Inter-rater agreement for these ratings was high (Cronbach’s alph

Inter-rater agreement for these ratings was high (Cronbach’s alpha for men rating women, men rating men, women rating women, and women rating men were all >0.90). Participants also completed the TDDS (Table 1). Responses on the three TDDS subscales were scored following selleck chemicals llc Tybur et al. (2009). Higher scores represent greater disgust sensitivity. The TDDS and face ratings were completed in a fully randomized order. Male and female faces were presented in separate, randomly ordered

blocks of trials in the face-rating task, and, within each block, trial order was fully randomized. The order of TDDS items was also fully randomized in the questionnaire block. As in previous research (Tybur, Bryan, Lieberman, Caldwell Hooper, & Merriman, 2011), women reported greater sexual (t(61) = 7.10, p < 0.001, d = 0.90) and pathogen (t(61) = 2.20, p = 0.032, d = 0.28) disgust than men. Women and men did not differ significantly in moral disgust (t(61) = −0.23,

p = 0.82, d = 0.03). Partners’ scores for sexual disgust were positively correlated (r = 0.38, N = 62, p = 0.002), but partners’ scores for pathogen (r = −0.01, N = 62, selleck inhibitor p = 0.95) and moral (r < 0.01, N = 62, p > 0.99) disgust were not. For each participant, we first calculated the correlation between (1) their attractiveness rating for each of the 50 men’s faces and those 50 men’s rated facial adiposity (mean r = −0.14, SD = 0.14), (2) their attractiveness rating for each of the 50 men’s faces and those 50 men’s BMI (mean r = −0.09, SD = 0.14), (3) their attractiveness rating for each of the 50 women’s faces and those 50 women’s rated facial adiposity (mean r = −0.19, SD = 0.13), and (4) their

attractiveness rating for each of the 50 women’s faces and those 50 women’s BMI (mean r = −0.24, SD = 0.12). Note that this procedure produces four correlation coefficients for each participant (representing their preferences for perceived adiposity in male faces, cues of BMI in male faces, perceived adiposity in female faces, and cues of BMI in female faces, respectively). These preference scores (i.e., correlation CYTH4 coefficients) served as the dependent variables in subsequent analyses. For each of these preference scores, larger positive values indicate stronger preferences for facial cues of heavier weight and larger negative values indicate stronger preferences for facial cues of lower weight. In order to establish whether preferences for rated adiposity and preferences for cues of BMI measure similar constructs, we analyzed men’s and women’s preference scores for own-sex and opposite-sex faces using factor analysis.

However, further changes were identified by participants that cou

However, further changes were identified by participants that could make it more accommodating for low literacy groups: ‘There were a couple of words in it that I thought might need thinking about…‘discuss’, I wonder whether ‘talk about’ would be more appropriate?’ (AL, 55 years, female, degree level education). Changes were also made to the spacing between and within lines to improve readability. As demonstrated in Table 2, nearly all statements were answered correctly by at least 80% of the participants. However, the statement on the meaning of an abnormal result remained problematic (8. ‘People with an abnormal result

always have cancer’ [F]). At a participant level, a mean of 7.1 out of 8 statements were answered correctly (range = 4–8). Changes to the layout selleck inhibitor of the leaflet were made in response to difficulties with remembering all of the information that they have just read, ‘I think it’s ok, but it’s remembering what you read. If you read something and don’t remember, it doesn’t do you any benefit does it?’ (DW, 52 years, female, no formal qualifications). Changes included placing boxes around text that related to each sub-heading, reducing the number

of bullet points on the final page, changing the colour of the background and increasing the size of the font on the front page to increase the readability of the text for individuals with eyesight difficulties (‘It’s very clear. Maybe I would say, it could be done in more bigger letters, you know if somebody’s old or something’ (SF, 51 years, female, no formal qualifications)). These changes were particularly Antiinfection Compound Library chemical structure apparent on the final page which assisted participants

when searching for the correct answer to the statement that did not meet the threshold. The text relating to this statement was altered: ‘For most people, the Atezolizumab in vivo follow-up test will show there is no bowel cancer’ in an attempt to improve comprehension. Participants reported being confused about the age of eligibility for screening: ‘That’s all clear and it’s explained further, all very simple. But this I couldn’t get [age extension]. That’s like a random statement. It’s not really backed up or [explained] why’ (VY, 45 years, male, advanced high school qualifications). Participants also wanted reassurance that the test was simple, as some felt that it might be complicated and that people may be less likely to participate as a result. This resulted in changes to the text concerning the age that people are invited to screening, as well as an additional sentence highlighting ‘The FOB test is easy to do’. The title of the booklet (‘A two minute guide’) was changed as this may have been perceived as intimidating by less literate and slower readers: ‘This is meant to be a two minute guide. Well people read at their own pace and you know they might think well, oh.

, 2010) Interesting, the results presented here for the MjTX-II

, 2010). Interesting, the results presented here for the MjTX-II can clarify this issue. As discussed in the item 3.2,

the structure of MjTX-II presents PEG4K molecules in its hydrophobic channels at the same regions where fatty acids are found in the MjTX-II/stearic acid structure. Therefore, this finding suggests that the Cys29-Lys122 interaction is not exclusive for Lys49-PLA2s-fatty acid bound structures. Additionally, comparison between BthTX-I/PEG4K (Fernandes et al., 2010) and MjTX-II/PEG4K (this work) structures reveals important features of MjTX-II in comparison to BthTX-I and other bothropic Lys49-PLA2s myotoxins. Despite the high sequential and structural similarity between MjTX-II and BthTX-I

(they share 95% of identity), MAPK inhibitor and the presence of two PEG4K molecules in the hydrophobic channels of both structures, their superposition clearly demonstrates the ligand way of binding at these proteins are somewhat different (Fig. 1C). The reason seems to be the insertion of the residue Asn120 and the Leu32Gly mutation since these characteristics apparently shifts the orientation of PEG molecules inside the hydrophobic channel by modification of the channel ends. Interestingly, Asn120 insertion and Leu32Gly mutation are only found in MjTX-II when comparing this protein to all the other bothropic Lys49-PLA2s whose structures are solved to date (Fig. 4). Therefore, the Asn120 insertion is probably the responsible for the binding of the Afatinib mouse interchain PEG 3 molecule since this insertion leads to a distortion of the protein protomers (Table 3). This evidence is enhanced by the fact that other Lys49-PLA2s toxins that presents 121 amino acids do not bind this interchain PEG4K or PEG3350 (Fernandes et al., 2010) whereas MjTX-II (122 residues) Glutamate dehydrogenase allow a PEG4K interaction at this region. It is important to highlight that bothropic Lys49-PLA2s

that do not have structures solved yet but present mutations and/or insertions at the positions 32 and 120 are known (Fig. 4); however their structural characteristics upon ligand binding will just be evidenced when these structures are elucidated. The C-termini of Lys49-PLA2s toxins has been pointed as containing their myotoxic site (Arni and Ward, 1996, Magro et al., 2003 and Ward et al., 2002). Afterward, dos Santos and colleagues reviewed several native and complexed Lys49-PLA2s and proposed that Arg118, Lys20 and Lys115 residues constitute these toxins myotoxic site (dos Santos et al., 2009). In the same study, the authors propose a two-step mechanism for Lys49-PLA2s which allow the destabilization of biological membranes. The first step of the mechanism would be the interaction of the Lys20, Lys115 and Arg118 of these proteins with the phospholipid head group region (dos Santos et al.

Five hundred msec after the fixation point vanished, a pair of di

Five hundred msec after the fixation point vanished, a pair of digits appeared and remained visible until the participant responded or for 5,000 msec. The next trial began 1,000 msec after the disappearance of the stimulus. Data collection and stimuli presentation

were controlled by a Compaq computer with an Intel Pentium III central processor. Stimuli were presented on a Compaq S510 monitor. Participants sat approximately 60 cm from the computer screen. A QWERTY keyboard was placed on a table between them and the monitor, and they were asked to respond manually by pressing the key attributed to the numerically larger digit. In the horizontal version, the participants were instructed to press a left key (“”F”") if the left digit was larger, and to press a right key (“”J”") if the right digit MEK phosphorylation was larger. In the vertical version, the participants were instructed to press a bottom key (“”B”") if the bottom digit was larger, and to press a top key (“”Y”") if the top digit

was larger. To avoid a possible artifact in the vertical block, all participants were asked to use their right index finger for the top key and the left index finger for the bottom key. Mean RTs of correct responses were calculated for each participant in each condition for the numerical and physical comparisons, separately. These mean values were subjected to 3-way analysis of variance (ANOVA), with physical-numerical congruency (congruent, neutral and incongruent), and number-line compatibility (compatible and incompatible) as within-subject factors and with group (synesthetes and controls) as a between-subject factor. Incorrect, very short (≤150 msec) or very long responses (≥2,000) were excluded from the

RT analysis. Mean RTs and ERs (error rates) in the various conditions are presented in Table 2. The results for the vertical presentation corresponded perfectly with our expectations. A significant main effect was found for dimension congruency [F (1, 15) = 57.5, MSE = 834, p < .0001]. That is, RTs for congruent trials were significantly faster than RTs for the neutral trials, which were significantly faster than RTs for the incongruent trials. Nearly significant effects were found for number-line compatibility [F Alanine-glyoxylate transaminase (1, 15) = 4.3, MSE = 1882, p = .05] as RTs for the compatible condition were faster than RTs for the incompatible condition. No other main effects or interactions were found; meaning the numerical comparison groups did not significantly differ in their patterns of behavior ( Fig. 1A). A significant main effect was found for dimension congruency [F (1, 15) = 19.2, MSE = 866, p < .0001]. The interaction between congruency and number-line compatibility was found significant as well [F (2, 30) = 13.5, MSE = 600, p < .0001]. Importantly, these two variables also interacted with group [F (2, 30) = 4, MSE = 600, p < .05].

The lysate was centrifuged at 12 000 × g for 10 min at 4 °C, afte

The lysate was centrifuged at 12 000 × g for 10 min at 4 °C, after which the supernatant was withdrawn and stored at − 20 °C until use. The methanol extract was evaporated to dryness, and the dried extract dissolved in selleck chemicals llc an aliquot of filtered sea water. Bloom extracts, culture extracts and the medium of batch cultures (extracellular exudates) were diluted with sterilized sea water to give a dilution series of 1, 2, 3, 5, 10, 20, 50 and 100%. Sterilized sea water was used as the control. 500 μl of each

dilution was added to a 5 ml culture tube containing 25 nauplii of 48 h-hatched cysts of A. salina. The tubes were incubated at 20 °C under a continuous light flux of 90 μmol photons m− 2 s− 1. After 48 h, the percentage mortality of nauplii was calculated compared to controls. The LC50 value was determined by probit analysis ( Finney 1963). Haemolytic activity was

tested by erythrocyte lysis assay (ELA) according to Eschbach et al. (2001) and its modification by Ling & Trick (2010). ELA was carried out on bloom samples, on algal cells and on extracellular exudates of exponentially growing cultures (6 days after inoculation) of H. akashiwo. An aliquot with a known number Ibrutinib of Heterosigma cells was centrifuged (6000 × g for 10 min at 4 °C), and the supernatant containing extracellular exudates following filtration through a 0.45 μm pore size GF/C filter was collected. Algal samples were prepared following the protocols of Eschbach et al. (2001), modified Isoconazole by Ling & Trick (2010). The cells of bloom samples (10 ml) and pellets of centrifuged cultures were ruptured in ELA buffer, prepared as

described by Eschbach et al. (2001) (150 mM NaCl, 3.2 mM KCl, 1.25 mM MgSO4, 3.75 mM CaCl2 and 12.2 mM TRIS base; pH adjusted to 7.4 with HCl) by sonication for 60 s at 20 °C in a bath-type sonicator. Complete cell rupture was confirmed by microscopic observation. Ultrasonicated algal samples and supernatants were kept in the freezer until use. The dry methanol extract of H. akashiwo cells prepared for the Artemia salina assay was re-dissolved in ELA buffer before use in ELA. Blood freshly collected from a rabbit was immediately mixed with 0.1 ml 10% sodium citrate to prevent it from coagulating. For the ELA, erythrocytes were harvested from the blood by centrifugation in a 1.5 ml microcentrifuge tube at 1500 × g for 5 min at 4 °C. The pelleted erythrocytes were washed twice with ELA buffer by vortexing and centrifugation at 1500 × g for 5 min at 4 °C. Erythrocyte suspensions were adjusted to the appropriate cell density (5 × 106) in ELA buffer with a haemocytometer. The ELA method was basically that of Eschbach et al. (2001) with modifications by Ling & Trick (2010). Briefly, 0.5 ml of erythrocyte suspension and 0.5 ml of cell extract or extracellular exudates of H. akashiwo were added to 1.

Handa et al , 2010, reported that H pylori infection stimulates

Handa et al., 2010, reported that H. pylori infection stimulates inflammatory cells within the gastric tissue to release ROS ( Handa et al., 2010) which correlates with higher levels of DNA repair in gastric epithelial cells ( Machado et al., 2010). Studies by Allen et al. (2005), showed that H. pylori infection interferes on the activity of human neutrophil NADPH oxidase leading to extracellular release of ROS ( Allen, 2001). Here, we demonstrated that rHPU-activated neutrophils release ROS extracellularly potentially contributing

to damage the gastric tissue. The half-life of human neutrophils is typically of 12 h, as a result of the constitutive expression of pro-apoptosis selleck chemicals llc proteins and almost non-detectable levels of anti-apoptosis proteins (Witko-Sarsat et al., 2011). Neutrophils release proteolytic enzymes and ROS that inflict local tissue damage and are removed from the inflammatory site by induction of apoptosis. Thus fine regulation of pro- and anti-apoptosis proteins that control neutrophil

lifespan is a critical process for the resolution of inflammation. Our data show that rHPU delays neutrophils apoptosis, prolonging their survival and contributing to the underlying local tissue inflammation, as seen in the mouse paw edema assay. Increased lifespan of rHPU-activated neutrophils was accompanied by reduced levels of the pro-apoptotic protein Bad and induction of expression of the anti-apoptotic protein Bcl-XL, a situation that would ultimately lead to a persistent inflammatory status. In agreement with our data, other groups have demonstrated that products from click here of H. pylori exert an important role in maintaining inflammation, by suppressing human neutrophil apoptosis ( Cappon et al., 2010; Kim et al., 2001). Interestingly, other studies demonstrated that H. pylori can induce apoptosis in gastric epithelial cell lines ( Ashktorab et al., 2008), contributing to the worsening of the gastroduodenal illness. Lipoxygenase products contribute to the

anti-apoptotic property as well as to chemotaxis induced by HPU as indicated by the AA861 pretreatment of neutrophils. HPU-treated neutrophils had increased levels of lipoxygenases(s) but no alteration of cyclooxygenase(s) content. Our data show that lipoxygenases play an important role in mediating the cell-activating property of HPU (Table 1). Altogether our data demonstrate that HPU, besides its well known role in allowing bacterial gastric colonization, also displays potent pro-inflammatory activity modulated by lipoxygenase-derived eicosanoids. The increased lifespan of HPU-activated neutrophils and its ability to attract more neutrophils toward the injured tissues, acting together with other bacterial factors, potentially amplify the gastric inflammatory process. These findings could be particularly relevant to the mechanisms leading to gastrointestinal disease caused by H.

Kunkel Calvin Kuo Tomoyuki Kuwaki James Lane Lena Lavie David J

Kunkel Calvin Kuo Tomoyuki Kuwaki James Lane Lena Lavie David J. Leehey Merry Lindsey Stephen Littleton Sumei Liu Zhiping selleck chemicals llc Liu Dakai Liu Sumei Liu Xiaowen Liu Gang Liu Joseph Loftus Dwight Look David Lynch Adriano Marchese Nathanial Marchetti Ali Marian Cary N. Mariash Koji Matsuo Michael Matthay Pascale

Mazzola-Pomietto Edwin McCleskey Herbert J. Meiselman Robert Mentzer Robert Mentzer Joe Miano John Millar York Miller Amparo Mir Harald Mischak Toshihiro Mitaka Monty Montano Nils Morganthaler Patrick Mueller Alvin Mushlin Lakshmi Nair Bahram Namjou Patrick Nana-Sinkam Marek Napierala Mark Noble Simon Noble Imre Noth Irene Oglesby Yukio Ozaki Dipak Patel Subramaniam Pennathur Dudley Pennell Keith Pennypacker Stefano Piccolo Steven Pipe David Rabago Daniel J. Rader Mahboob Rahman Nithya Ramnath Leon Raskin Laura Rasmussen-Torvik Fabio Recchia Raju Reddy Eugene Redmond Alan Remaley Giuseppe Remuzzi Bruce Richardson Troels Ring Frank Robb Michael Robbins Robert Roberts Andrea Romani Sharon Rosenberg Guy Rutter Amin Sabet Paul W. Sanders

Jeff Scherrer Anne Schott Pamela Schreiner Johannes Schwarz Jonathan Shaffer James Sham Jordan Shavit Yan-Ting Shiu Lalit P. Singh Mary Siotto Melissa Snyder Shinichi Someya Robert Soufer Thomas Stamos Clifford ERK inhibitor Steer Steve Steiner David Stowe Arthur Strauch Howard Strickler Yousin Suh Liou Sun Olga Syrkina Stefano Taddei Ira Tager Ali Taher Andrew Talal Toshiko Gemcitabine mw Tanaka Bor Luen Tang

Chris Tikellis James Timmons Gail Tominaga Jorn Tongers Ignacio Torres-Aleman Antonella Tosti Mats Ulfendahl Luca Valenti Ramakrishna Vankayalapati David Varon Richard Verrier Germaine Verwoert John M. Vierling Anitha Vijayan Jil Waalen Jin Wang Jin Wang Douglas Wangensteen Joel M. Weinberg Stephen J. Weiss Babette B. Weksler Christof Westenfelder Christof Westenfelder Adam Whaley-Connell Robert White Benjamin Wilfond Lance Wilson Xifeng Wu Michael Mingzhao Xing Michiro Yamamoto Nina Yang Xiao-Ru Yang Fujiyama Yoshihide Young You Xin Yu Peter Zage Robert Zee Jing Zheng “
“Lactic acid bacteria are a major part of the commensal microbial flora of the human gastrointestinal tract and are frequently used as probiotics for fermentation of food products (Fooks et al., 1999). Dietary supplementation with such beneficial (live) bacteria promotes health and reduces the risk of various diseases (Ahrne et al., 1998). In addition to demonstrating the efficacy of probiotics in improving human health, safety characteristics must be taken into consideration. It has been reported that lactic acid bacteria-cultured skim milk has antimutagenic activity (Hosono et al., 1986), that a multispecies probiotic mixture does not have mutagenic effects on various organisms (Chiu et al., 2013), and that LP20 powder made from heat-killed Lactobacillus plantarum L-137 has no genotoxic properties both in vitro and in vivo ( Hirose et al., 2009).

1 All experiments followed the ethical standards for animal expe

1. All experiments followed the ethical standards for animal experiments in toxinological research recommended by the International Society of Toxinology and was approved by the Committee for Ethics in Animal Utilization of Ribeirão Preto – Universidade de São Paulo (N° 08.04.2008). Although the primary structure of Ts15 shares homology with other toxins specific for potassium channels, its effect was tested on a wide variety of potassium and sodium channels using patch clamp and two-microelectrode voltage clamp techniques. The results on sodium currents showed that Ts15 has no affinity for these channels (data not shown, including the DRG experiments). The results on potassium

currents showed a significant effect on Kv1.2, Kv1.3, Shaker IR, KV1.6 isoforms with 73%, 50%, 30% and 22% of block, respectively, after Ts15 addition (0.5 μM). The toxin failed Ipilimumab clinical trial to inhibit Kv1.1, Kv1.4, Kv1.5, Kv2.1, Kv3.1, Kv4.2, Kv4.3 and hERG, when tested in the same concentration ( Fig. 3 and Fig. 4). The IC50 values were 196 ± 26 nM

for Kv1.2 (Fig. 5A) and 508 ± 66 nM for Kv1.3 (Fig. 5B). The current/voltage (I/V) curves (Fig. 5C) showed that the inhibition of Kv1.2 channels observed in the presence of Ts15 is not associated with a change in the shape of the I/V relationship. The V1/2 of activation was not significantly shifted for Kv1.2. Intriguingly, for Kv1.3 the V1/2 of activation was significantly shifted (p < 0.05) as observed in Fig. 5D. Fig. 5E and F show the voltage-dependence between Ts15 and Kv1.2 and Kv1.3 channels, respectively. As illustrated, the Ts15 induced blocking effect is not voltage-dependent in the tested range. The blocking effect observed on both isoforms was completely recovered by perfusing the oocytes with free toxin bath solution ( Fig. 5G and H). Comparing the interaction/reversibility graphs of Kv1.2 and Kv1.3 ( Fig. 5G and H) it can be observed that for Kv1.2 the association step N-acetylglucosamine-1-phosphate transferase Ts15/Channel

is slow (400 s) but that the dissociation is fast. For Kv1.3 the association Ts15/channel is faster (150 s) with a slower dissociation. These results indicate that the interaction of Ts15 with Kv1.3 is stronger than its interaction with Kv1.2. Most known scorpion toxins active on potassium channels adopt a similar 3-D structure formed by an α-helix and two β-strands linked by three disulfide bridges. An important structural feature of high affinity KV channel blocking scorpion toxins is the functional dyad, which has a strategically positioned lysine and an aromatic residue separated by 6.6 Å (Dauplais et al., 1997). Although the importance of this pharmacophore is generally acknowledged, toxins lacking the functional dyad with significant effect on potassium channels have been described, illustrating the existence of other important regions of the toxin that mediate their interaction with Kv channels (Batista et al., 2002). Papp et al.

The findings of this study support the use of TVR twice daily reg

The findings of this study support the use of TVR twice daily regardless of fibrosis stage or IL28B genotype, thus offering the potential of simplified TVR dosing to G1 HCV-infected patients, including those with advanced fibrosis or cirrhosis. The authors thank the patients and investigators who participated in the phase 3 study for their participation and support; the members of the Janssen telaprevir team (in particular, J. Mrus, E. O’Neil, I. Dierynck, A. Ghys, and Y. Wyckmans) for their input; and the members of the data and safety monitoring board: chairperson

Francesco Negro, MD; Dominique Larrey, MD; Tim Friede, PhD; and Christian Funck-Brentano, MD, PhD. Writing Idelalisib assistance was provided by Sally Gray (Gardiner-Caldwell Communications, Macclesfield, England) and funded by Janssen Pharmaceuticals. “
“The mammalian gastrointestinal tract harbors a dense and diverse community of an estimated 10−100 trillion micro-organisms1, 2 and 3 consisting of 500−1000 different

species, of which the vast majority are bacteria.2 and 4 It is well accepted that in inflammatory bowel disease (IBD), the mucosal immune system reacts inappropriately toward the commensal microbiota.5 No particular microbial species has been consistently linked to IBD pathogenesis or prevention; however, some symbiotic bacterial species have been shown HSP targets to prevent inflammatory host responses.2, 6, 7, 8 and 9

Numerous animal models have been generated to experimentally investigate human IBD,10 including erosive models of acute colitis (eg, dextran sodium sulfate [DSS]-induced colitis), spontaneous models of chronic colonic, and/or small bowel inflammation induced by targeted gene deletion (eg, interleukin [IL]10−/− mice) or induction by disruption of T-cell homeostasis (eg, Rag1−/− mice). 10 As chronic colitis results from a dysregulated immune response to components of the normal intestinal Gefitinib manufacturer microbiota, it is reasonable to suggest that the T-cell−dependent models are significantly more relevant to human disease than are the erosive models of acute colitis, if one wishes to investigate the immunologic mechanisms inducing, perpetuating, or preventing chronic colitis. 10 Microbe-associated molecular pattern, such as lipopolysaccharide (LPS) or flagellins, are recognized by different pattern recognition receptors. However, there is a dichotomic role for Toll-like receptor (TLR) in intestinal inflammation. 11 For example, IL2−/−MyD88−/− mice develop colitis independent of TLR signaling, and IL10−/−MyD88−/− mice remain healthy, indicating an inflammation promoting effect of MyD88-dependent TLR.

Za pracę naukową i organizacyjną został wyróżniony odznaczeniem z

Za pracę naukową i organizacyjną został wyróżniony odznaczeniem za wzorową pracę w służbie zdrowia (1984), medalem za zasługi dla neurologii dziecięcej (1996), certyfikatem Nowojorskiej Akademii Nauk (1995) i certyfikatem Polskiego Towarzystwa Epileptologicznego (1997), a w roku 2014 medalem Profesora Władysława Szenajcha z okazji 100-lecia założenia Szpitala im. Karola i Marii w Warszawie. Sirolimus mw Był wieloletnim członkiem komitetów naukowych czasopism medycznych: „Pediatrii

Polskiej” oraz „Neurologii Wieku Dziecięcego”. Miałem zaszczyt znać prof. Romana Michałowicza od ponad 50 lat, tj. od roku 1963, kiedy to odbywałem staż podyplomowy w Klinice Terapii Chorób Dzieci AM w Warszawie. Jemu zawdzięczam rozbudzenie zainteresowania pracą naukową i dydaktyczną. Pod jego kierunkiem i we współpracy z nim powstały moje pierwsze publikacje dotyczące zmian neurologicznych w przebiegu biegunek toksycznych u niemowląt oraz powikłań neurologicznych

u dzieci z chorobą Schoenleina i Henocha. Do końca jego życia utrzymywaliśmy przyjazny kontakt. Z zainteresowaniem śledził moją drogę zawodową i cieszyły go moje kolejno zdobywane stopnie i tytuły naukowe. Był miłośnikiem podróży, antycznych mebli i starego malarstwa oraz muzyki operowej i literatury pięknej. Prof. Roman Michałowicz zmarł 26 kwietnie 2014 r. na 4 tygodnie przed ukończeniem 88 roku życia, po krótkiej find more i do końca nierozpoznanej chorobie. Został pochowany w grobie rodzinnym na Starych Powązkach Warszawie. W uroczystościach pogrzebowych wzięło udział liczne grono jego przyjaciół oraz współpracowników z IP Centrum Zdrowia Dziecka. “
“Co może łączyć medycynę sądową z pediatrią? Z pewnością nagła, nieoczekiwana śmierć dziecka i konieczne badania pośmiertne. Czy poza tanatologią coś więcej? Profesor Edmund Chróścielewski (Ryc. 1), wieloletni kierownik Katedry i Zakładu Medycyny Sądowej AM w Poznaniu (1952–1985), którego setna rocznica urodzin przypada na 2014 rok, był przykładem, że rozległa problematyka

dzieci i młodzieży może heptaminol obejmować także ten pozornie odległy obszar zainteresowań medyka sądowego. Ta strona działalności profesjonalnej Profesora nie jest znana większości pediatrów, nawet środowiska poznańskiego. 100-lecie urodzin to znakomita okazja, aby przybliżyć tę istotną część badań i opracowań sądowo-lekarskich Profesora. Również problematyka okupacyjna i wojenna dzieci i młodzieży polskiej zawsze była mu bliska. Będąc więźniem obozu koncentracyjnego w Oświęcimiu i uczestnikiem czynnej walki z okupantem, miał też osobiste bolesne doświadczenia. Jako specjalista medycyny sądowej i patomorfologii wiele swych prac z początku lat pięćdziesiątych ubiegłego wieku poświęcił zagadnieniom pośmiertnych badań dzieci z wrodzonymi wadami rozwojowymi. były to przepukliny przeponowe, niedrożność przełyku, wady serca.