There were no significant changes in hemogram, serum activities of AST, ALT, GGT, and ALP, or serum concentrations of total protein, urea, and creatinine.

Goat 5 was euthanized 8 days after the start of the experiment. At necropsy, the walls of the small and large intestines were distended with edema, and the intestinal content was liquefied. Peyer’s patches were enlarged and hyperemic. The mesenteric lymph nodes were enlarged and edematous; the medullary region was disorganized with low cellularity and presence of homogeneous eosinophilic material (protein) and macrophages with hemosiderin in the cytoplasm. Congestion of blood vessels and dilated lymphatic vessels were observed in the pre-stomachs, abomasum, and large Ku-0059436 solubility dmso and small intestines. Edema of the submucosa was also observed in the abomasum, and small and large R428 ic50 intestines. Ileal Peyer’s patches showed disorganization with the deposition of protein material and the infiltration of macrophages and plasma cells. The diagnosis of poisoning by J. ribifolia was based

on epidemiological, clinical, and pathological findings and was confirmed by the experimental reproduction of the disease. In the outbreaks reported in this paper, poisoning by J. ribifolia revealed high morbidity (10–48%) and mortality (6–40%) rates in goats that were reared exclusively in the areas invaded by plant. To the best of our knowledge, this is the first report of an outbreak of Jatropha spp. poisoning in livestock Cediranib (AZD2171) grazing standing and unprocessed Jatropha spp. Previous reports of Jatropha spp. poisoning in ruminants involved the ingestion of J. Curcas seeds by confined animals ( Völker, 1950; Torres and Fernandes, 1941), or the experimental administration of J. gossypiifolia leaves ( Oliveira et al., 2008), J. Curcas seeds ( Adam and Magzoub, 1975; Ahmed and Adam, 1979a and Ahmed and Adam, 1979b), and the fruits and leaves of Jatropha glauca and Jatropha aceroides ( Barri et al., 1983). J. curcas was also experimentally toxic to mice, rats and fish ( Ferreira et al., 2011; Becker and Makkar, 1998;

Panigrahi et al., 1984). The clinical signs and lesions that are caused by J. ribifolia primarily affects the digestive system and are similar to those observed in experiments with other species of Jatropha in ruminants ( Völker, 1950; Adam and Magzoub, 1975; Ahmed and Adam, 1979a; Barri et al., 1983; Oliveira et al., 2008; Ferreira et al., 2011). Nevertheless, histological lesions can be defined as slight and nonspecific. Curcin and phorbol esters are the two main substances that have been associated with the toxicity of Jatropha spp. ( Makkar et al., 1997; Barahona et al., 2010). Initially, the toxic effect of J. curcas was attributed to curcin. However, the products of J. curcas mineral oil extract, which are detoxified by heat and that are curcin-free, are also toxic, showing that the toxicity of Jatropha spp.

NO can sensitize tumor cells to immune-mediated killing through Fas-, tumor necrosis factor (TNF)-related apoptosis-inducing ligand, and TNF-α–dependent mechanisms. The mechanism by which NO increases Fas sensitivity is due to inhibition of NF-κB and Yin Yang 1 that allows for increased levels of death-inducing Fas on the surface of tumor cells [48]. Reduction of the transcriptional repressor Yin Yang 1 also allows for increased expression of Trail on tumors and hence enhanced sensitivity to Trail-mediated apoptosis [49]. Because many tumors

have mechanisms to circumvent apoptosis, elevated levels of NO could theoretically resensitize tumors to the induction of apoptosis. NTG, or GTN, is an approved see more antianginal NO-donating nitrate ester [50] repurposed for evaluation as a single agent and chemosensitizer in late-stage cancer clinical trials. In a phase II study, patients with prostate cancer who had failed primary therapy were treated with a low dose of sustained delivery GTN resulting in a significant decrease in prostate-specific antigen. Natural Product Library The authors suggested that, although low-dose NO had no direct cytotoxic effect, NO decreased the emergence of a more malignant phenotype, including invasion and metastases [2], potentially by “normalizing” or “boosting” NO to physiological ranges. An alternative hypothesis supporting these observations is

that prolonged and sustained delivery of NO paradoxically resulted in inhibition of NO signaling through tachyphylaxis due to feedback inhibition of GC [2]. The latter possibility suggests itself as a consequence of the observations of Sonveaux et al., who have demonstrated that ionizing radiation activates proangiogenic signaling cascades through up-regulation of NOS in endothelial cells and NO production in the tumor vascular bed [51]. These studies suggest that it may be necessary to exceed a minimum threshold dose of NO before a switchlike response from a tumor stimulant to cytotoxicant is elicited. The effect of NO supplementation on the efficacy of chemotherapy

was studied in a double-blind phase II randomized study of 120 patients with stage IIIB/IV non small cell lung selleck compound cancer (NSCLC) [52], randomly assigned to a hybrid regimen of alternating courses of vinorelbine and cisplatin with either an NTG patch or placebo. Both time to disease progression and overall response rate were found to be significantly increased in the NTG arm. This marked effect of NO could be attributed to a normalization of NO levels from low to a normal physiological range in the tumor or, alternatively, an effect on GC and cyclic guanosine monophosphate production through feedback inhibition. Both scenarios would lead to disruption of the proangiogenic redox signaling circuitry.

The formula C12H14N4O13 was determined by HRESIMS (m/z 423.0631 as [M + H]+; calcd. 422.0508). The ESI-MS/MS spectrum in the positive mode for nigriventrine revealed main fragment ions with m/z 405.0052, 388.9932, 361.0143, 349.0632, 317.0211, 299.9906, 248.0321, 233.9894, 189.0235, 172.9785, 130.8851, 102.8918, and 75.0012 as [M + H]+ ( Fig. 4A). The pattern of fragmentation revealed that the ions of m/z 349.0632, 361.0143, 388.9932

and 405.0052 resulted from the fragmentation of the intact compound, whereas the ions of m/z 75.0012, 102.8918, 130.8851, 172.9785, 189.0235, ABT-199 manufacturer 233.9894, 248.0321, 299.9906 and 317.0211 resulted from the fragmentation of the molecule that lost two oxygens from one of the piperidinyl moieties [M + H – 32] (m/z 370.0631), as represented in Fig. 4B. The pattern of fragmentation proposed in Fig. 4B fitted well with the chemical structure proposed for nigriventrine in Fig. 3A and corroborated the structure proposed by NMR analysis. Nigriventrine was ICV administered to male Wistar rats, and the c-Fos-immunoreactive (ir) neurons were counted in all active brain regions. Examination Volasertib research buy of the four coronal sections sliced from the rat brains revealed that seven brain regions expressed the c-Fos protein; therefore, the Fos-ir neurons of all these regions were mapped (Fig. 5 and Fig. 6) and counted (Fig. 7). Comparing the counting of nigriventrine-treated and saline-treated neurons

revealed that the brain areas stimulated by nigriventrine were the motor cortex, sensory cortex, piriform cortex, median preoptic nucleus, dorsal endopiriform nucleus, lateral septal nucleus and hippocampus. The counting

of Fos-ir neurons in these regions indicated that the stimulation of the piriform cortex was particularly high compared to the other regions (Fig. 5E and F; Fig. 7). The widespread activation of c-Fos by nigriventrine in different populations ifenprodil of neurons of rat brain could be due to secondary actions resulting from the activation of specific brain regions because of the connectivity and network structure between spatially distributed brain areas. This finding has been previously reported for the spatiotemporal spreading of Fos induction by different types of stimuli (McIntosh et al., 2003 and Tchelingerian et al., 1997). Different brain regions present different propensities for generating epileptiform activity in the presence of convulsant stimuli. The piriform cortex and the hippocampus have strong tendencies to generate epileptiform events. Specifically, the piriform cortex has a propensity to generate spontaneous interictal spikes, which in turn may result in epileptic events (Namvar et al., 2008 and Rigas and Castro-Alamancos, 2004). It is interesting to note that the piriform cortex was the most intensely labelled region of c-Fos expression in the rat brain after treatment with nigriventrine (Fig. 7).

, 2012). The system not only allows one to determine the extent to which a mutation compromises p53 wild-type function ( Odell et al., 2013) but may also provide a powerful tool to study the response of cells carrying mutant p53 to cellular stress and DNA damage. Recent findings have indicated that wild-type p53 can impact on the bioactivation of environmental carcinogen and drugs indicating that the cellular TP53 status is linked to Epigenetics Compound Library the regulation of xenobiotic-metabolising enzymes (XMEs) ( Goldstein et al., 2013, Hockley et al., 2008 and Simoes

et al., 2008). Thus as mutant p53 expressed in preneoplastic and/or neoplastic cells severely limits or abolishes the capacity of p53 to regulate its target genes ( Freed-Pastor and Prives, 2012), mutant p53 may also impact on the expression of XMEs. Prior to studying carcinogen-induced cellular responses of p53 mutated ES cells and MEFs derived from the PLF mouse it must be ensured that they are metabolically competent to activate the carcinogen studied. We showed previously that primary HUFs have the metabolic capacity to activate some environmental carcinogens including BaP, AAI and the air pollutant 3-nitrobenzanthrone (3-NBA), all of which have also been studied in the HUF immortalisation assay

and are capable of inducing TP53 mutations ( Liu et al., 2004, Liu et al., 2005, Nedelko et al., 2009, Reinbold et al., 2008 and Brocke et al., 2009). However, little is known about the metabolic competence

of mouse ES cells with regard to environmental carcinogens. In the present study we have compared ES cells and MEFs derived from GSI-IX mice on a C57Bl/6 background, the same genetic background as the PLF mouse, for their ability to metabolically activate the carcinogens BaP, 3-NBA and AAI. Thus, these results are important for future studies using ES cells and MEFs derived from the PLF mouse carrying mutant p53. DNA adduct formation was assessed by 32P-postlabelling and the DNA damage response proteins p53 and p21 were evaluated by Western blotting. We also determined by quantitative real-time PCR (qRT-PCR) the GNE-0877 gene expression of two selected enzymes, cytochrome P450 1a1 (Cyp1a1) and NADP(H)quinone oxidoreductase (Nqo1). Benzo[a]pyrene (BaP) and aristolochic acid I (AAI, as sodium salt) were obtained from Sigma Aldrich (Gillingham, UK). 3-Nitrobenzanthrone (3-NBA) was synthesised as described ( Arlt et al., 2002). In the PLF mouse, exons 2-9 of the mouse Trp53 gene have been replaced by a PGK-neomycin resistance gene cassette to allow efficient exchange of the PGK-neo cassette with an incoming human TP53 sequence of interest ( Wei et al., 2011 and Wei et al., 2012). The modified Trp53 allele is the designated platform (plf) allele, where the plf/plf genotype is nominally p53 null and plf/Trp53 retains one functional mouse Trp53 allele along with the plf allele.

[129] und Chen [130] sowie In-vitro-Experimente von Syversen [131]. Jacobsen et al. [95] und Syversen et al. [132] beobachteten degenerative Veränderungen am endoplasmatischen Retikulum, und diese morphologischen Befunde bestätigten die biochemischen Veränderungen. Der einzige Bericht über eine gesteigerte Synthese von DNA, RNA und

Proteinen im Gehirn wurde von Brubaker et al. [133] publiziert. Syversen [125] gelang es, aus dem Cerebellum und dem Kortex von MeHg-vergifteten Ratten mit Neuronen angereicherte Zellfraktionen zu isolieren. Die Proteinsynthese in vivo war in den Körnerzellen und Purkinje-Zellen Dasatinib purchase im Cerebellum sowie in kortikalen Neuronen reduziert. Interessanterweise erholte sich die Proteinsynthese in zwei Zelltypen, nicht jedoch

in den cerebellären Körnerzellen. Diese Daten weisen darauf hin, dass in manchen Zellen, nicht aber in anderen, wichtige Reparaturmechanismen für Makromoleküle wirksam sein könnten und dass die Kapazität für die Reparatur des ersten Insults entscheidend dafür sein könnte, welche Zellen degenerieren. Das gleiche Prinzip der Zellselektion aufgrund einer eingeschränkten Reparaturkapazität wurde auch von Jacobs et al. [95] und von Sarafian et al. [134] vorgeschlagen. Einer der wichtigsten Mechanismen der MeHg-bedingten Toxizität ist die Bildung reaktiver Sauerstoffverbindungen (ROS) und die Depletion von GSH [135]. Das Gleichgewicht zwischen oxidativen und reduktiven zellulären Prozessen ist entscheidend im Zusammenhang mit der MeHg-induzierten Neurotoxizität. Nach Exposition gegenüber MeHg gehen erniedrigte see more GSH-Konzentrationen in der Regel mit erhöhten ROS-Konzentrationen

einher [136], [137], [138] and [139]. In einer epidemiologischen Studie, in der ein Zusammenhang zwischen oxidativem PLEKHM2 Stress und MeHg-Exposition hergestellt wurde [140], wurden bei erhöhtem Gesamt-Hg-Gehalt sowohl erhöhte als auch erniedrigte GSH-Konzentrationen bestimmt. Diese Ergebnisse legen nahe, dass MeHg die Bildung von ROS steigern kann, die wiederum entweder die GSH-Konzentration erniedrigen oder durch die Erhöhung der GSH-Konzentration eine adaptive Reaktion auf oxidativen Stress auslösen kann. Darüber hinaus wurde gezeigt, dass die Induktion einer gesteigerten GSH-Synthese [123], [141] and [142] gegen MeHg-induzierte Neurotoxizität schützen kann. Wichtige Inhaltsstoffe aus Fisch und Meeresfrüchten, wie z. B. Fettsäuren, Selen und Antioxidanzien, schützen nachgewiesenermaßen ebenfalls gegen MeHg-induzierte ROS [71], [143] and [144]. Im Gehirn scheinen Interaktionen zwischen Neuronen und Gliazellen eine wichtige Rolle bei der Neurotoxizität von MeHg zu spielen. Die Astrozyten versorgen die Neuronen mit verschiedenen Faktoren wie Cystein, Glyzin und Glutamin für die GSH-Synthese [145]. Der erhöhte Gehalt an GSH in kortikalen im Vergleich zu cerebellären Astrozyten war Publikationen zufolge verantwortlich für die erhöhte Produktion von ROS in cerebellären Astrozyten [123].

Unter diesen Umständen haben see more sich komplexe Mechanismen zur Aufrechterhaltung der Eisenhomöostase entwickelt mit dem doppelten Ziel, den Organismus einerseits mit ausreichend Eisen zu versorgen und andererseits empfindliche Strukturen vor eisenvermitteltem oxidativem Stress zu schützen. Wenn die Kapazität dieser regulatorischen Mechanismen überschritten wird, zeigen sich Symptome des Eisenmangels oder der Eisentoxizität; beides kann schwere

Gesundheitsschäden verursachen. Die Entwicklung von Eisenpräparaten mit hoher Bioverfügbarkeit und deren Einsatz als Nahrungsergänzungsmittel und zur Fortifikation von Nahrungsmitteln stellt eine Herausforderung für die Kapazität der Eisenhomöostase dar. Das Angebot verarbeiteter Lebensmittel in Industrieländern umfasst ausreichend Fleisch und Früchte, um die Bioverfügbarkeit des Eisens in der Nahrung nachhaltig zu verbessern. So ging die Prävalenz des Eisenmangels in Dänemark weiter zurück, auch als die obligatorische Nahrungsmittelfortifikation CDK inhibitor 1987 beendet wurde [3]. Gleichzeitig ist Eisenmangel in Entwicklungsländern immer noch weit

verbreitet. Im Versuch, angesichts von Eisenquellen mit hoher Bioverfügbarkeit die Risiken des Eisenmangels und der Eisenüberladung auszubalancieren, hat eine Reihe nationaler und regionaler Institutionen Empfehlungen für die Eisenaufnahme Isotretinoin erarbeitet, die hier mit Bezug auf ihren physiologischen, epidemiologischen oder toxikologischen Hintergrund dargestellt werden sollen. Eisenmangel ist der am weitesten verbreitete Nährstoff-Mangelzustand, betrifft weltweit etwa 2 Milliarden Menschen [4] und beeinträchtigt die Funktion eisenabhängiger Enzyme und Proteine [5]. Eisenmangelanämie entsteht, wenn zu wenig Eisen im Knochenmark zur Verfügung steht und führt zu eisendefizienter Hämatopoese. Im Knochenmark sammelt sich dann vermehrt Zn-Protoporphyrin an, obwohl die Hämoglobinkonzentration u. U. immer noch adäquat ist. Eine offenkundige Eisenmangelanämie entwickelt sich im nächsten Schritt. Eisenmangelanämie ist am weitesten verbreitet unter Frauen

im gebärfähigen Alter; die Prävalenzen liegen hier zwischen 35 und 75% in Entwicklungsländern und bei etwa 18% in Industrieländern [6]. Kleinkinder im Alter von 6 bis 24 Monaten sind eine weitere Risikogruppe mit einer Prävalenz von 25 bis 46% weltweit [4] and [7]. In Deutschland ist die Prävalenz der Eisenmangelanämie auf 2 und 5% bei erwachsenen Männern bzw. Frauen geschätzt worden [8]. Die körperliche und die intellektuelle Leistungsfähigkeit werden durch Hämoglobin- und Myoglobinmangel [5] sowie reduzierte Expression des eisenabhängigen Cytochroms c und der ATP-Produktion beeinträchtigt. So war das Einkommen von Tee- und Kaffeepflückern in hochgelegenen Anbaugebieten Guatemalas ihrem Eisenstatus direkt proportional [9].

Supplementary Appendix C details which studies contributed to each theme. Activities included active pursuits, such as walking, playing games, such as golf or baseball, gardening and doing tasks (in the dementia-specific therapeutic garden),17, 25 and 31 and passive enjoyment of the surroundings, such as sitting and relaxing, sunbathing, eating, picnicking, looking around the garden, and talking about the trees and flowers.25, 26 and 27 Staff reported that these visits to the garden raised the spirits

of the residents and of the staff who accompanied them. Member of staff – “….We can bring them out here just to relax… It is more fun to come to work as well. They’re happier and so are we.” (Edwards et PD0325901 datasheet al 17, p. 13, reviewer edit) mTOR inhibitor In most cases, residents were accompanied into the gardens by staff or visitors: Member of staff – “… what they normally do there is to go out and have a picnic type of thing. Drinks and ice cream, snacks and that type of thing. And I’ve seen some family members joining the group.

I think this is a very good courtyard.” (Hernandez 25, p. 139, reviewer edit) Very rarely were residents reported to visit gardens of their own accord by themselves or with other residents. In some cases, residents were reported to be able to continue to garden, when other activities were no longer possible for them: Family member – “He can’t

concentrate on anything for very long. So, television is not effective for him because he can’t follow the story line. He doesn’t read stories or books. These are activities he did before but he’s not able to continue them because of the progression of the dementia. But gardening is something that he can still do and enjoy very much.” (Raske 27, p. 343, edits in the original) It is not clear whether the level of engagement affects the level of benefit a resident can gain. Although some authors suggest that as Gemcitabine manufacturer all the residents with dementia in their study improved their agitation irrespective of their level of engagement with the garden, it may be enough to just take in the view of a garden, the smells, and the light.17 and 25 Staff and family members (and some residents) reported that the residents’ interaction with the garden seemed to improve their well-being and, in some cases, also improved their interactions with visitors and staff.16, 17, 25, 27, 29 and 31 The garden does not just affect the residents but changes the way staff and visitors feel about the care home, as it changes the possibilities for their interaction with residents too.

However, the presence of nitro toxins might exasperate the toxicological problems encountered with animals grazing I. lespedezioides. This work was supported by National Institute

for Science and Technology for the Control of Plant Poisonings, CNPq, grant 573534/2008-0. “
“Serine proteases are essential key enzymes in a broad diversity of physiologic and pathologic processes, and their overexpression is tightly blocked by endogenous inhibitors to maintain homeostasis. The disruption of this equilibrium is the basis for disease genesis, and therefore, serine protease inhibitors (SPI) are targets of the synthetic development of drugs (Cuccioloni et al., 2009; Perzborn et al., 2011). The family of Kunitz-type serine

protease inhibitors (Kunitz-type SPI) comprise more than twenty members, which include bovine pancreatic trypsin inhibitor, Alzheimer’s AC220 price amyloid precursor protein (APP), and tissue factor pathway inhibitors 1 and 2 (TFPI-1 and 2) (Chand et al., 2005). They are competitive protease inhibitors, with one or more Kunitz-type domains, characterized by intrachain disulfide bonds conserved in all family members (Laskowski and Quasim, 2000). The relation of Kunitz-type SPI with cancer development and PD-166866 cost metastases has been shown by reduced levels of endogenous TFPI-2 in some aggressive cancer types (Sierko et al., 2007; Ran et al., 2009) and by reduced tumor cell migration and invasion by TFPI-2 recombinant therapy or TFPI-2 overexpression (Yanamandra et al., 2005; Ran et al., 2009). The proposed mechanisms are related to the inhibition of the expression of matrix metalloproteinase

enzymes and activities (MMPs) Alanine-glyoxylate transaminase (Rao et al., 1999; Kong et al., 2004; Ran et al., 2009), tumor cell cytotoxicity (Wong et al., 2007; Kemparah and Kisiel, 2008), reduction of tumor cell lymphatic spread (Sierko et al., 2010), and impairment of angiogenesis (Yanamandra et al., 2005; Provençal et al., 2008; Ran et al., 2009). Angiogenesis or neovascularization is a highly complex pathophysiological process, where pre-existing endothelial cells must break through the basement membrane, migrate and proliferate in response to angiogenic factors. The new outgrowths have to reorganize into a patent three-dimensional tubular structure, which will create the new vessel (Risau, 1997). All steps of the process are influenced by a strongly controlled balance of positive or negative modulators, secreted by different cell types, and by the expression of cell membrane adhesion molecules, which allows the perfect cell–cell and cell–extracellular matrix interactions (Ramjaun and Hodivala-Dilke, 2009).

A second important consideration concerns the electric dielectric losses associated with RF irradiation at these very high frequencies, and their potential heat-deposition characteristics. In general, the effects of static and radiofrequency fields and of magnetic field gradients on sensory functions and on absorbed power in general, will have to be a topic of comprehensive research that is to accompany the development of 1H MRI and MRS at Larmor frequencies beyond 500 MHz. Fortunately, previous studies at 7 T have coped with this problem for the proton frequency range of 300 MHz, thereby solving

this complication for the other nuclei Olaparib price listed in Table 1 – all Bleomycin purchase the way up to the 20 T frontier. In addition to these RF heating and penetration problems, insertion of fish, birds or mammals at very high magnetic fields bring physiological complications

of their own. The development of MRI, fMRI and MRS in humans since 1973 has led to major new physiology information and significant improvements in diagnoses and treatments. The magnetic fields employed for human studies have increased from 0.04 T to 11.74 T over the last 40 years, and further possibilities would be opened by still higher fields. This motivates an initiative to develop magnets in the 12–20 T field range, with capabilities to image and perform spectroscopy on the human head and on large animals. Although this development would be for research and not for clinical applications, and although a number of technical complications going beyond the magnet-building aspects will have to be dealt with to enable ultra-high field MRS, MRI and fMRI technologies, this research could lead to important clinical benefits. For instance, at 20 T imaging the human cortex using proton MRI should be possible at a 50 μm resolution. The susceptibility differences between Alzheimer’s plaques and adjacent tissues size should allow visualization of plaque-invested tissues even for particles of 20 μm size. fMRI studies at 7 T give

confidence that fMRI above 12 T in combination with new rapid acquisition techniques will allow nearly Acyl CoA dehydrogenase whole-brain connectivity analyses. The acquisition times required to achieve SNR data under contemporary standards will be reduced by a factor of 8 from those currently achieved at 7 T, and by a factor of 33 vis-à-vis acquisitions at 3 T. Changes in spectral dispersion and relaxation times will allow investigations of metabolites in vivo that cannot be observed by current 1H MRS methods. A further horizon opened by 20 T is that of MR on nuclei such as 13C, 15N, 17O, 23Na, 31P, 37Cl, 39K and nuclei other than 1H. Particularly promising area will be opened in in vivo spectroscopy, thanks to the polarization and detection enhancements at higher fields.

Gostaria de recordar que Cruz et al.2 publicaram em 1986, na Revista de Gastrenterologia, um trabalho com idêntico nome: «Doença de Whipple associada a giardíase: coerente ou coincidente?». Numa revisão da literatura, Fenollar, que é citado no presente trabalho, menciona, para além deste caso nacional, em cujo estudo tive o gosto de participar, apenas mais 15 com coinfeção pela giardia3. A particularidade referida pelos autores como sendo uma originalidade deste caso clínico, especificamente, não terem sido identificadas lesões no duodeno sugestivas do

diagnóstico, pode ser devida a insuficiência de amostragem de material de biópsia, ao facto da colheita ter sido realizada por pinça e não por cápsula de Crosby, ao facto de não ter sido efetuado estudo ultraestrutural, ou por ter sido efetuada terapêutica

prévia com find more antibiótico, o que ocasiona migração dos macrófagos da lâmina própria para a submucosa conforme documentamos em publicação no Gastroenterology 4. Em editorial recentemente publicado nesta revista sobre a importância de um Centro de Registo de dados, foi referido: «É certamente reconhecida por todos a importância e a necessidade do conhecimento da realidade nacional no que respeita à patologia do foro gastrenterológico»5. Com efeito, pensamos que seria relevante que a SPG promovesse o levantamento nacional da doença de Whipple, tal como aconteceu recentemente em Espanha6. Na eventualidade de tal selleck screening library estudo estar em curso e para memória futura, acrescentamos referências sobre os casos que estudamos7, 8 and 9. Registo com apreço que este doente foi estudado com o recurso a novos métodos de diagnóstico, nomeadamente ao diagnóstico molecular. “
“O Carcinoma do Cólon e Reto (CCR) em Portugal constitui o tumor mais frequente e o however segundo com maior mortalidade1. Todos os dias no nosso país morrem 9 a 10 pessoas por CCR. Na verdade, apesar de existir tratamento curativo, o diagnóstico é habitualmente realizado numa fase sintomática e assim, o prognóstico é reservado e a sobrevivência global aos 5 anos não ultrapassa 50%. O

rastreio é a única estratégia que pode alterar esta situação, porque ao ser realizado obrigatoriamente numa fase assintomática, permite reduzir a mortalidade. Múltiplas guidelines dirigidas ao rastreio do CCR têm sido publicadas. Em 2008, pela primeira vez, os testes foram divididos em dois grupos em função dos seus objetivos2. Num grupo foram incluídos os testes de fezes e num segundo grupo os exames estruturais (radiológicos e endoscópicos). Os testes de fezes permitem apenas diagnosticar o carcinoma e os exames estruturais permitem não só o diagnóstico do carcinoma, mas também da lesão precursora, o adenoma. Qualquer dos exames ao diagnosticar o CCR numa fase precoce permite reduzir a mortalidade. A endoscopia, porque permite ainda, a ressecção dos pólipos reduz simultaneamente, a mortalidade e a incidência do CCR.