aureus can develop resistance to any antibiotic. As seen in the old derivation of mecA in the history of life on the earth, antibiotic resistance is the natural consequence of the production of antibiotics. Based on this principle, we should design a new chemotherapeutic strategy. The bacteria of our time is drastically changed as compared to that of the 1940s, when more than half of the hospital-associated S. aureus is methicillin-resistant, and more than 80% VISA are quinolone-resistant [59]. Given this, it is much more promising to develop an antibiotic that

has stronger activity against the S. aureus strains resistant to extant antibiotics rather than against wild-type S. aureus strains which are still susceptible to them. If such anti-resistance Dinaciclib nmr antibiotics were used in combination with the extant antibiotics, most of the S. aureus infections would become

treatable. By screening 1928 culture supernatants of Actinobacteria, we identified a curious substance that possessed a strong bactericidal activity against fluoroquinolone-resistant VISA strain Mu50, whereas only a weak activity against fluoroquinolon-, and methicillin-susceptible VSSA strain FDA209P [59]. The substance was found out to be an old antibiotic Nybomycin (NYB) that had been reported in 1955 [60]. We found that NYB strongly inhibited the function of the mutated DNA gyrase of CDK inhibitors in clinical trials quinolone-resistant Mu50, but did not inhibit the function of the wild-type DNA gyrase of quinolone-susceptible S. aureus [59]. Docking simulation study revealed stable binding of NYB to the quinolone-binding pocket of the GyrA having gyrA(S84L) mutation ( Fig. 6). On the other

hand, fluoroquinolone antibiotics cannot bind to it due to the mutational loss of the Serine residue, which is important to retain hydrogen-bond network for the stabilization of quinolone molecule in the quinolone-binding pocket ( Fig. 6). Bacteria always find the way to develop resistance to any antibiotic. As is expected, NYB was not exempt from the emergence of resistance, either. Mu50 did generate NYB-resistant mutants (temporarily defined by MIC ≥ 4 mg/L), although at extremely low frequencies: the unless appearance rates were 0.663–15.3 × 10−11[59]. However, surprisingly, all of the nine independently obtained resistant mutant strains were susceptible to fluoroquinolone antibiotics [59]. Nucleotide sequencing revealed that their gyrA genes of the resistant mutants were back mutated to the wild type. Therefore the resistant mutants were genetic revertants [59]. Accordingly, we designated NYB as a ‘Reverse Antibiotic’ (RA) against quinolone-resistant bacteria [59]. Recently, we found that some of the flavones as well are RAs against fluoroquinolone-resistant bacteria (Morimoto, Y. et al. in preparation). Flavones are known as natural antibiotics produced by plants [61]. NYB is also a natural antibiotic.

Furthermore, this technique has been proved valuable Y-27632 in vitro for the examination of traumatic nerve lesions, nerve sheath tumors and several types of polyneuropathies. The most common cause of focal neuropathies is entrapment of a nerve while passing through an osseo-fibrous tunnel, such as the carpal tunnel at the wrist and the cubital tunnel at the elbow. The pathophysiological feature of nerve compression comprises disturbed vascular microcirculation, impaired axonal transport, edema within the nerve, and thickening of perineurium resulting in

an enlargement of the nerve diameter, which is typically located proximally to the entrapment site [3]. Consequently, changes in nerve cross-sectional area are the most relevant sonographic findings in entrapment neuropathies (Supplementary Fig. 1; to view the figure, please visit the online supplementary file in ScienceDirect). In patients with carpal tunnel syndrome (CTS), numerous studies demonstrated high accuracy for both, the maximum cross-sectional area of the median nerve proximal to the entrance of the carpal tunnel and the GSK1120212 nmr ratio of the median nerve area at the wrist to the area of the nerve at the forearm [4], [5], [6], [7], [8], [9], [10] and [11]. For example,

according to a cut-off value for the cross-sectional area of 10 mm2, sensitivity and specificity were 82% and 87% in a study by Ziswiler

et al. [6]. Increasing the cut-off value to 12 mm2 resulted in a 100% specificity at the expense of a lower sensitivity of 44%. Secondary findings in patients with CTS are nerve flattening within the carpal tunnel and bowing of the flexor retinaculum [2]. In contrast to electrodiagnosis, ultrasonography has the capability to rule out secondary causes of CTS such as tenosynovitis, ganglion cysts, accessory muscles or tumors [4] and [5]. In case the nerve branches proximal to the carpal tunnel, ultrasonography can further demonstrate a bifid median nerve [11] or a persistent median artery (Fig. 1) [12]. If symptoms persist or worsen after surgery, ultrasonography may be valuable to assess incomplete splitting of the retinaculum Depsipeptide or intra-operative injuries of the ulnar branch of the median nerve (Fig. 2). However, in contrast to NCS, ultrasonography is obviously not suitable for post-treatment follow-up of CTS since Lee et al. [13] pointed out that the cross-sectional area of the median nerve remained unchanged 6 months after surgery. Supplementary Fig. 1.  Cross-sectional (a) and longitudinal (b) view of the median nerve (dotted line) at the wrist in a patient with carpal tunnel syndrome. Cross-sectional area of the nerve is enlarged to 16 mm2. Arrows indicate the retinaculum flexorum.

212, p = .076). Using an adaptation of Steiger’s Z test ( Hoerger, 2013 and Steiger, 1980), ICG-001 we found the two correlations between F1 and anxiety and F2 and anxiety to be significantly different from each other (ZH = −2.86, p = .004). Total hardiness and all its domains correlated significantly with anxiety (Total: r = −.568, p = <.001; Commitment: r = .−471, p < .001; Control r = −.363, p = .002, Challenge: r = −.280, p = .019). Multiple mediation analyses,

with commitment, control and challenge as mediators, were performed to investigate the indirect effect of psychopathy on anxiety through hardiness (see Fig. 1). No significant direct relationship was found, neither between PCL-R F1 and anxiety nor between PCL-R F2 and anxiety. Significant indirect effects of both PCL-R factors were found, partly mediated through the commitment facet of DRS-15-R. All indirect effects are reported in Table 2. Since only the commitment dimension of psychological hardiness contributed

significantly to the mediation of the relationship between psychopathy and anxiety, a simple mediation model was then calculated to assess the effect size of commitment as a mediator. The indirect effect of commitment in this simple model was −.079 for F1 and .159 for F2 (BootLLCI [95% CI] = -.260, BootULCI [95% CI] = −.024, k2 = .112 for F1; BootLLCI [95% CI] = .048, selleckchem BootULCI [95% CI] = .324, k2 = .155 for F2). Kelley’s Kappa-Squared (k2; Hayes, 2013) was used as a measure of effect size. It is interpreted as the indirect effect relative to its maximum possible value in the data, and the measure is bound between 0 and 1, with values closer to 1 signifying bigger effects ( Hayes, 2013 and Preacher and Kelley, 2011). As a deprivation of liberty, imprisonment is believed to be perceived as unpleasant, and incarceration as a major life event has also been linked to illnesses associated with stress (Massoglia, 2008). Since both psychopathy and psychological hardiness have been associated with the ability to remain relatively unaffected by daily stressors, this study examined

how the characteristics of psychological hardiness were PDK4 related to, and possibly mediated, the relationship between psychopathy and anxiety. Our initial correlational analysis did not reveal any significant relationship between the total score for psychopathy and anxiety. When psychopathy was divided into the separate dimensions of the two-factor model, however, a negative relationship emerged between F1 and anxiety. A positive, but not significant relationship was also found between F2 and anxiety. While these correlations are not significant at the conventional p < .05 level, they are significantly different from each other and also consistent with other studies ( Hansen et al., 2013 and Harpur et al., 1989). Moreover, a one-tailed analysis yields a significant correlation (p = .025/p = .038).

We also noticed that signals for Orc[1-11] were also reduced with inclusion of the inhibitor cocktail. Upon carrying out multiple trials making use of the inhibitor cocktail, we consistently found reduced levels of both Orc[1-11]-OMe and Orc[1-11] when the inhibitor was present; however, inhibition was never complete. Regardless, these results provide evidence to support the hypothesis that an enzyme

participates in production of the Orc[1-11]-OMe product. Heat has been used an effective means to reduce proteolytic degradation of proteins when processing vertebrate tissue samples [9], Sirolimus manufacturer [12], [13] and [44]. Working from the hypothesis that an enzyme plays a role in promoting the formation of Orc[1-11]-OMe during extraction of eyestalk tissues, we attempted to deactivate enzymatic components with heat. To test this approach we removed the paired eyestalk ganglia from one lobster. The ganglion from a single eyestalk was placed in a microcentrifuge tube with 50 μL of extraction solvent and the tightly capped tube was placed in a boiling Olaparib mw water bath for 5 min. Concurrently, the ganglia from the second

eyestalk of the same lobster were placed in extraction solvent and left at room temperature for 5 min. Both eyestalk tissue samples were then homogenized, sonicated, and centrifuged prior to MALDI-FTMS analysis. While the control eyestalk extract showed the Orc[1-11]-OMe-derived peaks at m/z 1270.57, 1253.54, 894.43, 876.42, and 537.28 (see Fig. 11A), no evidence for these peaks was found for the tissue/extraction solvent mixture that was placed in the boiling water bath for 5 min ( Fig. 11B and C). We also did not detect

IKBKE the truncated peptide, Orc[1-11]. When this approach was replicated (n > 6), the treatment consistently eliminated the production of Orc[1-11]-OMe and Orc[1-11]. We also tried freezing eyestalk ganglion tissues in liquid nitrogen before homogenizing and adding extraction solvent, but found that this treatment did not measurably reduce production of Orc[1-11]-OMe. Many enzymes are known to function in aqueous-methanolic solvent mixtures [2] and [38]; however, enzymatic activity is generally reduced or eliminated when the water content is reduced [22] and [25]. We hypothesized that, if an enzyme plays a role in the production of Orc[1-11]-OMe, production of the peptide would be reduced if the extraction solvent contained a lower percentage of water. To determine if the percentage of water in the extraction solvent influenced the extent of methylation, we extracted eyestalk ganglia in solvents containing 1–30% water.

Among these health-beneficial roles, its role in protecting and stimulating nerve cells, however, is the most sought after characteristic out of all the other edible mushrooms with medicinal value. Extracts of H.

erinaceus, such as hericenones C-H [18] and [19] and erinacines A-I [20], [21], [22] and [23], have all shown to induce the expression of NGF in cultured rodent astrocytes. Erinacine A, the main representative of the compounds in H. erinaceus extracts, has demonstrated epinephrine-stronger NGF-inducing activities in vitro and in vivo [24]. Furthermore, such NGF stimulating effects have been augmented by the increased availability of the active compound (up to 8 mg/kg body weight) [24], and it has also been achieved via

Sirolimus solubility dmso oral administration [25]. Hence, there is potential in developing H. erinaceus enriched with erinacine A (EAHE) as an ingredient in medicinal foods or products to help in the reduction or even the prevention of age-related neurodegenerative diseases. To our knowledge, there PD98059 molecular weight have been no reports on the mutagenicity of H. erinaceus prior to this paper. Furthermore, mushroom mycelium has an identity distinct from mushrooms, which are categorized into two specific classes of compounds: hericenones and erinacines, where they can only be extracted from the fruit body and the cultured mycelium, respectively. Our previous

28-day sub-chronic toxicity test in Sprague-Dawley rats showed no evidence of systemic toxicity attributable to EAHE administration [26]. It was estimated that NOAEL (no adverse effect level) of EAHE mycelium is greater than 3 g/kg of body weight/day, which is 171.4 times the recommended daily intake for humans (1.05 g/60 kg of body weight/day). Additional research on EAHE, including an assessment of its ADP ribosylation factor mutagenic and carcinogenic potential, however, should be included to further support the safety of its consumption. Evaluation of the genotoxic properties is important in the context of EU and international legislations aiming to protect human health. For an adequate assessment of the genotoxic potential, three endpoints need to be considered: gene mutations, structural chromosome aberrations, and numerical chromosome aberrations. Hence, the present study was undertaken to determine the mutagenicity and genotoxicity effects of EAHE mycelium conducted in three standard battery of tests (reverse mutation, chromosomal aberration, and micronuclei tests) according to the latest guidelines in order to meet all international regulatory requirements and provide information on the safety of this new and promising natural remedy. H.

“
“Beggiatoaceae are conspicuous members of

microbial mats at Guaymas Basin, a sedimented mid-ocean spreading center in the Gulf of California ( Jannasch et al., 1989). Hydrothermal fluid percolates to the surface through a complex system of heavily sedimented basaltic sills and dikes underlying the basin ( Albertin, 1989 and Aragón-Arreola et PI3K Inhibitor Library screening al., 2005); subsurface mineral precipitation from these fluids ( Von Damm et al., 1985) can further complicate the flow paths. Sediment geochemistry therefore varies from site to site and over time ( Simoneit et al., 1992 and Sturz et al., 1996), sometimes on time scales of a year or less ( McKay et al., 2012). The rising hydrothermal fluids interact with abundant organic carbon deposited from the surrounding land and productive overlying waters, producing natural gas and petroleum ( Didyk and Simoneit, 1989 and Bazylinski et al., 1988) which likewise migrate toward cooler surface

sediment layers. Some proportion of these is consumed as microbial growth substrates ( Bazylinski et al., 1989, Pearson et al., 2005, Marchand et al., 1994 and Goetz and Jannasch, 1993). Beggiatoaceae mats at Guaymas Basin are found around the stalks of Riftia colonies; in areas of moderate surface Trametinib molecular weight temperature on the flanks of carbonate structures; and on sediment patches where surface temperatures are moderate (ca. 10–15 °C) but hydrothermal flow supports temperatures of ca. 100 °C at 40 cm depth ( McKay et al., 2012). Orange and white Beggiatoaceae filaments are typically found together in the central portion of mats, where subsurface temperature gradients are steepest, surrounded by mat dominated by white filaments, and then by non-mat covered surfaces ( McKay et al., 2012). Marine Beggiatoaceae filaments collected from tropical, temperate, and Arctic sites and studied in the laboratory each have an optimum temperature for gliding motility ( Dunker et al., 2010), and a strain collected from reef corals has been shown to reverse direction less frequently in zones of high

oxygen or sulfide concentration ( Dunker et al., 2011). These behaviors tend to maintain filaments within a mat, and – given different thresholds buy Dolutegravir for different morphotypes – could also help maintain zonation by filament color. Little is known about the physiology of pigmented versus non-pigmented Beggiatoaceae. White Gulf of Mexico filaments are reported to have RuBisCO (CO2 fixation) activity, whereas colored filaments have little ( Nikolaus et al., 2003 and Wirsen et al., 1992), which would be consistent with greater reliance by the pigmented cells toward the center of sediment-surface mats on hydrocarbons or microbially produced organic compounds from the underlying sediments. The filaments tested were not axenic, however, so carbon dioxide fixation by other bacteria in the samples cannot be ruled out.

However, there were considerable differences between Reef Groups, Distances and Seasons. learn more At Group A, at the reef edge (0 m) and during the summer, nearly half of measurements indicated hypoxia (<0 mV). This contrasted markedly with 4 m distance, at the same reef group, where none of the stations were

hypoxic and during winter where the proportion indicating hypoxia/anoxia, at the reef edge, was much lower (23%) ( Table 2, Fig. 2). This trend, of increased hypoxia during summer, and as a function of reef-proximity, was also seen, but of reduced magnitude, at Group B but virtually absent at Group D ( Table 2, Fig. 2). However, at Group D there was a trend of increased proportions of samples that were ‘transition’ (sensu Wildish et al., 2001) as a function of season and reef-proximity ( Table 2, Fig. 2). In close proximity to the reef, redox was highly variable, for example on Group A, during the summer, redox varied between −160 and +190 mV at the reef edge (Fig. 2). In terms of the random effects, within reef groups, there were

differences between modules (Table 3). There was also higher variability in redox during summer months compared with winter months (standard deviation multiplier ranged between 0.50 and 1.3) Metformin order and 1.6 × the variability in redox at 0 m compared with 4 m (see weightings in Table 3). In terms of the modelled fixed effects, mean redox differed between distances but this was influenced by both the reef location and season (Fig. 3). Redox was lower in close proximity to the reef (compare zero and 1 m distance, Fig. 3), and this difference was maximal during the summer, particularly at Group A, with projected means, at the reef-edge, being lower by 40–120 mV (95% CI) (Fig. 3). This affect was still discernible, but of reduced magnitude, at Group B, Protirelin but only during the summer (Fig. 3). At Group D there were negligible differences in mean redox as a function of distance regardless of season (Fig. 3) but, across all Groups and Distances, there was a general trend of redox levels being lower in the summer compared to winter (Fig. 2).

The exception to this seasonal trend occurred during February 2005, at Group A (0 m), where negative redox values were recorded (Fig. 2). The confidence intervals shown in Fig. 3, for distances 1 and 4 m, are entirely overlapping at all combinations of Season and Group and this is interpreted as indicating that the discernible impacts, on redox, of the reef did not extend beyond 1 m. The measurable impacts of the LLR, on sedimentary oxygenation status, did not extend more than 1 m from the reef edge. At the reef edge, redox levels were highly variable with a mean expected reduction of 80 mV during the summer, at Group A. At other reef groups reef-proximity had less of an effect and there was a clear trend of decreasing change in mean redox from Group A to B to D and from summer to winter.

The structural similarity of chromate to phosphate and sulfate facilitates its uptake with potential risks of cancer in humans (Costa, 1997). In vitro studies suggest Cr(VI) compounds are cytotoxic and genotoxic, and form Cr-DNA adducts (Biedermann and Landolph, 1987, Biedermann and Landolph, 1990, Patierno et al., 1988, Zhitkovich, 2005 and Zhitkovich, 2011), while others suggest that Cr(VI)-induced carcinogenicity may involve epigenetic mechanisms (Arita and Costa, 2009 and Sun et al., 2011). Although, environmental levels of CrV(VI) are thought to pose

a minimal risk due to reduction to less toxic Cr(III) by bodily fluids and cellular constituents (De Flora et al., 1997, Proctor et al., 2002 and U.S. EPA, 1991), chronic exposure to high concentrations of Cr(VI), in the form of sodium dichromate dihydrate (SDD), resulted in intestinal tumors in mice but not rats (NTP, 2008). To further investigate the key events involved in the mode of action (MOA) of intestinal Angiogenesis inhibitor tumor development, a complementary series of comparative selleck compound drinking water studies was conducted in female F344 rats and B6C3F1 mice (Kopec et al., 2012, Thompson et al., 2011a, Thompson et al., 2011b and Thompson et al., 2012). Both species exhibit similar

biochemical and histological evidence of oxidative stress, villous cytotoxicity, and crypt hyperplasia. Our mouse intestinal epithelial gene expression study reported SDD-elicited dose-dependent differential gene expression consistent with the proposed MOA (Thompson et al., 2011b), as well as identified other over-represented functions and affected pathways (Kopec et al., 2012). FAD Given the similarity of several responses in mice and rats following exposure to SDD in drinking water, comparative studies were designed to investigate species-specific effects that may explain the different tumor outcomes. More specifically, the same study design and treatment regimen (7 and 90 days) was used to obtain duodenal and jejunal epithelial tissues from SDD-treated rats for whole-genome microarray profiling. In addition to analysis for over-represented functions and phenotypically anchoring differential gene expression to gross physiology,

histopathology, and biochemical effects from complementary studies (Thompson et al., 2012), rat and mouse gene expression data were systematically compared using the same analysis methods (Kopec et al., 2012). Qualitative and quantitative differences in the number and types of differentially expressed genes were identified that not only support a proposed MOA involving oxidative stress, cytotoxicity, cell proliferation, and DNA modification but also suggest that the rat is less responsive to SDD. These differences in SDD-elicited differential gene expression may contribute to the different tumor outcomes. Detailed descriptions of the test substance, animal husbandry, and study design have been described (Thompson et al., 2011b and Thompson et al., 2012).

“
“Electrical

cortical activity is segregated in discrete frequency bands (Buzsaki, 2006). Among the five mayor frequency bands, alpha and theta frequencies fluctuate predictably during the menstrual cycle, indicating an association between sex hormone fluctuations and neural activity (Becker Lapatinib et al., 1982, Creutzfeldt et al., 1976 and Brötzner et al., 2014). Analysis of EEG data reveal a lower frequency in the alpha band in late follicular phase, when estradiol is elevated but progesterone is low, compared to early follicular phase, when estradiol as well as progesterone is low, or luteal phase, when estradiol as well as progesterone is elevated (Brötzner et al., 2014). Theta oscillations show a higher frequency in the follicular compared to the luteal menstrual cycle phase (Becker

et al., 1982). How endogenous changes in sex hormone levels during the menstrual cycle contribute to inter- as well as intra-individual differences in cognitive performance and its underlying neural selleck products activity remains a fundamental issue. Previous studies correlated cognitive performance either with an event-related potential (ERP) or sex hormone level. Following presentation of visual stimuli, the temporal sequence of an ERP consists of C1, P1, and N1. This sequence may represent sensory processing (C1), early categorization (P1), and identification of objects (N1) (Klimesch, 2011). Among the three components, P1, with a post-stimulus latency of approximately 100 ms, may be the earliest equivalent for top-down modulation of sensory input. In goal-directed top-down

attention paradigms, expected perceptive contents are categorized as relevant or irrelevant information within a tenth of second (Thorpe et al., 1996 and Rousselet et al., 2007; for review see Klimesch, 2011). Furthermore, Hanslmayr and colleagues describe that during a visual discrimination task enhanced early ERP components (P1 and N1 amplitude) are related to good performance (Hanslmayr et al., 2005). Several lines of arguments indicate that at least a fraction of P1 equals synchronized alpha oscillations: (1) P1 latency and period of alpha oscillation are approximately 100 ms, (2) P1 is predicted by phase alignment in alpha (Gruber et al., 2005) and (3) similar time domain of alpha oscillations and crotamiton attentional blink (Hanslmayr et al., 2011). One influential interpretation of P1 is the inhibition model (Klimesch et al., 2007). According to the inhibition model, phasic synchronization of alpha oscillation is associated with an increase in signal to noise ratio for relevant information, but tonic synchronization with suppression of irrelevant information. Both processes improve working memory and attention performance (Klimesch et al., 2007). Ovarian steroid hormones modulate neural circuits and cognitive performance not directly related to reproductive behavior.

No exame objetivo destacou-se pele e mucosas ligeiramente desidratadas, temperatura axilar de 37,2 °C e dor abdominal difusa ligeira a moderada. Analiticamente, apresentava hemoglobina (Hb) de

13,2 g/dl, com leucocitose de 14 100 cél/mm3 e elevação da proteína C reativa (PCR) com 5,2 mg/dl. Nesta altura, a doente iniciou em ambulatório ciprofloxacina (500 mg de 12/12H via oral) e terapêutica sintomática com antiemético e antipirético, aconselhando-se reforço hídrico e dieta com restrição de gorduras, resíduos e lactose. Todavia, foi observado um agravamento PI3K inhibitor da sintomatologia ao longo das primeiras 96 horas após o início da antibioterapia com aumento do número de dejeções diárias (6-7) com presença esporádica de sangue, persistência das cólicas abdominais, anorexia e astenia marcada. Nesta ocasião encontrava-se desidratada, pálida, febril (38,0°-38,5 °C), taquicárdica PI3K Inhibitor high throughput screening (112 bpm), hipotensa (TA – 95/47 mmHg), apresentando o abdómen distendido e doloroso à palpação sem evidência de irritação peritoneal. Laboratorialmente, destacava-se descida da Hb (11,8 g/dl), agravamento dos parâmetros inflamatórios (leucócitos – 15 400 cél/mm3; PCR – 15,1 mg/dl; velocidade de sedimentação – 40 mm/hora), insuficiência renal ligeira (creatinina – 1,4 mg/dl; ureia – 72 mg/dl) e hipocaliémia (K+ – 3,1 mmol/L). A radiografia do abdómen em

pé mostrou distensão do cego e transverso com cerca de 4,5 cm de diâmetro, sem níveis hidroaéreos. A ecografia filipin abdominal e a tomografia computorizada abdominal revelaram espessamento parietal

de todo o cólon, mais exuberante no cego, e adenopatias na raiz do mesentério. Neste contexto, a doente foi internada iniciando-se correção hidroeletrolítica, terapêutica sintomática antipirética e analgésica (paracetamol) e antibioterapia com ciprofloxacina e metronidazol. Nas primeiras 48 horas do internamento, a doente manteve quadro clínico com 7 dejeções diárias associadas a quadro de toxicidade sistémica com febre, taquicárdia (100-110 bpm) e persistência dos parâmetros inflamatórios elevados. Repetiu radiografia do abdómen, que mostrou aumento da dilatação cólica ao nível do cego e cólon transverso, atingindo este último um diâmetro de 6,5 cm, compatível com quadro de megacólon tóxico (fig. 1). Nesse mesmo dia, realizou retossigmoidoscopia flexível, com insuflação mínima e progressão somente até aos 35 cm, registando-se em toda a mucosa observada a presença de múltiplas erosões e ulcerações superficiais com exsudado mucopurulento, associadas a marcada hiperémia e perda da rede vascular da mucosa (fig. 2). Foi colocada a hipótese diagnóstica de uma primeira manifestação de CU com atividade grave complicada com megacólon tóxico, não sendo possível nesta altura a exclusão de etiologia infecciosa.