In some

situations, especially in patients with liver cirrhosis and portal hypertension, a diffuse pattern and involvement of gastric mucosa are seen with both GAVE and severe PHG. The diagnosis in such cases is hard to determine on visual inspection, and thus, biopsy and histologic evaluation can be used to help differentiate GAVE from PHG. Index 849 “
“Gary W. Falk Edward V. Loftus Jr Maneesh Dave, Konstantinos A. Papadakis, and William A. Faubion Jr Inflammatory bowel disease (IBD) is an immune-mediated selleckchem disease and involves a complex interplay of host genetics and environmental influences. Recent advances in the field, including data from genome-wide association studies and microbiome analysis, have started

to unravel the complex interaction between host genetics and environmental influences in the pathogenesis of IBD. A drawback of current clinical trials is inadequate or lack of immune phenotyping of patients. However, recent advances in high-throughput technologies provide an opportunity to monitor the dynamic and complex immune system, which may to lead to a more personalized treatment approach in IBD. Jennifer Jones and Juan Nicolás Peña-Sánchez The therapeutic approach in inflammatory bowel disease has evolved to target end-organ inflammation MLN0128 solubility dmso to heal intestinal mucosa and avoid structural damage. Objective therapeutic monitoring is required to achieve this goal. Earlier intervention with biologic therapy has been shown, indirectly, to be associated with higher clinical response and remission rates. A personalized approach to risk stratification with consideration of key clinical factors and inflammatory biomarker concentrations is recommended when deciding whether or not to start a patient on biologic therapy. Parambir S. Dulai, Corey

A. Siegel, and Laurent Peyrin-Biroulet Inflammatory bowel disease (IBD) treatment has progressed significantly over the past decade with the advent of biologics. Anti-tumor necrosis factor (anti-TNF) agents are the most widely available biologics, Demeclocycline but the optimal approach when using them remains unclear. In this review, we highlight the currently available evidence regarding the use of anti-TNF monotherapy versus combination therapy with an immunomodulator. We focus on those patients at greatest risk for adverse events and outline the clinical approach when considering the use of combination therapy. We review the available tools through which providers may efficiently communicate these data to patients in the clinical setting. Siddharth Singh and Darrell S. Pardi Anti-tumor necrosis factor-α (TNF) agents, including infliximab, adalimumab, and certolizumab pegol, are effective medications for the management of moderate to severe Crohn disease (CD).

No entanto, apenas a PSOF e a SF foram avaliados em estudos controlados e randomizados. Estes estudos, porque constituem os de maior grau de evidência estatística são obrigatórios para demonstrar a eficácia de qualquer estratégia. Na verdade, os estudos com PSOF anual ou de dois em dois anos demonstraram redução da mortalidade (15-33%)4, 5, 6 and 7 e os estudos com uma única SF demonstraram redução da mortalidade (44-70%)8, 9 and 10 e da incidência (55%)8. Portanto, o CCR MK-8776 in vitro cumpre todas as regras indispensáveis que permitem definir um programa de rastreio

eficaz: Mortalidade elevada, tratamento curativo, história natural longa e conhecida e testes eficazes. Mas existe uma outra variável que é essencial para definir a eficácia duma estratégia de rastreio, a adesão. Tem sido conceptualmente aceite que a adesão tem de ser superior a 50%, para que a estratégia utilizada seja eficaz. Numa meta-análise muito antiga que selleck chemicals inclui

130 artigos, os autores constataram que a adesão era muito baixa para a PSOF (40% a 50%) e muito variada para a Sigmoidoscopia (2% a 69%)11. Mas se é possível calcular a adesão em programas de rastreio com uma base populacional bem definida, a nível nacional é uma variável impossível de definir. Habitualmente, utiliza-se a taxa de utilização. Um estudo europeu publicado em 2010 avaliou a utilização de endoscopia digestiva baixa e PSOF em 11 países europeus12. Os autores constataram uma taxa de utilização next muito baixa e muito variada, não só para a endoscopia

(6,1-25,1%), mas também para a PSOF (4,1-61,1%). Os autores verificaram que o país, idade, educação, rendimento, estado civil, residência principal, hábitos tabágicos e perceção do seu estado de saúde constituíram fatores preditivos com significado estatístico em relação à utilização dos testes. No estudo publicado neste número do Jornal Português de Gastrenterologia13, os autores pretendem identificar fatores que possam contribuir para a baixa taxa de utilização ao rastreio do CCR, numa população residente em 15 freguesias da cidade do Porto. Estudaram fatores como as características sociodemográficas, conhecimentos acerca do CCR, atitudes relativas ao CCR, comportamentos acerca dos cuidados de saúde e tipo de informação sobre o CCR. Concluíram que apesar da população estudada evidenciar falta de conhecimentos em relação à importância do rastreio e portanto, com uma prática de rastreio reduzida, mostrou-se recetiva ao mesmo. Terminam chamando a atenção para a importância da prevenção secundária através do acesso gratuito ao rastreio. São muitas as barreiras que o rastreio do CCR tem de ultrapassar. Estas barreiras estão relacionadas não apenas com os cidadãos, mas também com os médicos, as instituições que legalizam, patrocinam e onde o rastreio é realizado e obviamente os testes.

Based on these data, −11.5 and −12.5 °C were designated as the DTemps for juvenile and

mature larvae, respectively. Survival of larvae exposed to the DTemp for 8 h increased following prior acclimation to −5 °C for 1 h, and gradual cooling (+4 °C to the ABT-263 in vitro DTemp at 0.2 °C min−1), but not after acclimation for 1 h at 0 °C (Fig. 3). The highest survival was seen after gradual cooling for both juvenile (74%) and mature (83%) larvae. This was significantly different from their survival after direct transfer to the DTemp (F1,4 = 26.156, P < 0.05; F1,4 = 48.400, P < 0.05, respectively). Under all treatments, the strength of the RCH response was not significantly different between juvenile and mature larvae (P > 0.05 Tukey’s multiple range test). RCH lowered the lower lethal temperature (LLT) by 2.5 and 6.5 °C in mature and juvenile larvae, respectively (Fig. 4). Survival Obeticholic Acid ic50 ⩾80% at the DTemp (−12.5 °C) was also extended by at least 14 h in mature larvae following RCH and some individuals even survived 48 h under the same treatment (Fig. 5). Mature larvae acclimated to a model Signy Island thermoperiod (+6 to −1 °C over a 24 h cycle) exhibited increased survival of the DTemp for 8 h (Fig. 6). However, this was not significant (P > 0.05 Tukey’s multiple

range test). Survival was also not significantly different within or between −1 and +6 °C conditioned groups across all 3 days tested (P > 0.05 Tukey’s multiple range test). In contrast, mature larvae acclimated to a model Anchorage Island thermoperiod (+4 to −3 °C over a 24 h cycle) showed significantly higher survival of the DTemp for 8 h following removal at −3 °C after 2 d (F1,4 = 8.915, P < 0.05) and 3 d

(F1,4 = 9.291, P < 0.05) ( Fig. 7). There was a significant decline in cold tolerance during the warming phase at +4 °C on day 2, but cold tolerance was regained during the subsequent cooling phase on day 3 ( Fig 7) The tolerance accrued over 3 d was maintained during the day 3 warming phase, with significantly higher survival exhibited at the DTemp when larvae were Progesterone removed at 4 °C on day 3 (F1,4 = 11.560, P < 0.05). The mean SCP of mature larvae following RCH (0.2 °C min−1) was −5.54 °C. While slightly lower, this was not significantly different to the mean SCP of larvae cooled at 1 °C min−1 (−5.07 °C) and larvae directly transferred to the DTemp (−5.73 °C) (table 1, P > 0.05 Tukey’s multiple range test). Juvenile larvae cooled at 0.2 °C min−1 (SCP: −7.29 °C) also showed no significant difference in their SCP when compared with those directly transferred to the DTemp (SCP: −5.86 °C) ( Table 1, P > 0.05 Tukey’s multiple range test). The difference in survival between mature larvae that were held frozen at −7 °C for 4 min (20% survival) or frozen for 1 h 4 min (13% survival) was not statistically significant (F1,4 = 0.308, P > 0.05), indicating that RCH was not induced after the organisms froze.

, 19., 20., 21., 22., 23., 24., 25., 26., 27., 28., 29., 30., 31., 32. and 33.. The role of nutrition in the etiology of non-syndromic orofacial clefts has been appreciated since the beginning of 20th century, when JQ1 in vivo Strauss

suggested a possible link between diet without fresh meat for jaguars, and delivering cubs with a cleft palate [34]. We are living in a society that is over-fed and undernourished, with deficiencies apparent from a so-called “well-balanced” diet. This topic is the subject of an excellent recent review by Glenville [35]. Vitamin E deficiency-associated teratogenicity has been suggested by Cheng and Thomas in 1952 [36]. A significant reduction of the incidence of maternal diabetes-related fetal malformations including orofacial clefts

has been reported in rodents supplemented with vitamin E [37]. In a study aimed to evaluate the association between vitamin E and clefting, the ratio of α-tocopherol to total serum cholesterol were analyzed in 26 mothers of children with isolated find more cleft lip and 36 control mothers [20]. The ratio, as well as α-tocopherol level in erythrocytes, was significantly lower in Polish mothers of cleft-affected children. Interestingly further studies on vitamin E in mothers of children with CL/P showed: 1) The distribution of results to the clusters was significantly dependent on type of the cleft: isolated cleft lip or cleft lip with cleft palate (p=0.03), which may suggest etiological distinction between them [38]; 2) The multiple linear regression model with body mass index (BMI), BMI2, age, concentration of plasma retinol, and fish consumption as independent variabs predicted a 40% of variance in Phosphatidylinositol diacylglycerol-lyase the plasma α-tocopherol concentration [39]. These findings indicating a variance of α-tocopherol concentration should be considered in future studies. It has not yet been proven whether the teratogenic effects of an α-tocopherol deficiency are due directly to a deficiency of the vitamin, or whether they indirectly occur through modulators associated with α-tocopherol homeostasis. Moreover, future studies are recommended to test whether isolated cleft lip and cleft lip and palate have distinct

etiologies, which has also been suggested by other investigators [40]. Maternal intake of vitamin A from supplements >10,000 IU has been shown to cause CL/P in addition to other malformations [15, 41]. Vitamin A intoxication results in a multitude of alternations in mammalian embryos and several genes involved in palate development (i.e. muscle segment homeobox homolog 1, MSX1 and transforming growth factor β3, TGFβ3) interact or can be modified in expression by vitamin A and its analogs [41]. It is noteworthy that among unsupplemented Polish women high plasma retinol levels, exceeding the upper laboratory norm, were detected in mothers of children with orofacial cleft at two times that of control mothers, 11.5% (11/96) vs. 5.8% (3/52), respectively [19].

The compound has been indeed detected in the plasma of healthy young adults using body-lotion cosmetics

in concentrations up to 4.1 μg/L ( Hutter et al., 2005). However, even at such a concentration, galaxolide should not substantially interfere with the endogenous ligand progesterone (Kexp = 3.7 nM, Kcalc = 22 nM). False-positive predictions may, thus, occur in all cases where the kinetic stability of a protein–ligand complex is lower than the thermodynamic selleck chemical and—probably more relevant—when the ADME predisposition is unfavorable. We therefore plan to augment our technology with a series of corresponding pre-filters in the near future. False-negative predictions may occur for at least three reasons. Firstly (and most frequently), learn more when the adverse effect of a compound is triggered mechanisms other than those currently tested in the VirtualToxLab. Examples include Ochratoxin A (OcA), a

well known mycotoxin which does not significantly bind to any of our target proteins and is associated with a toxic potential of 0.519 suggesting only a moderate toxicity. While the toxic mechanism of OcA has not yet been fully disclosed (see, for example, Sorrenti et al., 2013), a critical step of the toxic pathway is the long residence time of OcA at the plasma protein serum albumin. Secondly, a toxic response may be triggered by a metabolite rather than by the parent compound. While our technology does not automatically generate feasible metabolites (several pieces of third-party software have been developed for this very purpose), at least primary metabolites should always be tested along with a parent compound.

In an earlier study, we have analyzed the activity of cyclo-diBA (a condensation product of glycidyl ether and bisphenol A) metabolites—a compound that is unintentionally Ureohydrolase formed as by-product during the coating of food cans and, due to its lipophilic character, migrates from the epoxy resin of the coating into the fatty tissues e.g., of canned fish ( Biedermann et al., 2013). Another example includes the metabolites of the mycotoxin zearalenone, which are known to display estrogenic activity (see, for example, Takemura et al., 2007 and Metzler et al., 2010). While the VirtualToxLab suggests a toxic potential of 0.409 for the parent compound, one of its metabolites, β-zearalanol, is estimated at 0.504. Fig. 13 compares the identified binding modes for the parent compound zearalenone and its metabolite β-zearalanol. Another reason for a false-negative prediction may lie in the fact that our sampling of the ligand at the protein’s binding site while extensive (cf. above) is not exhaustive. Thus, the correct binding mode may simply not been have generated within the 6000–12,000 trials. Finally, molecules that trigger a substantial induced fit (i.e., including changes in the protein’s main-chain conformation) are currently beyond our computational time scale.

parahaemolyticus strains containing

tdh1 and tdh2 genes is mainly caused by TDH2. The dominant expression of tdh2 is due to differences in the promoter regions between the two gene variants ( Okuda and Nishibuchi, 1998). To study cell-free expression of TDH2 separately, we therefore cloned the tdh2 gene in an E. coli vector and used the resulting recombinant plasmid pJET2-tdh2 as a template for the first step E-PCR1 amplification of the coding sequence of preTDH and mTDH. As expected the cell-free synthesis yielded only one protein band for the mature toxin Entinostat cost (and the preprotein). This was demonstrated by incorporation of 14C labeled leucine ( Fig. 8). The toxin synthesis rate in these experiments was within the same range as the synthesis rate with the chromosomal template. TCA precipitation yielded toxin synthesis rates for the CRM containing mature TDH2-His of approx. 300 μg/ml and in the supernatant a concentration of approx. 150 μg/ml could

be detected. Functionality was demonstrated by hemolysis on rabbit erythrocytes in hemolysis assays (see Supplementary Fig. S4). In this study, we describe the successful cell-free expression of functional thermostable direct hemolysin which is a major virulence factor of V. parahaemolyticus. Since the mid of the 1990s the pandemic O3:K6 clone of this pathogen has caused seafoodborne gastrointestinal see more diseases in Asia and America, but is also now spreading to European coasts and was detected in mussels in UK, Italy, France and Spain. For identification of pathogenic V. parahaemolyticus strains assays for toxin detection are of interest for food laboratories. The detection of the toxin requires easy systems to produce the toxin for application as reference materials or for use as antigen for the generation of antibodies. For functional studies or crystallographic investigations of the mature TDH variants it would be preferable to express the protein individually instead of

a combined aminophylline expression. In this study we showed that TDH can be synthesized in significant amounts in the prokaryotic E. coli system. The synthesis rate is nearly 100fold above the production achieved under optimized conditions with V. parahaemolyticus ( Nishibuchi et al., 1991). The synthesis can be easily performed by using chromosomal DNA or by using plasmids as a template for the two step E-PCR ( Merk et al., 2003). Additionally, no cloning steps are necessary for the expression of toxins and therefore the whole expression procedure is devoid of the generation of genetically modified organisms. In our study, the parallel synthesis of two closely related toxin variants (TDH1 and TDH2) was achieved from one genomic DNA template, which is advantageous for the fast and efficient generation of antibodies. In conclusion, cell-free expression offers a time saving and cost effective technology for the production of biologically active toxins. We thank Prof. Dr. R. T.

Folate supplementation has been reported to reduce serum Hsp70 levels in patients with type 2 diabetes (Hunter-Lavin et al., 2004b). In addition, supplementation with folic acid has been reported to increase the plasma total glutathione levels (Arnadottir et al., 2000), indicating that folate, like vitamin D and vitamin B12 can influence the production AT13387 mw of Hsp70 by augmenting the level of glutathione. Because a low vitamin D status will decrease resorption of calcium, and may induce PTH secretion, we also investigated the serum levels of calcium and PTH in relation to Hsp70 serum levels. An up-regulation of intracellular Hsp70 gene transcription caused by PTH via

endogenous PTH receptor was previously shown in LLC-PK1 renal epithelial cells and in osteoblastic cell lines (Fukayama et al., 1996). Whether this intracellular increase in Hsp70 transcripts can reflect the protein level and, moreover, the extracellular protein level, as measured in serum, is not known. In the present study, we found a negative correlation between the serum levels of Hsp70 and the levels of PTH. It is well known that PTH acts to increase the concentration of calcium in the blood. this website Further, an increased intracellular calcium level caused by thapsigargin

was shown to decrease the protein levels of Hsp70, in a chondrocytic cell line (Elo et al., 2000), even though, other authors reported the reverse to be true (Cheng and Benton, 1994). Thus it is possible that recruitment of calcium by PTH might have a modulating effect on the production of Hsp70. Because Hsp70 expressed by invading parasites are potent antigens that can elicit an immune response including the heat shock response (Polla, 1991, Kaufmann, 1992 and Maresca and Kobayashi, 1994), and because elevated levels of the Hsp70 family Fossariinae have been reported in some disease conditions such as parasitosis and autoimmune diseases (Minota et al., 1988), we investigated the relationship between

the serum concentration of Hsp 70 and the titer of anti-malarial antibodies. There was no particular link between the serum concentration of Hsp70 and the presence of anti-malarial antibodies. Noteworthy, the area where the study was performed was endemic for malaria and all the participants had very high titers of the anti-malarial antibodies, obscuring any possible relationship between the Hsp 70 serum level and exposure to malaria. A similar situation existed for infestation with filaria. Examination of blood smears or skin snips showed that at least half of the women and a third of the men had filariasis. This very high prevalence might have obscured the relationship between the serum concentration of Hsp70 and the presence of filariasis. Although no definite reference values for Hsp70 serum concentrations can be put forward, we found clearly higher values in the present study than observed in a study of Belgian geriatric patients (an average value of 5.5 ± 4.

A link between reduced protein thiol levels and cytotoxicity has been demonstrated in a study conducted with the chemical menadione (Di Monte et al., 1984). In our laboratory, studies with isolated mitochondria showed that DHM, but not MCT, has the ability to oxidize protein thiol groups (Santos et al., 2009). Therefore, to investigate whether this would also happen in hepatocytes, we incubated the isolated hepatocytes with MCT and observed a significant oxidation of –SH groups of proteins at 90 min of incubation. However, when DTT was added, the oxidation of these groups was prevented. Thiol groups, in addition to participating in the Venetoclax supplier antioxidant defense system previously mentioned,

regulate various aspects of cellular Linsitinib supplier function. Among these is the induction of cell death by apoptosis, an activity regulated by the redox state of the thiol groups (Sato et al., 1995). One of the pathways that mediate apoptosis is the mitochondrial pathway (Green and Reed, 1998 and Lemasters et al., 1999), which involves the MPT, a calcium-dependent inner mitochondrial membrane permeabilization. This permeability of the inner membrane is associated with the opening of a pore called the permeability transition

pore. The opening of the pore results in the potential loss of the mitochondrial membrane, swelling of the mitochondria and rupture of the mitochondrial outer membrane (Zoratti and Szabò, 1995 and Halestrap et al., 2002), and it is sufficient to promote the release

of cytochrome c (a component of the electron transport chain that allows the transfer of electrons between complex III and IV) into the cytoplasm of the cell (Kroemer, 1997). Cytochrome c in turn interacts with apoptotic protease activating factors (Apaf), triggering the cascade of activation of pro-caspases by proteolytic cleavage and causing death by apoptosis. By assessing the effects of MCT on the induction of apoptosis with the dye Hoechst 33342 in parallel with monitoring the decrease in cell viability by changes in the pattern of release of the enzyme ALT, we found that MCT is C59 mw able to induce programmed cell death. A possible cause for this observed effect can be found in our previous work with isolated mitochondria (Mingatto et al., 2007). We demonstrated that DHM inhibits NADH-dehydrogenase, causing a significant reduction in the synthesis of ATP, which is a critical event for the development of cell damage by necrosis or apoptosis (Nicotera et al., 1998). In addition, DHM causes the oxidation of thiol groups of proteins from mitochondria, resulting in the release of cytochrome c (Santos et al., 2009), which initiates the cascade of induction of programmed cell death. Accordingly, Copple et al. (2004) showed that MCT kills cultured hepatic parenchymal cells by apoptosis, with activation of caspase 3.

It is concluded that in children with prolonged immobilization kidney stone formation may occur with possible significant consequences that should be considered in differential diagnosis. In patients with neurological disease with narrowed logical contact the special attention should be paid for accompanying sparse symptoms. MS – essential contribution to the concepts and design work, data collection and interpretation, critical reviewing work for important intellectual content, final acceptance for publication. AZ-B, JM-P – data collection and interpretation. PA, EK – essential

contribution to the concepts and design work, critical reviewing SRT1720 chemical structure work for important intellectual content. ET-D, ZG – literature search. AP – essential contribution to the concepts and design work. KZ – critical reviewing work for important intellectual content krytyczne zrecenzowanie pod katem istotnej zawartosci intelektualnej akceptacja ostatecznej wersji do opublikowania, final acceptance for publication. None declared. None declared. The work described in this article has been carried out in accordance with The Code of Ethics of the World Medical Association (Declaration of Helsinki) for experiments involving humans; EU Directive 2010/63/EU for animal experiments; Uniform Requirements for manuscripts submitted

to Biomedical journals. “
“Figure options Download full-size image Download this website as PowerPoint slide W dniu 26 kwietnia 2014 r. zmarł w Warszawie nestor polskiej neurologii dziecięcej prof. dr hab. n. med. Roman Michałowicz, wieloletni członek Komitetu Naukowego Pediatrii Polskiej. Roman Michałowicz urodził się w Warszawie dnia 20 maja 1926 r. Ojciec jego Aleksander był urzędnikiem państwowym, a matka Stanisława z Pietrasów administratorem nieruchomości. Starsza o 4 lata siostra Stefania Wielądek jest wybitnym architektem. W Warszawie ukończył szkołę powszechną, Gimnazjum pod D-malate dehydrogenase wezwaniem św. Stanisława Kostki, a następnie

Liceum Przyrodnicze im. A. Mickiewicza w ramach tajnego nauczania w okupowanej przez Niemców Polsce. W roku 1943 po uzyskaniu matury rozpoczął studia na tajnym Wydziale Lekarskim Uniwersytetu Warszawskiego, słynnej szkole docenta Zaorskiego. Po wojnie studia lekarskie kontynuował początkowo na Uniwersytecie Warszawskim, później na Uniwersytetach Łódzkim (1946–47) i Wrocławskim (1947–48), a tytuł lekarza, po zdaniu egzaminów dyplomowych, uzyskał na Uniwersytecie Marii Curie-Skłodowskiej w Lublinie 2 lipca 1949 roku. Po studiach został powołany do wojska i otrzymał przydział w szpitalu wojskowym w Szczecinie. Jednocześnie, jako wolontariusz, pracował w klinice chorób wewnętrznych. Tu w roku 1952 po napisaniu rozprawy pt.

Here are 3 example MAPK inhibitor of such titles from this journal: • The coral reef crisis: The critical importance of <350 ppm CO2 Titles

can also be tantalizing/catchy/cool, again making readers want to learn more. Here are 2 examples of such titles from this journal: • Famines, food insecurity and coral reef ‘Ponzi’ fisheries But titles only attract readers. Titles are not enough, no matter how interesting your subject matter, if you do not present it well. The next most important component of a paper is the Abstract. Abstracts need to be short, easy to read, and informative. More importantly, they need to answer five key questions, not necessarily in the order shown: 1. What did you do? Answer these five questions not just in the Abstract but in the paper. Answer these questions simply, in short sentences that a layperson can understand. Remember,

you are telling a story. That story needs to be reader-friendly, with no unnecessary words. After the Abstract, the next most likely parts of your paper to be read are the Introduction and Conclusions. If your parents or other non-technical relatives cannot understand the Abstract, Introduction, or Conclusions, rewrite them until they can; get them to help you in rewriting. Note that when we speak we tend to do so in HCS assay short, simple sentences. However, we too often write in long, complex sentences. Which sentences would you rather read? If you cannot write simply, talk into a voice recorder and transcribe what you said. You will be surprised at how short and simple your sentences now are. Winston Churchill is a great example of an author who wrote in short, simple, easily read and understood sentences. When preparing your paper avoid the LPU (Lowest Publishable Unit). LPUs do not lend themselves to interesting

titles or Abstracts and do no credit to Rapamycin clinical trial authors’ reputations. Methods should be provided in sufficient detail that your work could be independently repeated. Methods sections should be kept short, using Supplementary Information. Reference the methodology without unnecessary repetition. Results will be based on your figures and tables, which must be fully understandable on their own. Again, use Supplementary Information to keep your Results section short and focused. The first sentence of each paragraph in the Discussion should summarize the contents of that paragraph. In the Discussion, as in the Abstract, Introduction, and Conclusions, create interest and awareness of the importance and relevance of your work. Answer the “so what?” question. Choose the journal you want to publish in with care; it should be reputable and well-respected, as is this journal. Make sure your paper will appear before the right audience and fit the scope of the journal. Impact factors are unfortunately important, particularly for academic advancement. Also important is speed of publication.