| 1. |
- Albertsson, Anna-Maj, et al.
(författare)
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The effect of osteopontin and osteopontin-derived peptides on preterm brain injury.
- 2014
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Ingår i: Journal of neuroinflammation. - : Springer Science and Business Media LLC. - 1742-2094. ; 11:1
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Tidskriftsartikel (refereegranskat)abstract
- BackgroundOsteopontin (OPN) is a highly phosphorylated sialoprotein and a soluble cytokine that is widely expressed in a variety of tissues, including the brain. OPN and OPN-derived peptides have been suggested to have potential neuroprotective effects against ischemic brain injury, but their role in preterm brain injury is unknown.MethodsWe used a hypoxia-ischemia (HI)-induced preterm brain injury model in postnatal day 5 mice. OPN and OPN-derived peptides were given intracerebroventricularly and intranasally before HI. Brain injury was evaluated at 7days after the insults.ResultsThere was a significant increase in endogenous OPN mRNA and OPN protein in the mouse brain after the induction of HI at postnatal day 5. Administration of full-length OPN protein and thrombin-cleaved OPN did not affect preterm brain injury. This was demonstrated with both intracerebroventricular and intranasal administration of OPN as well as in OPN-deficient mice. Interestingly, both N134¿153 and C154¿198 OPN-derived peptides increased the severity of brain injury in this HI-induced preterm brain injury model.ConclusionsThe neuroprotective effects of OPN are age-dependent, and, in contrast to the more mature brain, OPN-derived peptides potentiate injury in postnatal day 5 mice. Intranasal administration is an efficient way of delivering drugs to the central nervous system (CNS) in neonatal mice and is likely to be an easy and noninvasive method of drug delivery to the CNS in preterm infants.
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| 2. |
- Albertsson, Anna-Maj, et al.
(författare)
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The immune response after hypoxia-ischemia in a mouse model of preterm brain injury.
- 2014
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Ingår i: Journal of neuroinflammation. - : Springer Science and Business Media LLC. - 1742-2094. ; 11:1
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Tidskriftsartikel (refereegranskat)abstract
- BackgroundPreterm brain injury consists primarily of periventricular leukomalacia accompanied by elements of gray-matter injury, and these injuries are associated with cerebral palsy and cognitive impairments. Inflammation is believed to be an important contributing factor to these injuries. The aim of this study was to examine the immune response in a postnatal day (PND) 5 mouse model of preterm brain injury induced by hypoxia-ischemia (HI) that is characterized by focal white and gray-matter injury.MethodsC57Bl/6 mice at PND 5 were subjected to unilateral HI induced by left carotid artery ligation and subsequent exposure to 10% O2 for 50 minutes, 70 minutes, or 80 minutes. At seven days post-HI, the white/gray-matter injury was examined. The immune responses in the brain after HI were examined at different time points after HI using RT-PCR and immunohistochemical staining.ResultsHI for 70 minutes in PND 5 mice induced local white-matter injury with focal cortical injury and hippocampal atrophy, features that are similar to those seen in preterm brain injury in human infants. HI for 50 minutes resulted in a small percentage of animals being injured, and HI for 80 minutes produced extensive infarction in multiple brain areas. Various immune responses, including changes in transcription factors and cytokines that are associated with a T-helper (Th)1/Th17-type response, an increased number of CD4+ T-cells, and elevated levels of triggering receptor expressed on myeloid cells 2 (TREM-2) and its adaptor protein DNAX activation protein of 12 kDa (DAP12) were observed using the HI 70 minute preterm brain injury model.ConclusionsWe have established a reproducible model of HI in PND 5 mice that produces consistent local white/gray-matter brain damage that is relevant to preterm brain injury in human infants. This model provides a useful tool for studying preterm brain injury. Both innate and adaptive immune responses are observed after HI, and these show a strong pro-inflammatory Th1/Th17-type bias. Such findings provide a critical foundation for future studies on the mechanism of preterm brain injury and suggest that blocking the Th1/Th17-type immune response might provide neuroprotection after preterm brain injury.
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| 3. |
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| 4. |
- Cheng, Ye, et al.
(författare)
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Genetic variants in the HLA region contribute to the risk of cerebral palsy
- 2024
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Ingår i: BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE. - 0925-4439 .- 1879-260X. ; 1870:3
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Tidskriftsartikel (refereegranskat)abstract
- Cerebral palsy (CP) is the most common physical disability in childhood, and genetic factors play an important role in its pathogenesis. However, the genetic contributions remain incompletely elucidated. Here, we conducted a two-stage association study between 1090 CP cases and 1100 healthy controls after whole exome sequencing. The human leukocyte antigen (HLA) allelic predispositions were further analyzed in overall CP and subgroups using multivariate logistic regression. We found a strong signal in the HLA region on chromosome 6, where rs3131787 harbored the most significant association with CP (P = 2.05 x 10-14, OR = 2.22). In comparison to controls, the carrier frequencies of HLA-B*13:02 were significantly higher in children with CP (9.82 % in control vs 19.27 % in CP, P = 1.03 x 10-4, OR = 2.17). Furthermore, the effect of HLA-B*13:02 on increasing the risk of CP mainly existed in cryptogenic CP without exposure to premature birth, low birth weight, birth asphyxia, or periventricular leukomalacia. This study indicated a strong association of HLA variants with CP, which implied that immune dysregulation resulting from immunogenetic variants might underlie the pathogenesis of CP. Our findings provide genetic evidence that an immunomodulator may serve as a promising therapeutic intervention for patients with CP by reinstating the neuroinflammation hemostasis.
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| 5. |
- Liu, Xueqi, et al.
(författare)
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Study on charge transportation in the layer-structured oxide composite of SOFCs
- 2018
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Ingår i: International journal of hydrogen energy. - : Elsevier. - 0360-3199 .- 1879-3487. ; 43:28, s. 12773-12781
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Tidskriftsartikel (refereegranskat)abstract
- In the past few years, triple (H+/O2-/e(-)) conducting materials have been regarded as one of the most promising electrode categories for solid oxide fuel cells (SOFCs). In this work, a layer-structured LiNi0.8Co0.15Al0.05O2-delta (LNCA) with triple conduction has been studied. The semiconductor-ionic conductor (SIC) LNCA-SDC composite has been fabricated by compositing the LNCA material with ionic conductor, i.e., samarium doped ceria (SDC). The electrochemical performance of the LNCA-SDC composite was studied by electrochemical impedance spectroscopy, while its electronic conductivity was confirmed by d.c. polarization method. It is found that the ionic conductivity of the composite is higher than the electronic conductivity by several orders of magnitude. The charge carriers and transportation properties of LNCA-SDC were studied using H+ and O2- blocking layer cells respectively. Results prove that the LNCA-SDC composite is a hybrid oxygen ion-proton conducting material. The oxygen ion conduction is dominated at low temperature (425 -500 degrees C), however, it is comparable with H+ conduction at high temperature (550 degrees C). Additionally, the formation of Li2CO3 under fuel cell operation environment was observed and the mechanism of the hybrid conductivity of LNCA-SDC was studied.
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| 6. |
- Wang, Yangong, et al.
(författare)
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TEP1 is a risk gene for sporadic cerebral palsy
- 2021
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Ingår i: Journal of genetics and genomics. - : Elsevier BV. - 1673-8527. ; 48:12, s. 1134-1138
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 7. |
- Yu, Yang, et al.
(författare)
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Apolipoprotein M gene single nucleotide polymorphisms discovery in patients with chronic obstructive pulmonary disease and determined by the base-quenched probe technique
- 2017
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Ingår i: Gene. - : Elsevier BV. - 0378-1119. ; 637, s. 9-13
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Tidskriftsartikel (refereegranskat)abstract
- Background It has been reported increased serum apoM levels seen in the patients suffered from obstructive sleep apnoea and chronic obstructive pulmonary diseases. In the present, we further examine the prevalence of apoM gene SNPs in COPD patients. And a new method base-quenched probe technique is established. Methods In the present study, we first used the Roche 454 GS Junior high-throughput sequencer to analyze 6 COPD samples and 6 control samples, in these samples we found 3 interesting SNPs (rs805264, rs707922 and rs707921) and then we designed primers and probes to establish a simple and quick screening method that is a base-quench probe technique and the genotype was confirmed by melting curves. With this new technique, we further determined 252 COPD samples and 248 normal subjects were applied as controls. Results A total of 19 high-confidence mutations were detected in the Roche 454, 6 mutations among them were not been reported in NCBI, but the mutation frequency was < 20%. Four mutations occurred only in COPD patients, rs751064723 is located in the first exon of transcript 1 and the rest are located in either apoM gene promoter or intron region. The results of melting curve showed that the wild-type and homozygous mutants of rs805264, rs707922 and rs707921 presented melting valley at two different melting temperatures, and the results were consistent with those of DNA sequencing (K = 1, P = 0.000). Conclusions The detection of apoM gene SNPs laid the foundation for the study of the relationship between COPD and apoM, and the base-quenched probe technique is simple, economic and accurate, and it is suitable for a large number of apoM genotyping studies.
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