Differences in worst-case scenarios calculated by fixed length and rolling average methods in professional soccer match-play

The aims of this study were to describe the worst-case scenarios (WCS) in professional soccer players calculated by fixed length and rolling average methods with regards to each playing position. This was done, firstly, by comparing total distance (TD covered in the WCS; secondly, by comparing high-speed running distance (HSRD); and thirdly, by comparing sprint distance (SPD). The study was conducted over a three-mesocycle competitive period. The WCS of three distance-related variables (TD, HSRD, SPD) in four time windows (1, 3, 5, 10 minutes) were calculated according to playing position (central defender; full-back; midfielder, wide midfielder, and forward) using fixed length and rolling average methods. A significant effect of the type of method used to calculate the WCS in TD (F_{(1, 142)} = 151.49, p < 0.001, ηp² = 0.52), HSRD (F_{(1, 138)} = 336.95, p < 0.001, ηp² = 0.71) and SPD (F_{(1, 138)} = 76.74, p < 0.001, ηp² = 0.36) was observed. In addition, there was a significant interaction between type of method and WCS duration in TD (F_{(1.36, 193.53)} = 41.95, p < 0.001, ηp² = 0.23), HSRD (F_{(2.28, 315.11)} = 21.77, p < 0.001, ηp² = 0.14) and SPD (F_{(2.59, 358.41)} = 6.93, p < 0.001, ηp² = 0.05). In conclusion, the use of fixed length methods of different durations significantly underestimated the WCS of TD, HSRD and SPD across the most common playing positions in professional soccer players. Therefore, the application of rolling averages is recommended for an appropriate WCS analysis in professional soccer match-play.     

The first,second, and third most demanding passages of play in professional soccer: a longitudinal study

The study aimed to compare the physical demands required during the first, second, and third most demanding passages (MDP) of play considering the effect of playing position, type of passage, and passage duration. A longitudinal study for three mesocycles was conducted in a professional soccer team competing in LaLiga123. Tracking systems collected total distance covered (DIS), high-speed running distance (HSRD), sprinting distance (SPD), total of high-intensity accelerations (ACC_HIGH), and total of high-intensity decelerations (DEC_HIGH). The results confirmed that a significant effect of the type of passage (first, second or third MDP of play) on DIS (F_{(1.24, 178.89)} = 115.53; p = 0.01; ηp² = 0.45), HSRD (F_{(1.35, 195.36)} = 422.82; p = 0.01; ηp² = 0.75), SPD (F_{(1.43, 206.59)} = 299.99; p = 0.01; ηp² = 0.68), ACC_HIGH (F_{(1.45, 209.38)} = 268.59; p = 0.01; ηp² = 0.65), and DEC_HIGH (F_{(1.45, 209.38)} = 324.88; p = 0.01; ηp² = 0.69) was found. In addition, a significant interaction between playing position, type and duration of the passage was observed in DIS (F_{(12.60, 453.47)} = 1.98; p = 0.02; ηp² = 0.05) and ACC_HIGH (F_{(13.99, 503.78)} = 1.92; p = 0.03; ηp² = 0.06). In conclusion, significant differences in physical demands between the first, second, and third MDP of play were observed. However, there were some cases (DIS and ACC_HIGH) in which no significant differences were found between these passages. Therefore, coaches should consider not only the magnitude of these peak intensity periods (e.g., distance covered per minute) but also the number of passages that players may experience during match play.     

COPS5 Protein Overexpression Increases Amyloid Plaque Burden,Decreases Spinophilin-immunoreactive Puncta,and Exacerbates Learning and Memory Deficits in the Mouse Brain

Brain accumulation of neurotoxic amyloid β (Aβ) peptide because of increased processing of amyloid precursor protein (APP), resulting in loss of synapses and neurodegeneration, is central to the pathogenesis of Alzheimer disease (AD). Therefore, the identification of molecules that regulate Aβ generation and those that cause synaptic damage is crucial for future therapeutic approaches for AD. We demonstrated previously that COPS5 regulates Aβ generation in neuronal cell lines in a RanBP9-dependent manner. Consistent with the data from cell lines, even by 6 months, COPS5 overexpression in APΔE9 mice (APΔE9/COPS5-Tg) significantly increased Aβ40 levels by 32% (p < 0.01) in the cortex and by 28% (p < 0.01) in the hippocampus, whereas the increases for Aβ42 were 37% (p < 0.05) and 34% (p < 0.05), respectively. By 12 months, the increase was even more robust. Aβ40 levels increased by 63% (p < 0.001) in the cortex and by 65% (p < 0.001) in the hippocampus. Similarly, Aβ42 levels were increased by 69% (p < 0.001) in the cortex and by 71% (p < 0.011) in the hippocampus. Increased Aβ levels were translated into an increased amyloid plaque burden both in the cortex (54%, p < 0.01) and hippocampus (64%, p < 0.01). Interestingly, COPS5 overexpression increased RanBP9 levels in the brain, which, in turn, led to increased amyloidogenic processing of APP, as reflected by increased levels of sAPPβ and decreased levels of sAPPα. Furthermore, COPS5 overexpression reduced spinophilin in both the cortex (19%, p < 0.05) and the hippocampus (20%, p < 0.05), leading to significant deficits in learning and memory skills. Therefore, like RanBP9, COPS5 also plays a pivotal role in amyloid pathology in vivo.     

Effects of Thiazolidinedione Therapy on Inflammatory Markers of Type 2 Diabetes: A Meta-Analysis of Randomized Controlled Trials

Background

Inflammation is a common feature in patients with type 2 diabetes mellitus (T₂DM). This meta-analysis aimed to assess the influence of thiazolidinedione (TZD) therapy on the circulating levels of inflammatory markers in patients with T₂DM.

Methods and Results

We searched the databases Medline, Embase, ScienceDirect, Web of Science, SpringerLink, and the Cochrane Library for randomized controlled trials (RCTs) that examined the effects of thiazolidinedione vs. a placebo on patients with T₂DM. The main outcomes were absolute changes in levels of circulating inflammatory markers. Twenty-seven RCTs were included and data were analyzed using a fixed-effect model or a random-effect model based on heterogeneity. Pooled results indicated that circulating levels of high-sensitivity C reactive protein (hsCRP; SMD = –0.65, 95% CI = –0.98 to –0.32, p < 0.01), monocyte chemoattractant protein-1 (MCP-1; WMD = –54.19, 95% CI = –73.86 to –34.52, p < 0.01), von Willebrand factor% (vWF%; WMD = –8.18, 95% CI = –13.54 to –2.81, p 0.01), fibrinogen (SMD = –0.26, 95% CI = –0.41 to –0.11, p < 0.01) and E-selectin(WMD = –3.57, 95% CI = –5.59 to -1.54, p <0.01) were significantly decreased after TZD therapy. However, interleukin-6 (IL-6), matrix metalloproteinase-9 (MMP-9), soluble CD40 ligand, plasminogen activator inhibitor 1 (PAI-1) and intercellular adhesion molecule (ICAM-1) were not significantly affected. Subgroup analyses of PAI-1, vWF% and fibrinogen in terms of trial drugs showed significant reductions for rosiglitazone (all p valuses< 0.05), but not pioglitazone treatment. Conversely, the E-selectin (p < 0.01) lowering effect only existed in the pioglitazone group. Further, rosiglitazone and pioglitazone treatment reduced serum hsCRP and MCP-1 but had no marked effects on MMP-9, IL-6 and ICAM-1.

Conclusions

Limited evidence suggested that TZD therapy had anti-inflammatory property that might contribute to its beneficial effect on inflammatory state in patients with type 2 diabetes.     

Angiotensin II Stimulates Thick Ascending Limb Superoxide Production via Protein Kinase Cα-dependent NADPH Oxidase Activation

Angiotensin II (Ang II) stimulates thick ascending limb (TAL) O production, but the receptor(s) and signaling mechanism(s) involved are unknown. The effect of Ang II on O is generally attributed to the AT₁ receptor. In some cells, Ang II stimulates protein kinase C (PKC), whose α isoform (PKCα) can activate NADPH oxidase. We hypothesized that in TALs, Ang II stimulates O via AT₁ and PKCα-dependent NADPH oxidase activation. In rat TALs, 1 nm Ang II stimulated O from 0.76 ± 0.17 to 1.97 ± 0.21 nmol/min/mg (p < 0.001). An AT₁ antagonist blocked the stimulatory effect of Ang II on O (0.87 ± 0.25 nmol/min/mg; p < 0.006), whereas an AT₂ antagonist had no effect (2.16 ± 0.133 nmol/min/mg; p < 0.05 versus vehicle). Apocynin, an NADPH oxidase inhibitor, blocked Ang II-stimulated O by 90% (p < 0.01). Ang II failed to stimulate O in TALs from p47^phox−/− mice (p < 0.02). Monitored by fluorescence resonance energy transfer, Ang II increased PKC activity from 0.02 ± 0.03 to 0.13 ± 0.02 arbitrary units (p < 0.03). A general PKC inhibitor, GF109203X, blocked the effect of Ang II on O (1.47 ± 0.21 versus 2.72 ± 0.47 nmol/min/mg with Ang II alone; p < 0.03). A PKCα- and β-selective inhibitor, Gö6976, also blocked the stimulatory effect of Ang II on O (0.59 ± 0.15 versus 2.05 ± 0.28 nmol/min/mg with Ang II alone; p < 0.001). To distinguish between PKCα and PKCβ, we used tubules expressing dominant-negative PKCα or -β. In control TALs, Ang II stimulated O by 2.17 ± 0.44 nmol/min/mg (p < 0.011). In tubules expressing dominant-negative PKCα, Ang II failed to stimulate O (change: −0.30 ± 0.27 nmol/min/mg). In tubules expressing dominant-negative PKCβ1, Ang II stimulated O by 2.08 ± 0.69 nmol/min/mg (p < 0.002). We conclude that Ang II stimulates TAL O production via activation of AT₁ receptors and PKCα-dependent NADPH oxidase.     

Single-Channel Kinetics,Inactivation, and Spatial Distribution of Inositol Trisphosphate (IP3) Receptors in Xenopus Oocyte Nucleus

Single-channel properties of the Xenopus inositol trisphosphate receptor (IP₃R) ion channel were examined by patch clamp electrophysiology of the outer nuclear membrane of isolated oocyte nuclei. With 140 mM K⁺ as the charge carrier (cytoplasmic [IP₃] = 10 μM, free [Ca²⁺] = 200 nM), the IP₃R exhibited four and possibly five conductance states. The conductance of the most-frequently observed state M was 113 pS around 0 mV and ∼300 pS at 60 mV. The channel was frequently observed with high open probability (mean P _o = 0.4 at 20 mV). Dwell time distribution analysis revealed at least two kinetic states of M with time constants τ < 5 ms and ∼20 ms; and at least three closed states with τ ∼1 ms, ∼10 ms, and >1 s. Higher cytoplasmic potential increased the relative frequency and τ of the longest closed state. A novel “flicker” kinetic mode was observed, in which the channel alternated rapidly between two new conductance states: F₁ and F₂. The relative occupation probability of the flicker states exhibited voltage dependence described by a Boltzmann distribution corresponding to 1.33 electron charges moving across the entire electric field during F₁ to F₂ transitions. Channel run-down or inactivation (τ ∼ 30 s) was consistently observed in the continuous presence of IP₃ and the absence of change in [Ca²⁺]. Some (∼10%) channel disappearances could be reversed by an increase in voltage before irreversible inactivation. A model for voltage-dependent channel gating is proposed in which one mechanism controls channel opening in both the normal and flicker modes, whereas a separate independent mechanism generates flicker activity and voltage- reversible inactivation. Mapping of functional channels indicates that the IP₃R tends to aggregate into microscopic (<1 μm) as well as macroscopic (∼10 μm) clusters. Ca²⁺-independent inactivation of IP₃R and channel clustering may contribute to complex [Ca²⁺] signals in cells.     

Educational Attainment Influences Levels of Homozygosity through Migration and Assortative Mating

Individuals with a higher education are more likely to migrate, increasing the chance of meeting a spouse with a different ancestral background. In this context, the presence of strong educational assortment can result in greater ancestry differences within more educated spouse pairs, while less educated individuals are more likely to mate with someone with whom they share more ancestry. We examined the association between educational attainment and F _roh (= the proportion of the genome consisting of runs of homozygosity [ROHs]) in ~2,000 subjects of Dutch ancestry. The subjects’ own educational attainment showed a nominally significant negative association with F _roh (p = .045), while the contribution of parental education to offspring F _roh was highly significant (father: p < 10^-5; mother: p = 9×10^-5), with more educated parents having offspring with fewer ROHs. This association was significantly and fully mediated by the physical distance between parental birthplaces (paternal education: p _mediation = 2.4 × 10^-4; maternal education: p _mediation = 2.3 × 10^-4), which itself was also significantly associated with F _roh (p = 9 × 10^-5). Ancestry-informative principal components from the offspring showed a significantly decreasing association with geography as parental education increased, consistent with the significantly higher migration rates among more educated parents. Parental education also showed a high spouse correlation (Spearman’s ρ = .66, p = 3 × 10^-262). We show that less educated parents are less likely to mate with the more mobile parents with a higher education, creating systematic differences in homozygosity due to ancestry differences not directly captured by ancestry-informative principal components (PCs). Understanding how behaviors influence the genomic structure of a population is highly valuable for studies on the genetic etiology of behavioral, cognitive, and social traits.     

Serum levels of appetite-regulating hormones and pro-inflammatory cytokines are ameliorated by a CLA diet and endurance exercise in rats fed a high-fat diet

[Purpose]

This study examined whether conjugated linoleic acid (CLA) supplementation and endurance exercise affect appetite-regulating hormones and pro-inflammatory cytokines in rats.

[Methods]

Seven-week-old male Sprague-Dawley rats were divided randomly into the high-fat diet sedentary group (HS, n=8), the 1.0% CLA supplemented high-fat diet sedentary group (CS, n=8), and the 1.0% CLA supplemented high-fat diet exercise group (CE, n=8). Rats in the CE group swam 60 min/day, 5 days/week for 4 weeks.

[Results]

Leptin and insulin levels in the CS and CE groups were significantly lower than those in the HS group (p<0.001), whereas leptin (p<0.01) and insulin (p<0.05) levels decreased significantly in the CE compared to those in the CS group. Interleukin (IL)-1β (p<0.001) and IL-6 (p<0.01) levels in the CS and CE groups decreased significantly compared to those in the HS group. Leptin (IL-1β: r=0.835, p<0.001), IL-6 (r=0.607, p<0.05), insulin (IL-1β: r=0.797, p<0.01), and IL-6 (r=0.827, p<0.01) levels were positively related with pro-inflammatory cytokine levels.

[Conclusion]

Endurance exercise may play an important role during CLA supplementation of rats on a high-fat diet.     

Task-specific performance fatigability and the bilateral deficit during isokinetic leg extensions

Objectives:The purpose of the present study was to compare the fatigue-induced changes in performance fatigability, bilateral deficit, and patterns of responses for the electromyographic (EMG) and mechanomyographic (MMG) amplitude (AMP) and mean power frequency (MPF), during unilateral and bilateral maximal, fatiguing leg extensions.Methods:Nine men (Mean±SD; age =21.9±2.4 yrs; height =181.8±11.9 cm; body mass =85.8±6.2 kg) volunteered to perform 50 consecutive maximal, bilateral (BL), unilateral dominant (DL), and unilateral non-dominant (NL) isokinetic leg extensions at 180°·s^-1, on 3 separate days. Electromyographic and MMG signals from both vastus lateralis (VL) muscles were recorded. Repeated measures ANOVAs were utilized to examine mean differences in normalized force, EMG AMP, EMG MPF, MMG AMP, MMG MPF and the bilateral deficit.Results:The results demonstrated a Condition × Repetition interaction for normalized force (p=0.004, η²_p=0.222) and EMG MPF (p=0.034, η²_p=0.214) and main effects for Repetition for EMG AMP (p=0.019, η²_p=0.231), MMG AMP (p<0.001, η²_p=0.8550), MMG MPF (p=0.009, η²_p=0.252), and the bilateral deficit (p<0.001, η²_p=0.366).Conclusions:The findings demonstrated less performance fatigability during the BL than the unilateral tasks, likely due to a reduced relative intensity via interhemispheric inhibition that attenuated the development of excitation-contraction coupling failure during the BL task.     

Simulation of Interstitial Fluid Flow in Ligaments: Comparison among Stokes,Brinkman and Darcy Models

In this paper, we use Stokes, Brinkman and Darcy equations to approximate the porous continuum media of ligament tissues respectively, simulate the flow field with FLUENT software, and study the shear stress on the cell surface due to the interstitial fluid flow. Since the Brinkman equation approaches Stokes equation well in high hydraulic permeability (k_p) condition (k_p ≥1.0×10^-8 m² in our numerical simulation), and it is an approximation to Darcy model in low k_p condition (k_p ≤5.0×10^-12 m² in our numerical simulation), we used the Brinkman model to simulate the interstitial fluid flow in the ligament where k_p is approximately 1.0×10^-16 m². It shows k_p and anisotropic property have a little effect on the flow field, but have a great effect on the shear stress on the membrane of interstitial cells (τ_cell). There is a linear relationship between τ_cell and , when k_p =1.0×10^-16 m² and the maximum τ_cell (τ_cell,max) is approximately 10 Pa. The anisotropic property will affect τ_cell''s distribution on the cell surface. When k_x/k_y>1, low τ_cell dominates the cell, while when k_x/k_y<1, high τ_cell dominants the cell.     

Relationship between the Autoantibody and Expression of β3-Adrenoceptor in Lung and Heart

Background

Evidences suggest that β₃ -adrenoceptor (β₃-AR) plays an important role in heart failure (HF), although no data is reported indicating how these effects may change with the increasing age. Pulmonary congestion and edema are the major life-threatening complications associated with HF. The purpose of this study is to explore the relationship between the anti-β₃-AR autoantibody and the expression of β₃-AR in the lungs and heart for both aged patients and rats with HF.

Methods

Synthetic β₃-AR peptides served as the target antigens in ELISA were used to screen the anti-β₃-AR autoantibody in aged patients and rats. Two aged rat models were constructed based on aortic banding and sham-operation. The expression of β₃-AR mRNA and protein in the lung and heart was measured in intervention and non-intervention groups by Western blot analysis at the baseline, 5^th, 7^th, 9^th and 11^th week, respectively.

Results

The frequency and titer of anti-β₃-AR autoantibody in aged patients and rats with HF were higher than those in the control group (p<0.05). The expression of β₃-AR mRNA and protein in pulmonary tissues decreased continually from the 7^th week (p<0.05), followed by HF observed during the 9^th week. The expression of β₃-AR in myocardial tissues continued to increase after the 9^th week (p<0.05), and the expression of both β₃-AR mRNA and protein in the BRL group [HF group with BRL37344 (4-[-[2-hydroxy-(3-chlorophenyl)ethyl-amino] phenoxyacetic acid) (a β₃-AR agonist) injection] was positively correlated with BRL37344 when compared with non-BRL group (HF group without BRL37344 injection) (p<0.05).

Conclusion

Anti-β₃-AR autoantibody was detected in aged patients and rats with HF. The expression of β₃-AR mRNA and protein in pulmonary tissues decreased continually, and began earlier than in the heart, but its expression in myocardial tissues increased continually and could be further promoted by β₃-AR agonist.     

Acute effect of a static- and dynamic-based stretching warm-up on standing long jump performance in primary schoolchildren

The aim of the present study was to compare the acute effect of a static- vs dynamic-based stretching warm-up on standing long jump (SLJ) performance in primary schoolchildren. The sample was composed of 76 schoolchildren, 43 girls and 33 boys, aged 9–10 years old from three fourth-grade classes of Primary Education. The three groups were cluster-randomly assigned to the control (CG), static (SG) or dynamic (DG) groups. All the schoolchildren performed a standardized warm-up consisting of mobility exercises (five minutes), jogging (five minutes) and the SLJ test. Afterwards the CG schoolchildren received jump theory (eight minutes), the SG performed static stretching (eight minutes) and the DG performed dynamic-bounces stretching (eight minutes). Afterwards, all of them performed the SLJ test again. The results of the one-way ANOVA (F_2,73 = 34.184; p < 0.001; η²p = 0.484), followed by the pairwise comparisons with the Bonferroni adjustment, showed that the DG students (M_Δ = 11.07, SE = 1.42) made a significant statistical improvement in their SJL levels compared with the CG (M_Δ = -3.00, SE = 1.89; p < 0.001, d = 1.51) and SG students (M_Δ = -1.85, SE = 0.67; p < 0.001, d = 1.38). However, statistically significant differences between the CG and SG students were not found (p > 0.05, d = 0.12). The dynamic-bouncing stretch as a final part of a warm-up improves explosive strength performance in primary schoolchildren, and seems to be a good option before carrying out explosive strength activities of the lower body.     

The Zinc Transporter Slc30a8/ZnT8 Is Required in a Subpopulation of Pancreatic α-Cells for Hypoglycemia-induced Glucagon Secretion

SLC30A8 encodes a zinc transporter ZnT8 largely restricted to pancreatic islet β- and α-cells, and responsible for zinc accumulation into secretory granules. Although common SLC30A8 variants, believed to reduce ZnT8 activity, increase type 2 diabetes risk in humans, rare inactivating mutations are protective. To investigate the role of Slc30a8 in the control of glucagon secretion, Slc30a8 was inactivated selectively in α-cells by crossing mice with alleles floxed at exon 1 to animals expressing Cre recombinase under the pre-proglucagon promoter. Further crossing to Rosa26:tdRFP mice, and sorting of RFP⁺: glucagon⁺ cells from KO mice, revealed recombination in ∼30% of α-cells, of which ∼50% were ZnT8-negative (14 ± 1.8% of all α-cells). Although glucose and insulin tolerance were normal, female αZnT8KO mice required lower glucose infusion rates during hypoglycemic clamps and displayed enhanced glucagon release (p < 0.001) versus WT mice. Correspondingly, islets isolated from αZnT8KO mice secreted more glucagon at 1 mm glucose, but not 17 mm glucose, than WT controls (n = 5; p = 0.008). Although the expression of other ZnT family members was unchanged, cytoplasmic (n = 4 mice per genotype; p < 0.0001) and granular (n = 3, p < 0.01) free Zn²⁺ levels were significantly lower in KO α-cells versus control cells. In response to low glucose, the amplitude and frequency of intracellular Ca²⁺ increases were unchanged in α-cells of αZnT8KO KO mice. ZnT8 is thus important in a subset of α-cells for normal responses to hypoglycemia and acts via Ca²⁺-independent mechanisms.     

The Effects of Hyperbaric Oxygen Therapy on Post-Training Recovery in Jiu-Jitsu Athletes

Objectives

The present study aimed to evaluate the effects of using hyperbaric oxygen therapy during post-training recovery in jiu-jitsu athletes.

Methods

Eleven experienced Brazilian jiu-jitsu athletes were investigated during and following two training sessions of 1h30min. Using a cross-over design, the athletes were randomly assigned to passive recovery for 2 hours or to hyperbaric oxygen therapy (OHB) for the same duration. After a 7-day period, the interventions were reversed. Before, immediately after, post 2 hours and post 24 hours, blood samples were collected to examine hormone concentrations (cortisol and total testosterone) and cellular damage markers [creatine kinase (CK), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH)]. Moreover, the rating of perceived exertion (RPE) and recovery (RPR) scales were applied.

Results

Final lactate [La] values (control: 11.9 ± 1.4 mmol/L, OHB: 10.2 ± 1.4 mmol/L) and RPE [control: 14 (13–17 a.u.), OHB: 18 (17–20 a.u.)] were not significantly different following the training sessions. Furthermore, there was no difference between any time points for blood lactate and RPE in the two experimental conditions (P>0.05). There was no effect of experimental conditions on cortisol (F_1,20 = 0.1, P = 0.793, η² = 0.00, small), total testosterone (F_1,20 = 0.03, P = 0.877, η² = 0.00, small), CK (F_1,20 = 0.1, P = 0.759, η² = 0.01, small), AST (F_1,20 = 0.1, P = 0.761, η² = 0.01, small), ALT (F_1,20 = 0.0, P = 0.845, η² = 0.00, small) or LDH (F_1,20 = 0.7, P = 0.413, η² = 0.03, small). However, there was a difference between the two experimental conditions in RPR with higher values at post 2 h and 24 h in OHB when compared to the control condition (P<0.05).

Conclusions

Thus, it can be concluded that OHB exerts no influence on the recovery of hormonal status or cellular damage markers. Nonetheless, greater perceived recovery, potentially due to the placebo effect, was evident following the OHB condition.     

Role of IL-17 Variants in Preeclampsia in Chinese Han Women

Previous studies have suggested an important role for IL-17, mainly secreted by Th17 cells, in the development of systemic inflammation in preeclampsia (PE). This study therefore investigated the association between genetic variants in IL-17A, IL-17F, and IL-17RA and susceptibility to PE in Chinese Han women. We recruited 1,031 PE patients and 1,298 controls of later pregnant women, and used TaqMan allelic discrimination real-time PCR to genotype the polymorphisms of IL17A rs2275913, IL-17F rs763780, and IL-17RA rs4819554. No significant differences in genotypic or allelic frequencies were found at all three polymorphic sites between PE patients and controls (rs2275913: genotype χ² = 0.218, p = 0.897 and allele χ² = 0.157, p = 0.692, OR = 1.024, 95%CI 0.911–1.152; rs763780: genotype χ² = 1.948, p = 0.377 and allele χ² = 1.242, p = 0.265, OR = 0.897, 95%CI 0.741–1.086; rs4819554: genotype χ² = 0.633, p = 0.729 and allele χ² = 0.115, p = 0.735, OR = 1.020, 95%CI 0.908–1.146). There were also no significant differences in genetic distributions between mild/severe PE or early/late-onset PE and control subgroups. Our data indicate that the genetic variants of rs2275913 in IL-17A, rs763780 in IL-17F, and rs4819554 in IL-17RA may not play a role in the pathogenesis of PE in Chinese Han women. However, these findings should be confirmed in other ethnic populations.     

Hypoxia-inducible Factor-1α (HIF-1α) Protein Diminishes Sodium Glucose Transport 1 (SGLT1) and SGLT2 Protein Expression in Renal Epithelial Tubular Cells (LLC-PK1) under Hypoxia

In this work, we demonstrated the regulation of glucose transporters by hypoxia inducible factor-1α (HIF-1α) activation in renal epithelial cells. LLC-PK₁ monolayers were incubated for 1, 3, 6, or 12 h with 0% or 5% O₂ or 300 μm cobalt (CoCl₂). We evaluated the effects of hypoxia on the mRNA and protein expression of HIF-1α and of the glucose transporters SGLT1, SGLT2, and GLUT1. The data showed an increase in HIF-1α mRNA and protein expression under the three evaluated conditions (p < 0.05 versus t = 0). An increase in GLUT1 mRNA (12 h) and protein expression (at 3, 6, and 12 h) was observed (p < 0.05 versus t = 0). SGLT1 and SGLT2 mRNA and protein expression decreased under the three evaluated conditions (p < 0.05 versus t = 0). In conclusion, our results suggest a clear decrease in the expression of the glucose transporters SGLT1 and SGLT2 under hypoxic conditions which implies a possible correlation with increased expression of HIF-1α.     

State Transitions in the Green Alga Scenedesmus Obliquus Probed by Time-Resolved Chlorophyll Fluorescence Spectroscopy and Global Data Analysis

Decay-associated fluorescence spectra of the green alga Scenedesmus obliquus have been measured by single-photon timing with picosecond resolution in various states of light adaptation. The data have been analyzed by applying a global data analysis procedure. The amplitudes of the decay-associated spectra allow a determination of the relative antenna sizes of the photosystems. We arrive at the following conclusions: (a) The fluorescence kinetics of algal cells with open PS II centers (F₀ level) have to be described by a sum of three exponential components. These decay components are attributed to photosystem (PS) I (τ ≈ 85 ps, λ_max^em ≈ 695-700 nm), open PS II α-centers (τ ≈ 300 ps, λ_max^em = 685 nm), and open PS II β-centers (τ ≈ 600 ps, λ_max^em = 685 nm). A fourth component of very low amplitude (τ ≈ 2.2-2.3 ns, λ_max^em = 685 nm) derives from dead chlorophyll. (b) At the F_max level of fluorescence there are also three decay components. They originate from PS I with properties identical to those at the F₀ level, from closed PS II α-centers (τ ≈ 2.2 ns, λ_max^em = 685 nm) and from closed PS β-centers (τ ≈ 1.2 ns, λ_max^em = 685 nm). (c) The major effect of light-induced state transitions on the fluorescence kinetics involves a change in the relative antenna size of α- and β-units brought about by the reversible migration of light-harvesting complexes between α-centers and β-centers. (d) A transition to state II does not measurably increase the direct absorption cross-section (antenna size) of PS I. Our data can be rationalized in terms of a model of the antenna organization that relates the effects of state transitions and light-harvesting complex phosphorylation with the concepts of PS II α,β-heterogeneity. We discuss why our results are in disagreement with those of a recent lifetime study of Chlorella by M. Hodges and I. Moya (1986, Biochim. Biophys. Acta., 849:193-202).     

Expectant Mothers Maximizing Opportunities: Maternal Characteristics Moderate Multifactorial Prenatal Stress in the Prediction of Birth Weight in a Sample of Children Adopted at Birth

Background

Mothers’ stress in pregnancy is considered an environmental risk factor in child development. Multiple stressors may combine to increase risk, and maternal personal characteristics may offset the effects of stress. This study aimed to test the effect of 1) multifactorial prenatal stress, integrating objective “stressors” and subjective “distress” and 2) the moderating effects of maternal characteristics (perceived social support, self-esteem and specific personality traits) on infant birthweight.

Method

Hierarchical regression modeling was used to examine cross-sectional data on 403 birth mothers and their newborns from an adoption study.

Results

Distress during pregnancy showed a statistically significant association with birthweight (R² = 0.032, F _{(2, 398)} = 6.782, p = .001). The hierarchical regression model revealed an almost two-fold increase in variance of birthweight predicted by stressors as compared with distress measures (R² Δ = 0.049, F _{(4, 394)} = 5.339, p < .001). Further, maternal characteristics moderated this association (R² Δ = 0.031, F _{(4, 389)} = 3.413, p = .009). Specifically, the expected benefit to birthweight as a function of higher SES was observed only for mothers with lower levels of harm-avoidance and higher levels of perceived social support. Importantly, the results were not better explained by prematurity, pregnancy complications, exposure to drugs, alcohol or environmental toxins.

Conclusions

The findings support multidimensional theoretical models of prenatal stress. Although both objective stressors and subjectively measured distress predict birthweight, they should be considered distinct and cumulative components of stress. This study further highlights that jointly considering risk factors and protective factors in pregnancy improves the ability to predict birthweight.