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Molecular knowledge of human gastric corpus epithelium remains incomplete. Here, by integrated analyses using single-cell RNA sequencing (scRNA-seq), spatial transcriptomics, and single-cell assay for transposase accessible chromatin sequencing (scATAC-seq) techniques, we uncovered the spatially resolved expression landscape and gene-regulatory network of human gastric corpus epithelium. Specifically, we identified a stem/progenitor cell population in the isthmus of human gastric corpus, where EGF and WNT signaling pathways were activated. Meanwhile, LGR4, but not LGR5, was responsible for the activation of WNT signaling pathway. Importantly, FABP5 and NME1 were identified and validated as crucial for both normal gastric stem/progenitor cells and gastric cancer cells. Finally, we explored the epigenetic regulation of critical genes for gastric corpus epithelium at chromatin state level, and identified several important cell-type-specific transcription factors. In summary, our work provides novel insights to systematically understand the cellular diversity and homeostasis of human gastric corpus epithelium in vivo.
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Humans , Epigenesis, Genetic , Gastric Mucosa/metabolism , Chromatin/metabolism , Stem Cells , Epithelium/metabolism , Fatty Acid-Binding Proteins/metabolismABSTRACT
each group were sacrificed, respectively. Distributions of BrdU positive cels and ChAT positive cels were detected by S-P immunohistochemical method. The learning and memory abilities of rats were detected by Morris water maze system. RESULTS AND CONCLUSION:BrdU positive cels were mainly distributed in the cortex and hippocampus, especialy around the blood vessels, and there was the presence of focal aggregation. A smal amount of BrdU positive cels were observed in the basal ganglia and thalamus as wel as in the ependyma. BrdU positive cels were counted at different time after operation. The number of BrdU positive cels decreased with time, and only a smal number of BrdU positive cels were observed at 60 days after transplantation. The number of ChAT positive cels at different time after transplantation was ranked as folows: neural stem cel transplantation group > model group > sham operated group (P < 0.05). Compared with the model group, the time for searching the platform was significantly lower in the neural stem transplantation group and sham operated group, but the number of crossing the platform was significantly higher in the neural stem cel transplantation group and sham operated group (P < 0.05). The results show that neural stem cels could be transplanted into the rats with vascular dementia, and the cels could survive and migrate in the brain of rats and significantly improve the learning and memory ability. This mechanism may be related to the differentiation and growth of cholinergic neurons in the hippocampus.
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Objective To study the pathological alterations,such as oxidative stress,cell proliferation and insulin resistance,especially autophagy,in Alzheimer' s disease (AD) complicated with type 2 diabetes (AD + T2DM).Methods The mouse models of T2DM,AD and AD + T2DM were used in the study,and totally 80 mice were divided into four groups:control group,T2DM group,AD group and AD + T2DM group.Morris water maze was applied to test the ability of learning and memory among the above mentioned groups.In the meantime,insulin resistance index,the expression of insulin receptor substrate 2,oxidative stress,cell proliferation and autophagy were observed with chemical analysis,immunofluorescent labeling,transmission electron microscopy and Western blotting.Results On day 4,the difference of time to find Morris water maze in control group,T2DM group,AD group and AD + T2DM group ((26.08 ±4.93) s,(38.46 ± 4.07) s,(47.32 ± 5.86) s,(53.01 ± 6.12) s,F =2.454,P =0.025) was statistically significant,and the time in AD + T2DM group was longer than that in AD group (t =-3.624,P =0.033).Compared with control group,insulin resistance occurred in T2DM group,AD group and AD + T2DM group (4.35 ± 0.48,16.12 ± 3.57,7.03 ± 3.11,18.78 ± 5.06,F =5.602,P =0.009),and the reduction of insulin receptor substrate 2 expression,the oxidative stress reaction,neural proliferative suppression and autophagy (F =418.344,222.514,436.250,113.934,23.772,35.469,all P ＜ 0.05) were induced in T2DM group,AD group and AD + T2DM group,which were more serious in AD + T2DM group than in AD group (t =-2.796,21.723,-8.041,9.037,-4.403,-32.011,-26.593,all P ＜0.05).Conclusion AD + T2DM mice suffered more serious cognitive impairment than AD and T2DM mice.The oxidative stress levels of AD + T2DM mice were upregulated,and thus led to the inhibition of cell proliferation,eventually leading to promotion of autophagy.
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Objective To investigate the clinical influence about levetiracetam on cognitive function and emotional influence in the patients with partial epilepsy.Methods A total of 62 patients with partial epilepsy were divided into carbamazepine group (30 cases) and levetiracetam group (32 cases) by random digits table method,carbamazepine group was treated by carbamazepine while levetiracetam group was treated by levetiracetam.The patients were assessed before treatment and 4,8,12,16 weeks after treatment by the Montreal cognitive assessment scale (MoCA),self rating anxiety scale (SAS) and self rating depression scale (SDS).Results There was no significant difference in MoCA score between two groups before treatment and 4 weeks after treatment (P ＞ 0.05).MoCA score at 8,12,16 weeks after treatment in levetiracetam group was better than that in carbamazepine group [(22.6 ± 2.1) scores vs.(20.8 ± 2.6) scores,(23.5±2.7) scoresvs.(21.3± 2.8) scores,(24.6±4.7) scoresvs.(21.2±3.0) scores],the difference was statistically significant (P ＜ 0.05).There was no significant difference between SAS score,SDS score between two groups before and after treatment (P ＞ 0.05).Conclusion In the process of treating the patients with partial epilepsy by drug,levetiracetam is superior to carbamazepine on the improvement of cognitive function,but the mood improvement is not obvious.
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BACKGROUND: The role of inflammatory reaction and inflammatory factors and the mechanism of pathophysiology of restenosisfollowing the stent implantation remains controversial. OBJECTIVE: To observe the changes of platelet activation markers and correlated factors following carotid artery stenting in rabbits. DESIGN, TIME AND SETTING: Observation experiment was performed at the Institute of Neurobiology of Henan University fromMarch to September 2008. MATERIALS: A total of 26 rabbits, male or female, weighing 2.1-2.9 kg, were included. The alloy stent was made of 90% platinumand 10% iridium with wire diameter of 0.13 mm and monofilament winding spiral structure. The alloy stent was submerged 100 g/Lgelatin solution, and made into protein-coated stent after dried. METHODS: Animals were anesthetized by sodium pentobarbital (30 mg/kg), and the right carotid artery was exposed. The stent was inserted in the proximal end after administration of aspirin and clopidogrel dual antiplatelet therapy. Penicillin was intravenously injected, 800 000 IU per day. MAIN OUTCOME MEASURES: The platelet-activating factor (PAC-1 and CD62P) of peripheral blood, platelet-monocyte aggregates and interleukin (IL-6) immediately before and 0.5 hour, 6 days, 1 month and 6 months after implantation were determined.RESULTS: Twenty-six rabbits were included in the final analysis. The level of PAC-1, CD62P and platelet-monocyte aggregates at 0.5 hour, 6 days and 1 month after inserting were significantly elevated compared with the levels immediately before inserting (P
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Stent-assisted angioplasty of intracranial and extracranial arteries is a complex pathophysiologic process.Therefore,understanding of related factors is significant for guiding clinical treatment and reducing restenosis rate.Intravascular stent as a foreign body leads to platelet activation and aggregation,cytokine secretion,resulting in thrombosis and leukocyte aggregation at vessel injury site to produce cytokine and inflammatory reaction.In addition,the smooth muscle cells migrate to injury site and proliferate,leading to intimal hyperplasia,vessel wall reconstruction and intra-stent restenosis.Moreover,the restenosis following stenting is related to stent type and medicine supportive treatment.Drug-eluted stent with anti-inflammation and vascular smooth muscle cell proliferation can reduce body inflammation intensity and duration,and postoperative medicine supportive treatment can reduce incidence of intravascular restenosis.