All participants underwent clinical examination prior to arthroscopy. A subgroup of participants also underwent MRI investigation prior to arthroscopy. The decision to undertake an MRI investigation was made at the surgeons’ discretion. The order of the provocative tests and MRI was dictated by convenience, but both the provocative tests and MRI were completed before the arthroscopy. All provocative tests were performed as close as possible to arthroscopy. The longest delay was 21 days. Provocative tests were conducted blind to the results of MRI, and MRIs were interpreted blind to the results of the provocative tests. The surgeons performing the arthroscopies were blinded to the results

of the provocative tests but not to the results of the MRIs. Clinical examinations were performed primarily (87%) by one hand therapist (RP) with 27 years of experience. The other clinical examinations were performed by two therapists with 20 and 10 years of find more experience. Initially, a subjective assessment was undertaken and included questions to determine the time of injury, location of pain, and the functional demand on the wrist. The functional demand placed on the wrist by work and activities of daily living was

classified by participants on a 3-point scale designed for this study. On this scale ‘light’ reflected sedentary or office work, ‘moderate’ reflected Enzalutamide supplier intermittent use with heavier activities such as gardening, and ‘heavy’ reflected manual work or participation in manual sports such as martial arts and racquet sports on a regular basis. Participants were also asked to self-rate perceived wrist stability on a 4-point scale designed for this study. The levels of the scale were ‘does not give way’, ‘gives way with heavy activity’, ‘gives way with moderate activity’, and ‘gives way with light activity’. Pain and function were assessed with the Patient-Rated Wrist and science Hand Evaluation questionnaire (MacDermid and Tottenham, 2004). The physical examination consisted of an assessment of the integrity of various wrist ligaments, the TFCC, and the lunate

cartilage. The tests used were the SS test, LT test, MC test, TFCC test, TFCC comp test, DRUJ test, and the GRIT (LaStayo and Weiss, 2001). Both asymptomatic and symptomatic wrists were tested to establish if there was hypermobility in the symptomatic wrist with respect to the asymptomatic wrist and to determine if there was pain. The outcomes of tests were reported as positive, negative or uncertain except for the GRIT which was only reported as positive or negative. A test was only reported as positive if it reproduced the participant’s pain (with or without hypermobility compared to the contralateral side). A test was reported as uncertain if there was hypermobility (compared to the contralateral side) or if the pain produced was not the primary pain that the participant presented with.

That firing rates do not adapt to zero but rather to a relatively high rate indicates that trafficking (superlinear component) is rapidly accessible under physiological conditions. Similar to the response described in Figure 5, under physiological conditions the processes tend to merge but vesicle release shows a reduction in slope initially that becomes sustained. The level of neural adaptation may in part be determined by how rapidly each synapse is capable of recruiting

vesicles between pools—the faster the recruitment, RG-7204 the less adaptation is observed. In fact, it may be argued that steady-state firing requires recruitment of vesicles such that the rate of release at any given synapse may be dictated by access to the reserve pool of vesicles. Thus it may be that spontaneous firing rates are regulated

by resting calcium currents and vesicles in the RRP and recycling pool, while stimulated release is more dependent upon vesicle recruitment from the reserve pool and the ability to modulate release of stored calcium (Guth et al., 1991). In summary, we used real-time capacitance measurements to identify saturable pools of vesicles and discovered a superlinear release component requiring recruitment of vesicles to release sites. We suggest that Ca2+-dependent vesicle trafficking Trichostatin A chemical structure is responsible for this movement, which is required for hair cell synapses to maintain high rates of sustained vesicle fusion. We postulate that the superlinear release component reflects synapses operating at maximal rates of release and trafficking Mannose-binding protein-associated serine protease and that release of an as yet undefined internal pool of Ca2+ may be required. These characteristics of synaptic vesicle recruitment and release make hair cell ribbon

synapses quite unique as compared to other synapses. The auditory papilla from red-eared sliders (Trachemys scripta elegans) were prepared as previously described ( Schnee et al., 2005) by using methods approved by the IACUC committee at Stanford University and following standards established by NIH guidelines. Tectorial membranes were removed as previously described by using a hypertonic and hypercalcemic (10 mM Ca2+) solution ( Farris et al., 2006). The external recording solution contained 125 mM NaCl, 0.5 mM KCl, 2.8 mM CaCl2, 2.2 mM MgCl2, 2 mM pyruvate, 2 mM creatine, 2 mM ascorbate, 6 mM glucose, and 10 mM N-(2-hydroxy-ethyl) piperazine-N′-(2-ethanesulfonic acid) (HEPES) with pH adjusted to 7.6 and osmolality maintained at 275 mosml/kg. One hundred nanometers apamin was included in the external solution to block SK potassium currents ( Tucker and Fettiplace, 1996). Cells were imaged with a BX51 fixed-stage upright microscope (Olympus) with bright-field optics. Conventional epifluorescence was used for the Ca2+ imaging.

The relative gene transfer was calculated by dividing the % value of each treatment by the % value for the standard. Here transconjugants serve as standard. Data were analyzed using Graph Pad InStat-3 and expressed as mean ± standard

deviation (SD) of three independent experiment. The continuous variables were tested with one-way analysis of variance (ANOVA) and Dunnett’s test. Values < 0.05 was considered statistically significant. Re-identification of all of the clinical isolates were done and found to be of A. baumannii, C. braakii, E. coli, P. aeruginosa and K. pneumoniae. A. baumannii and C. braakii were positive for both qnrA and qnrB gene, whereas E. coli, P. aeruginosa and K. pneumoniae were positive for qnrB gene and none of the clinical isolates harbored qnrS ( Fig. 1). As shown in the Table 1, Potentox emerged as the most active antibacterial against A. baumannii, P. aeruginosa, E. coli and K. pneumoniae with MIC values 8 μg/ml. http://www.selleckchem.com/products/PD-173074.html The corresponding MIC for C. braakii was 16 μg/ml. The imipenem MIC values for A. baumannii and K. pneumoniae were 256 μg/ml each; 64 μg/ml for P. aeruginosa and C. braakii and 32 μg/ml for E. coli. The meropenem MIC values for A. baumannii, and K. pneumoniae were 128 μg/ml

each and 32 μg/ml for C. braakii and P. aeruginosa whereas 16 μg/ml for E. coli. For the other comparator drugs, the overall MIC values ranged from 32 to 1024 μg/ml. On the other hands, P. aeruginosa and K. pneumoniae found to be resistant to cefoperazone + sulbactam, amoxicillin plus clavulanic acid and levofloxacin; A. baumannii also showed resistant to amoxicillin plus clavulanic c-Met inhibitor acid. There was a significant (p < 0.01) reduction in the MIC values of Potentox when compared

with the other comparator antibacterial agents ( Table 2). The zones of inhibition were calculated in millimeter for all strains and presented in the Table 3. Potentox was found to be sensitive against all clinical isolates as evident by zone of inhibition values, 23.5 ± 1.2, 20.8 ± 2.8, 25.8 ± 3.0, 27.2 ± 2.8, 23.2 ± 2.5 for A. baumannii, C. braakii, P. aeruginosa, E. coli and K. pneumoniae, respectively. Imipenem was found to be sensitive only against E. coli, Montelukast Sodium whereas meropenem was sensitive against P. aeruginosa and E. coli. Piperacillin plus tazobactam and cefoperazone plus sulbactam exhibited sensitivity toward C. braakii and E. coli. Cefepime was found to be sensitive only against C. braakii. Other tested drugs including amoxicillin plus clavulanic acid, moxifloxacin, levofloxacin and amikacin were observed to be resistant against all of the clinical isolates. The statistical analysis of AST values of Potentox vs other comparator drugs are shown in Table 4. Following conjugation, transconjugants were selected on MacConkey agar plates containing sodium azide and streptomycin. Analysis of transconjugants through PCR confirmed that transconjugants carrying the same gene as donor (Fig. 2).

075 s, spatial resolution: 0.33 mm, table speed: 458 mm/s; ferret thorax acquisition times ≈0.22 s; enables accurate scanning of living ferrets without the necessity of breath-holding, respiratory gating, or electrocardiogram (ECG)-triggering) as previously described [28] and [29]. Briefly, all animals of group 1 (saline; infection control), group 2 (TIV; parenteral control) and of group 4 (nasal Endocine™ formulated split antigen, 15 μg HA) were scanned 6 days prior to virus inoculation (day 64) to define the uninfected baseline status of high throughput screening compounds the respiratory system, and after challenge on 1, 2, 3 and 4 days

post inoculation (dpi). During in vivo scanning the anesthetized ferrets were positioned in dorsal recumbency CB-839 in a perspex biosafety container of approximately 8.3 l capacity that was custom designed and built (Tecnilab-BMI). The post-infectious reductions in aerated lung volumes were measured from 3-dimensional CT reconstructs using lower and upper thresholds in substance densities of −870 to −430 Hounsfield units (HU). Differences between the groups immunized with the Endocine™

adjuvanted H1N1/California/2009 vaccine preparations (groups 3–6) were analyzed statistically using the Kruskal–Wallis test. Differences between the sham (saline) immunized control group and the immunized groups were statistically analyzed using the two-tailed Mann–Whitney test. One intranasal immunization with Endocine™ adjuvanted split, or whole virus antigen induced high homologous HI antibody titers: in all ferrets of groups 3 and 5 (5 and 30 μg HA split antigen; titers 160–1120 and 400–3200, respectively) and in 5 out of 6 ferrets of groups 4 and 6 (15 μg HA split and whole virus antigen at; titers

≤5–5760 and 5–1280, respectively). A second immunization increased HI antibody titers in all ferrets, Dipeptidyl peptidase irrespective of antigen and antigen dose (groups 3–6, titers 1120–2560, 1120–5760, 640–3840 and 100–2880, respectively) (Fig. 1A). A third intranasal immunization did not substantially boost the HI immune response further (groups 3–6, titers 1280–3840, 1920–4480, 1280–3200 and 160–2560, respectively). The differences in HI antibody titers between the 3 split antigen HA doses (groups 3, 4 and 5) were not significant (p > 0.05). However, mean HI antibody titers in group 4 (15 μg HA split antigen) were significantly higher than those in group 6 (15 μg HA whole virus antigen); p = 0.01 and p = 0.02 after 2 and 3 immunizations, respectively. Cross-reactive HI antibodies were measured against the distant H1N1 viruses A/Swine/Ned/25/80, H1N1 A/Swine/Italy/14432/76 and H1N1 A/New Jersey/08/76 (Fig. 1B–D, respectively). The highest cross-reactive HI antibody titers were measured in group 4 (15 μg HA split antigen) after 2 immunizations.

Our estimate of rotavirus outpatient visits are lower than those estimated by Parashar and colleagues [8] and [9] because a conservative ratio of rotavirus outpatient visits to hospitalization obtained from a phase III rotavirus vaccine trial cohort of 1500 children observed for two years was used in which two-thirds of children had received a rotavirus vaccine. The ratio of outpatient rotavirus gastroenteritis visits to rotavirus gastroenteritis

admission in the phase III clinical trial population was 3.75, and may have been lower because of the prompt administration of rehydration solutions at home decreasing mild or moderate disease, which points again to higher need for healthcare due to rotavirus disease than has previously been estimated. These are findings Panobinostat order that must be considered as policy makers shift from impact estimation based on mortality alone to disease reduction. This study has several limitations.

First, four of the five cohorts that contributed to the estimation of rotavirus related morbidity were from a single site in Vellore. It is likely that morbidity rates and health-seeking characteristics of this population differs from higher mortality INCB024360 mw regions of India and limits the validity of extrapolations from these geographically limited cohorts. Nonetheless, given that health characteristics and health care access in Tamil Nadu are better than most other parts of India, it is likely that the estimates based on Tami Nadu are very conservative. Second, the <5 mortality rate is the number of <5 deaths per 1000 live births in a year and does not provide a direct estimate of probability of death between 0 and 5 years required for calculating deaths averted and NNV. Third, there is limited information on the rate of rotavirus morbidity in the 3–5 year age group. This analysis assumes a constant rate of events in the 4 months to 2 years age group L-NAME HCl and applies an adjusted estimate to the 3–5 year age group where no or limited direct estimates are available. Similarly we applied the ratio of outpatient to inpatient rotavirus gastroenteritis

among the clinical trial participants to estimate the number of ambulatory rotavirus gastroenteritis visits. Despite there being no active referral to hospital for diarrheal episodes, free and better healthcare access in the clinical trial environment could have inflated the number of outpatient visits. This must be considered against the underestimation of the impact on society due to rotavirus disease that occurs when outpatient and hospitalization rates do not account for barriers in access to appropriate levels of healthcare. Furthermore, the increased access to ambulatory care might, by early diagnosis and treatment, prevent progression of disease to more severe presentation and thus contribute to lower estimates of mortality and hospitalization. Fourth, this analysis assumes that vaccine efficacy approximates effectiveness.

12 Hydrophilic polymers are commonly used as rate-controlling polymers for extended release matrix-type dosage forms. Hydroxypropyl methylcellulose (HPMC) is a hydrophilic polymer used in the matrix type systems for the prolonged drug release. HPMC matrix tablets may be affected

by several formulation variables, such as polymer concentration, molecular weight, drug levels and solubility, type of excipient and tablet shape and size. 13, 14, 15 and 16 Usually HPMC upon contact with aqueous media begins to hydrate, swell, coalesce, and form a viscous phase around the surface of the tablet. For hydrophilic matrix tablets comprised of water-soluble, swellable polymers such as HPMC, the release kinetics are described by drug diffusion and polymer erosion. Drug GSI-IX release is dependent on the relative contribution of diffusion and erosion release mechanisms. 17 The matrix geometry is also one of the important factors for drug release from extended-release dosage

forms. 18 Specifically for HPMC matrix tablets, the effect of Rigosertib purchase matrix geometry on drug release has also been studied in detail. 19 Poly (ethylene oxide) (PEO) is a hydrophilic polymeric excipient that can be used in formulations for different purposes. 20 PEOs are mostly used to produce controlled release solid dosage forms such as matrices, reservoirs or coated cores. Due to their chemical structure, in the presence of water, control the release of the active moiety either by swelling or by eroding and swelling forming a hydrogel. In both cases, the water triggers the process starting the erosion and/or the swelling. PEO has been used in association with HPMC to delay the release of a drug by controlling the extent and rate of swelling of the polymers. 21 However, there appears a scanty

literature available on XR formulations of lamivudine. Punna Rao Sitaxentan et al prepared lamivudine matrix tablets using HPMC and Prakash et al prepared lamivudine microcapsules using various cellulose polymers.22 and 23 The purpose of this study was to design oral XR tablet formulations of lamivudine using HPMC and PEO as the drug retarding polymers. The tablets were formulated by direct compression method, and their physical and in vitro release characteristics were evaluated. The effect of formulation factors such as polymer proportion, polymer type on the release characteristics was studied in order to optimize the formulation. The optimized formulation was applied for in vivo bioavailability studies in rabbits upon oral administration. Lamivudine (LAMI) was obtained as a gratis sample from Alkem laboratories Ltd., Mumbai, India. Hydroxypropyl methylcellulose K100M (HPMC) from Colorcon Asia Private Ltd., and Poly (ethylene oxide) (Polyox WSR 303, PEO) from The DOW Chemical Company were purchased in Mumbai, India.

Despite the poor level of bra fit

and breast support in these adolescent athletes, only low levels of breast discomfort selleck compound during exercise were reported. Furthermore, this did not significantly improve, despite improvement in bra fit and level of breast support. The relatively small average breast size of the participants (12B) and their age may explain this finding, as breast discomfort during exercise is more problematic in females with large breasts (Gehlsen and Albohm 1980). In addition, changes in the mechanical properties of the tissues supporting the breasts or the habitual lack of adequate breast support over time in adult females may decrease their anatomical level of breast support, although this notion requires further investigation. The improvement in level of support post-intervention in the experimental group shows that the improvement in knowledge was accompanied by an improvement in choice of bra (in terms of design

and lifespan) relative to the level of physical activity and breast size. For this age group, the improved breast support may be more effective in decreasing the embarrassment of physical appearance, a known barrier to physical activity in adolescence (James 1998, Robbins et al 2003, Shaw 1991, Taylor et al 1999a), by reducing breast bounce during exercise rather than breast discomfort. Of FG-4592 mouse interest, 25% of participants reported knowing that their bra did not fit, yet they still

wore this bra during vigorous exercise. This result suggests that adolescent females do not perceive wearing an ill-fitting bra as problematic. Comments included ‘This is the bra I wore to school and I came to training straight after school’ and ‘I wear my good bras for competition, not training’. Although poorly fitted bras in this young cohort were not associated with high levels of discomfort, in order to prevent the development of musculoskeletal disorders from insufficient breast support (Ryan 2000, BeLieu 1994, Kaye 1972, Wilson and Sellwood 1976, Maha 2000) and to promote physical activity Oxymatrine (Lorentzen and Lawson 1987, Mason et al 1999, Gehlsen and Albohm 1980) education on bra fit is warranted. Since 75% of the participants reported never having been fitted for a bra professionally, bra education enabling them to fit themselves independently is particularly important. Physiotherapists are in an ideal position to provide education to adolescent females on the importance of wearing a well-designed, supportive and comfortable bra when participating in physical activity. They can prevent the development of poor bra wearing habits, which may impact negatively upon their health and lifestyle in later years. An improvement in bra knowledge was sufficient to improve the ability to fit a correct bra independently with appropriate support for the level of physical activity and breast size.

The control group included children born at full term, adequate for gestational age, with no neonatal complications, discharged from the maternity unit at two to four days of life and in follow up at a pediatric outpatient clinic. The exclusion criteria were: congenital malformation, children of HIV-infected mothers, primary immunodeficiency, children who received plasma or immunoglobulin transfusions five months before or three weeks after the booster dose or received the tetanus booster vaccination prior to being invited to participate in the study. Infants included in the study were vaccinated according to the Brazilian

immunization recommendations. Briefly, the routine vaccine schedule in Brazil is: BCG at birth; Hepatitis B at birth, 1, 2 and

6 months of age (the 1-month dose, only for children this website born with less than 2 kg); tetanus and diphtheria toxoids and pertussis (DTP) at 2, 4, 6 months and 4–6 years; H. influenzae type b (Hib) at 2, 4 and 6 months; oral poliovirus at 2, 4, 6 months and 4–6 years; rotavirus at 2 and 4 months; 10-valent pneumococcal conjugate vaccine at 3, 5, 7, 15 months; meningococcal C conjugate vaccine (Men C) at 3, 5, and 12 months; yellow Selleckchem Raf inhibitor fever vaccine at 9 months; measles–mumps–rubella vaccine at 12 months and 4–6 years of age. Maternal demographic and clinical characteristics as well as children’s data related to the period of Phosphoprotein phosphatase hospitalization in the neonatal unit and clinical complications in the first year of life were collected. Gestational age was determined either by the best obstetric estimate or using the New Ballard method [11]. The adjustment of birth weight to gestational age was performed using the curve proposed by Alexander et al. [12]. Clinical severity score in the first

12 h of life was determined using the Score for Neonatal Acute Physiology, Perinatal Extension, Version II (SNAPPE II) [13]. Nutritional status at the time of vaccination was determined based on the recommendations of the World Health Organization [14]. Four mililiters of blood was collected for the determination of humoral and cellular immunity against tetanus toxoid at 15 months of age (prior to the booster vaccine dose against tetanus, diphtheria and whooping cough) and at 18 months of age (post-vaccination). Double-antigen enzyme-linked immunosorbent assay (ELISA) was used to determine humoral immunity, as described by Kristiansen et al. [15]. The results were expressed in international units per milliliter (IU/mL) by comparisons of the curves of the plasma samples tested and the international reference standard. Concentrations of anti-tetanus antibodies equal to or greater than 0.1 IU/mL were considered optimal protective levels against tetanus, concentrations between 0.01 and 0.

Analyses were performed using GraphPad Prism, version 4.00 (GraphPad Software). Linear data was expressed as means ± SEM, whereas logarithmic data was expressed as geometric means ± 95% confidence interval. Statistical differences between groups were

calculated using one-way ANOVA with Tukey’s multiple comparison posttest to compare groups by pairs. Differences between groups in relation to time were analyzed by two-way ANOVA with Bonferroni’s posttest for comparison of pairs. Paired Student’s t-test was used to compare two groups. Differences were considered significant at P ≤ 0.05. Multiple types of YC-NP emulsified with different surfactants were BMS-907351 concentration screened for low cell toxicity, efficient cellular uptake, and good protein adsorption (data not shown). Three different YC-NP were selected that met these criteria: YC-SDS (yellow carnauba-sodium dodecil sulphate), YC-NaMA (sodium myristate acetate), and YC-Brij700-chitosan. The latter NP was emulsified

with Brij700, a surfactant with a long carbon chain (C18) that contains 100 ethylenoxide (EO) units, and then mixed with medium molecular weight chitosan during the oil-in-water melting process to provide the NP surface with a positive charge. The zeta potential (Z) of the different YC-NP, a measurement in mV of the magnitude of repulsion or attraction between particles, was: YC-SDS, −47.7; YC-NaMA, −64.1; and YC-Brij700chitosan, +19.5. The size of the NP ranged between 387.0 and 675.0 nm, with mean size ± SD for each NP as follows: YC-SDS, 406.5 ± 27.94, n = 6; YC-NaMA, 478.8 ± 100.9, n = 5; and YC-Brij700-chitosan, 588.0 ± 123.0, n = 2. The NP polydispersity index (PDI) GW3965 nmr was YC-SDS: 0.21 ± 0.033; YC-NaMA: 0.17 ± 0.05; and YC-Brij700chitosan 0.41 ± 0.23. Representative SEM pictures of YC-SDS, YC-NaMA, and YC-Brij700chitosan particles are shown

in Fig. 1A. Nanoparticles showed high stability at 5 °C also and 25 °C in terms of particle size, ZP, and viscosity for up to 12 months after preparation ( Fig. 1B), demonstrating good colloidal stability. Zeta potential of the Ags, as expected, varied widely depending on the pH due to the amphoteric characteristics of the proteins. However, all three Ags (BSA, TT, and gp140) showed negative ZP at pH ranging between 7 and 8. Interestingly, whereas the ZP at this pH interval was about −10 mV for BSA and gp140, that of TT reached −30 mV. These results suggest that, at physiological pH, adsorption of Ags to the NP may vary depending on both NP and protein surface charge. However, all three Ags bound to anionic and cationic NP (data not shown and Fig. 1C). Binding of gp140 to negatively (YC-SDS and YC-NaMA) and positively (YC-Brij700-chitosan) charged NP is shown in Fig. 1C as indicated by the change in ZP of NP after incubation with gp140. We believe that association of these Ags with the YC-NP may be dominated by both electrostatic and hydrophobic interactions [25].

Pro-susceptible mice had higher numbers of circulating leukocytes, and leukocyte number and IL-6 release correlated negatively with social interaction ratio, indicating a predictive relationship. Increased leukocyte

number is likely driven by an increase in blood CD11b+ monocytes, as significant differences in proportions of leukocyte subtypes between susceptible and resilient mice were observed only in monocytes. Generation of chimeric mice via transplantation of bone marrow hematopoietic progenitor cells from a susceptible donor produced a robust social avoidance phenotype compared learn more to control bone marrow chimeras. In contrast, chimeras generated via transplantation of progenitors from an IL-6−/− donor demonstrated behavioral resilience to CSDS, behaving similarly to IL-6−/− mice and mice treated with an IL-6 antibody, which binds and neutralizes IL-6 in the peripheral circulation. These findings suggest that peripherally derived IL-6 drives susceptibility to CSDS, and that susceptible and resilient mice display baseline differences in leukocyte number and responsiveness. The mechanisms contributing to pre-existing

differences in stress responsive IL-6 release and circulating PD-0332991 in vivo leukocyte number are under investigation and will inform our understanding of immune regulation in resilience. Experiments investigating whether peripheral blood leukocytes of mice susceptible to CSDS, like splenic leukocytes in mice exposed to SDR, display glucocorticoid resistance may prove particularly fruitful. As mentioned above, increased levels of CD11b+ monocytes in blood and spleen are both a risk factor for susceptibility to CSDS and a consequence of RSD in mice. A likely Levetiracetam mechanism underlying this increased number of monocytes/macrophages is direct sympathetic nervous system innervation of bone marrow and control of bone marrow hematopoiesis via β-adrenergic signaling. Two recent studies propose that stress promotes proliferation and egress of immature,

pro-inflammatory myeloid cells from the bone marrow. Powell et al. (Powell et al., 2013) reported that in mice subjected to RSD, stress induces a transcriptional pattern that ultimately leads to myelopoiesis favoring immature, proinflammatory monocytes and granulocytes that express high and intermediate levels, respectively, of the surface marker Ly6c. RSD results in a 4-fold higher prevalence of monocytes in blood and spleen as well as a 50–70% increase in monocytic and granulocytic bone marrow progenitor cells. Post-RSD genome-wide analysis of the peripheral blood mononuclear cell transcriptome revealed a transcriptional mechanism underlying this phenomenon—enhanced expression of proinflammatory genes and genes related to myeloid cell lineage commitment accompanied by decreased expression of genes related to terminal myeloid differentiation.