H2 Group Research Articles

Occlusion of dentinal tubules on periodontally involved teeth by dentifrice containing stannous fluoride and sodium fluoride.

This study examined the occlusion effect of a dentifrice containing stannous fluoride (SnF2) and sodium fluoride (NaF) on periodontally involved teeth in comparison with healthy teeth using scanning electron microscopy (SEM) in comparison with a dentifrice containing NaF alone. Sixty dentine samples obtained from single-rooted premolars, 15 of them extracted for orthodontic reasons (Group H) and 15 because of periodontal destruction (Group P), were included in the study. Each group of specimens was further divided into subgroups: HC and PC (control), H1 and P1 (treated with SnF2 and NaF), and H2 and P2 (treated with NaF). The samples were brushed twice a day for 7 days, kept in artificial saliva, and examined by SEM. The diameters of open tubules and the numbers of tubules were assessed at ×2,000 magnification. The H and P groups showed similar diameters of open tubules. The numbers of open tubules in Groups H1, P1, H2, and P2 were significantly lower than in Groups HC and PC (P < 0.001), and consistent with the percentages of occluded tubules. Group P1 had the highest percentage of occluded tubules. Although both dentifrices were found to successfully occlude dentinal tubules, the dentifrice containing SnF2 and NaF provided the highest degree of occlusion in periodontally involved teeth.

Особенности микробиома кишечника при некротизирующим энтероколите у недоношенных новорожденных и доношенных новорожденных с врожденными пороками сердца по данным метагеномного секвенирования

Necrotizing enterocolitis (NEC) is a serious disease that predominantly affects premature infants with a birth weight of less than 1500 g. Newborns with ductus-dependent congenital heart disease (CHD) are also at risk of developing NEC, which is associated with impaired mesenteric perfusion and hypoxemia. Objective. To identify features of the intestinal microbiome composition of preterm neonates and full-term neonates with ductusdependent CHD, depending on the development of NEC. Patients and methods. A prospective observation of neonates and a retrospective “case-control” analysis (1:1 ratio) of the intestinal microbiome composition depending on the development of NEC were performed. In neonates with NEC, specimens were collected at the onset of NEC (±2 days), in patients without NEC – on the day of life, corresponding to the onset of the disease in newborns with NEC (±3 days) matched by gestational age. The intestinal composition was analyzed in 31 preterm newborns with stage IB–III NEC (subgroup N1 with early-onset NEC (days 1–7 of life) (n = 19); subgroup N2 with late-onset NEC (days 13–34 of life) (n = 12)), as well as in 31 preterm neonates without NEC (subgroup C1 of patients with specimens collected on days 2–7 of life (n = 19), subgroup C2 of patients with specimens collected on days 11–36 of life (n = 12)). Also, an analysis of the microbiome composition was performed in 14 full-term newborns with ductus-dependent CHD who developed NEC (group H1), and 14 full-term newborns with ductus-dependent CHD without NEC (group H2). Fecal specimens were collected from diapers into sterile tubes and stored at -40°C. Analysis of the intestinal microbiome was performed on Illumina MiSeq by prokaryotic 16S rRNA sequencing of amplicons with primers F515/R806 to the V4 16S rRNA variable region. A Naive Bayes classifier trained on the NCBI 16S RefSeq database was used for ASV taxonomic classification. Results. NEC stages of preterm neonates: IB – 5 children, IIA – 19, IIB – 4, III – 3. Stages of NEC in newborns with ductusdependent congenital heart disease: IB – 3 children; IIA – 11. There were no statistically significant differences in the Shannon alpha diversity index between groups (N1 and C1, N2 and C2, H1 and H2). Neonates with antibiotic exposure (ABT) at specimen collection had different beta diversity (PERMANOVA F-value: 24.534; R-squared: 0.21997; p = 0.001) and had a higher alpha diversity (Shannon index: 2.0 (0.8–2.8) vs. 1.2 (0.8–1.5), p = 0.004), primarily due to representatives of opportunistic flora. Analysis of the intestinal microbiome did not reveal bacteria, which could be interpreted as a universal marker for the development of NEC, but some features were identified. Among neonates from the “early” groups (N1 and C1), the dominant genera were more often Staphylococcus, Serratia, and Corynebacterium. Neonates with early-onset NEC (N1) had a significantly lower relative abundance of Enterococcus, Lacticaseibacillus, Clostridium, Fusobacterium, Limosilactobacillus, Agrococcus, Alkalibacterium, Ancrocorticia, Blautia, Brachybacterium, Brevibacterium, Carnobacterium, Citricoccus, Flaviflexus, Garicola, Lactococcus, Microbacterium, Phocaeicola, Propionimicrobium, Ruoffia, Stenotrophomonas compared to subgroup C1. Preterm neonates with late-onset NEC (N2) had a lower relative abundance of Bifidobacterium (p = 0.027) and Streptococcus (p = 0.037) than the comparison subgroup (C2) had. Neonates with late-onset NEC (N2) had a significantly higher relative abundance of Enterococcus than in early-onset NEC (N1) (7.83 (0.09–46.15) % vs. 0 (0–0.18) % resp., p = 0.0004), no differences were found between the comparison subgroups (C2 and C1). Preterm neonates with a longer NEC duration (n = 16, nil per os 20 (16–27) days) compared to children with a shorter duration (nil per os 10 (9.5–11) days) had several pathobionts/pathogens in fecal specimens at the NEC onset: Alkalibacterium, Brevibacterium, Flaviflexus and Ruo (Facklamia). Full-term neonates with ductus-dependent CHD and NEC (H1) had a higher relative abundance of Staphylococcus (p = 0.029), Serratia ( p = 0.011; OR = 14 (95% CI 1.43–137.3)), Pelomonas ( Roseateles) (p = 0.017), Methylobacterium (p = 0.017), and Nitrincola (p = 0.017) than neonates with CHD without NEC (H2). Conclusion. Intestinal dysbiosis may act as a predisposing background for the development of NEC, but not its main cause. The dysbiosis by antibiotic exposure is not a sufficient factor for NEC development; the mother's health, fetal development status, and the early postnatal period play a significant role. Early correction of antibiotic-induced dysbiosis may be a reasonable approach to preventing NEC. Probiotics, prebiotics, postbiotics/metabolites, live biotherapeutic products, and phages may be potential microbiome-modulating agents in neonates. Key words: necrotizing enterocolitis, ductus-dependent congenital heart disease, metagenomics, 16S rRNA sequencing, intestinal microbiome

CMC and CGC surfaces in Lorentz Heisenberg group H3

The aim of this paper is to study the characterization of some constant mean curvature (CMC) and constant Gauss curvature (CGC) A-net surfaces in the 3-dimensional Lorentz-Heisenberg group H3 endowed with a left invariant Lorentzian metric gi in the three following cases : 1. g1 = -dx2 + dy2 + (xdy + dz)2, 2. g2 = dx2 + dy2 - (xdy + dz)2. 3. g3 = dx2 + (xdy + dz)2 - [(1 - x)dy - dz]2. Using Levi-Civita connection, we will calculate the mean curvature H and the Gaussian curvature K in order to study CMC and CGC A-net surfaces in (H3, g1), (H3, g2) and (H3, g3).

Hardy spaces and quasiconformal maps in the Heisenberg group

We define Hardy spaces Hp, 0<p<∞, for quasiconformal mappings on the Korányi unit ball B in the first Heisenberg group H1. Our definition is stated in terms of the Heisenberg polar coordinates introduced by Korányi and Reimann, and Balogh and Tyson. First, we prove the existence of p0(K)>0 such that every K-quasiconformal map f:B→f(B)⊂H1 belongs to Hp for all 0<p<p0(K). Second, we give two equivalent conditions for the Hp membership of a quasiconformal map f, one in terms of the radial limits of f, and one using a nontangential maximal function of f. As an application, we characterize Carleson measures on B via integral inequalities for quasiconformal mappings on B and their radial limits. Our paper thus extends results by Astala and Koskela, Jerison and Weitsman, Nolder, and Zinsmeister, from Rn to H1. A crucial difference between the proofs in Rn and H1 is caused by the nonisotropic nature of the Korányi unit sphere with its two characteristic points.

Effects of Postmortem Hemolysis and Ultrafiltration on Creatinine Detection Results.

To investigate the interference of postmortem hemolysis on the detection of creatinine and whether ultrafiltration can reduce the interference. A total of 33 non-hemolyzed whole blood samples from the left heart were collected. Hemolyzed samples with 4 hemoglobin mass concentration gradients H1-H4 were artificially prepared. Ultrafiltration was performed on each hemolyzed sample. Creatinine concentrations in non-hemolyzed serum (baseline serum), hemolyzed samples and ultrafiltrate were detected. Bias (B), Pearson correlation and receiver operator characteristic (ROC) of baseline creatinine concentration between before and after ultrafiltration were analyzed. As the hemoglobin mass concentration increased, B of the hemolyzed samples in the H1-H4 groups gradually increased, the |B| was 2.41(0.82, 8.25)-51.31(41.79, 188.25), reaching a maximum of 589.06%, and there was no statistically significant between the creatinine concentration and the baseline creatinine concentration (P=0.472 7, r=0.129 5). After ultrafiltration of hemolyzed samples, the interference of creatinine concentration in ultrafiltrate was significantly reduced, the |B| was 5.32(2.26, 9.22)-21.74(20.06, 25.58), reaching a maximum of 32.14%, and there was a positive correlation with baseline creatinine concentration (P<0.05, r=0.918 2). In the hemolyzed samples of H3 and H4 groups, there were 7 false-positive samples and 1 false-negative sample; in the ultrafiltrate samples, there were no false-positive sample and 1 false-negative sample. ROC analysis results showed the hemolyzed samples were lack of diagnostic value (P=0.117 5). The postmortem hemolysis significantly interferes creatinine detection results of blood samples, ultrafiltration can reduce hemolysis-induced interference in postmortem creatinine detection.

A double-blinded, randomized controlled clinical trial of hydrogen inhalation therapy for idiopathic sudden sensorineural hearing loss.

Hydrogen (H2) has been reported to be effective in reducing hearing loss due to several causes in animal studies. However, no study has examined the effectiveness of H2 in treating hearing loss in humans. Thus, we investigated whether H2 is effective for the treatment of idiopathic sudden sensorineural hearing loss (ISSNHL). We conducted a double-blind randomized controlled trial at six hospitals between June 2019 and March 2022. The study protocol and trial registration have been published in the Japan Registry of Clinical Trials (jRCT, No. jRCTs06119004). We randomly assigned patients with ISSNHL to receive either H2 (H2 group) or air as a placebo (control group) through inhalation combined with the administration of systemic glucocorticoids and prostaglandin E1. The primary outcome was the hearing threshold and changes in hearing threshold 3 months after therapy. In contrast, the secondary outcomes included the proportion of patients with a good prognosis (complete recovery or marked improvement). Sixty-five patients with ISSNHL (31 and 34 in the H2 and control groups, respectively) were included in this study. The hearing threshold 3 months after treatment was not significantly different between the groups; 39.0 decibels (dB) (95% confidence interval [CI]: 28.7-49.3) and 49.5 dB (95% CI: 40.3-58.7) in the H2 and control groups, respectively. In contrast, the changes in hearing threshold 3 months after treatment was 32.7 dB (95% CI: 24.2-41.3) and 24.2 dB (95% CI: 18.1-30.3) in the H2 and control groups, respectively. Consequently, the changes in hearing threshold were significantly better in the H2 group than in the control group (P = 0.048). However, no adverse effects due to the inhalation of H2 gas have been reported. This is the first study to investigate the efficacy of H2 for the treatment of ISSNHL in humans. The results suggest that H2 therapy may be effective for ISSNHL treatment. [https://jrct.niph.go.jp/re/reports/detail/10442], identifier [jRCTs06119004].

Immediate versus early (24-hours) urinary catheter removal after elective minimally invasive colonic resection: study protocol for a randomized, multicenter, non-inferiority trial

BackgroundEnhanced Recovery After Surgery (ERAS) represents the standard of care in colorectal surgery. Among ERAS items, early removal of urinary catheter (UC) is considered a key issue, though adherence to this specific item still varies among centers. UC placement allows for monitoring of post-operative urinary output but relates to an increased risk of urinary tract infection (UTI), reduced mobility, and patient’s discomfort. Several studies investigated the role of early UC removal specifically looking at the rate of acute urinary retention (AUR) but most of them were retrospective, single-center, underpowered, cohort studies. The main purpose of this study is to compare the rate of AUR after immediate (at the end of the surgery) versus early (within 24 h from the completion of surgery) removal of UC in patients undergoing minimally invasive colonic resection (MICR). The secondary outcomes focus on goals that could be positively impacted by the immediate removal of the UC at the end of the surgery. In particular, the rate of UTIs, perception of pain, time-to-return of bowel and physical functions, postoperative complications, and length of hospital stay will be measured.MethodsThis is a prospective, randomized, controlled, two-arm, multi-center, study comparing the rate of AUR after immediate versus early removal of UC in patients undergoing MICR. The investigators hypothesize that immediate UC removal is non-inferior to 24-h UC removal in terms of AUR rate. Randomization is at the patient level and participants are randomized 1:1 to remove their UC either immediately or within 24 h from the completion of surgery. Those eligible for inclusion were patients undergoing any MICR with an anastomosis above the peritoneal reflection. Those patients who need to continue urinary output monitoring after the surgery will be excluded. The number of patients calculated to be enrolled in each group is 108 based on an expected AUR rate of 3% for the 24-h UC removal group and considering acceptable an AUR of 9% for the immediate UC removal group.DiscussionThe demonstration of a non-inferiority of immediate versus 24-h removal of UC would call into question the usefulness of urinary drainage in the setting of MICR.Trial registrationClinicalTrials.gov NCT05249192. Prospectively registered on February 21, 2022.

Application of humic acid and hydroxyapatite in Cd-contaminated alkaline maize cropland: A field trial

Soil quality is critical to the quality and safety of agricultural products, and remediation of heavy metal contaminated soils is an urgent task to be implemented. This study applied hydroxyapatite (HAP) and humic acid (HA) as remediation materials to Cd-contaminated alkaline cropland. Data on soil pH, electrical conductivity (EC), cation exchange capacity (CEC), soil organic matter (SOM), diethylenetriamine pentaacetic acid (DTPA) extraction, and improved BCR sequential extraction were obtained for different periods. The joint application of HAP and HA enhanced the soil's buffering capacity. During the experiment, treatment groups CK, H1, H2, H3, and H4 showed changes in pH of 0.29, 0.28, 0.21, 0.24, and 0.32, respectively, and changes in the conductivity of 341.4, 183.0, 133.1, 104.6 and 320.2 μS/cm. Soil organic matter had a positive effect on soil's effective phosphorus content. HAP and HA both reduced the BCFgrain/soil of Cd for the maize, but the impact of HA was more substantial (20.19 % reduction compared to CK). HA increased the yield of maize by 44.20 %. The combination of HA and HAP was recommended.

Phosphorylation-mediated PI3K-Art signalling pathway as a therapeutic mechanism in the hydrogen-induced alleviation of brain injury in septic mice.

Our previous studies illustrated that 2% H2 inhalation can protect against sepsis-associated encephalopathy (SAE) which is characterized by high mortality and has no effective treatment. To investigate the underlying role of protein phosphorylation in SAE and H2 treatment, a mouse model of sepsis was constructed by caecal ligation and puncture (CLP), then treated with H2 (CLP + H2 ). Brain tissues of the mice were collected to be analysed with tandem mass tag-based quantitative proteomics coupled with IMAC enrichment of phosphopeptides and LC-MS/MS analysis. In proteomics and phosphoproteomics analysis, 268 differentially phosphorylated proteins (DPPs) showed a change in the phosphorylated form in the CLP + H2 group (p < 0.05). Gene ontology analysis revealed that these DPPs were enriched in multiple cellular components, biological processes, and molecular functions. KEGG pathway analysis revealed that they were enriched in glutamatergic synapses, tight junctions, the PI3K-Akt signalling pathway, the HIF-1 signalling pathway, the cGMP-PKG signalling pathway, the Rap1 signalling pathway, and the vascular smooth muscle contraction. The phosphorylated forms of six DPPs, including ribosomal protein S6 (Rps6), tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein gamma (Ywhag/14-3-3), phosphatase and tensin homologue deleted on chromosome ten (Pten), membrane-associated guanylate kinase 1 (Magi1), mTOR, and protein kinase N2 (Pkn2), were upregulated and participated in the PI3K-Akt signalling pathway. The WB results showed that the phosphorylation levels of Rps6, Ywhag, Pten, Magi1, mTOR, and Pkn2 were increased. The DPPs and phosphorylation-mediated molecular network alterations in H2 -treated CLP mice may elucidate the biological roles of protein phosphorylation in the therapeutic mechanism of H2 treatment against SAE.

Hydrogen gas alleviates lipopolysaccharide-induced acute lung injury and inflammatory response in mice

BackgroundChronic inflammation and oxidant/antioxidant imbalance are two main pathological features associated with lipopolysaccharide (LPS)-induced acute lung injury (ALI). The following study investigated the protective role of hydrogen (H2), a gaseous molecule without known toxicity, in LPS-induced lung injury in mice and explored its potential molecular mechanisms.MethodsMice were randomly divided into three groups: H2 control group, LPS group, and LPS + H2 group. The mice were euthanized at the indicated time points, and the specimens were collected. The 72 h survival rates, cytokines contents, pathological changes, expression of Toll-like receptor 4 (TLR4), and oxidative stress indicators were analyzed. Moreover, under different culture conditions, RAW 264.7 mouse macrophages were used to investigate the potential molecular mechanisms of H2 in vitro. Cells were divided into the following groups: PBS group, LPS group, and LPS + H2 group. The cell viability, intracellular ROS, cytokines, and expression of TLR4 and nuclear factor kappa-B (NF-κB) were observed.ResultsHydrogen inhalation increased the survival rate to 80%, reduced LPS-induced lung damage, and decreased inflammatory cytokine release in LPS mice. Besides, H2 showed remarked anti-oxidative activity to reduce the MDA and NO contents in the lung. In vitro data further indicated that H2 down-regulates the levels of ROS, NO, TNF-α, IL-6, and IL-1β in LPS-stimulated macrophages and inhibits the expression of TLR4 and the activation of nuclear factor kappa-B (NF-κB).ConclusionHydrogen gas alleviates lipopolysaccharide-induced acute lung injury and inflammatory response most probably through the TLR4-NF-κB pathway.

Accelerated Fatigue Model for Predicting Composite Restoration Failure

An empirical method is proposed to predict the clinical performance of resin composite dental restorations by using laboratory data derived from simple specimens subjected to chemical degradation and accelerated cyclic fatigue. Three resin composites were used to fill dentin disks (2-mm inner diameter, 5-mm outer diameter, and 2 mm thick) made from bovine incisor roots. The specimens (n = 30 per group) were aged with different durations of a low-pH challenge (0, 24, and 48 h under pH 4.5) before being subjected to diametral compression with either a monotonically increasing load (fast fracture) or a cyclic load with a continuously increasing amplitude (accelerated fatigue). The data from 1 material were used to establish the relationship between laboratory time (number of cycles) and clinical time to failure (years) via the respective survival probability curves. The temporal relationship was then used to predict the clinical rates of failure for restorations made of the other 2 materials, and the predictions were compared with the clinical data to assess their accuracy. Although there were significant differences in the fast fracture strength among the groups of materials or durations of chemical challenge, fatigue testing was much better at separating the groups. Linear relationships were found between the laboratory and clinical times to failure for the first material (R2 = 0.90, 0.90, and 0.62 for the 0-, 24-, and 48-h low-pH groups, respectively). The clinical life of restorations made of the other 2 materials was best predicted with data from the 48-h low-pH groups. In conclusion, an accelerated fatigue model was successfully calibrated and applied to predict the clinical failure of resin composite restorations, and the predictions based on data obtained from chemically aged specimens provided the best agreement with clinical data.

Quantitative Analysis of Renal Perfusion in Rhabdomyolysis-Induced Acute Kidney Injury Using Contrast-Enhanced Ultrasound: An Experimental Study.

The aim of this study was to evaluate renal perfusion changes in rats with acute kidney injury induced by rhabdomyolysis, using quantitative parameters obtained with contrast-enhanced ultrasound (CEUS). Sprague-Dawley (SD) rats were randomly divided into an experimental group (n=40) and a control group (n=20). Each group was further divided into four subgroups (0.5-, 6-, 24- and 72-h groups). Time-intensity curves and related quantitative parameters of the renal cortex and medulla were obtained by CEUS, and the contrast characteristics analyzed for different time points. In the experimental group, the CEUS quantitative parameters for the renal medulla of time to peak (TTP), descending time/2 (DT/2) and area under the curve (AUC) increased, whereas ascending slope (AS) and descending slope (DS) decreased. Similarly, renal cortical AS, DS and AUC in the experimental group differed significantly from those in the control group. With respect to the CEUS quantitative parameters for the renal cortex, AUC increased, and AS and DS decreased. These parameters differed significantly between the experimental and control groups. CEUS is sensitive to change in renal perfusion in rhabdomyolysis-induced acute kidney injury and, thus, has diagnostic value.

VP.49 Total sleep deprivation leads to changes in neuromuscular junction of soleus muscle in male wistar rats

Skeletal muscle atonia is a prominent feature of rapid eye movement sleep. Neuromuscular junction exhibits high morphological and functional plasticity. Sleep deprivation (SD) may influence NMJ morphology at presynaptic and postsynaptic terminals levels. In the present study, we have looked into the ultrastructural changes in the rat soleus muscle NMJ after sleep, sleep deprivation and recovery sleep. A total of 18 rats were divided into three groups. Group I rats had normal sleep wake cycle, group II rats were subjected to 24 h SD by running wheel method and group III rats had 24h recovery sleep. At the end of the study, soleus muscles were collected for electron microscopic and neurochemical study. Morphometry was performed and neurotransmitters were measured by ELISA. The study was conducted as per the guidelines of the Institutional Animal Ethics Committee (960/IAEC/16). Electron microscopic observation revealed a significant increase in mitochondrial density in 24h SD (p<0.01) as compared to control in presynaptic terminal. Further, in post synapse we found similar increase in SD (p<0.0002). Within group comparison of intact versus altered mitochondria exhibited a significant increase in the diameter of altered mitochondria in all the experimental groups (p≤0.0001). Moreover, within group comparison of area of intact versus altered mitochondria showed significant increase in area of altered mitochondria only in control (p= 0.01) and 24h SD (p= 0.02). Synaptic vesicle density we found to be significantly increased in 24h SD as compared to control (p=0.002), but not in recovery sleep at presynaptic terminal. Interestingly, the number of junctional folds per synapse profile was significantly increased in the 24h SD group as compared to control, (p= 0.002). Also, there was a significant difference between 24hr SD and recovery group (p= 0.002). Concentration of acetylcholine in 24 h sleep deprivation was decreased (p=0.02). In addition, but acetylcholine esterase activity was significantly increased (p= 0.02). The acetylcholine esterase activity did not come back to control level even after 24h of recovery sleep. Pearson correlation between acetylcholine and vesicular density showed found a negative correlation (r= 0.07, p<0.05) in 24h SD. These findings suggest that there are significant changes in neuromuscular junction of soleus muscle after24hr SD. We conclude that sleep plays a key role in NMJ homeostasis.

VP.37 Sleep deprivation induces aging like changes in antigravity muscles of young adult male wistar rats

Sleep is essential for the cellular, organic and systemic functions of an organism. Sleep deprivation is associated with metabolic dysfunction and ageing is so. Muscle health at elderly age is one of the major risk factor. Poor muscle health is associated with a series of chronic and metabolic conditions that are prevalent in individuals who chronically experience poor-quality sleep. But there is no study deciphering the role of sleep deprivation on muscle ageing. Therefore, in the present study we have measured the ultrastructure, histopathology, and oxidative stressors in soleus muscle of wistar rat after sleep deprivation and recovery sleep. The experiments were conducted in18 rats of three groups. Group I rats had normal sleep wake cycle, Group II rats were subjected to 24 h sleep deprivation (SD) by gentle handling method1 and Group III rats had recovery sleep after 24 h SD. At the end of the sleep, sleep deprivation and recovery period, soleus muscle tissue was collected for ultrastructural, histological and oxidative stress markers. Oxidative damage was assessed by lipid peroxidation, catalase activity, reduced glutathione and nuclear labelling of 8-OHdG. The study was conducted as per the guidelines of the Institutional Animal Ethics Committee (960/IAEC/16). The data demonstrated that SD leads to ultrastructural changes in soleus muscle which includes sarcolemmal and mitochondrial alterations. In case of histopathological and histomorphological changes there was signs of tissue degeneration, inflammatory infiltrate in type I fibers and muscle atrophy was observed in soleus muscles. There was significant increase in level of 8-OHdG (p=0.02) and malondialdehyde in 24h SD (p=0.02) than control and recovery sleep groups. Moreover, the catalase activity and reduced glutathione level was significantly decreased in 24h SD group (p≤0.02) than control and recovery sleep. Therefore, we conclude that 24hr sleep deprivation leads to an ageing like state in the skeletal muscle, which was recovered after sleep rebound.

Optimal administration time of vitamin C after 131I therapy in differentiated thyroid cancer based on propensity score matching.

ObjectivesThis study aimed to investigate the protection of the salivary glands by vitamin C administration at 2 and 24 h after an initial treatment using iodine-131 (131I) in patients with differentiated thyroid cancer (DTC) and examined the optimal administration time of vitamin C to protect the salivary glands from radiation injury.MethodThe clinical data of patients with differentiated thyroid carcinoma who had been treated with 131I in the Department of Nuclear Medicine in Shanxi Bethune Hospital from January 2014 to December 2020 were retrospectively analyzed. The propensity score matching method was adopted to match patients who received the administration of vitamin C at 2 h with those receiving administration at 24 h. A total of 230 pairs/460 patients were enrolled in the study. The chi-squared (χ2) or Fisher's exact test was used to compare the indicators representing the incidence of salivary gland injury between the two groups.ResultsThe incidence of salivary gland injury (17.39%) with acidic substances at 2 h was lower compared with administration at 24 h (26.96%). The incidence of acute salivary gland injury (15.22%) and chronic salivary gland injury (26.09%) in the 24-h group were higher than those in the 2-h group (4.78% and 18.26%, respectively). The differences in the left submandibular gland concentrate index and right submandibular gland concentrate index were statistically significant before and after treatment in both the 2 and the 24-h groups; these functions had been impaired after treatment.ConclusionsFollowing treatment with 131I, the protective effect of acidic substances administered at 2 and 24 h on the salivary glands were different. The incidence of salivary gland injury in the 2 h acid stimulation group was lower than in the 24 h acid stimulation group. The present study revealed that 131I treatment did cause some injury to the salivary glands and that the protective effect of administering vitamin C at 2 and 24 h may be limited. Accordingly, protection against salivary gland injury should be conducted using comprehensive measures.

Effects of PUMA knockout on the apoptosis of H9C2 cardiomyocytes induced by high glucose

To investigate the effects of p53 upregulated modulator of apoptosis (PUMA) on the apoptosis of H9C2 cardiomyocytes induced by high glucose and its mechanisms. H9C2 cardiomyocytes were treated with 5.5mmol/L (control group) or 35 mmol/L glucose (HG group) for 6 h, 12 h, 24 h or 48 h respectively to induce apoptosis, each group sets 5 multiple wells. Apoptosis was tested by TUNEL assay. PUMA mRNA was measured by RT-PCR and protein expression was measured by Western blot assay. The mitochondrial membrane potential was detected by JC-1 method. The expressions of cleaved caspase-3 and cytochrome C (Cyt C) protein in mitochondria and cytoplasm were determined by Western blot assay. H9C2 cardiomyocytes were randomly divided into four groups, control group (5.5 mmol/L), HG (35 mmol/L) group, HG+si-scramble group(si-scramble treatment for 24 h, then 35 mmol/L high glucose treatment for 24 h) and HG-si-PUMA group (si-PUMA treatment for 24 h, then 35mmol/L high glucose treatment for 24 h). Si-PUMA was transfected into cardiomyocytes and the effects of PUMA on high glucose-induced apoptosis were studied. Compared with the control group, high glucose increased cardiomyocyte apoptosis and enhanced PUMA mRNA and protein expressions significantly (P＜0.05 or P＜0.01). Cell injury and increased PUMA expression were time-dependent and there was no significant difference between the high glucose 24 h group and the high glucose 48h group. The following experiment used high glucose 24 h as the stimulation time. The cardiomyocytes transfected with si-PUMA to inhibit PUMA expression had decreased apoptotic rate and cleaved caspase-3, increased mitochondria membrane potential and decreased Cyt C release (P＜0.05 or P＜0.01). There were no significant differences between the HG+si-scramble group and the high glucose group (P＞0.05). PUMA mediates high glucose-induced cardiomyocyte apoptosis suggesting PUMA may be an important target gene of diabetic cardiomyopathy.

The Formal Affine Demazure Algebra and Real Finite Reflection Groups

In this paper, we generalize the formal affine Demazure algebra of Hoffnung-Malagón-López-Savage-Zainoulline to all real finite reflection groups. We begin by generalizing the formal group ring of Calmès-Petrov-Zainoulline to all real finite reflection groups. We then define and study the formal Demazure operators that act on the formal group ring. Using these results and constructions, we define and study the formal affine Demazure algebra for all real finite reflection groups. Finally, we compute several structure coefficients that appear in a braid relation among the formal Demazure elements, and we conclude this paper by computing all structure coefficients for the reflection groups I2(5), I2(7), H3, and H4.

Establishment and assessment of postoperative cognitive impairment in intermittent hypoxia rats.

Obstructive sleep apnea hypopnea syndrome (OSAHS) is a chronic disease characterized by repeated episodes of apnea or hypopnea, accompanied by intermittent awakening and sleep disturbances. The incidence of OSAHS is increasing and has become a serious disease. In recent years, more and more evidence shows that OSAHS is closely related to postoperative neurocognitive disorders, and the preparation of models of postoperative cognitive impairment in intermittent hypoxia animals is an important way to study its pathogenesis and intervention targets. This study aims to explore the establishment and evaluation of the animal model of postoperative cognitive impairment in intermittent hypoxia rats. A total of 108 male SD rats were randomly divided into 8 groups: a control group (C group, n=27), a surgery group (S group, n=27), an intermittent hypoxia 7 d group (H1 group, n=9), an intermittent hypoxia 14 d group (H2 group, n=9), an intermittent hypoxia 21 d group (H3 group, n=9), an intermittent hypoxia 7 d operation group (O1 group, n=9), an intermittent hypoxia 14 d operation group (O2 group, n=9), and an intermittent hypoxia 21 d operation group (O3 group, n=9). The rats in the H1, H2 and H3 group treated with intermittent hypoxia for 7, 14, and 21 d, respectively. The rats in the O1, O2 and O3 groups received left lateral hepatic lobectomy after 7, 14, and 21 d intermittent hypoxia, respectively. The rats in each group were subjected to open field test, new object recognition test, and Barnes Maze test. The expression of IL-1β mRNA in hippocampus of rats was detected at the 1st day after the surgery. Compared with the C, S, and H2 groups, the discrimination index in novel object recognition test 6 h and 1 d after the surgery of the O2 group was significantly lower (P<0.05), the latency and errors in Barnes maze at the 1st day and 2nd day after the surgery were increased significantly (P<0.05) and the expression of IL-1β mRNA in hippocampus was significantly increased at the 1st day after the operation (P<0.05). However, there was no difference in the preference index in NORT 6 h and 1 d after the surgery, the latency and errors in Barnes maze and the expression of IL-1β mRNA in hippocampus between the O1 group and the H1 group, the H3 group and the O3 group (all P>0.05). The rate with intermittent hypoxia 14 d pretreatment with anesthesia and laparotomy could be established the animal model of postoperative cognitive impairment.

Hydrogen Gas Inhalation Attenuates Acute Impulse Noise Trauma: A Preclinical In Vivo Study.

Molecular hydrogen (H2) has shown therapeutic potential in several oxidative stress-related conditions in humans, is well-tolerated, and is easily administered via inhalation.The aim of this preclinical in vivo study was to investigate whether impulse noise trauma can be prevented by H2 when inhaled immediately after impulse noise exposure. Guinea pigs (n = 26) were subjected to impulse noise (n = 400; 156 dB SPL; 0.33/s; n = 11; the Noise group), to impulse noise immediately followed by H2 inhalation (2 mol%; 500 ml/min; 1 hour; n = 10; the Noise + H2 group), or to H2 inhalation (n = 5; the H2 group). The acoustically evoked ABR threshold at 3.15, 6.30, 12.5, 20.0, and 30.0 kHz was assessed before and 4 days after impulse noise and/or H2 exposure. The cochleae were harvested after the final ABR assessment for quantification of hair cells. Noise exposure caused ABR threshold elevations at all frequencies (median 35, 35, 30, 35, and 35 dB SPL, the Noise group; 20, 25, 10, 13, and 20 dB SPL, the Noise + H2 group; P < .05) but significantly less so in the Noise + H2 group (P < .05). Outer hair cell (OHC) loss was in the apical, mid, and basal regions 8.8%, 53%, and 14% in the Noise group and 3.5%, 22%, and 1.2% in the Noise + H2 group. The corresponding inner hair cell (IHC) loss was 0.1%, 14%, and 3.5% in the Noise group and 0%, 2.8%, and 0% in the Noise + H2 group. The difference between the groups was significant in the basal region for OHCs (P = .003) and apical (P = .033) and basal (P = .048) regions for IHCs. Acute acoustic trauma can be reduced by H2 when inhaled immediately after impulse noise exposure.

Drinking hydrogen water improves photoreceptor structure and function in retinal degeneration 6 mice

Retinitis pigmentosa (RP) is a genetically heterogeneous group of inherited retinal disorders involving the progressive dysfunction of photoreceptors and the retinal pigment epithelium, for which there is currently no treatment. The rd6 mouse is a natural model of autosomal recessive retinal degeneration. Given the known contributions of oxidative stress caused by reactive oxygen species (ROS) and selective inhibition of potent ROS peroxynitrite and OH·by H2 gas we have previously demonstrated, we hypothesized that ingestion of H2 water may delay the progression of photoreceptor death in rd6 mice. H2 mice showed significantly higher retinal thickness as compared to controls on optical coherence tomography. Histopathological and morphometric analyses revealed higher thickness of the outer nuclear layer for H2 mice than controls, as well as higher counts of opsin red/green-positive cells. RNA sequencing (RNA-seq) analysis of differentially expressed genes in the H2 group versus control group revealed 1996 genes with significantly different expressions. Gene and pathway ontology analysis showed substantial upregulation of genes responsible for phototransduction in H2 mice. Our results show that drinking water high in H2 (1.2–1.6 ppm) had neuroprotective effects and inhibited photoreceptor death in mice, and suggest the potential of H2 for the treatment of RP.