Association between vitamin B2 intake and prostate-specific antigen in American men: 2003-2010 National Health and Nutrition Examination Survey.

BACKGROUND: Accumulating evidence suggests a pivotal role of vitamin B2 in the pathogenesis and progression of prostate cancer (PCa). Vitamin B2 intake has been postulated to modulate the screening rate for PCa by altering the concentration of prostate-specific antigen(PSA). However, the relationship between vitamin B2 and PSA remains indeterminate. Hence, we conducted a comprehensive evaluation of the association between vitamin B2 intake and PSA levels, utilizing data from the National Health and Nutrition Examination Survey (NHANES) database. METHODS: From a pool of 20,371 participants in the NHANES survey conducted between 2003 and 2010, a cohort of 2,323 participants was selected for the present study. The male participants were classified into four distinct groups based on their levels of vitamin B2 intake. We employed a multiple linear regression model and a non-parametric regression method to investigate the relationship between vitamin B2 and PSA levels. RESULTS: The study cohort comprised of 2,323 participants with a mean age of 54.95 years (± 11.73). Our findings revealed a statistically significant inverse correlation between vitamin B2 intake (mg) and PSA levels, with a reduction of 0.13 ng/ml PSA concentration for every unit increase in vitamin B2 intake. Furthermore, we employed a fully adjusted model to construct a smooth curve to explore the possible linear relationship between vitamin B2 intake and PSA concentration. CONCLUSIONS: Our study in American men has unveiled a notable inverse association between vitamin B2 intake and PSA levels, potentially posing a challenge for the identification of asymptomatic prostate cancer. Specifically, our findings suggest that individuals with higher vitamin B2 intake may be at a greater risk of being diagnosed with advanced prostate cancer in the future, possibly indicating a detection bias. These results may offer a novel explanation for the observed positive correlation between vitamin B2 intake and prostate cancer.

Neuropilin-1 is up-regulated by cancer-associated fibroblast-secreted IL-8 and associated with cell proliferation of gallbladder cancer.

We previously demonstrated that cancer-associated fibroblasts (CAFs) promoted the proliferation of gallbladder cancer (GBC) cells, but the mechanism is not clear. Neuropilin-1 (NRP-1) plays an important role in various malignancies as transmembrane glycoprotein. Our goal was to reveal the relationship between CAFs and NRP-1 and their potential functions in GBC. In this study, we found NRP-1 was overexpressed in GBC tissue, associated with poor survival and was up-regulated by CAFs. The cytokine array cluster analysis revealed IL-8 secreted by CAFs facilitated the up-regulation of NRP-1 in tumour cells. NRP-1 knockdown suppressed tumour growth in vivo. Gene expression microarray analysis showed 581 differentially regulated genes under NRP-1 knockdown conditions. Ingenuity pathway analysis demonstrated that NRP-1 knockdown may inhibit tumour progression by affecting cell proliferation. We then confirmed that NRP-1 knockdown in NOZ and GBC-SD cells significantly inhibited cell proliferation. Additionally, the IL-8 mediated MDM2 and CCNA2 expression were affected by NRP-1 knockdown. Our findings suggested that NRP-1 was up-regulated by CAF-secreted IL-8, which subsequently promoted GBC cell proliferation, and these molecules may serve as useful prognostic biomarkers and therapeutic targets for GBC.

Therapeutic hypercapnia reduces blood-brain barrier damage possibly via protein kinase Cε in rats with lateral fluid percussion injury.

BACKGROUND: This study investigated whether therapeutic hypercapnia (TH) ameliorated blood-brain barrier (BBB) damage and improved the neurologic outcome in a rat model of lateral fluid percussion injury (FPI), and explored the possible underlying mechanism. METHODS: Rats underwent lateral FPI and received inhalation of 30%O2-70%N2 or 30%O2-N2 plus CO2 to maintain arterial blood CO2 tension (PaCO2) between 80 and 100 mmHg for 3 h. To further explore the possible mechanisms for the protective effects of TH, a PKC inhibitor staurosporine or PKCαß inhibitor GÖ6976 was administered via intracerebral ventricular injection. RESULTS: TH significantly improved neurological function 24 h, 48 h, 7 d, and 14 d after FPI. The wet/dry ratio, computed tomography values, Evans blue content, and histological lesion volume were significantly reduced by TH. Moreover, numbers of survived neurons and the expression of tight junction proteins (ZO-1, occludin, and claudin-5) were significantly elevated after TH treatment at 48-h post-FPI. TH significantly increased the expression of protein kinase Cε (PKCε) at 48-h post-FPI, but did not significantly change the expression of PKCα and PKCßII. PKC inhibitor staurosporine (but not the selective PKCαß inhibitor-GÖ6976) inhibited the protective effect of TH. CONCLUSIONS: Therapeutic hypercapnia is a promising candidate that should be further evaluated for clinical treatment. It not only protects the traumatic penumbra from secondary injury and improves histological structure but also maintains the integrity of BBB and reduces neurologic deficits after trauma in a rat model of FPI.

Effect of the menstrual cycle on circulation during combined spinal-epidural anaesthesia.

BACKGROUND: From adolescence to menopause, hormone levels during the menstrual cycle affect various body systems, from the cardiovascular system to the water and electrolyte balance. This study investigated the effect of different phases of the menstrual cycle on circulatory function relative to changes in body position and combined spinal-epidural anaesthesia (CSEA). METHODS: Forty-six women were selected who underwent scheduled gynaecological surgery, were classified as American Society of Anesthesiology (ASA) I-II, and met the test criteria. The sample was divided into the follicular and corpus luteal groups. Preoperative heart rate and blood pressure measurements were taken from the supine and standing positions. Heart rate measurements as well as systolic, diastolic, and mean blood pressure measurements were taken upon entering the operating room, at the beginning of the spinal-epidural anaesthesia, and 10, 20, and 30 min after anaesthesia was administered. RESULTS: The heart rates of patients in the corpus luteal group were higher than those of patients in the follicular group both before and after anaesthesia (P <  0.05). Significantly more ephedrine was used during the first 30 min of CSEA in the corpus luteal group than in the follicular group (P <  0.05). CONCLUSIONS: Although the effect was slight, women in the follicular phase were better able to compensate and tolerate circulatory fluctuations than those in the luteal phase.

Decision of surgical approach for advanced gallbladder adenocarcinoma based on a Bayesian network.

BACKGROUND AND OBJECTIVES: To determine whether radical resection can benefit patients with advanced gallbladder adenocarcinoma using a Bayesian network (BN) with clinical data. METHODS: In total, 362 patients who had undergone surgical treatment of gallbladder adenocarcinoma at a tertiary institute were evaluated to establish two BN models using a tree-augmented naïve Bayes algorithm. We then chose 250 patients with T3-4N0-2M0 stage gallbladder adenocarcinoma to test the posterior probability after the surgical type was taken into account. RESULTS: In total, 170 patients (≤7 months) and 137 patients (>7 months) were correctly classified in the median survival time model (accuracy, 84.81%), and 204 patients (≤12 months), 15 patients (12-36 months), 17 patients (36-60 months), and 34 patients (>60 months) were correctly classified in the 1-, 3-, and 5-year survival model (accuracy, 74.59%), respectively. Every posterior probability in the two models upregulated the ratio of the longer survival time and suggested a better prognosis for gallbladder adenocarcinoma that can be improved by R0 resection. CONCLUSIONS: These BN models indicate that stages T4 and N2 gallbladder adenocarcinoma are not contraindications for surgery and that R0 resection can improve survival in patients with advanced gallbladder adenocarcinoma.

[Surgical treatment of advanced penile cancer without distant metastasis].

OBJECTIVE: To investigate the effect of surgery on advanced penile cancer without distant metastasis and the factors influencing the prognosis. METHODS: Between September 2007 and July 2015, we treated 8 cases of advanced penile cancer without distant metastasis by penectomy and lymph node dissection. The patients were aged 37－67 (mean 51.1) years. We followed up the patients for 4－60 (mean 19.25) months postoperatively and analyzed the surgical effects and the factors affecting the prognosis. RESULTS: Three of the patients remained alive while the other 5 (62.5%) died at 4－13 (mean 9) months after surgery. No significant complications were observed and myocutaneous flap repair showed good prognosis in 4 of the patients with largearea skin defect. CONCLUSIONS: Surgery is comparatively a valuable option for the treatment of advanced penile cancer without distant metastasis, though with a poor prognosis, and the important factor affecting its prognosis is lymph node metastasis. Flap repair can solve the problem of largearea skin defect after surgery. However, evidence is not yet sufficient to prove the effectiveness of multimodality therapy of this malignancy.

[Supplemental role of thrombospondin-1 in the diagnosis of prostate cancer].

OBJECTIVE: To employ enzyme-linked immunosorbent assay (ELISA) to measure the serum level of thrombospondin-1 (TSP-1) and analyze its diagnostic value for prostate cancer. METHODS: The serum levels of TSP-1 were measured by human TSP-1 ELISA kit in 50 patients with organ-confined prostate cancer (n = 22) and non-organ-confined prostate cancer (n = 28). And the subjects of benign prostatic hyperplasia (BPH, n = 20) and healthy controls (n = 16) were selected. RESULTS: The average serum concentration of TSP-1 was (200 ± 49) µg/L in prostate cancer group, (281 ± 53) µg/L in BPH group and (323 ± 56) µg/L in healthy control group. There were significant inter-group differences in the serum levels of TSP-1 (both P < 0.05). The average serum concentration of TSP-1 was (216 ± 34) µg/L in organ-confined prostate cancer (including stages I and II) and (188 ± 49) µg/L in non-organ-confined prostate cancer (including stages III and IV) respectively (P = 0.030). The level of TSP-1 was also correlated with Gleason score (r = -0.32, P = 0.023). However, the relationship between TSP-1 levels and lymph node metastasis remained elusive (P = 0.189). The diagnostic sensitivity and specificity of TSP-1 and prostate specific antigen (PSA) for prostate cancer were 72%, 90% and 64%, 70% respectively (both P < 0.05). The area under the receiver operating characteristic curve (ROC) of TSP-1 and PSA were 0.886 and 0.719 respectively (P = 0.028). CONCLUSION: As a relatively ideal predictor of prostate cancer, the serum concentration of TSP-1 can not only distinguish prostate cancer from BPH, but also correlate with tumor stage and Gleason grade.

Molecular Hydrogen Mediates Neurorestorative Effects After Stroke in Diabetic Rats: the TLR4/NF-κB Inflammatory Pathway.

Diabetes is an independent risk factor for stroke and amplifies inflammation. Diabetic stroke is associated with a higher risk of death and worse neural function. The identification of effective anti-inflammatory molecules with translational advantages is particularly important to promote perioperative neurorestorative effects. Applying molecular hydrogen, we measured blood glucose levels before and after middle cerebral artery occlusion (MCAO), 48-h cerebral oedema and infarct volumes, as well as 28-day weight, survival and neurological function. We also measured the levels of TLR4, NF-κB p65, phosphorylated NF-κB p65, catecholamines, acetylcholine and inflammatory factors. All measurements comprehensively showed the positive effect and translational advantage of molecular hydrogen on diabetic stroke. Molecular hydrogen improved the weight, survival and long-term neurological function of rats with diabetic stroke and alleviated changes in blood glucose levels before and after middle cerebral artery occlusion (MCAO), but no difference in circadian rhythm was observed. Molecular hydrogen inhibited the phosphorylation of NF-κB and significantly reduced inflammation. Molecular hydrogen mediates neurorestorative effects after stroke in diabetic rats. The effect is independent of circadian rhythms, indicating translational advantages. The molecular mechanism is related to the TLR4/NF-κB pathway and inflammation. Molecular hydrogen (H2) affects outcomes of ischemic stroke with diabetes mellitus (DM).

Erratum: Long non-coding RNA SNHG5 affects the invasion and apoptosis of renal cell carcinoma by regulating the miR-363-3p-Twist1 interaction.

[This corrects the article on p. 697 in vol. 12, PMID: 32194916.].

Effect and Mechanism of Sodium Butyrate on Neuronal Recovery and Prognosis in Diabetic Stroke.

Ischemic stroke is a cerebrovascular lesion caused by local ischemia and hypoxia. Diabetes mellitus (DM) is a chronic inflammatory disease that disturbs immune homeostasis and predisposes patients to ischemic stroke. The mechanism by which DM exacerbates stroke remains unclear, although it may involve disturbances in immune homeostasis. Regulatory T cells (Tregs) play a regulatory role in many diseases, but the mechanism of Tregs in diabetes complicated by stroke remains unclear. Sodium butyrate is a short-chain fatty acid that increases Treg levels. This study examined the role of sodium butyrate in the prognosis of neurological function in diabetic stroke and the mechanism by which Tregs are amplified in the bilateral cerebral hemispheres. We evaluated the brain infarct volume, observed 48-h neuronal injury and 28-day behavioral changes, and calculated the 28-day survival rate in mice. We also measured Treg levels in peripheral blood and brain tissue, recorded changes in the blood‒brain barrier and water channel proteins and neurotrophic changes in mice, measured cytokine levels and peripheral B-cell distribution in bilateral hemispheres and peripheral blood, and examined the polarization of microglia and the distribution of peripheral T-cell subpopulations in bilateral hemispheres. Diabetes significantly exacerbated the poor prognosis and neurological deficits in mice with stroke, and sodium butyrate significantly improved infarct volume, prognosis, and neurological function and showed different mechanisms in brain tissue and peripheral blood. The potential regulatory mechanism in brain tissue involved modulating Tregs/TGF-ß/microglia to suppress neuroinflammation, while that in peripheral blood involved improving the systemic inflammatory response through Tregs/TGF-ß/T cells.

Molecular hydrogen alleviates lung injury after traumatic brain injury: Pyroptosis and apoptosis.

BACKGROUND: Traumatic brain injury (TBI)-induced acute lung injury (ALI) is a critical condition, and inflammation and apoptosis play essential roles. Molecular hydrogen (H2) exerts anti-inflammatory and anti-apoptotic effects. Our previous work has shown that 42% H2 can improve TBI. In the current study, we tested the hypothesis that inhalation of hydrogen (42% H2, 21% O2, balanced nitrogen) for 1 h per day can improve TBI-induced ALI. METHODS: Sprague-Dawley male rats were randomly divided into 3 groups. Except for the sham group (group S), rats were subjected to a fluid percussion injury (FPI) and the H2 treatment group were given inhaled hydrogen for 1 h per day. We evaluated the lung function, pyroptosis and apoptosis at 24 h, 48 h and 72 h. RESULTS: Compared with group S, the rats in the TBI group (group T) showed obvious pulmonary edema after a TBI. Inhalation of high-concentration hydrogen significantly improved the rats. During this process, rats had some tendency to heal on their own, and H2 also accelerated the self-healing process. Lung injury scores, oxygenation index and pulmonary edema were consistent. Compared with group S, the pyroptosis-related proteins Caspase-1, apoptosis-associated speck-like protein containing CARD (ASC) and Gasdermin-D (GSDM-D) in the lung tissues of the rats in group T were significantly increased after a TBI. In the H2 treatment group (group H), these proteins were significantly decreased. The levels of IL-1ß and IL-18 were significantly increased after TBI while in group H were significantly decreased. At the same time, cleaved caspase-3 and BCL-2/Bax were also changed after H2 treatment. These demonstrates the powerful ameliorating effect of H2 on pyroptosis, apoptosis and systemic inflammation. However, rats also had tendency to heal on their own, and H2 also accelerated the self-healing process at the same time. CONCLUSIONS: H2 improves TBI-ALI, and the mechanism may be due to the decrease of both pyroptosis and apoptosis and the alleviation of inflammation. These findings provide a reference and evidence for the use of H2 in TBI-ALI patients in the intensive care unit (ICU).

Anti-tumor effect of lentivirus-mediated gene transfer of alphastatin on human glioma.

Alphastatin, an endogenous angiogenesis inhibitor, has recently been used as an anticancer agent in several tumor models. This study was to investigate whether local sustained long-term expression of alphastatin could serve to diminish tumor growth of a human xenograft glioma model. We found that the recombinant alphastatin lentiviruses were able to stably infect HUVECs, and infected HUVECs could sustainably secrete alphastatin, which exhibited potent inhibitory effects on HUVECs migration, differentiation but not proliferation induced by vascular endothelial growth factor (VEGF) or basic fibroblast growth factor(bFGF). And the expression of secreted protein alphastatin markedly decreased tumor vascularization and inhibited tumor growth. Additionally, alphastatin inhibited VEGF- or bFGF-induced initial stage of angiogenesis by reducing JNk and ERK phosphorylation in vitro. Taken together, these data demonstrate that secreted protein alphastatin inhibits VEGF- or bFGF-induced angiogenesis by suppressing JNK and ERK kinases activation pathways in HUVECs, and markedly inhibits tumor angiogenesis in vivo. Consequently lentivirus-mediated gene transfer might represent an effective strategy for expression of alphastatin to achieve inhibition of human malignant glioma proliferation and tumor progression.

Chronic ß-adrenoceptor antagonists upregulate the rat alveolar macrophage adrenergic system through the ß1-subtype.

BACKGROUND: Previous studies demonstrate that macrophages synthesis and release catecholamines, which regulate the immune responses in an autocrine manner. These responses are mediated in part by ß-adrenoceptors expressed on macrophages. Some ß-adrenoceptor antagonists are commonly used in clinical conditions. Here we investigated whether the chronic administration of ß-adrenoceptor antagonists upregulate adrenergic system of alveolar macrophage and the potential mechanims. METHODS: Propranolol (30 mg/kg·d) or atenolol (5 mg/kg·d) was administered by gavage to rats for 4 weeks. Then alveolar macrophages were isolated and the expression of ß(1) or ß(2)-adrenoceptor was detected by flow cytometric analysis. Dopamine ß-hydroxylase expression was assessed by Western blot assay and the concentrations of noradrenaline, IL-6, and TNF-α in cell supernatants were measured using ELISA after 2 h or 24 h exposure of alveolar macrophages to 100 ng/ml lipopolysaccharide (LPS). RESULTS: Propranolol increased the mean fluorescence intensity (MFI) of ß(1), ß(2)-adrenoceptor and the frequency of ß(1)-,ß(2)- adrenoceptor positive macrophages. However, only the MFI of ß(1)-adrenoceptor and the frequency of ß(1)-adrenoceptor positive macrophages were increased by atenolol. Furthermore, both propranolol and atenolol promoted LPS-mediated dopamine ß-hydroxylase protein expression and increased noradrenaline production in rat alveolar macrophages. This was accompanied by increased LPS-mediated IL-6 and TNF-α production in cell supernatants of alveolar macrophages. CONCLUSION: These findings demonstrate that propranolol or atenolol upregulates alveolar macrophage adrenergic system, and the response may be ß(1)-adrenergic receptor subtype dependent.

{µ-6,6'-Dimeth-oxy-2,2'-[butane-1,4-diylbis(nitrilo-methanylyl-idene)]diphenolato}trinitratocopper(II)samarium(III).

In the monomeric dinuclear title complex, [CuSm(C(20)H(22)N(2)O(4))(NO(3))(3)], the four-coordinate Cu(II) ion has a square-planar geometry involving two O atoms and two N atoms of the deprotonated Schiff base ligand. The Sm(III) ion is ten-coordinate, chelated by four O donor atoms of the Schiff base and two O atoms each from three bidentate nitrate groups, one of which is disordered over two sites in a 0.55 (7):0.45 (7) ratio.

Inhibition of nitric oxide synthase aggravates brain injury in diabetic rats with traumatic brain injury.

Studies have shown that hyperglycemia aggravates brain damage by affecting vascular endothelial function. However, the precise mechanism remains unclear. Male Sprague-Dawley rat models of diabetes were established by a high-fat diet combined with an intraperitoneal injection of streptozotocin. Rat models of traumatic brain injury were established using the fluid percussion method. Compared with traumatic brain injury rats without diabetic, diabetic rats with traumatic brain injury exhibited more severe brain injury, manifested as increased brain water content and blood-brain barrier permeability, the upregulation of heme oxygenase-1, myeloperoxidase, and Bax, the downregulation of occludin, zona-occludens 1, and Bcl-2 in the penumbra, and reduced modified neurological severity scores. The intraperitoneal injection of a nitric oxide synthase inhibitor N(5)-(1-iminoethyl)-L-ornithine (10 mg/kg) 15 minutes before brain injury aggravated the injury. These findings suggested that nitric oxide synthase plays an important role in the maintenance of cerebral microcirculation, including anti-inflammatory, anti-oxidative stress, and anti-apoptotic activities in diabetic rats with traumatic brain injury. The experimental protocols were approved by the Institutional Animal Care Committee of Harbin Medical University, China (approval No. ky2017-126) on March 6, 2017.

{µ(2)-6,6'-Dimeth-oxy-2,2'-[butane-1,4-diylbis(nitrilo-methyl-idyne)]diphenolato}trinitratocopper(II)neodymium(III).

In the title complex, [CuNd(C(20)H(22)N(2)O(4))(NO(3))(3)], the Cu(II) ion is coordinated in a distorted square-planar environment by two O atoms and two N atoms of a tetra-dentate Schiff base ligand. The Nd(III) ion is ten-coordinated by three bis-chelating nitrate groups and four O atoms of the Schiff base ligand. The atoms of one of the nitrato ligands are disordered over two sets of sites, with refined occupancies of 0.567 (13) and 0.433 (17).

[Construction of eukaryote expression vector carrying human pulmonary surfactant-associated protein C and its expression in vitro].

OBJECTIVE: To clone human pulmonary surfactant-associated protein C (SP-C) and construct an eukaryote expression vector pcDNA3.1(+)/SP-C, and then to examine the SP-C expression in vitro, which may provide a reliable way of massive production of SP-C. METHODS: The total RNA of normal lung tissue neighboring lung cancer from patients undergoing operation was extracted, and SP-C cDNA was then obtained by reverse transcription-polymerase chain reaction (RT-PCR). Both SP-C cDNA sequence and plasmid pcDNA3.1(+) were digested with NotI and XhoI, then connected by T4 DNA ligase after recycling agarose. After identification by restriction analysis and DNA sequencing, the recombinant was transfected into human breast cancer MCF-7 cells by using lipofectin reagent, and then the expression of SP-C was examined by RT-PCR and Western blotting. RESULTS: Human SP-C cDNA could be correctly cloned into the plasmid pcDNA3.1(+), and SP-C protein may be expressed in MCF-7 cells after transfection. CONCLUSION: By in vitro recombination, the eukaryote expression vector pcDNA3.1(+)/SP-C was successfully constructed and expressed SP-C in vitro, which rendered preparation for the construction of specific expression vector of human SP-C, and it laid the foundation of massive production of SP-C through mammary gland bioreactor.

Long non-coding RNA SNHG5 affects the invasion and apoptosis of renal cell carcinoma by regulating the miR-363-3p-Twist1 interaction.

Non-coding RNA dysregulation is associated with many human diseases, including cancer. This study explored the effects of lncRNA SNHG5 on clear cell renal cell carcinoma (ccRCC). We found that lncRNA SNHG5 is upregulated in human ccRCC tissues and that lncRNA SNHG5 inhibition reduced ccRCC cell invasion and promoted apoptosis in vitro. Bioinformatics database searching revealed that lncRNA SNHG5 is predicted to regulate the interaction between miR-363-3p and Twist1. We further verified a ccRCC biomarker panel, which consists of lncRNA SNHG5, miR-363-3p, and Twist1 in ccRCC tissue samples. The direct SNHG5-miR-363-3p and Twist1-miR-363-3p interactions were confirmed via dual-luciferase reporter assays. Additionally, functional assays demonstrated that SNHG5 promotes cell invasion and inhibits apoptosis, while miR-363-3p inhibits cell invasion and promotes apoptosis via an interaction with Twist1. Furthermore, we found that Twist1 promotes tumor metastasis by regulating matrix metalloproteinase (MMP)2 and MMP9 levels. Together, these results suggest that lncRNA SNHG5 may predict ccRCC patient clinical outcome and serve as a novel anti-ccRCC therapeutic target.

Effects of a high concentration of hydrogen on neurological function after traumatic brain injury in diabetic rats.

Reactive oxygen species, inflammation, and apoptosis are major contributors to secondary injuries that follow traumatic brain injury (TBI) in diabetic patients. Hydrogen (H2) can selectively neutralize reactive oxygen species and downregulate inflammatory and apoptotic factors. Therefore, we investigated the effects of inhaled high and low concentrations of hydrogen on neurological function after TBI in diabetic rats and the potential mechanism. We found that the inhalation of high concentrations of H2 significantly improved outcomes following TBI in diabetic rats. The inhalation of 42% H2 for one hour per day for 48 h significantly reduced brain edema, decreased the extravasation of sodium fluorescein, and reduced oxidative stress markers (p < 0.05). In addition, the inhalation of a high concentration of H2 (42% for one hour per day for 7 days) improved neurological deficits (p < 0.05) and reduced the expression of apoptotic protein markers (p < 0.05). However, the inhalation of 3% H2 did not yield significant effects. These results showed that the inhalation of 42% H2 can alleviate nerve damage and improve neurological function after TBI in diabetic rats. Therefore, the inhalation of a high concentration of H2 may be associated with the treatment of traumatic brain injuries.

{µ-6,6'-Dimeth-oxy-2,2'-[propane-1,3-diylbis(nitrilo-methyl-idyne)]diphenolato}trinitratocopper(II)erbium(III) acetone solvate.

In the title complex, [CuEr(C(19)H(20)N(2)O(4))(NO(3))(3)]·CH(3)COCH(3), the Cu(II) ion is coordinated in a square-planar environment by two O atoms and two N atoms of a Schiff base ligand. The Er(III) ion is bis-chelated by three nitrate ligands and coordinated by four O atoms of the Schiff base ligand in a slightly distorted bicapped square-anti-prismatic environment.