However, some limitations of this study should be acknowledged. One of the limitations is that the effects of many factors,

such as population, social and economic status, health services and environmental hygiene, were not quantified precisely. Moreover, due to a lack of detailed laboratory information, we did not analyze the pathogens and the difference in pathogens, and the impact of pathogens on the different relative risks among the cities. A study analyzing the epidemic and aetiological character of bacillary dysentery in Henan Province from 2005 selleck products to 2009 found that Shigella flexneri was the dominant strains in the province where the study cities located, and the dominant sertypings were S. flexneri 2a, S. flexneri 4c Adriamycin price and S. flexneri 1a. 47 These strains may be associated with floods in the three cities during the study period. In addition, under reporting was inevitable in passive disease surveillance systems such as where we obtained our data for the current study and the notified cases were those with severe symptoms that chose to visit doctors in a hospital. 48 Some people with mild clinical symptoms and self-treated cases might not seek medical help. This could lead to an

underestimation of the risk of dysentery due to floods. This study has, for the first time, quantified the effects of floods on dysentery in a region including several cities. Flooding can significantly increase the risk of dysentery in the study areas. Moreover, results reveal that the risk of floods could be different between different areas. Additionally, the risk for dysentery may be higher during and after a sudden and severe flooding than a prolonged and moderate flooding. Our findings have significant implications for developing strategies to prevent and reduce health impact of floods. This work was supported by the National Basic Research Program of China (973 Program) (Grant No. 2012CB955502). We thank Chinese Center for Disease Control and Prevention, National Meteorological Information Center of China, and Data center for Institute of Geographic Sciences and Natural Resources Research of China sharing

with us the data needed for this study. “
“The incidence of pneumococcal meningitis in adults is estimated to be 0.1–1/100,000 in well-resourced countries1 and 2; Sclareol in sub-Saharan Africa where there are few surveillance data, the incidence is estimated to be 12/100,000 adult population3. In addition to the increased burden of disease in this region, the adult mortality rate from pneumococcal meningitis is 54%, compared to 30% in Europe.4 and 5 High Streptococcus pneumoniae bacterial load in the cerebrospinal fluid (CSF) has been associated with increased mortality in children with meningitis in Malawi and Finland, higher bacterial loads in the blood of adults with pneumococcal sepsis in Europe are also associated with poor outcome.

Selenoenzyme selleck products 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 selleck 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 Selleck Gefitinib 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].

alba enzyme is most closely related to those from other Gammaproteobacteria (not shown), and the genes encoding it (including sdhDE) are found together in a possible operon. The three BOGUAY subunits selleck chemical identified, on the other hand, are interior to three different contigs. Succinate dehydrogenase also plays a role in oxidative phosphorylation (see Section 3.4.2). The BOGUAY isocitrate dehydrogenase

(IcdA; Fig. S4D) likewise has a complex inferred history, being most closely related to sequences from hydrothermal vent gammaproteobacterial endosymbionts, the Chlorobium Chloroherpeton thalassium, and an uncultured archaeon (Thermoplasmatales archaeon SCGC AB-549-N05 Lloyd et al., 2013). Two enzymes are specific to the oxidative TCA cycle, citrate synthase and pyruvate dehydrogenase. Bacterial citrate synthases may be either Type I (homodimeric) or Type II (hexameric) (Nguyen et al., 2001). The B. alba and BgP genomes encode putative copies of both types (Table S5), but only Type I is found in the BOGUAY genome. It is closely related to the B. alba but not the BgP Type I sequence (Fig. S5A), and to sequences from other Gammaproteobacteria.

Unusually, it is also related to a sequence reportedly derived from sponge chromosomal DNA; no further information is available on this, but BLASTX matches to other regions of this scaffold (XP_003390620.1) are overwhelmingly this website bacterial (not shown). It may either be a contaminating sequence in the sponge genome, or recently acquired by lateral transfer. All three genomes possess putative pyruvate dehydrogenase genes (Table S5), whose phylogenies appear dissimilar, with the BOGUAY and BgP derived amino acid sequences more closely related to each other

and to sequences from a great diversity of other bacteria (Fig. S5B, C) than to the B. alba sequence. For BOGUAY, no gene for 2-oxoglutarate dehydrogenase (SucAB) was identified; however, this gap can be filled by the “reductive” KorAB in some bacteria (e.g., Baughn et al., 2009). No gene for the succinate dehydrogenase/fumarate reductase membrane anchor (SdhD) could be found, but the oxidative pathway is otherwise complete. Three enzymes are specific to the rTCA pathway: ATP citrate lyase (AclAB), 2-oxoglutarate ferredoxin oxidoreductase (KorAB), and pyruvate oxidoreductase (PorABCD). Of the three relatively complete Beggiatoaceae Cell press genomes, only orange Guaymas Beggiatoa possesses a complete set of these ( Fig. 5, Table S5), and their inferred phylogenies suggest histories of horizontal transfer via different routes. The putative BOGUAY AclA and AclB amino acid sequences (Fig. S6A, B) are both most closely related to sequences from a small cluster of other Gammaproteobacteria (Thioflavicoccus mobilis 8321, a tubeworm endosymbiont, and a hydrothermal vent environmental sequence), but beyond that to sequences from diverse proteobacteria. For the pyruvate:ferredoxin oxidoreductase KorAB (Fig.

Under these premises, the use of RDCs to yield the relative orientation of components in the complex might Proteases inhibitor not be always successful. Nevertheless, in a recent study of the ADAR2 dsRBM-RNA complex (MW ∼50 kDa), the Allain group has derived the structure of the whole particle by assembling the two sub-complexes under the guidance of only 45 N–HN RDCs. The

success of the approach in this particular case was helped by the additional constraint imposed on the complex structure by the long RNA stem [32]. Even in the case that enough RDCs can be collected for each component, the data from one alignment medium do not uniquely define the mutual orientation of two molecules; rather, four clusters are obtained where the two molecules are related by 180° rotations around the axis

of the alignment tensor [33]. To lift this ambiguity, RDCs should be obtained from at least two alignment media leading to independent alignment tensors. In practice, we find it often difficult to obtain good quality RDCs for large RNP assemblies, not least because the dissolution of supra-molecular particles in orienting media can lead to the disassembly or the rearrangement of unstable parts of the complex. We prefer to use RDCs to confirm or refine the structural models of the single components, before proceeding to the collection Navitoclax in vitro of intermolecular restraints [34]. In the past decade, the NMR community has witnessed a renaissance of paramagnetism, namely of magnetic dipoles generated by unpaired electrons. In general, the presence of a paramagnetic center influences the chemical shift and the relaxation properties

of the neighboring nuclei. Here I would like to concentrate on the effect of paramagnetic Suplatast tosilate relaxation enhancement   (PRE) on nuclear spins. Two mechanisms are responsible for increased nuclear relaxation rates in the presence of an unpaired electron: the first mechanism, called Solomon relaxation, is a dipole–dipole interaction between the electron and the nucleus and is prominent for slowly tumbling molecules (long rotational correlation time τ  c) and long-lived electron spin states; the Curie relaxation, instead, is important for fast relaxing electrons, and generates from the interaction of the nuclear dipole with the averaged static magnetic moment of the electron [35]. Both relaxation mechanisms depend on the distance between the electron spin and the nucleus according to r−6. Quantification of the paramagnetic relaxation enhancement effect (PRE=R2para) at the site of the nucleus yields a measure of the distance between the electron and the nucleus and can be translated into structural information. For methyl groups detected in a 13C–1H HMQC spectrum, the PRE effects are quantified from the cross peak intensity ratio (Ipara  /Idia  ) of samples with the spin label in the paramagnetic (oxidized, Ipara  ) and diamagnetic (reduced, Idia  ) state.

2D). Both the pharmacological AMPK inhibitor compound C (Figs. 3A, B)

and transfection with AMPK shRNA (Figs. 3C, D) also suppressed osteogenic differentiation of hDP-MSC. The shRNA silencing of AMPK early during hDP-MSC activation (day 1) prevented activation of AMPK/Raptor and restored the activity of the negative autophagy regulators mTOR/S6K, resulting in the inhibition of LC3-II increase (Fig. 3E). On the other hand, late inhibition of AMPK at day 3 by compound C completely failed to block osteogenic differentiation (day 7 ALP values: 2.07 ± 0.10 and 2.11 ± 0.06 in control and compound C-treated hDP-MSC, respectively; n = 3, p > 0.05). Similarly, autophagy inhibitors bafilomycin and chloroquine were also ineffective in preventing hDP-MSC differentiation if added at day this website Selleck Ixazomib 3 (ALP values: 1.82 ± 0.15, 1.76 ± 0.10 and 1.74 ± 0.08 in control, bafilomycin and chloroquine-treated hDP-MSC; n = 3, p > 0.05). Therefore, it appears that early AMPK-dependent autophagy is required for optimal differentiation of hDP-MSC to osteoblasts. Finally, we explored the role of Akt/mTOR activation in AMPK-dependent osteogenic differentiation of hDP-MSC. The selective Akt antagonist DEBC (Figs. 4A, B), as well as pharmacological mTOR inhibitor rapamycin (Figs. 4C, D) or

transfection with mTOR siRNA (Fig. 4E), inhibited hDP-MSC differentiation to osteoblasts, as confirmed by alkaline phosphatase assay and RT-PCR/immunoblot analysis of osteocalcin, Runx2 and BMP2. Similar effect, although somewhat Casein kinase 1 less pronounced, was observed even if DEBC or Akt were added at day 3 (day 7 ALP values: 1.47 ± 0.09, 1.20 ± 0.05 and 1.28 ± 0.01 in control, DEBC- or rapamycin-treated hDP-MSC; n = 3, p < 0.05) or even day 5 of differentiation (data not shown). The suppression of Akt phosphorylation

in DEBC-treated hDP-MSC prevented activation of mTOR/S6K at day 5 of differentiation, while AMPK activation remained largely unaffected ( Fig. 5A). Both the mTOR siRNA and rapamycin reduced the phosphorylation of mTOR/S6K without affecting the activation of either Akt or AMPK ( Figs. 5A, B). Finally, AMPK downregulation with compound C or shRNA mimicked the inhibitory effects of DEBC on the activation status of Akt and mTOR/S6K in differentiating hDP-MSC at day 5 ( Figs. 5A, C), indicating AMPK as an upstream signal for Akt activation and subsequent increase in mTOR/S6K activity. These data demonstrate that the optimal osteogenic transformation of hDP-MSC requires AMPK-dependent phosphorylation of Akt and consequent activation of mTOR at the latter stages of differentiation. The present study demonstrates a central role of the intracellular energy sensor AMPK in the osteogenic differentiation program of hDP-MSC.

W drugą rocznicę jego śmierci Rada Miejska Nowej Soli w uznaniu jego zasług dla rozwoju miasta nazwała jego imieniem miejscowe rondo. Zapamiętamy go jako dobrego człowieka i sumiennego lekarza, o wysokiej kulturze osobistej, niezwykle życzliwego dla wszystkich

potrzebujących pomocy. “
“Pleural effusions are common complications of pediatric bacterial pneumonias. Improving pediatric care does not eliminate pleural empyema (PE) – a life-threatening condition which may also result in the permanent deterioration of lung function. There is debate about treatment options. Simple chest tube drainage is often inadequate in complicated parapneumonic effusions due to presence of viscous fluid with fibrinous debris clogging the tube [1]. Patients with poor response to antibiotics and tube thoracostomy may require surgical decortications [1] and [2]. Length of stay and long-term morbidity this website are reduced by this more aggressive approach. Video-assisted thoracoscopic surgery (VATS) closely imitates open thoracotomy and drainage, and is an effective and less-invasive replacement for the decortications procedure [3]. We performed a retrospective review of the records of 11 consecutive patients who needed surgical treatment because of pleural empyema in regional referral children’s hospital between January

2004, and December 2010. There were 4 boys and 7 girls, and all had postpneumonic empyemas. Their ages ranged from 1 to 19 years (mean 8.9). Before having been referred learn more to our department, all children were managed for sustained pneumonia Reverse transcriptase by local pediatricians using broad-spectrum antibiotics for 1 to 9 weeks (mean 3 weeks). Next, children were ineffectively treated in general hospitals using conventional pleural drainages maintained for 1 day to 2 months (mean 12 days). On the admission three youngest children

– boys aged 1, and 4, and girl aged 1 showed clinical signs and symptoms of a septic condition. All patients had anteroposterior and lateral chest radiographs and all patients had computed tomographic scans to guide interventional procedures (Fig. 1, Fig. 2, Fig. 3, Fig. 4 and Fig. 5). VATS is performed under general anesthesia. Intra-operative monitoring includes an arterial pressure line, large bore intravenous access, a Foley catheter, and pulse oximetry. The patient is positioned as for a posterolateral thoracotomy. The camera port is placed in the 7th or 6th intercostal space in the line of the anterior superior iliac spine or just anterior to this. VATS decortication can be performed through 2 or 3 ports. The working port should be placed over the 5th intercostal space between the mid and anterior axillary lines. The intercostal incision should allow 3 fingers. A third port can be placed posteriorly, positioned to allow access to the anterior part of the pleural cavity. Once the chest is entered, a suction is used to drain the chest of effusion.

The maturation arrest observed in the present study which is represented by few numbers of spermatogenic layers and few sperms in the group treated with MSG was reinforced by El-Wessemy [52] who correlated this arrest to the testosterone inhibition which caused stopping of spermatogenesis.

Previous researches have explained the mechanisms by which MSG inhibited the spermatogenesis in the current experiment. Glutamate receptors are present in different tissues: the hypothalamus, spleen, thymus, liver, kidneys, endocrine system, ovaries, etc. [53]. Our results came in harmony with other studies that proved the presence of functional glutamate transporters and receptors in testes selleck inhibitor of rats [54] and [55] in mice. One of the mechanisms may be a direct effect of MSG via glutamate receptors and transporters on the epithelial cells of the seminiferous tubules. Selenium can strengthen antioxidant ability by enhancing activities of antioxidant enzymes and by increasing contents of the antioxidants [56]. Inorganic Se such as sodium selenite is commonly used with vit. E for supplementation in animals diagnosed with Se deficiency or in animals residing in Se deficient areas [57]. In this study, the protective efficacy of selenium on MSG toxicity may be due to its antioxidant

effects. Selenium is present in biological systems as selenoproteins, PCI32765 which characteristically are oxidoreductases. These selenoenzymes have a variety of activities [58] and many of them, including the GPx and the thioredoxin reductases, have oxidant defense functions. Under conditions of selenium deficiency, tissue levels of these enzymes fall and oxidative stress conditions develop [59]. This increases the susceptibility of cells to certain types of oxidative and this is greatly was in harmony with our results as the

oxidative stress level was low in Se- treated group while it was higher in group treated with MSG. Our results are in agree with Rao and Sharma [60] and [61] who had reported that co-administration of mercuric chloride and vit E was protective effect in their study. Because the major criterion of irreversibility of cell injury is damage to the plasma membrane, vit E becomes essential else in the protection against chemical insult [62]. In the present study, vit E showed protective effect against MSG. This effect may be due to impaired absorption of MSG in the gastrointestinal tract and/or its antioxidant effect [63]. Vitamin E prevents oxidative damage to sensitive membrane lipids by destroying hydroperoxide formation, acting in conjunction with Se, and protects cellular membranes and lipid containing organelles from peroxidative damage by oxidative Stress [64]. In this work, biochemical and histopathological alterations observed in testis tissues of rats exposed to MSG.

The presence of executive functioning deficits may moderate the response to treatment, and metacognitive strategy training may AZD0530 clinical trial need to be incorporated in these interventions. Finally, there is evidence from numerous studies indicating

that cognitive rehabilitation is effective during the postacute period, even many years after the initial injury. Additional research is needed to investigate the patient characteristics that influence treatment effectiveness. In our initial review, we indicated that cognitive rehabilitation should be directed at achieving changes that improve persons’ functioning in areas of relevance to their everyday lives. The majority of studies have relied on changes in cognitive functioning, assessed by standardized neuropsychologic

testing or other cognitive measures, as proximal outcomes of cognitive rehabilitation. Our reviews are consistent with the view that cognitive rehabilitation check details is effective in helping patients learn and apply compensations for residual cognitive limitations, although several studies suggest that intervention may directly improve underlying cognitive functions.10, 15 and 99 Our systematic reviews provide more limited evidence regarding improvements at the level of functional activities, participation, or life satisfaction after cognitive rehabilitation. Although improvements at the level of social participation and quality of life are valued as the distal health-related outcomes of cognitive rehabilitation, it is often not possible to observe improvements on these more global outcomes within

the limited timeframes used in most investigations of cognitive Y27632 rehabilitation. The possible reasons for this include the relatively brief periods of intervention, limited opportunity to address the application of interventions to everyday functioning, lack of follow-up assessing community functioning, or failure to include the relevant outcome measures. A number of studies have evaluated treatment effects based on observations of everyday functioning or performance on tasks derived from activities of daily living, which provide evidence for the effects on daily functioning. Studies of comprehensive-holistic cognitive rehabilitation provide the best evidence for improvements in health-related outcomes, such as social participation and quality of life. Since our prior reviews, more sophisticated criteria have been developed for evaluating the level of evidence beyond basic study design (eg, blinding of outcome assessments). We recognize that the failure to employ these additional criteria has influenced the classification of studies and is a limitation of this review. We elected to retain our initial criteria in order to be consistent with our prior reviews.

2 to − 4.8%. Four susceptibility QTL were detected on Chrs.A7, D3, D5 and D8 based on the RDIs of the CSILs. The additive effect of the decrease in G. hirsutum cv. TM-1 resistance to V. dahliae D8092 ranged from 8.28 to 11.04 and the percentage of PV ranged from 2.3 to 4.1%. There were seven QTL for resistance to V. dahliae V991 on the At subgenome, which was more than the three found on the Dt subgenome ( Table 4). However, there was no significant difference between the numbers of resistance QTL on At and Dt subgenome chromosomes (P = 0.21) by chi-square test ( Table 4). The total additive effect and PV of the V.

dahliae V991 resistance QTL on the At subgenome chromosomes were − 61.63 and 16.6%, respectively, and the total additive effect and PV of those on the Dt subgenome were EPZ5676 ic50 − 25.06 and 6.3%, respectively. The values for the other two V. dahliae isolates were similar to those obtained for the V991 isolate. These results indicate that the resistance effects of the QTL on the At subgenome are greater than those of the QTL on the Dt subgenome. There were 10 QTL for susceptibility to all of the V. dahliae isolates in the At subgenome and nine in the Dt subgenome ( Table 5). There was no significant difference in

the numbers of susceptibility QTL located on At and Dt subgenome chromosomes click here (P = 0.82) ( Table 5). The total additive effect and PV of the QTL for susceptibility to V. dahliae V991 on At subgenome chromosomes were 81.31% and 22.7%, respectively, and those of the susceptibility QTL on the Dt sub-genome was 75.94 and 23.0%, respectively. The RDIs of five CSILs and G. hirsutum cv. TM-1 corresponding

to 11 QTL are given in Table 6. Based on the RDIs, IL055 contained one introgressed segment on Chr.A5 and was resistant to V. dahliae D8092, tolerant to V. dahliae V991, from but susceptible to V. dahliae V07DF2; IL162 contained one introgressed segment on Chr.D12 and was resistant to V991, tolerant to D8092, but susceptible to V07DF2; IL154 contained one introgressed segment on Chr. D11 and was resistant to V07DF2 and D8092 but susceptible to V991; IL009 contained two introgressed segments on Chrs.A8 and D1 and was resistant to D8092, tolerant to V07DF2, but susceptible to V991; and IL089 contained three introgressed segments on Chrs.A7, D7, and D11 and was resistant to D8092 and V991 and tolerant to V07DF2. Clearly, the CSILs showed variable resistance to each of the different V. dahliae isolates, suggesting that there might exist an additional effect between each resistance QTL and the different fungal strains. The genotypes and resistance performances of three CSILs and G. hirsutum cv. TM-1 (recipient parent) are illustrated in Fig. 3. IL095 and IL154 each contained one introgressed segment, located on Chrs.D7 and D11, respectively; whereas IL089 contained three introgressed segments located on Chrs.A7, D7 and D11, respectively ( Fig. 3-A). The two introgressed segments in IL089 on Chrs.

Cell recovery and viability were measured in blood samples during the CMI protocol using the following combination of experimental conditions: TTP (2, 7 or 24 h) and RsT (none, 2, 6 or 18 h). These measurements were used as input in a polynomial prediction model, to further calculate optimal combinations for these experimental conditions on cell viability. The same approach was used for cell recovery and measurements of CMI responses. The study

Dinaciclib research buy was conducted in accordance with the Good Clinical Practice Guidelines and the Declaration of Helsinki. Written informed consent was obtained from each participant prior to the performance of any study-specific procedures. This study has been registered at www.clinicaltrials.gov

(NCT01610427). A summary of the protocol is available at http://www.gsk-clinicalstudyregister.com (GSK study 116329). Participants were ART− HIV + eligible adults between 18 and 55 years of age at the time of enrollment, who were not eligible for ART treatment as per established guidelines. Participants had to have an HIV-1 RNA viral load (VL) level between and including 2000 and 100,000 copies/mL and a CD4+ T-cell Phospholipase D1 count > 500 cells/μL at screening. Participants

who at screening had any clinically relevant medical condition or grade 3 or 4 abnormalities as defined EPZ015666 cost by Division of Acquired Immunodeficiency Syndrome (DAIDS) grading were not enrolled. No planned hematotoxic, investigational or non-registered product, nor vaccine not foreseen in the protocol was allowed during the study period. No pregnant or lactating women were included in the study. The primary objective of this study was to model lymphocyte viability according to TTP and RsT conditions and to select the best combination of these two parameters with the aim to maximize the post-ICS viability in PBMC samples collected from ART− HIV+ individuals. The secondary objectives were: (i) to describe the impact of absence or presence of the resting step before ICS on the proportion of viable lymphocytes and on the CMI responses in PBMC samples, and (ii) to describe the proportion of viable lymphocytes and the magnitude of the CMI responses following 6 h (as compared to overnight) antigen stimulation before ICS. The impact of TTP and RsT on the total cell recovery has been evaluated as a post-hoc analysis.