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- Niemi, MEK, et al.
(författare)
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- 2021
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swepub:Mat__t
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- Kanai, M, et al.
(författare)
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- 2023
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swepub:Mat__t
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- Gong, XZ, et al.
(författare)
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Tetramethylpyrazine prevents contrast-induced nephropathy by inhibiting p38 MAPK and FoxO1 signaling pathways
- 2013
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Ingår i: American journal of nephrology. - : S. Karger AG. - 1421-9670 .- 0250-8095. ; 37:3, s. 199-207
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Tidskriftsartikel (refereegranskat)abstract
- <b><i>Background:</i></b> Apoptosis is recognized as an important mechanism in contrast-induced nephropathy (CIN). As tetramethylpyrazine (TMP) has been recently found to be renoprotective and anti-apoptotic in multiple kidney injuries, we hypothesized that TMP would prevent CIN. <b><i>Methods:</i></b> An experimental model of CIN was established in rats. Serum creatinine, blood urea nitrogen, plasma cystatin C, urinary N-acetyl-β-glucosaminidase, and urinary γ-glutamyl transpeptidase were measured to evaluate kidney function. Apoptosis was assessed by transmission electron microscopy, transferase-mediated deoxyuridine triphosphate nick end-labeling staining, and poly-ADP-ribose polymerase cleavage. Fork-head box O1 transcriptional factor (FoxO1) mRNA expression was evaluated by quantitative real-time PCR. Phospho-p38 mitogen-activated protein kinase (MAPK) protein expression was assessed by immunohistochemistry and Western blotting. <b><i>Results:</i></b> TMP significantly attenuated the resulting renal dysfunction and renal tubular cell apo-ptosis. Mechanistically, TMP decreased the expression of phospho-p38 MAPK protein and attenuated the increased FoxO1 mRNA and nuclear protein expression. In addition, TMP inhibited inducible nitric oxide synthase and Bax protein expression while it upregulated Bcl-2. <b><i>Conclusion:</i></b> In summary, this study demonstrated the protective role of TMP against CIN and indicated the effects of TMP may be mediated by the inhibition of p38 MAPK and FoxO1 pathways. Thus, TMP may be a new potential therapeutic agent to prevent CIN.
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- Yuen, RKC, et al.
(författare)
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Genome-wide characteristics of de novo mutations in autism
- 2016
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Ingår i: NPJ genomic medicine. - : Springer Science and Business Media LLC. - 2056-7944. ; 1, s. 160271-1602710
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Tidskriftsartikel (refereegranskat)abstract
- De novo mutations (DNMs) are important in autism spectrum disorder (ASD), but so far analyses have mainly been on the ~1.5% of the genome encoding genes. Here, we performed whole-genome sequencing (WGS) of 200 ASD parent–child trios and characterised germline and somatic DNMs. We confirmed that the majority of germline DNMs (75.6%) originated from the father, and these increased significantly with paternal age only (P=4.2×10−10). However, when clustered DNMs (those within 20 kb) were found in ASD, not only did they mostly originate from the mother (P=7.7×10−13), but they could also be found adjacent to de novo copy number variations where the mutation rate was significantly elevated (P=2.4×10−24). By comparing with DNMs detected in controls, we found a significant enrichment of predicted damaging DNMs in ASD cases (P=8.0×10−9; odds ratio=1.84), of which 15.6% (P=4.3×10−3) and 22.5% (P=7.0×10−5) were non-coding or genic non-coding, respectively. The non-coding elements most enriched for DNM were untranslated regions of genes, regulatory sequences involved in exon-skipping and DNase I hypersensitive regions. Using microarrays and a novel outlier detection test, we also found aberrant methylation profiles in 2/185 (1.1%) of ASD cases. These same individuals carried independently identified DNMs in the ASD-risk and epigenetic genes DNMT3A and ADNP. Our data begins to characterize different genome-wide DNMs, and highlight the contribution of non-coding variants, to the aetiology of ASD.
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- Gong, XZ, et al.
(författare)
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Nephroprotective Effects of N-Acetylcysteine Amide against Contrast-Induced Nephropathy through Upregulating Thioredoxin-1, Inhibiting ASK1/p38MAPK Pathway, and Suppressing Oxidative Stress and Apoptosis in Rats
- 2016
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Ingår i: Oxidative medicine and cellular longevity. - : Hindawi Limited. - 1942-0994 .- 1942-0900. ; 2016, s. 8715185-
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Tidskriftsartikel (refereegranskat)abstract
- Contrast-induced nephropathy (CIN) is a leading cause of hospital-acquired acute kidney injury (AKI) due to apoptosis induced in renal tubular cells. Our previous study demonstrated the novel N-acetylcysteine amide (NACA); the amide form of N-acetyl cysteine (NAC) prevented renal tubular cells from contrast-induced apoptosis through inhibiting p38 MAPK pathway in vitro. In the present study, we aimed to compare the efficacies of NACA and NAC in preventing CIN in a well-established rat model and investigate whether thioredoxin-1 (Trx1) and apoptosis signal-regulating kinase 1 (ASK1) act as the potential activator for p38 MAPK. NACA significantly attenuated elevations of serum creatinine, blood urea nitrogen, and biomarkers of AKI. At equimolar concentration, NACA was more effective than NAC in reducing histological changes of renal tubular injuries. NACA attenuated activation of p38 MAPK signal, reduced oxidative stress, and diminished apoptosis. Furthermore, we demonstrated that contrast exposure resulted in Trx1 downregulation and increased ASK1/p38 MAPK phosphorylation, which could be reversed by NACA and NAC. To our knowledge, this is the first report that Trx1 and ASK1 are involved in CIN. Our study highlights a renal protective role of NACA against CIN through modulating Trx1 and ASK1/p38 MAPK pathway to result in the inhibition of apoptosis among renal cells.
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- Peng, Y, et al.
(författare)
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The effect of low volume high-intensity interval training on metabolic and cardiorespiratory outcomes in patients with type 2 diabetes mellitus: A systematic review and meta-analysis
- 2023
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Ingår i: Frontiers in endocrinology. - : Frontiers Media SA. - 1664-2392. ; 13, s. 1098325-
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Tidskriftsartikel (refereegranskat)abstract
- The present systematic review and meta-analysis of randomized controlled trials (RCTs) was conducted to investigate the effect of low volume high-intensity interval training (LVHIIT) on the metabolic and cardiorespiratory outcomes in patients with type 2 diabetes mellitus (T2DM).MethodsRelevant articles were sourced from PubMed, EBSCO, Web of Science, Embase, and the Cochrane Library from inception to October 2022. The study search strategy and all other processes were implemented in accordance with the PRISMA statement.ResultsFive randomized controlled trials that satisfied the inclusion criteria were included in this meta-analysis. The LVHIIT group had significantly lower fasting blood glucose levels (RR= -1.21; 95% CI= -2.02— -0.40, p = 0.0032) and HbA1c levels (RR= -0.65; 95% CI= -1.06— -0.23, p = 0.002) and higher levels of insulin resistance indicator HOMA-IR (RR= -1.34; 95% CI = -2.59— -0.10, p = 0.03) than the control group. Moreover, our results show that LVHIIT can reduce body mass (RR = -0.94, 95% CI = -1.37— -0.51, p<0.0001) and body mass index (RR = -0.31, 95% CI = -0.47— -0.16, p<0.0001). LVHIIT had a better therapeutic effect on blood lipid metabolism, such as total cholesterol, high-density lipoprotein, low-density lipoprotein and triglycerides. However, the change in fasting insulin levels was not statistically significant (RR= -1.43; 95% CI = -3.46— 0.60, p =0.17). Furthermore, LVHIIT reduced the systolic blood pressure (RR =-4.01, 95% CI = -4.82 – -3.21, p<0.0001) and improved peak oxygen uptake (VO2peak) compared to the control group (RR= 5.45; 95% CI = 1.38 – 9.52, p =0.009).ConclusionAfter a certain period of LVHIIT, glycaemic control, insulin resistance, body weight, lipid profile and cardiorespiratory outcomes were significantly improved in T2DM patients.
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