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Oligodendroglial heterogeneity in health,disease,and recovery:deeper insights into myelin dynamics

Neural Regeneration Research 2025年第11期20卷 3179-3192页

作者： Pieter-Jan Serneels Julie D.De Schutter Lies De Groef Lieve Moons Steven Bergmans KU Leuven Leuven Brain InstituteDepartment of BiologyAnimal Physiology and Neurobiology DivisionNeural Circuit Development&Regeneration Research GroupLeuvenBelgium KU Leuven Leuven Brain InstituteDepartment of BiologyAnimal Physiology and Neurobiology DivisionCellular Communication&Neurodegeneration Research GroupLeuvenBelgium

Decades of research asserted that the oligodendroglial lineage comprises two cell types:oligodendrocyte precursor cells and ***,recent studies employing single-cell RNA sequencing techniques have uncovered novel cell states,prompting a revision of the existing *** forward,the oligodendroglial lineage should be delineated into five distinct cell states:oligodendrocyte precursor cells,committed oligodendrocyte precursor cells,newly formed oligodendrocytes,myelin-forming oligodendrocytes,and mature *** new classification system enables a deeper understanding of the oligodendroglia in both physiological and pathological *** this uniform terminology will facilitate comparison and integration of data across ***,including the consolidation of findings from various demyelinating models,is essential to better understand the pathogenesis of demyelinating ***,comparing injury models across species with varying regenerative capacities can provide insights that may lead to new therapeutic strategies to overcome remyelination ***,by standardizing terminology and synthesizing data from diverse studies across different animal models,we can enhance our understanding of myelin pathology in central nervous system disorders such as multiple sclerosis,Alzheimer's disease,and amyotrophic lateral sclerosis,all of which involve oligodendroglial and myelin dysfunction.

关键词： animal models demyelination fish mammals multiple sclerosis myelin neurodegeneration oligodendrocytes oligodendroglial lineage remyelination

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Context-dependent role of sirtuin 2 in inflammation

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Neural Regeneration Research 2025年第3期20卷 682-694页

作者： NoemíSola-Sevilla Maider Garmendia-Berges MCarmen Mera-Delgado Elena Puerta Department of Pharmaceutical Sciences Division of PharmacologySchool of Pharmacy and NutritionUniversity of NavarraPamplonaSpain Navarra Institute for Health Research(IdiSNA) PamplonaSpain

Sirtuin 2 is a member of the sirtuin family nicotinamide adenine dinucleotide(NAD~+)-dependent deacetylases, known for its regulatory role in different processes, including inflammation. In this context, sirtuin 2 has been involved in the modulation of key inflammatory signaling pathways and transcription factors by deacetylating specific targets, such as nuclear factor κB and nucleotide-binding oligomerization domain-leucine-rich-repeat and pyrin domain-containing protein 3(NLRP3). However, whether sirtuin 2-mediated pathways induce a pro-or an anti-inflammatory response remains controversial. Sirtuin 2 has been implicated in promoting inflammation in conditions such as asthma and neurodegenerative diseases, suggesting that its inhibition in these conditions could be a potential therapeutic strategy. Conversely, arthritis and type 2 diabetes mellitus studies suggest that sirtuin 2 is essential at the peripheral level and, thus, its inhibition in these pathologies would not be recommended. Overall, the precise role of sirtuin 2 in inflammation appears to be context-dependent, and further investigation is needed to determine the specific molecular mechanisms and downstream targets through which sirtuin 2 influences inflammatory processes in various tissues and pathological conditions. The present review explores the involvement of sirtuin 2 in the inflammation associated with different pathologies to elucidate whether its pharmacological modulation could serve as an effective strategy for treating this prevalent symptom across various diseases.

关键词： interferon inflammation lipopolysaccharide neuroinflammation NLRP3 nuclear factorκB sirtuin 2

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Pathogenesis of NSAID-induced gastric damage:Importance of cyclooxygenase inhibition and gastric hypermotility

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World Journal of Gastroenterology 2012年第18期18卷 2147-2160页

作者： Koji Takeuchi Department of Pharmacology and Experimental Therapeutics Division of Pathological SciencesKyoto Pharmaceutical UniversityKyoto 607-8414Japan

This article reviews the pathogenic mechanism of nonsteroidal anti-inflammatory drug(NSAID)-induced gastric damage,focusing on the relation between cyclooxygenase(COX) inhibition and various functional ***,such as indomethacin,at a dose that inhibits prostaglandin(PG) production,enhance gastric motility,resulting in an increase in mucosal permeability,neutrophil infiltration and oxyradical production,and eventually producing gastric *** lesions are prevented by pretreatment with PGE 2 and antisecretory drugs,and also via an atropine-sensitive mechanism,not related to antisecretory *** neither rofecoxib(a selective COX-2 inhibitor) nor SC-560(a selective COX-1 inhibitor) alone damages the stomach,the combined administration of these drugs provokes gastric ***-560,but not rofecoxib,decreases prostaglandin E 2(PGE 2) production and causes gastric hypermotility and an increase in mucosal ***-2 mRNA is expressed in the stomach after administration of indomethacin and SC-560 but not *** up-regulation of indomethacin-induced COX-2 expression is prevented by atropine at a dose that inhibits gastric *** addition,selective COX-2 inhibitors have deleterious influences on the stomach when COX-2 is overexpressed under various conditions,including adrenalectomy,arthritis,and Helicobacter *** summary,gastric hypermotility plays a primary role in the pathogenesis of NSAID-induced gastric damage,and the response,causally related with PG deficiency due to COX-1 inhibition,occurs prior to other pathogenic events such as increased mucosal permeability;and the ulcerogenic properties of NSAIDs require the inhibition of both COX-1 and COX-2,the inhibition of COX-1 upregulates COX-2 expression in association with gastric hypermotility,and PGs produced by COX-2 counteract the deleterious effect of COX-1 inhibition.

关键词： Non-steroidal anti-inflammatory drug Gastric damage Pathogenesis Gastric motility Neutrophil

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Genomic and genetic alterations influence the progression of gastric cancer

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World Journal of Gastroenterology 2011年第3期17卷 290-299页

作者： Stefania Nobili Lorenzo Bruno Ida Landini Cristina Napoli Paolo Bechi Francesco Tonelli Carlos A Rubio Enrico Mini Gabriella Nesi Department of Preclinical and Clinical Pharmacology University of Florence Department of Critical Care Medicine and Surgery University of Florence Department of Clinical Physiopathology University of Florence Department of Pathology Karolinska Institute and University Hospital division of pathological anatomy Department of Critical Care Medicine and SurgeryUniversity of Florence

Gastric cancer is one of the leading causes of cancerrelated deaths worldwide, although the incidence has gradually decreased in many Western countries. Two main gastric cancer histotypes, intestinal and diffuse, are recognised. Although most of the described genetic alterations have been observed in both types, different genetic pathways have been hypothesized. Genetic and epigenetic events, including 1q loss of heterozygosity (LOH), microsatellite instability and hypermethylation, have mostly been reported in intestinal-type gastric carcinoma and its precursor lesions, whereas 17p LOH, mutation or loss of E-cadherin are more often implicated in the development of diffuse-type gastric *** this review, we summarize the sometimes contradictory findings regarding those markers which influence the progression of gastric adenocarcinoma.

关键词： Gastric cancer Gene alterations Prognosis Molecular pathology

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Role of copper in central nervous system physiology and pathology

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Neural Regeneration Research 2025年第4期20卷 1058-1068页

作者： Martina Locatelli Cinthia Farina Institute of Experimental Neurology Division of NeuroscienceIstituto di Ricovero e Cura a Carattere Scientifico(IRCCS)San Raffaele Scientific InstituteMilanItaly Vita-Salute San Raffaele University MilanItaly

Copper is a transition metal and an essential element for the organism,as alterations in its homeostasis leading to metal accumulation or deficiency have pathological effects in several organs,including the central nervous *** copper dysregulations have been evidenced in two genetic disorders characterized by mutations in the copper-ATPases ATP7A and ATP7B,Menkes disease and Wilson’s disease,respectively,and also in multifactorial neurological disorders such as Alzheimer’s disease,Parkinson’s disease,amyotrophic lateral sclerosis,and multiple *** review summarizes current knowledge about the role of copper in central nervous system physiology and pathology,reports about unbalances in copper levels and/or distribution under disease,describes relevant animal models for human disorders where copper metabolism genes are dysregulated,and discusses relevant therapeutic approaches modulating copper ***,alterations in copper metabolism may contribute to the etiology of central nervous system disorders and represent relevant therapeutic targets to restore tissue homeostasis.

关键词： astrocytes central nervous system copper cuprizone multiple sclerosis myelin neurodegenerative disorders

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Norepinephrine transporter (NET) is expressed in cardiac sympathetic ganglia of adult rat

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Cell Research 2001年第4期11卷 317-320页

作者： LI HE, SUN KAI MA , XIAO PING HU , GOU YUAN ZHANG , JIAN FEI Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China Cardiovascular division of Changzheng Hospital, Shang Institute of Biochemistry and Cell Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences Shanghai China Cardiovascular division of Changzheng Hospital Shanghai China pathological division of Pu Nan Hospital Shanghai China

The sympathetic nervous system plays a cardinal role in regulating cardiac function through releasing the neurotransmitter norepinephrine (NE). In comparison with ceniral nervous system, the molecular mechanism of NE uptake in myocardium is not clear. In present study we proved that in rat the CNS type of NE transporter (NET) was also expressed in middle cervical-stellate ganglion complex (MC-SG complex) which is considered to control the activity of heart, but not expressed in myocardium. The results also showed that NET expression level in right ganglion was significantly higher than in the left, rendering the greater capacity of NE uptake in right ventricle, a fact which may contribute to the maintenance of right ventricular function under pathologic state.

关键词： Norepinephrine transporter gene expression cardiac sympathetic ganglion, rat.

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Contemporary grading of prostate cancer:2017 update for pathologists and clinicians

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Asian Journal of Andrology 2019年第1期21卷 19-23页

作者： Silvla Gasparrini Alessia Clmadamore Marina Scarpelli Francesco Massari Andrea Doria Roberta Mazzucchelli Liang Cheng Antonio Lopez-Beltran Rodolfo Montironi Section of pathological anatomy Polytechnic University of the Marche RegionSchool of MedicineUnited HospitalsAnconaItaly division of Oncology S.Orsola-Malpighl HospitalBolognaItaly Department of Pathology and Laboratory Medicine Indiana University School of MedicineIndianapolisINUSA Department of Pathology and Surgery Faculty of MedicineCordobaSpain.

The Gleason grading system for prostate cancer(PCa)*** in the 1960s by DF *** to changes in PCa detection and treatment,the application of the Gleason grading system has changed considerably in pathology routine *** consensus conferences were held in 2005 and in 2014 to update PCa Gleason *** review provides a summary of the changes in the grading of PCa from the original Gleason grading system to the prognostic grade grouping,as well as a discussion of the clinical significance of the percentage of Gleason patterns 4 and 5.

关键词： Gleason grading Gieason system prognostic grade grouping prostate cancer tertiary pattern

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Rate of local tumor progression following radiofrequency ablation of pathologically early hepatocellular carcinoma

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World Journal of Gastroenterology 2017年第17期23卷 3111-3121页

作者： Yoshiteru Hao Kazushi Numata Tomohiro Ishii Hiroyuki Fukuda Shin Maeda Masayuki Nakano Katsuaki Tanaka Gastroenterological Center Yokohama City University Medical Center division of Gastroenterology Yokohama City University Graduate School of Medicine pathological Department Shonan Fujisawa Tokusyukai Hospital

AIM To evaluate whether pathologically early hepatocellular carcinoma(HCC) exhibited local tumor progression after radiofrequency ablation(RFA) less often than typical *** Fifty pathologically early HCCs [tumor diameter(mm): mean, 15.8; range, 10-23; follow-up days after RFA: median, 1213; range, 216-2137] and 187 typical HCCs [tumor diameter(mm): mean, 15.6; range, 6-30; follow-up days after RFA: median, 1116; range, 190-2328] were enrolled in this retrospective study. The presence of stromal invasion(namely, tumor cell invasion into the intratumoral portal tracts) was considered to be the most important pathologic finding for the diagnosis of early HCCs. Typical HCC was defined as the presence of a hyper-vascular lesion accompanied by delayed washout using contrastenhanced computed tomography or contrast-enhanced magnetic resonance imaging. Follow-up examinations were performed at 3-mo intervals to monitor for signs of local tumor progression. The local tumor progression rates of pathologically early HCCs and typical HCCs were then determined using the Kaplan-Meier *** During the follow-up period for the 50 pathologically early HCCs, 49(98%) of the nodules did not exhibit local tumor progression. However, 1 nodule(2%) was associated with a local tumor progression found 636 d after RFA. For the 187 typical HCCs, 46(24.6%) of the nodules exhibited local recurrence after RFA. The follow-up period until the local tumor progression of typical HCC was a median of 605 d, ranging from 181 to 1741 d. Among the cases with typical HCCs, local tumor progression had occurred in 7.0%(7/187), 16.0%(30/187), 21.9%(41/187) and 24.6%(46/187) of the cases at 1, 2, 3 and 4 years, respectively. pathologically early HCC was statistically associated with a lower rate of local tumor progression, compared with typical HCC, when evaluated using a log-rank test(P = 0.002). CONCLUSION The rate of local tumor progression for pathologically early HCCs after RFA was significa

关键词： Early hepatocellular carcinoma Local tumor progression Radiofrequency ablation Ablative margin Contrast-enhanced ultrasonography

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Development of cancer-initiating cells and immortalized cells with genomic instability

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World Journal of Stem Cells 2015年第2期7卷 483-489页

作者： Ken-ichi Yoshioka Yuko Atsumi Hitoshi Nakagama Hirobumi Teraoka division of Carcinogenesis and Cancer Prevention National Cancer Center Research Institute Department of pathological Biochemistry Medical Research InstituteTokyo Medical and Dental University

Cancers that develop after middle age usually exhibit genomic instability and multiple mutations. This is in direct contrast to pediatric tumors that usually develop as a result of specific chromosomal translocations andepigenetic aberrations. The development of genomic instability is associated with mutations that contribute to cellular immortalization and transformation. Cancer occurs when cancer-initiating cells(CICs), also called cancer stem cells, develop as a result of these mutations. In this paper, we explore how CICs develop as a result of genomic instability, including looking at which cancer suppression mechanisms are abrogated. A recent in vitro study revealed the existence of a CIC induction pathway in differentiating stem cells. Under aberrant differentiation conditions, cells become senescent and develop genomic instabilities that lead to the development of CICs. The resulting CICs contain a mutation in the alternative reading frame of CDKN2A(ARF)/p53 module, i.e., in either ARF or p53. We summarize recently established knowledge of CIC development and cellular immortality, explore the role of the ARF/p53 module in protecting cells from transformation, and describe a risk factor for genomic destabilization that increases during the process of normal cell growth and differentiation and is associated with the downregulation of histone H2 AX to levels representative of growth arrest in normal cells.

关键词： ARF/p53 module Cancer stem cells Cancerinitiatingcells Differentiation Genomic instability H2AX

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A New Early Gastric Cancer after Subtotal Gastric Resection for Early Cancer: Case Report and Review of the Literature

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Journal of Cancer Therapy 2014年第14期5卷 1450-1453页

作者： Lorenzo Bruno Lucia Barni Gabriella Nesi Sabrina Pacciani Gaia Masini Filippo Melli Gherardo Maltinti Tiku Zalla Lorenzo Dioscoridi Antonio Taddei Giancarlo Freschi Paolo Bechi Department of Surgery and Translational Medicine University of Florence Florence Italy division of pathological anatomy Department of Surgery and Translational Medicine University of Florence Florence Italy

Although the prognosis of early gastric cancer (EGC) is considered to be satisfactory, some patients experience tumor relapse after curative surgery. Both pathogenesis and risk factors of recurrence remain unclear. We describe a case report of a 49-year-old male who underwent subtotal gastric resection D2A for angular gastric cancer. Histological examination revealed gastric adenocarcinoma with low grade of differentiation and colloid areas, intramucosal, and absence of neoplastic proliferation in the surgical margins, in omental stroma and in the six examined lymph nodes (pT1, pN0). 11 years later, the same patient underwent D2 total gastrectomy for gastric cancer in the remnant stomach. New histological examination revealed again gastric adenocarcinoma, intramucosal, medium degree of differentiation, no documentable neoplastic proliferation within the limits of surgical resection, in the thirty-three examined lymph nodes and in the omentum (pT1, pN0).

关键词： Early Gastric Cancer Remnant Gastric Cancer Long Term Follow-Up

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