“Non-small cell lung cancer (NSCLC) is the most common

type of lung cancer, accounting for approximately 80% of lung cancers. NSCLC is attributed in part to somatic mutations of the epidermal growth factor receptor gene (EGFR) [1]. The most common mutations are an in-frame E746-A750 deletion in exon 19 and a single-point substitutional L858R mutation in exon 21, both of which are located in the tyrosine kinase domain of EGFR. These two mutations are observed in approximately 90% of EGFR mutations and are termed “activating mutations” [2]. EGFR-TKIs, such as gefitinib and erlotinib, block autophosphorylation of EGFR with subsequent inhibition of the downstream signaling Cediranib (AZD2171) pathways involving RAS/extracellular signal regulated kinase (ERK)1/2 and phosphoinositide 3-kinase (PI3K)/AKT, and show favorable activity in NSCLC patients with activating mutations of EGFR [3]. However, almost all patients eventually develop acquired resistance to EGFR-TKIs within several years [4]. Two genetic mechanisms of acquired resistance to EGFR-TKIs have been identified in EGFR-mutated NSCLC. A secondary mutation of T790M in exon 20 of EGFR and amplification of the MET oncogene are observed in approximately 50% and 5% of resistant cases, respectively [5], [6], [7] and [8]. Moreover, Yano et al. showed that overexpression of hepatocyte growth factor (HGF), a ligand for MET, induces acquired resistance by activating MET signals [9].

FTIR reflectance methods can be divided into Attenuated Total Reflectance Fourier Transform Infrared Spectroscopy (ATR-FTIR) and Diffuse Reflectance Fourier Transform Infrared Spectroscopy (DRIFTS). ATR collects information from the sample surface while DRIFTS provides information from the entire sample, being a combination of internal and external reflection. Both techniques have been employed for coffee analysis, with most of the ATR-based studies employing liquid samples, i.e., the coffee ABT-199 price beverage itself (aqueous extract) or some organic solvent extract (Briandet, Kemsley, & Wilson, 1996; Gallignani, Torres, Ayala, & Brunetto, 2008; Garrigues,

Bouhsain, Garrigues, & De La Guardia, 2000; Lyman, Benck, Dell, Merle, & Murray-Wijelath, 2003; Singh, Wechter, Hu, & Lafontaine, 1998; Wang, Fu, & Lim, 2011; Wang, Jun, Bittenbender, Gautz, & Li, 2009) whereas DRIFTS measurements employed solid samples, i.e., roasted and ground coffee (Briandet et al., 1996; Kemsley, Ruault, & Wilson, 1995; Ribeiro, Salva, & Ferreira, 2010; Suchánek, Filipová, Volka, Delgadillo, & Davies, 1996). The specific applications were discrimination between Arabica and Robusta varieties (Kemsley et al., selleck chemicals 1995; Suchánek et al., 1996), detection of glucose, starch or chicory as adulterants of freeze-dried instant coffees (Briandet et al.,

1996), determination of caffeine content (Gallignani et al., 2008; Garrigues et al., 2000; Singh et al., 1998), evaluation of roasting conditions (Lyman et al., 2003; Wang et al., 2011), geographical discrimination (Wang et al., 2009;

2011) and separation between decaffeinated and regular roasted coffees (Ribeiro et al., 2010). A few recent studies have compared ATR-FTIR and DRIFTS for analysis of solid samples, aiming at discrimination between high and low quality coffees prior to roasting (Craig, Franca, & Oliveira, 2011; Craig, Franca, & Oliveira, 2012a). In general, DRIFTS provided spectra that presented higher intensity of absorption in comparison to ATR-FTIR. Both techniques were satisfactory for discrimination between immature and mature coffees (Craig et al., 2011). However, even though DRIFTS provided complete discrimination between defective (low quality) and non-defective (high quality) coffees, P-type ATPase ATR-FTIR could not provide complete discrimination between non-defective and sour (fermented) coffees (Craig et al., 2012a). The previously mentioned study showed that DRIFTS presented a more effective performance in comparison to ATR-FTIR in the discrimination between crude coffees of different qualities. Furthermore, DRIFTS was shown to be appropriate for the analysis of roasted coffees, providing satisfactory discrimination between Arabica and Robusta varieties (Kemsley et al., 1995; Suchánek et al., 1996), between regular and decaffeinated coffees (Ribeiro et al.

Furthermore, there is general agreement that inhibitory processes involve frontal regions of the IWR-1 nmr brain, more specifically lateral regions of the right prefrontal cortex [1]. Interest in the neural bases of inhibitory processing is high because these processes have been found to be disrupted in a number of psychiatric disorders, including ADHD [2] and substance abuse disorders [3]. This review focuses on two issues that recently have spurred debate. While there is agreement that right lateral prefrontal regions play a prominent role in inhibitory control, the exact nature

of the specific computation or process that is being implemented by this region, especially that of the right inferior frontal gyrus (rIFG), is being debated (see Figure 1). The second issue Afatinib purchase revolves around the degree to which ‘inhibition’ is a unitary construct, which relies on a central

shared brain mechanism regardless of the domain — motoric, cognitive, or emotional — in which inhibition is exerted, or whether there are separate neural mechanisms for inhibitory control in each of these domains. Typically, inhibitory control is indexed by asking an individual to override, interrupt, or suppress an ongoing cognitive, emotional or behavioral response. Classically this ability has been measured by paradigms that assess inhibition in the motoric domain, such as the Go/No-Go paradigm, which induces a prepotent bias to respond, and which must be overridden when certain specific stimuli are present. Similarly, in the Stop-Signal paradigm, individuals Y-27632 2HCl make a forced-choice decision on the majority of trials, but on a minority a specific sensory signal

(e.g., auditory tone, perceptual cue) indicates that an ongoing process of responding must be aborted or interrupted [4]. Approximately a decade ago, it was proposed that the rIFG (also sometimes referred to as right ventrolateral cortex) plays a prominent role in inhibiting motor responses by sending a signal to the subthalamic nucleus of the basal ganglia, which in turn suppresses thalamocortical output so as to preclude motor responding [5•]. Since that time, compelling work using a variety of converging methods including that performed with patients with focal lesions, alteration of brain activation (rTMS, tDCS), neuroimaging and electrophysiological evidence has supported such a viewpoint [6••]. An expansion of this viewpoint suggests two distinct forms of motor inhibition, one invoked for stopping all responses, and another that is more selective, only stopping certain responses but not others [7]. It has been proposed that the global stopping mechanisms may be mediated by a hyperdirect pathway from the rIFG → STN → Globus Pallidus → Thalamus.

We are currently using P10 and PEPeS to investigate vitrification of the two-cell stage embryos of multiple strains. We are grateful to Dr. Tatsuji Nomura of the Central Institute for Experimental Animals, Public Utility Foundation, for his support in this study. We also thank Dr. Taichi Yamamoto of his critical discussion. “
“Ice expands ∼10% upon freezing when it crystallizes, which can destroy cell membranes by the simple expansion effect, coupled with the Selleck Proteasome inhibitor damaging effect of sharp edges from growing ice crystallites. This can be avoided by supercooling the water, chilling

it to a glassy state that does not go through the expansion process, and/or limiting the size of the ice crystals that do form. During the last 10 years the ABI Corporation (Chiba, Japan) has marketed a “Cells Alive System”, CAS, which claims to have improved the ability of much larger volumes of animal and vegetable matter to be frozen with minimal damage to cellular ultrastructure http://www.selleckchem.com/screening/epigenetics-compound-library.html from ice

crystal growth. The programmable CAS freezers expose samples to low-frequency oscillating electric and magnetic fields while controlling the supercooling of the materials in the critical 0 °C to −20 °C temperature interval by blowing refrigerated air on the samples [18], [34] and [35]. Published analyses suggest this technology can aid in the freezing and shipping of delicate fruits and vegetables, in the enhanced cryopreservation of human transplant tissues like teeth [1] and [28] and embryonic stem cells [29], and even promotes whole-organism survival of frozen small animals like drosophila [33]. Papers and patents published by the ABI group [17], [18], [34] and [35] postulate mechanisms of action that do not agree with basic biophysics. In particular, the oscillating electric and magnetic fields

are supposed to ‘wiggle’ water molecules directly to inhibit the nucleation of ice crystals in the supercooled state, as well as to promote rapid and isothermal cooling of the sample interiors. Wowk [44] pointed out in a recent critique that water molecules are diamagnetic, and will not produce any effect above thermal noise when exposed to the weak oscillating magnetic fields (<10 Gauss or Sirolimus research buy 1 mT) used in the CAS freezers. He also notes that electric fields are known to either inhibit or enhance ice crystal formation slightly, depending upon the conditions used, but not at the levels claimed for these devices. In a direct test of the magnetic aspect of the CAS freezers, Suzuki et al. [38] also report that the oscillating magnetic field treatments alone did not alter the cooling time curves for test samples of radish or sweet potatoes, and had no visible effect on cellular microstructures of the tissues they examined.

3, 95% CI 5.5-83.2, P < 0.001). The non-curative cases consisting mostly of non-surgically managed cases showed favorable long-term outcomes,

suggesting that non-surgical management is an acceptable option. In addition, the recognition of extensive LM positivity as a risk factor for residual/locally recurrent cancer would www.selleckchem.com/products/chir-99021-ct99021-hcl.html be helpful in selecting cases that may necessitate strict management such as immediate additional endoscopic treatment. Table 1. Relationship between various clinicopathological features and residual/recurrent cancer in the 85 lesions: univariate analyses “
“Endoscopic submucosal dissection (ESD) is accepted as a treatment for gastric neoplasms. Several trials have shown the efficacy of gastric acid secretion inhibitors for post-ESD ulcers. However, to date there has been no consensus regarding the optimal drug regimens. Irsogladine has previously been shown to accelerate the healing of

gastric ulcers after Helicobacter pylori (H. pylori) eradication therapy. Hence, we conducted a randomized controlled trial to compare proton pump inhibitor (PPI) and combination PPI plus irsogladine treatments. To assess the efficacy Sotrastaurin manufacturer of PPI and irsogladine combination therapy compared with PPI monotherapy for ESD-induced gastric ulcer healing. Ninety Six ESD-induced gastric ulcer patients

were enrolled in this study. In Group A(n=51), subjects received rabeprazole 10 mg/day and irsogladine 4 mg/day for 8 weeks and in Group B(n=45), subjects received rabeprazole 10 mg/day for 8 weeks. At 1, 4 and 8 weeks after ESD, we performed endoscopic examination to assess each gastric ulcer healing. There was no significant difference between group A and group B in the patient’s background. The ulcer healing rates at 4 weeks after ESD in group A were significantly higher than those in group B in the full analysis set (19.6% vs 5.13%; P < 0.05, chi-square test). The concomitant use of PPI and irsogladine was more effective than the PPI alone for treating Nutlin 3 ulcers within 4 weeks after ESD. Therefore, the combination therapy of PPI and irsogladine was favorable regimen in patients with artificial ulcer after ESD. “
“Subepithelial tumors (SETs) can be challenging to diagnose and treat by endoscopy. Biopsies may not reach the tumor and endoscopic ultrasound (EUS)-guided tissue acquisition can be difficult due to small lesion size and mobility. Resection has been reported, but carries inherent risks of bleeding and perforation. Loop ligation can achieve ischemic tumor ablation, but may not capture broad-based lesions, and does not address tissue acquisition for diagnosis.

The remaining sample size for the analysis was

132,352. Characteristics of the 132,352 patients included in the analysis are enumerated in Table 1. It can be seen that 67% of the patients were women, and the mean (± standard deviation [SD]) age was 52.9 ± 16.7 years. Gross abnormalities such as scalloping and decreased folds accounted for less than 2% of all gross descriptions. Marsh I or II lesions were noted in 5944 individuals (4.5%), whereas Marsh IIIA was found in 819 (0.6%), and Marsh IIIB/C was found in 628 (0.5%). When a pathological diagnosis of CD was defined as blunted or flat villi (Marsh IIIA/B/C), a total of 1447 individuals (1.1%) were categorized as having CD. The most common number of small-bowel check details specimens submitted during upper endoscopy was

2 (histogram; Fig. 1). The mean (± SD) number of specimens submitted was 3.1 ± 1.6, and the median number submitted was 3. Of the 132,352 patients undergoing upper endoscopy with small-bowel biopsy, ≥4 small-bowel specimens were submitted in 45,995 patients RG7204 in vivo (35%). The proportion of patients with ≥4 specimens submitted during endoscopy increased from 33.8% in 2006 to 37.2% in 2009 (P for trend < .0001). Of the 45,995 individuals with ≥4 specimens submitted, Rolziracetam a pathologic diagnosis of CD was present in 824 (1.8%), whereas among the 86,357 patients in whom <4 specimens were submitted, CD was present in 623 (0.7%; P < .0001). When treated as a continuous variable, the number of specimens submitted was directly correlated with the probability of a pathologic diagnosis of CD ( Fig. 2). Biopsy of the duodenal bulb was performed in 10% of patients; inclusion of a bulbar biopsy was not associated with an increased

proportion of adherence to ≥4 small-bowel specimens (P = .4309), nor was it associated with an increased probability of a pathological diagnosis of CD (OR 0.93; 95% confidence interval [CI], 0.78-1.11; P = .4373). Patients with abnormal gross duodenal findings on endoscopy had an increased prevalence of CD (3.2% vs 0.7%; OR 4.64; 95% CI, 3.80-5.67). The relationship between adherence to the standard of ≥4 specimens submitted and a pathologic diagnosis of CD stratified by gross endoscopic findings is presented in Table 2. Gross endoscopic findings modified the association between number of specimens submitted and the prevalence of CD (Breslow-Day test for homogeneity of ORs: P = .0015). This relationship was greater for those with abnormal gross findings (OR 3.67; 95% CI, 2.86-4.72) than for those with normal gross findings (OR 1.91; 95% CI, 1.38-2.63).

Just four days before that, I had received an e-mail from him in which he sounded pretty positive, so the news was a great shock. Looking back, it was about a year ago (July 23rd, 2010) that I

was humbly allowed the opportunity to present an address of congratulations to him, as an old friend. We were gathered to celebrate the Professor, who was basking in the glory of the Order of the Sacred Treasure, 2nd Class. This is the highest honor granted to civilians by the Cabinet Office, Government of Japan. Later, last May, at the 53rd General Assembly of the JSCN in Yokohama, an emergency Forum on “What we learned from this major disaster, and what we can draw on in the future” was held to discuss the role of child neurologists in facing with unprecedented selleck chemical devastating earthquake, tsunami and nuclear power plant explosions in Northwestern Japan last March. The Forum was planned jointly by JSCN and the Japan Foundation of Pediatric Research, the latter of which is a new organization PLX3397 purchase created by Japan Pediatric Society (JPS). As the chairperson, Board of Trustees, JPS, Dr.

Kamoshita had been dedicated himself to establish the Foundation. Thus, he delivered a closing remark at the aforementioned Forum. On both occasions, his complexion and tone of voice were quite normal, so I did not have the slightest anticipation to receive a news of his passing so early. His death is a great loss not only for our JSCN and other many medical societies around Japan, but to the entire nation and society of Japan. The late Professor Kamoshita was born in the Muroran City, Hokkaido, Japan in 1934. He graduated from the Faculty Orotic acid of Medicine, University of Tokyo in 1959, and completed postgraduate study at the same University, majoring in pediatrics. His subsequent career is summarized in Table 1. He was also

active on numerous committees of the governmental, ministerial and public organizations (Table 2). In addition, in the capacity of the chief of the 7th Section (Life Science), Science Council of Japan, he issued a series of recommendations/expert opinions to the public on various contemporary controversial problems in life science and biological ethics, low fertility societies, assisted reproductive treatment, including surrogate motherhood, and so on. As a committee chairperson of the Social Security Council, Ministry of Health, Labour and Welfare, he advocated an introduction of regionally autonomous, patient-oriented healthcare system, proposing a promotion of patient’s solidarity and information dissemination to broaden patient’s choices. Moreover, he played a pivotal role in numerous policies dealing with national and social issues such as medical education, health care systems, life ethics and children’s rights. He authored a number of influential books on fundamental mentality and thoughts, including biographees of modern great Japanese such as Inazo Nitobe [1], Shigeru Nambara [2] and Tadao Yanagihara [3].