0–62.9 mg/100 g), and corresponded to a mean of 29.6% of their total soyasaponins contents. These results agree with those reported selleckchem by Murphy et al. (2008), who found that the major soyasaponin was soyasaponin B-I, followed by soyasaponin B-II (54.7% and 23.0%, on mean,

respectively). The remaining group B soyasaponins (V, αg, βg and βa) corresponded to 22.3% of total soyasaponins content, which were not analysed in the present study, as mentioned before. To properly compare the contents of isoflavones and soyasaponins, values must be expressed on a molar basis, since the former have about half the mean molecular weight than the latter. While soyasaponins molar contents in soy-based formulas ranged from 16.1 to 65.2 μmol/100 g, isoflavones molar contents varied from 4.2 to 19.7 μmol/100 g. Aptamil 1 and Nursoy showed similar molar contents of isoflavones and soyasaponins, while Aptamil 2, Isomil 1, Isomil 2 and

RG7420 order Nan Soy contained approximately 3 times more soyasaponins than isoflavones, on a molar basis. Alergomed showed a unique profile of bioactive compounds, with soyasaponins present at a molar content 14 times higher than that of isoflavones. Murphy et al. (2008) reported that soy protein isolates, the source of protein used in infant formula’s manufacture, contained from 2 to 5 times more soyasaponins than isoflavones. The estimated daily intake of the isoflavones from soy-based infant formulas ranged from 0.2 to 1.5 mg/day/kg body weight of the infant, considering all products and ages, with a mean intake of 0.8 mg/day/kg (Table 5). These values are lower than data previously published inthe literature, ranging from 1.6 to 8.0 mg/day/kg (Genovese and Lajolo, 2002, Irvine et al., 1998 and Setchell et al., 1997). This difference is due to the low contents of isoflavones in the samples analysed

in the present study. The mean estimated intake in the present study was twice the estimated daily intake of isoflavones by the Japanese adult population (0.4 mg/day/kg) (Nakamura, Tsuji, & Tonogai, 2000). By measuring the rates of daily excretion of isoflavones in the urine of infants from 2 to 16 weeks and comparing with data from adults, Irvine et al. (1998) suggested Casein kinase 1 that infants of this age could digest, absorb and excrete genistein and daidzein from soy-based formulas as efficiently as adults who consumed soy products. On the other hand, Setchell et al. (2002) suggested that infants younger than 4 months are probably unable to absorb isoflavones, since they do not have a fully developed intestinal flora and isoflavone absorption is dependent of colonic microorganisms. Considering the high intake of isoflavones by infants fed with soy-based formulas, the potential bioactivity of these compounds and the contradictory data regarding their absorption by infants, further studies are necessary to assure the safety of the use of soy-based infant formulas.

Reduction in new-onset AF was driven by a large

bucindolol treatment effect in patients with a β1389 Arg/Arg genotype who had a 74% reduction (p = 0.0003) when treated with bucindolol compared to those treated with placebo. There was no reduction in event rate (HR: 1.01) in bucindolol patients who were β1389 Gly carriers, and the treatment × genotype group interaction p value was 0.008. Subdividing the β1389 Gly carrier genotype by α2c322–325 Wt/Del genotype appeared to further differentiate bucindolol response as it does for heart failure (12) and serious ventricular arrhythmia (13) endpoints, with a significant (p = 0.016) test for interaction when β1389 Arg/Arg patients were included in the 3-group analysis. Although differences in race and/or history of hypertension could have affected

KU-55933 molecular weight the analysis between genotypes, the (β1389 Gly carrier + α2c322–325 Wt/Wt) group had prevalence rates for black patients and cases of hypertension that were similar to those of the β1389 Arg/Arg group but markedly different HRs (0.94, p = 0.84 and 0.26, p = 0.0003, respectively). This indicates that the differentially enhanced treatment effect of bucindolol on AF prevention is mediated through β1389 Arg vs. Gly ARs and is not directly related to race or history of hypertension. There appears to be a class affect of β-blockers for reduction of new-onset AF in HFREF patients. A meta-analysis by Nasr Selleck Navitoclax et al. (7) of new-onset AF in HFREF trials demonstrated an average 27% reduction of

new-onset AF for five different β-blockers and evidence for a treatment effect for all β-blockers except nebivolol. This relatively modest reduction in new-onset AF across all β-blocker HFREF trials is in contrast to the marked 74% reduction in new-onset events in the β1389 Arg/Arg group IMP dehydrogenase observed in this analysis. Patients who developed AF had higher baseline NE levels than patients who remained free of AF, similar to data for AF development in an animal model of heart failure (18). Bucindolol’s well-known sympatholytic effects 14, 15 and 16 were observed in patients who developed AF and in those who did not and to the same extent in patients with β1389 Arg/Arg and β1389 Gly carrier genotypes. Thus, NE reduction by bucindolol may play a role in its AF prevention effects, but a difference in degree of sympatholysis does not explain the highly selective therapeutic effects of bucindolol in patients with the β1389 Arg/Arg genotype. In this genotype patients express only the β1389 Arg receptor, which is the “NE receptor” in the heart (12). A reduction in NE will therefore have a selectively greater therapeutic effect in this genotype, and patients are also protected from the adverse effects of marked sympatholysis (12). In the (β1389 Gly carrier + α2c322–325 Del carrier) group, relatively low prevalence (13.

It is parenthetically detected, asymptomatic, and treatment is not often indicated.

The first case of thoracic splenosis was reported in 1937 by Shaw and Shafi in a 20-year old selleck kinase inhibitor Egyptian man, and ever since, less than 50 new cases have been reported in the literature [1]. It involves 16%–67% of patients with past splenic trauma and or past splenectomy [2]. Pathogenesis of thoracic splenosis is depicted in Fig. 3[3]. Autotransplanted spleens have no hilum and the arterial supply can pass through any site in the capsule; however, accessory spleens have hilum where the arteries enter [4]. Splenosis is microscopically identical to normal spleen with both having thick capsule, trabeculae, and white and red pulp [4] and [5]. Although it is usually asymptomatic and diagnosed incidentally; it can occasionally present as hemoptysis and pleuritic chest pain [6]. Diagnosis can be challenging without knowledge of preceding

splenic injury, often leading to the use of biopsy, video-assisted thoracoscopic surgery (VATS) and even thoracotomy for diagnosis, causing significant morbidity and mortality among patient population [7] and [8]. There is a wide list of differentials for thoracic splenosis which include low grade lymphoma, thymoma, primary lung carcinoma, mesothelioma, thoracic endometriosis, mediastinal tumor, neurogenic tumors selleck and metastatic lesions. It may present as soliatary (25% cases) or multiple nodules (75% of cases) on CT scans [8]. Scintigraphy performed with heat-damaged 99Tc-labelled red blood cells is considered the most sensitive and specific imaging

modality for the diagnosis of splenosis [9], [10] and [11] and can demonstrate splenic tissue even when minimally present. This is because splenic tissue takes up more than 90% of damaged red blood cells [12] and [13]. Removal of thoracic splenic tissue is inadvisable especially in patients without functional abdominal splenic tissue may render the patient a splenic, increasing the risk of infection, although this notion is still debatable [14]. Surgical removal is considered in symptomatic patients and patients with hematological disease [3] and [8]. In conclusion, if a patient has an appropriate those history of splenic injury and multiple, asymptomatic, left-side pleural lesions, intrathoracic splenosis should be considered in the differential diagnosis. “
“Cardiovascular disease (CVD) is the leading cause of death globally. According to the World Health Organization, CVD was responsible for 30% of all deaths in 2005. Although typically considered a disease of developed countries, its incidence is increasing in the developing world as well. CVD usually stems from vascular dysfunction, for example, as a result of atherosclerosis, thrombosis, or high blood pressure, which then compromises organ function. Most notably, the heart and brain can be affected, as in myocardial infarction and stroke, respectively.

Because the

overarching objectives of forest restoration are frequently to influence ecological processes such as disturbance regimes and habitat connectivity operating at very large spatial scales (10,000’s–100,000’s of ha), a broader spatial perspective is required to evaluate the overall magnitude of ecological and planning needs. Without an understanding of regional scale restoration needs it is difficult to accurately quantify the magnitude of PD98059 price restoration funding needs for state and national entities or to set the context for prioritization of limited land management resources. It is also difficult to determine the cumulative, regional scale impact of current restoration efforts and evaluate whether these efforts are “making a difference”. Consequently, evaluation of restoration needs requires a perspective larger than individual watersheds or even individual national forests, and that

considers forested lands across all ownerships within a region. In this study we demonstrate a new approach for evaluating where, how much, and what types of treatments are currently needed to restore a Natural Range of Variability buy XL184 (NRV) in forest structure across eastern Washington, eastern Oregon, and southwestern Oregon. NRV is defined as a frequency distribution of ecosystem characteristics, including the appropriate spatial and temporal scales for those distributions and a reference period, typically prior to European settlement. These ecosystem characteristics may encompass a wide suite of terrestrial and aquatic considerations (Keane et al., 2009, Landres et al., 1999, Morgan et al., 1994 and USDA Forest Service, 2012a); here we focus on forest unless structure. We acknowledge the limitations of focusing on forest structure as an indicator of ecosystem health, and the NRV as the reference condition. Many biotic and abiotic components must be considered for

comprehensive restoration of forest ecosystems, including forest structure. Nevertheless, forest structure presents a tractable coarse filter to which many other aspects of biodiversity (e.g., terrestrial wildlife habitat, riparian and aquatic habitat, herbaceous diversity and productivity, and fire, insect, and disease frequency and severity) respond (Agee, 1993, Hessburg et al., 1999, Johnson and O’Neil, 2001 and Peterson et al., 2005). Ideally, we would also evaluate future range of variability (FRV) reference conditions that describe the expected response of forest ecosystems to climate change (Gartner et al., 2008 and Keane et al., 2009). FRV is an emerging concept, but FRV reference models are not yet consistently available at a regional scale. While the specific impacts of climate change are uncertain, restoring to a NRV is assumed to increase forests’ resilience and adaptive capacity (Agee, 2003, Hessburg et al., 1999, Keane et al., 2009, Millar et al., 2007, Stephens et al., 2013 and Stine et al., in press).

Of identified patients with behavioral or conduct problems, 22% were referred to an external mental health provider. At 6-month follow-up, more than a third (39%) had not attended an appointment with the referred provider, suggesting many behavioral problems identified in primary care

are left untreated. Subclinical or subthreshold disruptive, externalizing behavioral problems are also common among children who do not meet criteria for diagnosable disorders (Leflot et al., 2011 and Leijten et al., 2013). These children may present with problematic behaviors such as temper tantrums or disobedience. For both Selleckchem Lumacaftor diagnosable and subthreshold concerns, caregivers often utilize pediatricians as a resource for mental health care. Although pediatricians and other medical providers typically feel responsible for managing such mental health

issues (Stein et al., 2008), they are not often trained to adequately address these difficulties (Axelrad, Pendley, Miller, & Tynan, 2008). In order to address the mental health needs seen in primary care, medical and psychological services have increasingly been blended into an integrated model of health care delivery. This model aims to assist people with their behavioral health concerns at the time of their medical visits, avoiding the lag between an identified mental health need and its treatment (Strosahl, 1998). Effective service AZD2281 price delivery in an integrated primary care model calls for BCKDHB the joining of a variety of professionals working collaboratively as a team (Bachrach, 1996 and Blount, 2003). Patients across the lifespan—including families—are granted access to psychological services when they present to their primary care providers for medical concerns. The philosophy of integrated care differs from traditional mental health care in important ways. For instance, the goal of treatment is functional improvement of the patient rather than symptom amelioration. Furthermore,

behavioral health service providers are viewed as an integral member of the medical health team (Robinson & Reiter, 2007) and, therefore, patient rapport with their primary care provider (PCP) often assists in quick building of rapport with the mental health provider. In the integrated care model, behavioral health problems identified during a PCP visit trigger an in-the-moment referral to a BHC, also called a “warm hand-off.” BHCs will often conduct their interventions right in the medical examination room, so patients do not need to change locations or feel increased stigma for visiting with a BHC and discussing behavioral health concerns. The mechanics of service delivery in an integrated behavioral health care model also differ from traditional care.

5 μM and 0.08 μM respectively. However, their triphosphates were equally effective against HCV NS5B polymerase (IC50 values both 0.3 μM). In the replicon system, the triphosphate of the N-Nuc (MK608) was formed more efficiently than that of the C-Nuc1, thus explaining the lower activity of the C-Nuc1. However, in primary human hepatocytes, C-Nuc1 was phosphorylated to the triphosphate more efficiently than the N-Nuc (MK608). This illustrates the importance of using primary human cells. C-Nuc1 seemed to have a benign in vitro toxicity profile, including not inhibiting the mitochondrial DNA polymerase-gamma, but it had very significant toxicity

in animals. In a collaboration between Gilead and Craig Cameron at Pennsylvania State University, the researchers sought to identify the toxicity target(s) for ribonucleotide analogues, including C-Nuc1 and selleck kinase inhibitor others that had been stopped in Phase II trials. These studies showed a correlation between C-Nuc1 and the Phase II candidates, R1626, NM283 and BMS986094/IDX184. All the latter were efficiently incorporated into RNA by the mitochondrial RNA polymerase (>70% of the corresponding natural nucleotide). The triphosphate of C-Nuc1 was also an efficient substrate (22% the rate of ATP). In contrast, the active nucleotide analogs, formed by drugs approved

for the treatment of HCV, were poor substrates. Ribavirin was poorly incorporated (about 5%) and sofosbuvir was below the limit of detection (= 0.02%). More extensive Pictilisib clinical trial in vitro and cell culture evaluation of the compounds could have saved the expense of taking them into clinical trials. Understanding

that the mitochondrial RNA polymerase is an important target for ribonucleotide toxicity, the Gilead team sought analogs that were not incorporated by this polymerase. Adding a CN group to the 1′ position of C-Nuc1 did not change its activity as an HCV NS5B polymerase inhibitor (IC50 0.3 μM) but it did reduce incorporation in the mitochondrial RNA assay (<0.02%). However, in the absence of a nucleotide prodrug to bypass the first GNA12 phosphorylation step, the resulting di-substituted nucleoside analog would not be a drug candidate because it was not efficiently activated in cells. Application of a nucleotide prodrug strategy allowed this nucleotide to be pursued further. Oral absorption, delivery of the monophosphate into hepatocytes and high hepatic extraction were criteria used as part of the prodrug optimization process. A nucleotide prodrug, GS-464335 (a mixture of diastereoisomers at phosphorous) was well absorbed in dogs (>80%). Comparing the pre-hepatic and post-hepatic plasma drug levels, about 80% of the absorbed drug was taken up by the liver. Inside cells, GS-464335 was converted to the corresponding monophosphate which was efficiently converted to the triphosphate. At 24 h, the triphosphate levels remained about 2-fold above the IC90 value. A pure stereoisomer was selected and later named GS-6620.

3 μM for BIT225, NN-DNJ and Rimantadine, respectively, compared to IC90 values of 30, 30 and 1 μM for SA13/JFH (data not shown). The higher IC90 values reported here compared to previous studies most likely

reflect differences in the duration of treatment, with earlier studies treating infected cells for up to 72 h before measuring extracellular virus infectivity. Since Volasertib datasheet NN-DNJ can affect glycosylation of viral proteins we limited the duration of treatment to minimise such off-target effects. The efficacy of the inhibitors to limit HCV cell-to-cell transmission was tested using a recently developed single-cycle co-culture assay (Meredith et al., 2013). Since p7 has been reported to play a role in viral internalisation (Griffin et al., 2008) it is important to discriminate the effect of p7 inhibitors on virus assembly and entry. This assay allows one to assess the effect of p7 inhibitor treatment on infected ‘producer’ cells and enables the quantification of new infection events within 2 h of culturing infected and naïve hepatoma cells, which is essential given the reversible nature of p7 targeted compounds NLG919 molecular weight (Pavlovic et al., 2005 and Pavlovic et al., 2003). HCV J6/JFH or SA13/JFH infected Huh-7.5 cells were treated with 30 μM of either BIT225 or NN-DNJ and 3 μM Rimantadine for 24 h, concentrations previously shown to inhibit the level of infectious extracellular virus by 80–90%. The cells were washed to remove the compounds, labelled

with 5-Chloromethylfluorescein diacetate (CMFDA Cell Tracker Green, Invitrogen), and cultured with naïve Huh-7.5 targets at a 1:1 ratio as detailed in Fig. 1A. We confirmed that all compounds reduced the level of extracellular infectious virus in the co-culture ( Fig. 1B and C), consistent

with a reduction in J6/JFH and SA13/JFH cell-free transmission events. Although all three compounds inhibited 50–70% of J6/JFH cell-to-cell transmission, they had no detectable effect on SA13/JFH cell-to-cell transmission ( Fig. 1C). To determine how wide ranging this effect was, we screened a panel of diverse chimeric viruses expressing the structural proteins from genotype 1–7 for their sensitivity to all currently available p7 inhibitors, including NN-DGJ that does not affect host cell glycosylation pathways ( Chapel et al., 2006a, Chapel et al., 2006b and Chapel et al., 2006c). 4-Aminobutyrate aminotransferase Three viruses (JFH-1 – GT2; ED43/JFH – GT3 and QC69/JFH – GT7) showed limited transmission and were excluded from the analysis. The results show that all of the p7 inhibitors were significantly more effective at inhibiting cell-free infection than cell-to-cell transmission when all genotypes are considered ( Fig. 1D). The recent study by OuYang et al., suggest that amantadine binds the p7 ion-channel and locks it into a closed position (OuYang et al., 2013), preventing the de-acidification of the intravesicular compartments and leading to the secretion of non-infectious virus.

The conversion factor was the calculated as

the ratio of weight (kg) to volume (m3) for each core ( Fig. 8 and Table selleck chemicals llc 2). These values were imported into ArcGIS and gridded using the nearest-neighbor-gridding algorithm to provide a surface for a spatially integrated volume–weight calculation. Additional correction factors were taken into consideration: (1) core compaction (Cc), which was recorded during coring, and (2) inorganic sediment fraction (Co), which was determined from the LOI analysis. The methodology of applying correction factors is outlined in Fig. 8 with values for each core shown in Table 2. Interpolated and gridded values were multiplied as raster layers in ArcGIS and generated an estimate of dry sediment weight for the pond. An envelope of inferred minimum and maximum values for sediment weight in the pond was provided by using uniform values for the conversion and correction

factors based on min/max values of the empirical data, respectively. The resulting weight estimates serve as bounding values for internal error assessment. Regardless of C-factors used and resulting min/max pixel values the USLE model of the Lily Pond watershed shows erosion-rate variations that mimic LS-factor variations; this is particularly noticeable along the this website steep pond-proximal slopes ( Fig. 4). C-factor values of 0.001 and 0.42 provide an envelope of erosion estimates representing end-members of forested land-cover types described in the literature ( Table 1). Each metric was used as a constant C-value in repeated model runs. Using a C-factor of 0.001 produced an estimated total soil loss from 1974 to 2012 of 1087 kg while a C-factor of 0.42 yielded a total of 456,368 kg over the same time duration; the highest value possible for the C-factor ( Wischmeier and Smith, 1965) is 1 for bare soil; running the model using this C-factor generated an estimated total soil loss of 1,086,590 kg ( Table 3). The USLE models show that 60% of the estimated erosion is focused on the steep slopes

surrounding the pond, which make up only ∼10% of the watershed extent ( Fig. 1). The high-gradient hillslopes surrounding the pond to the north have the highest R-values while the more gently sloping terrain has values approximating Branched chain aminotransferase ‘0’ ( Table 3 and Fig. 4F). Collected pond cores range in length from 14 to 46 cm with compaction averaging ∼30% (Table 2). Depths to bedrock or till with respect to pond level were checked during the coring process and found in agreement with the 1974 excavation-survey maps, which detail a 1.5-m uniform pond depth and 2:1 aspect ratio along the sides (Fig. 7A). Sediment cores all contain low percentages of organic matter with near-surface intervals containing slightly higher weight percentages; organic-matter contributions to the sediment budget rarely exceed 2% in weight percent and are always below 5.5% (Table 2).

For nearly two millennia, it was a symptom and symbol of China’s never-ending problems with “frontier barbarians” who worked continuously to harvest some of the nation’s wealth for themselves (Barfield, 1989). It survives very visibly to the present, albeit now in greatly dilapidated condition except for a few limited restorations. The new Qin emperor also created for his personal afterlife a huge mounded tomb almost half a square km in extent, still unexcavated but, according to recorded legend, containing

a detailed replica of the royal palace surrounded by rivers of mercury. Well-digging in 1974 led to the discovery, about two km away from this location, of a fully equipped “spirit army” buried in two large pits that BMS-387032 cost included perhaps 3000 life-sized LBH589 concentration “terracotta warriors” and associated pottery models of horses, chariots, and weaponry. Excavations quickly captured world attention and the work continues, now sheltered and displayed beneath a vast metal hangar that could house a considerable fleet of the world’s largest jet airplanes (Fig. 2). The Zheng Guor Canal system, according to historical records created in 246 BC by the pre-imperial Qin State, was laid out over a course of some 200 km and linked two local rivers. It hugely expanded the agricultural output of the Qin region and helped afford its lord the economic wherewithal to gain

greater control next over his rivals. Beyond the constructions subsequently ordered by Emperor Qin Shihuangdi there were also infrastructural projects sponsored by other wealthy “houses” of the region that we still see attested archeologically – dams, canals, vast irrigated agricultural fields, and roads – that are not as well preserved as the displays of royal wealth we see in the Qin emperor’s funereal Terracotta Army. Nevertheless,

these modifications are evident on the landscape and referred to in written records of the time. A third-century historical source quoted by Elvin (1993) vividly portrays the busy cultural landscape of the Qin and following Han periods: “The households of the powerful are [compounds] where one finds hundreds of ridge beams linked together. Their fertile fields fill the countryside. Their slaves throng in thousands, and their [military] retainers can be counted in tens of thousands. Their boats, carts, and their merchants spread out in every direction…. The valleys between the hills cannot contain their horses, cattle, sheep, and swine. The great array of huge mounded earth tombs inside the boundaries of modern Xi’an, created by the Han emperors who followed Qin Shihuangdi, further attests the Imperial capacity of the time for enormously labor-intensive construction projects that created large areas of anthropogenic landscape in the Wei River Valley. Each Han tomb was an artificial mountain that took armies of men and animals years to build.

Selenoenzyme click here spielen eine wichtige Rolle beim Schilddrüsenhormonmetabolismus. Alle drei bekannten Deiodasen, D1 – D3, sind Selenoenzyme [18]. Die Schilddrüse ist wegen der verschiedenen Selenoenzyme, die für den normalen Schilddrüsenhormonmetabolismus von Bedeutung sind, das Organ mit dem höchsten Selengehalt. Die Aktivität dieser Enzyme in der Schilddrüse wird, im Vergleich zu anderen Geweben wie Leber, Niere oder der Haut, selbst unter Selenmangel äußerst effizient aufrechterhalten [19]. Das NTIS tritt in den meisten, nicht schilddrüsenassoziierten chronischen und akuten Krankheiten auf und ist durch einen raschen Abfall

des freien und gesamten T3 charakterisiert, begleitet von einem Anstieg des metabolisch inaktiven rT3 [20]. Abhängig vom Schweregrad der Erkrankung sind außerdem TSH und T4 reduziert und diese Veränderungen korrelieren mit der Prognose und der Mortalität. Die D1 ist verantwortlich für die Konversion von T4 zu T3, wohingegen die D3 die Umwandlung von T4 zu rT3 katalysiert. Die D1 katalysiert außerdem die Konversion und Clearance von rT3. Im Gegensatz zur D2, die ebenfalls die Aktivierung von T4 zu T3 katalysiert

und die im endoplasmatischen Retikulum lokalisiert ist, ist die MAPK inhibitor D1 in der Plasmamembran lokalisiert und wesentlich für die Bildung des zirkulierenden T3 verantwortlich [18]. Daher würde eine geringe D1-Aktivität allein einen niedrigen T3- und einen erhöhten rT3-Spiegel bei kritisch Kranken erklären [21]. Da die D1-Aktivität gegenüber der Verfügbarkeit von Selen empfindlicher ist und die D2 von ihren Substraten reguliert wird, wurde die Hypothese aufgestellt, dass der niedrige Selenspiegel bei kritisch kranken Patienten für die niedrige D1-Aktivität verantwortlich und damit die Ursache des niedrigen T3-Spiegels bei schweren akuten und chronischen Erkrankungen sein könnte [22]. Jedoch wird angenommen, dass der niedrige Selenspiegel bei akuten schweren Erkrankungen kein langfristiger Aprepitant Effekt, sondern ein schnelles Ereignis

ist, einhergehend mit der Schwere der Erkrankung. In einer prospektiven, randomisierten, placebokontrollierten Studie wurde gezeigt, dass eine Supplementierung mit hochdosiertem Natriumselenit bei operierten Patienten zu einem Anstieg des zirkulierenden Selens führt und dass dies mit einer rascheren Normalisierung des T4- und des rT3-Plasmaspiegels assoziiert ist. Antioxidanzien und Zink hatten dagegen keinen Effekt auf den Schilddrüsenhormonmetabolismus [22]. Kürzlich haben wir eine randomisierte, placebokontrollierte Studie an Patienten mit schwerer Entzündung und Sepsis durchgeführt, bei der wir zeigen konnten, dass unter adjunktiver Supplementierung mit Natriumselenit sich die Prognose der Patienten verbesserte. Zwar bestand unter Selensupplementierung keine Korrelation der Selenplasmaspiegel oder SePP mit dem T4-/T3-Verhältnis, wohl aber mit dem Clinical Activity Score [23].