A doente manteve metrotexato e prednisolona e iniciou messalazina

A doente manteve metrotexato e prednisolona e iniciou messalazina, ficando clinicamente estabilizada durante alguns meses. A decisão de iniciar messalazina

é questionável já que o seu benefício na DC não está suficientemente demonstrado9 and 10; admite-se que alguns subgrupos de doentes possam ter benefício11 e na prática selleck chemicals clínica corrente ainda é muito utilizada. A posologia do metotrexato está abaixo da recomendada para a DC, mas admitiu-se que o uso simultâneo de corticosteroides assegurava a imunossupressão. O posterior agravamento clínico, com astenia, anorexia, perda ponderal importante, náuseas e o aumento marcado da massa na FID num curto espaço de tempo, poderia até ser interpretado como um agravamento da atividade da DC; mas se os achados radiológicos da primeira enterografia sugeriam processo inflamatório ativo, em concordância com a impressão clínica, já a segunda enterografia

sugeria fortemente a presença de processo atípico do cólon, o que desde logo impunha uma reavaliação endoscópica e histológica. Foi realizada nova colonoscopia que mostrou aspeto inflamatório exuberante e ulcerações no ascendente distal condicionando estenose não franqueável (fig. 3). No transverso viu-se úlcera longitudinal extensa (fig. 4) com aspeto inflamatório, ocupando metade do lúmen, numa extensão de 15 cm. A histologia mostrou mucosa intestinal com extensas áreas ulceradas ALK inhibitor infiltradas por tecido de granulação, sem lesões causadas por micro-organismos, sem sinais de efeito citopático viral. Alguns fragmentos do cólon transverso estavam infiltrados por

toalhas de células redondas com imunorreatividade com CD20 e CD10 e não reativas com CD5, CD3, Bcl2 e ciclina D1, achados compatíveis com linfoma não-Hodgkin B difuso de grandes células. Foi referenciada para a consulta de hematologia onde a doença foi estadiada e classificada como estádio iv B. Protelou-se terapêutica cirúrgica devido ao mau estado geral da doente e à presença de trombose venosa profunda extensa no membro inferior esquerdo. Suspendeu metotrexato PAK6 e realizou 7 ciclos de quimioterapia com esquema R-CHOP (rituximab, ciclofosfamida, doxorrubicina, vincristina e prednisolona) com remissão completa até ao presente (17 meses). Os aspetos endoscópicos das 2 colonoscopias, realizadas com 2 anos de intervalo, diferiam bastante. No primeiro exame, a mucosa ileal congestionada com erosões aftoides era evocativa de DC. No segundo exame, o processo inflamatório exuberante da porção proximal do cólon com estenose poderia corresponder a uma atividade marcada da DC ou a um adenocarcinoma. A úlcera extensa do transverso, associada a congestão da mucosa, favorecia a DII, visto não corresponder ao aspeto mais habitual do adenocarcinoma cólico. A histologia revelou o diagnóstico final de linfoma B difuso de grandes células.

It is in these areas where natural floating objects are less abun

It is in these areas where natural floating objects are less abundant that fishers have subsequently

deployed the greatest number of artificial objects. FADs have a short life time (generally <6 months; [29]) and can sink or be appropriated by other vessels. Thus skippers constantly deploy new FADs or relocate older FADs (e.g. objects that have drifted into areas with poor fishing opportunities) and in doing so have effectively created a perpetual artificial floating object habitat across much of the northwest Indian Ocean. Selleckchem Sotrastaurin Seasonal patterns of fishing activity by the purse seine fleet follow a roughly cyclical movement around the western Indian Ocean that is largely influenced by the distribution of floating objects and by seasonal changes in fishing opportunities (T. Davies; unpublished data). The main FAD-fishing season extends from August to November and the fleet fishes predominantly in the northwest Indian Ocean to the east of Somalia. Although this northwest check details region is reasonably small, catches are high and almost exclusively made on floating objects.

The use of FADs in particular has consistently been high in this sector with a northwards extension of the fleet in the Arabian Sea region during the mid-1990s. It is interesting to note that these new northerly fishing grounds were discovered by FADs fitted with satellite buoys drifting into previously unfished (but productive) areas [29]. As primary productivity levels fall from November, catch rate on FADs decreases and the fleet moves into the equatorial

Indian Ocean (southeast Seychelles and Chagos regions) in search of free-swimming schools. At this time schools of yellowfin and bigeye tunas are generally feeding or spawning near the surface and thus ifoxetine are easier to find and catch [30]. However, the spatial distribution of schools can vary considerably and as a result there is marked variation in the proportion of catches on free schools in the Chagos region during this period; vessels enter the region to search for free schools but will also fish on FADs where available, resulting in a higher proportion of FAD catches when free schools are scarce. From March to July the fleet fishes mainly in the Mozambique Channel and northwest Seychelles region using a mixed strategy of floating objects (both natural and artificial) and free school sets. As there has always been an abundance of natural floating objects in this region [31] the proportion of catch on floating objects has always been reasonably high and the deployment of FADs has been more limited than further north in the Somali region. Although no distinction is made in the data, up until the late 1980s ‘floating objects’ are generally considered to be have been natural flotsam [3].

Despite the recent decrease in total catch compared with 10 years

Despite the recent decrease in total catch compared with 10 years ago, fish exports have increased constantly; this

increase seems to occur at the expense of local consumption and has caused significant increases in fish prices in local markets [44]. Artisanal fishing accounts for well over 90% of the total production [27]. The key fisheries resources, shown in Table 1, include pelagic fishery for tuna and tuna-like species and demersal fishery for fish, cuttlefish, shrimp, and lobster. Tuna and tuna-like species and cuttlefish are prevalent in the Gulf of Aden and the Arabian Sea, whereas demersal fish are more abundant in the Red Sea. Key pelagic species include yellowfin tuna, longtail tuna, little tuna, narrow-barred Spanish mackerel, Indian mackerel, anchovy, and sharks; key demersal fish species include emperors, groupers, snappers, and jacks [27] and [32]. Despite Venetoclax cell line the lack of comprehensive selleck products stock assessment studies and reliable catch statistics, it is believed that most fish stocks, except small pelagic species for which there is no market demand, are either fully exploited or overexploited [37]; interviews with fishermen and

different stakeholders confirm these beliefs. Cuttlefish (Sepia pharaonis) has been harvested since 1967 by industrial fleets in the Gulf of Aden and the Arabian Sea region. The intensive trawling on their spawning aggregations has led to overfishing and a major decline of the fishery by 1982–1983 with reported annual landings falling from around 9000 to 1500 t. Landings of the rock lobster (Panulirus homarus) virtually collapsed to near zero in the late 1990s from peaks of around 400 t in the early part of the decade. This collapse was attributed to the widespread use of nets rather than traps to capture lobsters [37]. Large-scale harvest of sea cucumbers started in 2003 with the advent of air compressors, which facilitated diving; this process

led, a few years later, to the collapse of the fishery [45]. Many important demersal fish stocks and some pelagic species, such as Indian Fenbendazole mackerel [41], narrow-barred Spanish mackerel, and sharks [40] and [46], have experienced severe overfishing and their production levels have been beyond the maximum sustainable yields. The lack of FMPs, widespread IUU fishing, uncontrolled growth of fishing effort, and weak compliance and enforcement arrangements have led to significant economic losses associated with the suboptimal use of the resources, which has in turn resulted from weak and ineffective governance and subsequent overfishing. Small-scale fishermen typically use two types of fishing boats: small fiberglass boats called huris, 7–16 m long, with outboard engines and 2–6 crew members, and larger wooden boats called sambuks, 10–20 m long, with inboard or outboard engines and with a crew from 10 up to 25 or more [4] and [27]. Huris were traditionally used for single day trips in inshore waters, within 40 km of the shore [4].

Cryobiology 44, 132–141 Zachariassen, K E , Einarson, S , 1993

Cryobiology 44, 132–141. Zachariassen, K.E., Einarson, S., 1993. Regulation of body-fluid compartments during dehydration of the tenebrionid beetle Rhytinota praelonga. Journal of Experimental Biology 182, 283–289. Zachariassen, K.E., Hammel, H.T., 1976. Nucleating-agents in hemolymph of insects tolerant to freezing. Nature 262, 285–287. Zachariassen, K.E., Hammel, H.T.,

1988. The effect of ice-nucleating agents on ice-nucleating activity. Cryobiology 25, 143–147. Zachariassen, K.E., Hammel, H.T., Schmidek, LEE011 W., 1979. Osmotically inactive water in relation to tolerance to freezing in Eleodes blanchardi beetles. Comparative Biochemistry and Physiology A – Physiology 63, 203–206. Zachariassen, K.E., Hammel, H.T., Schmidek, W., 1979. Studies on freezing injuries in Eleodes blanchardi ABT-737 in vivo beetles. Comparative Biochemistry and Physiology A 63, 199–202. Zachariassen, K.E., Husby, J.A., 1982. Antifreeze effect of thermal hysteresis agents protects highly supercooled insects. Nature 298, 865–867.

Zachariassen, K.E., Kamau, J.M.Z., Maloiy, G.M.O., 1987. Water-balance and osmotic regulation in the east-african tenebrionid beetle Phrynocolus petrosus. Comparative Biochemistry and Physiology A – Physiology 86, 79–83. Zachariassen, K.E., Kristiansen, E., 2000. Ice nucleation and antinucleation in nature. Cryobiology 41, 257–279. Zachariassen, K.E., Kristiansen, E., Pedersen, S.A., 2004. Inorganic ions in cold-hardiness. Cryobiology 48, 126–133. Zachariassen, K.E.,

Kristiansen, E., Pedersen, S.A., Hammel, H.T., 2004. Ice nucleation in solutions and freeze-avoiding insects – homogeneous or heterogeneous? Cryobiology 48, 309–321. Zachariassen, K.E., Li, N.G., Laugsand, A.E., Kristiansen, E., Pedersen, S.A., 2008. Is the strategy for cold hardiness in insects determined by their water balance? A study on two closely related families of beetles: else Cerambycidae and Chrysomelidae. Journal of Comparative Physiology B 178, 977–984. Zachariassen, K.E., Pedersen, S.A., 2002. Volume regulation during dehydration of desert beetles. Comparative Biochemistry and Physiology A 133, 805–811. Full-size table Table options View in workspace Download as CSV “
“The honey bee Apis mellifera L. is a model organism with a wide behavioral repertoire that serves as a baseline for studies of the complexity of cognitive functions in insect brains ( Giurfa, 2003 and Menzel, 2001). In addition to its behavioral organization, this honey bee has a set of putative genes that are highly related to vertebrate genes, including most of the genes that encode factors related to cell signaling/signal transduction ( Consortium, 2006, Nunes et al., 2004 and Sen Sarma et al., 2007). Studies of the honey bee brain have identified genes and proteins that are expressed in this tissue ( Calabria et al., 2008, Garcia et al., 2009, Peixoto et al., 2009, Robinson, 2002 and Whitfield et al.

These results, therefore, should not be used to determine stroke

These results, therefore, should not be used to determine stroke risk, and repeated examinations Ibrutinib nmr should be performed when the patient is stable. It is essential to use educational

intervention to target parents and caregivers as well as children about the importance of conducting systematic TCD examinations. The use of criteria other than ICA/MCA was analyzed in some studies; however, there is no consensus that allows us to recommend chronic transfusion. Nevertheless, we suggest attentiveness to changes in other arteries and a thorough understanding of “individual risk” thereby reducing the need for numerous exam repetitions. Children with abnormal ICA/MCA velocities and elevated anterior cerebral artery (ACA) velocities presented a risk of stroke more than twice that of those with abnormal ICA/MCA but normal ACA velocity [19]. There are similar findings with the basilar artery, vertebral, PCA and OA when compared with the ICA/MCA,

ERK screening however, the recommendations must be more uniform. Although in the majority of cases, velocities could go back to a normal range (MCA TAMMX < 170 cm/s) after a period of 30 months or longer, discontinuation can result in a high rate of reversion to abnormal blood-flow velocities on the TCD or even in stroke. The STOP II study concluded that we must maintain chronic transfusion indefinitely [17] and [18]. Other treatment regimens are now being tested [20]. TCD screening rates in children with SCD have increased after the publication of the STOP trial, and medical providers may be targeting those children at the highest stroke risk. Prospective follow-up of a larger sample will be required to assess the impact of this screening on stroke rates. TCD screening

itself only stratifies stroke risk, but does not prevent stroke; stroke prevention depends on the implementation of PDK4 chronic transfusion therapy. However, access to vascular laboratories appears to be a barrier to the implementation of this highly effective stroke prevention strategy, even among children with comprehensive health insurance. The main problems are difficulties in performing the examination, differences in imaging and nonimaging techniques, and interpretation of guidelines. The identification of sickle cell vasculopathy by MRI, MRA, and MR diffusion imaging has increased our understanding of sickle cell lesions. Silent infarction incidence could be as high as 17% and carries a risk of future infarctions as well [21]. The etiology of silent infarctions, however, remains unresolved, and the implications for preventive therapy continue to be studied. At present, we should attempt to increase the availability of TCD screening by physician training and TCD machine access in the locations of disease prevalence.

Because TGF-β can induce expression of CD103 in some cells, 14 a

Because TGF-β can induce expression of CD103 in some cells, 14 a potential explanation for the reduced ability of Itgb8 (CD11c-Cre) mice to induce iTregs is that lower CD103+ DC numbers are present in these mice owing to reduced TGF-β activation. However, we found that Itgb8 (CD11c-Cre) mice had comparable numbers of CD103+ DCs in all gut-associated Apoptosis Compound Library in vitro lymphoid tissue examined ( Figure 6C). Taken together with our in vitro data, these results strongly indicate that αvβ8-mediated TGF-β activation by specialized intestinal

CD103+ DCs is essential for the induction of tolerogenic Foxp3+ iTregs in the gut. Intestinal CD103+ DCs have emerged as key cells in maintaining gut tolerance, with recent data showing that these cells have the enhanced ability to induce gut-homing receptors on responding T cells15 and convert naïve T cells to immune-suppressive Foxp3+ iTregs.6 and 7 These important functions appear to be due to high expression of the retinal dehydrogenase aldh1a2 in CD103+ intestinal DCs, suggesting they have the capacity to metabolize retinal acid to RA. 6 However, our data now show that CD103+ gut DCs have an enhanced ability to induce iTregs that is independent of RA but completely Natural Product Library dependent on TGF-β function. These results strongly suggest that the enhanced ability of CD103+

intestinal DCs to induce iTregs is linked to an increased ability of these cells to produce active TGF-β. Indeed, we directly show for the first time that CD103+ intestinal

DCs are specialized to activate latent TGF-β and that elevated expression of the TGF-β–activating integrin αvβ8 by CD103+ intestinal DCs is responsible for the enhanced ability of these cells to activate latent TGF-β. Importantly, elevated integrin αvβ8-mediated TGF-β activation by CD103+ intestinal DCs is responsible for their increased ability to induce Foxp3+ Tregs both in vitro and in vivo. We have therefore identified a novel molecular pathway by which a specialized gut DC subset activates TGF-β to promote a tolerogenic environment via induction of Foxp3+ iTregs. Many different immune cells produce TGF-β (predominately the isoform TGF-β116) Dimethyl sulfoxide but always noncovalently bound to an N-terminal propeptide (LAP), preventing TGF-β binding to its receptor.8 Hence, TGF-β function is exquisitely regulated at the level of TGF-β activation. Strong evidence in vivo now supports a critical role for integrin receptors in activating latent TGF-β1 via interaction with an RGD integrin binding motif present in the LAP region of the latent complex.17 Our finding that the TGF-β–activating integrin αvβ8 is highly expressed and functionally important on specialized tolerogenic DCs in the intestine correlates with our previous findings that Itgb8 (CD11c-Cre) mice develop severe colitis associated with reduced levels of total Foxp3+ Tregs in the colonic lamina propria.

obliqua venom Nevertheless, biochemical markers of acute liver i

obliqua venom. Nevertheless, biochemical markers of acute liver injury (AST, ALT and γ-GT) were increased in the serum of animals after envenomation. As it is known that some of these enzymes are not specific to the liver, it is possible that they were derived from other sources, such as the red blood cells or skeletal muscle. For instance, increases in AST activity are also associated with damage

to cardiac and skeletal muscle and the kidneys ( Prado et al., 2010 and Shashidharamurthy et al., 2010). Despite these apparently conflicting observations, we cannot rule out the occurrence of liver injury, mainly because evidence of DNA damage was detected in liver cells using the comet assay. Probably, these findings indicate that the extent of acute hepatic injury in this model of envenomation was subtle and did not lead to gross histological alterations. As mentioned above, L. obliqua envenomation may have triggered an intense inflammatory response, SGI-1776 price which may be involved in several of the clinical manifestations. The activation of the kallikrein-kinin system and the consequent release of vasoactive mediators (mainly bradykinin, histamine and prostaglandins) seems to play an essential role in the edematogenic, nociceptive and vascular effects ( Bohrer et al., 2007). Accordingly, we have shown that during envenomation the animals experienced neutrophilic leukocytosis, indicating that a systemic inflammatory response had occurred. Histological

sections also provided evidence of inflammatory cell infiltrates

in the heart, lungs and kidneys. Corroborating these results, a clear activation in the vascular bed that Small molecule library was characterized by an increase in leukocyte rolling and adhesion to the endothelium was observed in hamster cheek pouch venules that had previously been incubated with low doses of LOBE ( Nascimento-Silva et al., 2012). The up-regulated expression of genes from pro-inflammatory mediators and adhesion molecules, such as IL-8, IL-6, CCL2, CXCL1, E-selectin, VCAM-1 and ICAM-3, was also detected in endothelial cells and fibroblasts after incubation with LOBE. Once released, these mediators acted as chemoattractants, inducing inflammatory cell migration to the sites of injury CHIR 99021 ( Pinto et al., 2008 and Nascimento-Silva et al., 2012). Recently, classical methods of genetic toxicology have been applied to the identification of potential therapeutic agents in animal venoms (mainly for the treatment of some types of cancer) and have also provided a better understanding of the toxic mechanisms of action of these venoms in the human body (Marcussi et al., 2011 and Marcussi et al., 2013). During envenomation, genotoxic damage can occur directly due to the cytotoxic activity of the venom or indirectly through the production of cytotoxic mediators (such as free radicals, for example) in response to tissue injury. In both cases, the damage could lead to DNA fragmentation and eventually, cell death.

, 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31

, 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 SCH772984 price 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 Obeticholic Acid ic50 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 stiripentol 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].

These aspects, however, merge when we remove marine space by putt

These aspects, however, merge when we remove marine space by putting in land claim for urban expansion. selleck kinase inhibitor Most importantly, this separation of the pressures affecting marine systems allows us to know and appreciate for human activities what, why and how we can and cannot manage. We have to ensure that we have robust and defendable science to

assess marine health and underpin marine management, hence be aware of the THREE aspects of science methodology – that we should define our Aims, as the big idea in the science, list our Objectives, as what we need to do to reach our Aims, and give our Hypotheses, as testable and scientifically rigorous questions. Following this, we can suggest there are THREE types of significance in our findings – firstly, and most easy to determine as long as we have sufficient data, is statistical significance. Secondly, and perhaps more importantly, is ecological or Birinapant supplier environmental significance, and thirdly we have the social significance of any change that we detect. For example, detecting the loss of a species amongst hundreds would be impossible statistically without a large and powerful statistical sampling design but that lost species could be ecologically relevant. Despite this, we might not be able to statistically

or ecologically detect a change because of noise (inherent variability) in the system but if society thinks a change has occurred then it should have the highest significance (see Gray and Elliott, 2009). If society thinks there is a problem then by definition there is one even if science cannot detect it. Consequently, The

Ecosystem Approach relies on good and proportionate Cyclin-dependent kinase 3 (fit-for-purpose) science to provide an ecosystem health assessment (or monitoring) programme consisting of FOUR elements – (i) an analysis of main processes and structural characteristics of ecosystem; (ii) an identification of known or potential stressors; (iii) the development of hypotheses about how those stressors may affect each ecosystem; and (iv) the identification of measures of environmental quality and ecosystem health to test hypotheses. In managing the environment we can no longer just be concerned with single sciences – for example, we can take ideas from the business literature which suggests that the environment of an organisation is summarised by the FOUR categories of PEST (Political, Economical, Social and Technological constraints) ( Palmer and Hartley, 2008). This has been expanded to the PESTLE analysis which includes the FIFTH, Legal aspect. We can then juxtapose this to reinforce the idea that the organisation and management of an environment is subjected to the same constraints. This recognises that while as natural scientists we may want to emphasise the natural science, we have to be aware of (and work with) wider disciplines.

All potential predictors with a P value of <0 1 in the univariate

All potential predictors with a P value of <0.1 in the univariate analysis were entered into the multivariate model. Survival curves were plotted using the Kaplan–Meier method and compared with the log-rank test. Statistical

significance was defined at a two-tailed P value of <0.05. The statistical analyses were performed using the SPSS Version 15.0 (SPSS Inc., Chicago, IL) and Stata Version 10.0 software packages. A total of 243 patients (164 males, 62.1 ± 17.9 years) were prospectively enrolled in this study. The baseline characteristics, comorbidities, laboratory data, and microbiologic and radiographic features are outlined in Table 1. Among them, 132 (54%) patients were sputum acid-fast smear-positive and 35 (14%) had mono-drug resistant tuberculosis. Chest radiographs showed the presence

of Rapamycin cavity and pleural effusion in 36 (15%) and 70 (29%) patients, respectively. Pexidartinib More than half (55%) of the patients had radiographic findings of moderately advanced disease, and far advanced disease was observed in only 14% of the patients. Disseminated TB was diagnosed in 23 (10%) patients. Overall, 39 (16%) patients died within 6 months after the diagnosis of PTB. The causes of death were multi-organ failure (n = 19), progressive respiratory failure (n = 11), acute myocardial infarction (n = 2), massive gastrointestinal bleeding (n = 2), hepatic failure (n = 2), malignancy (n = 2), and heart failure (n = 1). Univariate analysis revealed that the mortality was associated with older age, a lower serum albumin level, and the presence of cavitary lesion and pleural effusion MRIP on chest radiographs ( Table 1). There was no difference in sex, body mass index, habits of smoking

and drinking alcohol, comorbidities, microbiology, and other blood testing results between nonsurvivors and survivors. In PTB patients, mean serum levels of PCT, CRP, and sTREM-1 were 0.47 ± 2.60 ng/mL, 17.3 ± 37.2 mg/L, and 161 ± 185 pg/mL, respectively. Twenty-seven (11%) patients had PCT levels exceeding the normal cutoff value of 0.5 ng/mL and 105 (43%) had serum levels of CRP above the upper limit of normal of 5 mg/L. The PCT, CRP, and sTREM-1 levels on the diagnosis of PTB were higher in patients who died within 6 months (PCT: 2.22 ± 6.22 vs. 0.13 ± 0.31 ng/mL, P = 0.043; CRP: 42.1 ± 59.4 vs. 12.5 ± 29.1 mg/L, P = 0.004; sTREM-1: 332 ± 362 vs. 128 ± 98 pg/mL, P = 0.001). Fig. 1 displays serum levels of PCT, CRP, and sTREM-1 in 6-month survivors and nonsurvivors. To assess the potential of the three biomarkers to predict 6-month mortality, ROC curves were plotted (Fig. 2). The analysis identified the areas under the curves (AUCs) of 0.79 (95% confidence interval [CI], 0.71–0.87), 0.75 (95% CI, 0.67–0.83), and 0.76 (95% CI, 0.68–0.84) for PCT, CRP, and sTREM-1, respectively. Of note, the predictive potential of the three biomarkers was comparable (P = 0.571).