Minocycline ameliorates D-galactose-induced memory deficits and loss of Arc/Arg3.1 expression.

Dysfunction of learning and memory is widely found in many neurological diseases. Understanding how to preserve the normal function of learning and memory will be extremely beneficial for the treatment of these diseases. However, the possible protective effect of minocycline in memory impairment is unknown. We used the well-established D-galactose rat amnesia model and two behavioral tasks, the Morris water maze and the step-down task, for memory evaluation. Western blot and PCR were used to examine the protein and mRNA levels of Arc/Arg3.1. We report that minocycline supplementation ameliorates both the spatial and fear memory deficits caused by D-galactose. We also found that Arc/Arg3.1, c-fos, and brain-derived neurotrophic factor levels are decreased in the D-galactose animal model, and that minocycline reverses the protein and mRNA levels of Arc in the hippocampus, suggesting the potential role of Arc/Arg3.1 in minocycline's neuroprotective mechanism. Our study strongly suggests that minocycline can be used as a novel treatment for memory impairment in neurological diseases.

Toward enhanced photocatalytic activity of graphite carbon nitride through rational design of noble metal-free dual cocatalysts.

The g-C3N4-MoS2-M(OH)x ternary heterostructures were designed and fabricated for the first time. The embedding of noble-metal-free MoS2-M(OH)x dual cocatalysts over g-C3N4 nanosheets led to obvious synergistic effect for improving the transport as well as utilization efficiency of photo-generated charge carriers. Consequently, the optimal ternary heterostructure (g-C3N4-MoS2-Ni(OH)2) exhibited photocatalytic hydrogen production activity 4.5 times larger than the sum of the photocatalytic HER activity of g-C3N4-MoS2 and g-C3N4-Ni(OH)2. More significantly, even in the absence of the sacrificial agent, the g-C3N4-MoS2-Ni(OH)2 ternary heterostructure exhibited a photocatalytic HER activity of 0.3 mmol h-1 g-1 with considerable H2O2 production under UV-visible light.

Association of Bone Turnover Levels with MTHFR Gene Polymorphisms among Pregnant Women in Wuhan, China.

Pregnancy is a critical stimulator of bone mineral resorption. We used to find the MTHFR gene polymorphisms are related with blood lead levels among pregnant women. Pregnancy-stimulated bone turnover may be associated with MTHFR gene polymorphisms too. In this article, we aimed to determine the relationship between MTHFR gene polymorphisms and bone turnover rates among the pregnant women. The participants including pregnant and non-pregnant women were selected and recruited during their routine prenatal or physical examination from July to October in 2012. A total of 1000 participants, including 250 pregnant women in the first, second, and third trimesters and 250 non-pregnant women, were enrolled in the study. Finally, after excluding 27 participants unable to provide blood samples, 973 eligible participants (i.e., 234,249, and 248 pregnant women in the first, second, and third trimesters, respectively, and 242 non-pregnant women) were included in the research. The MTHFR gene 1298CC homozygote carriers were more susceptible to yield higher plasma homocysteine levels than the 1298AA/AC carriers, with standardized coefficients of 0.086 (P<0.05) and 0.104 (P<0.01) of all the participants and the pregnant women, respectively. The MTHFR gene 1793AA homozygote carriers more likely showed higher plasma osteocalcin levels (standardized ß=0.091,P<0.01) than the 1793GG/GA carriers among all the subjects. Plasma homocysteine levels were positively correlated with blood lead levels among the participants and the pregnant women with standardized coefficients of 0.320 (P<0.01) and 0.179 (P<0.01), respectively. Plasma osteocalcin levels were positively associated with blood lead levels among pregnant and non-pregnant women with standardized coefficients of 0.084 (P<0.05) and 0.125 (P<0.01), respectively. In conclusion, homocysteine and osteocalcin contents in plasma are associated with the MTHFR gene A1298C polymorphism and blood lead levels among pregnant women. The MTHFR gene A1298C polymorphism-related homocysteine is a possible risk factor for increased blood lead levels among Chinese women.

Underlying Mechanisms of Memory Deficits Induced by Etomidate Anesthesia in Aged Rat Model: Critical Role of Immediate Early Genes.

BACKGROUND: Etomidate (R-1-[1-ethylphenyl] imidazole-5-ethyl ester) is a widely used anesthetic drug that had been reported to contribute to cognitive deficits after general surgery. However, its underlying mechanisms have not been fully elucidated. In this study, we aimed to explore the neurobiological mechanisms of cognitive impairments that caused by etomidate. METHODS: A total of 30 Sprague-Dawley rats were used and divided into two groups randomly to receive a single injection of etomidate or vehicle. Then, the rats' spatial memory ability and neuronal survival were evaluated using the Morris water maze test and Nissl staining, respectively. Furthermore, we analyzed levels of oxidative stress, as well as cyclic adenosine 3',5'-monophosphate response element-binding (CREB) protein phosphorylation and immediate early gene (IEG, including Arc, c-fos, and Egr1) expression levels using Western blot analysis. RESULTS: Compared with vehicle-treated rats, the etomidate-treated rats displayed impaired spatial learning (day 4: 27.26 ± 5.33 s vs. 35.52 ± 3.88 s, t = 2.988, P = 0.0068; day 5: 15.84 ± 4.02 s vs. 30.67 ± 4.23 s, t = 3.013, P = 0.0057; day 6: 9.47 ± 2.35 s vs. 25.66 ± 4.16 s, t = 3.567, P = 0.0036) and memory ability (crossing times: 4.40 ± 1.18 vs. 2.06 ± 0.80, t = 2.896, P = 0.0072; duration: 34.00 ± 4.24 s vs. 18.07 ± 4.79 s, t = 3.023, P = 0.0053; total swimming distance: 40.73 ± 3.45 cm vs. 27.40 ± 6.56 cm, t = 2.798, P = 0.0086) but no neuronal death. Furthermore, etomidate did not cause oxidative stress or deficits in CREB phosphorylation. The levels of multiple IEGs (Arc: vehicle treated rats 100%, etomidate treated rats 86%, t = 2.876, P = 0.0086; c-fos: Vehicle treated rats 100%, etomidate treated rats 72%, t = 2.996, P = 0.0076; Egr1: Vehicle treated rats 100%, etomidate treated rats 58%, t = 3.011, P = 0.0057) were significantly reduced in hippocampi of etomidate-treated rats. CONCLUSION: Our data suggested that etomidate might induce memory impairment in rats via inhibition of IEG expression.

Expressions of E-cadherin, p120ctn, ß-catenin and NF-κB in ulcerative colitis.

This study was aimed to investigate the expressions of E-cadherin, p120ctn, ß-catenin and NF-κB in ulcerative colitis (UC) tissues and the implications of their expressions in the pathogenesis of UC. The expressions of E-cadherin, p120ctn, ß-catenin and NF-κB were detected by immunohistochemistry, and those of p120ctn and NF-κB by Western blotting in 23 cases of UC and 17 cases of normal colonic tissues. The relationship between the expression of E-cadherin or NF-κB and that of p120ctn was analyzed by Spearman rank correlation analysis. The results showed that in UC and normal colonic groups, the abnormal expression rate of E-cadherin, p120ctn, ß-catenin, and NF-κB was 52.2% vs. 0 (P<0.05), 73.9% vs. 23.5% (P<0.05), 65.2% vs. 17.6% (P<0.05) and 78.4% vs. 23.5% (P<0.05), respectively. p120ctn expression was positively correlated with E-cadherin expression (r=0.404, P<0.05), but negatively with nuclear NF-κB expression (r= - 0.347, P<0.05). Western blotting showed that as compared with the normal controls, the p120ctn protein level was significantly decreased (P<0.05), whereas the NF-κB protein level was increased (P<0.05) in UC tissues. It was concluded that in the colonic tissues of UC patients, the expressions of E-cadherin, p120ctn and ß-catenin are decreased, suggesting the mucosal barrier is impaired in UC. Moreover, NF-κB is increased and activated in the UC tissues, resulting in the inflammation in UC. p120ctn may influence the UC development through modulating intercellular adhesion and inflammatory response.