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Statins and Metformin Use Is Associated with Lower PSA Levels in Prostate Cancer Patients Presenting for Radiation Therapy

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Journal of Cancer Therapy 2017年第2期8卷 73-85页

作者： Xiaonan Liu Jing Li Steven E. schild michael H. schild William Wong Sujay Vora michael G. Herman Mirek Fatyga School of Computing Informatics Decision Systems Engineering Arizona State University Tempe AZ USA Department of Radiation Oncology Mayo Clinic Arizona Phoenix AZ USA Department of Radiation Oncology Mayo Clinic Rochester AZ USA

Background: A possible association between the level of prostate specific antigen (PSA) and the use of some commonly prescribed medications has been reported in recent studies. Most of these studies were carried out in general populations of men who were screened for prostate cancer using the PSA test. We reported on the association between the initial PSA level and the use of statins, metformin and alpha-blockers in patients who were diagnosed with prostate cancer and presented for radiation therapy. Methods: Three hundred and eighty one patients treated between the years of 2000-2005 and 2009-2012 were included in this retrospective study. The information about statin, metformin and alpha-blockers use was recorded immediately prior to treatment. Differences in PSA levels prior to treatment by medication status were estimated using univariate and multivariate linear regression on log PSA values. Results: Compared with men who were not on these medications, the PSA level at presentation was 20% lower for statin users (p = 0.002) and 33% lower for metformin users (p = 0.004). We did not observe statistically significant associations between the use of statins or metformin and cancer stage, National Comprehensive Cancer Network (NCCN) risk score, or therapy outcome. A statistically significant association between the NCCN risk score and the use of alpha-blockers was observed (p = 0.002). Conclusions: We found that statins and metformin were associated with lower PSA levels in prostate cancer patients to an extent that could influence management decisions. We found no statistically significant associations between the use of these medications and treatment outcomes.

关键词： PSA Statins Metformin Prostate Cancer

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Splenic-vasculature involvement is associated with poor prognosis in resected distal pancreatic cancer

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Gastroenterology Report 2021年第2期9卷 139-145,I0002页

作者： Feng Yin Mohammed Saad Jingmei Lin Christopher R.Jackson Bing Ren Cynthia Lawson Dipti M.Karamchandani Belen Quereda Bernabeu Wei Jiang Teena Dhir Richard Zheng Christopher W.Schultz Dongwei Zhang Courtney L.Thomas Xuchen Zhang Jinping Lai michael schild Xuefeng Zhang Hao Xie Xiuli Liu Department of Pathology and Anatomical Sciences University of MissouriColumbiaMOUSA Department of Pathology Indiana UniversityIndianapolisINUSA Department of Pathology Dartmouth-Hitchcock Medical CenterLebanonNHUSA Department of Pathology Pennsylvania State Health Milton S.Hershey Medical CenterHersheyPAUSA Department of Pathology Thomas Jefferson University HospitalPhiladelphiaPAUSA Department of Pathology and Laboratory Medicine University of Rochester Medical CenterRochesterNYUSA Department of Pathology Yale UniversityNew HavenCTUSA Department of Pathology and Laboratory Medicine Kaiser Permanente Sacramento Medical CenterSacramentoCAUSA Department of Pathology Duke UniversityDurhamNCUSA Department of Pathology Cleveland ClinicClevelandOHUSA Department of Gastrointestinal Oncology Moffitt Cancer CenterTampaFLUSA Department of Pathology Immunology and Lab MedicineUniversity of FloridaGainesvilleFLUSA

Background Distal pancreatic carcinoma is one of the most lethal cancers largely due to its high incidence of distant *** study aims to assess the prognostic value of splenic-vasculature involvement in resected distal pancreatic *** In this retrospective study,we collected the clinicopathologic information of 454 patients with pancreatic cancer and performed univariate and multivariate analyses to identify factors associated with progression-free survival(PFS)and overall survival(OS),with an emphasis on the prognostic value of splenic-artery and-vein *** Univariate analysis revealed that larger tumor size,non-intraductal papillary mucinous neoplasm(non-IPMN)-associated adenocarcinoma,poor differentiation,stage pT3,nodal metastasis,lymphovascular invasion,perineural invasion,and pathologic and radiographic evidence of splenic-vein invasion were significantly associated with shorter PFS and OS(all P<0.05).Multivariate analysis confirmed non-IPMN-associated adenocarcinoma,stage pT3,stage pN1-2,and postoperative adjuvant chemotherapy as independent risk factors for both PFS and OS,and larger tumor size and radiographic evidence of splenic-artery invasion as predictors of PFS *** Guidelines should be developed for a uniform approach with regard to the examination and reporting of the status of the splenic vasculature when dealing with distal-pancreatic-cancer specimens.

关键词： pancreatic cancer splenic artery splenic vein prognosis intraductal papillary mucinous neoplasm

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Like a G6-nal:transcriptional control of G-protein coupled receptors during oligodendroglial development

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Neural Regeneration Research 2025年第7期20卷 2001-2002页

作者： Tim Aberle michael Wegner Institut für Biochemie Friedrich-Alexander-Universität Erlangen-NürnbergErlangenGermany

Multilayered control of myelination:Quick,saltatory conduction of action potentials along nerve fibers requires the electrical insulation of axons by myelinating *** the central nervous system,this role is taken up by *** are marked by the expression of the lineage determinants Sox10 and Olig2 and arise from oligodendrocyte precursor cells(OPCs)during embryonal *** the majority of OPCs differentiate into mature oligodendrocytes when nearby axonal segments require myelination,a small subpopulation of OPCs persist as a progenitor ***,the timing of myelination and maintenance of the OPC pool both need to be precisely *** transcription factors either positively or negatively affect oligodendrocyte differentiation and maintenance of the OPC pool as components of a complex gene regulatory network(reviewed in Sock and Wegner,2021).Network activity is additionally influenced by extracellular signaling molecules that bind to receptors on the oligodendroglial cell surface and activate intracellular signaling *** the receptors are linked to the network is poorly understood so far,but pivotal to understanding the overall regulation of central nervous system(CNS)myelination in response to environmental *** insights were recently gained for Gpr37(Schmidt et al.,2024),a G-protein coupled receptor(GPCR)with known relevance in differentiating oligodendrocytes(Yang et al,2016).

关键词： gained insulation conduction

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Emerging structures and dynamic mechanisms ofγ-secretase for Alzheimer’s disease

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Neural Regeneration Research 2025年第1期20卷 174-180页

作者： Yinglong Miao michael S.Wolfe Computational Medicine Program and Department of Pharmacology University of North Carolina–Chapel HillChapel HillNCUSA Department of Medicinal Chemistry University of KansasLawrenceKSUSA

γ-Secretase,called“the proteasome of the membrane,”is a membrane-embedded protease complex that cleaves 150+peptide substrates with central roles in biology and medicine,including amyloid precursor protein and the Notch family of cell-surface *** inγ-secretase and amyloid precursor protein lead to early-onset familial Alzheimer’s disease.γ-Secretase has thus served as a critical drug target for treating familial Alzheimer’s disease and the more common late-onset Alzheimer’s disease as ***,critical gaps remain in understanding the mechanisms of processive proteolysis of substrates,the effects of familial Alzheimer’s disease mutations,and allosteric modulation of substrate cleavage byγ-*** this review,we focus on recent studies of structural dynamic mechanisms ofγ-*** mechanisms,including the“Fit-Stay-Trim,”“Sliding-Unwinding,”and“Tilting-Unwinding,”have been proposed for substrate proteolysis of amyloid precursor protein byγ-secretase based on all-atom molecular dynamics *** an incorrect registry of the Notch1 substrate was identified in the cryo-electron microscopy structure of Notch1-boundγ-secretase,molecular dynamics simulations on a resolved model of Notch1-boundγ-secretase that was reconstructed using the amyloid precursor protein-boundγ-secretase as a template successfully capturedγ-secretase activation for proper cleavages of both wildtype and mutant Notch,being consistent with biochemical experimental *** approach could be potentially applied to decipher the processing mechanisms of various substrates byγ-*** addition,controversy over the effects of familial Alzheimer’s disease mutations,particularly the issue of whether they stabilize or destabilizeγ-secretase-substrate complexes,is ***,an outlook is provided for future studies ofγ-secretase,including pathways of substrate binding and product release,effects of modulators on familial Alzheimer’s disease mutations

关键词： Alzheimer’s disease amyloid precursor protein cryo-EM structures drug design intramembrane proteolysis molecular dynamics Notch

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Validation of American Joint Committee on Cancer 8th edition of TNM staging in resected distal pancreatic cancer

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World Journal of Gastrointestinal Pharmacology and Therapeutics 2020年第2期11卷 25-39页

作者： Feng Yin Mohammed Saad Hao Xie Jingmei Lin Christopher R Jackson Bing Ren Cynthia Lawson Dipti M Karamchandani Belen Quereda Bernabeu Wei Jiang Teena Dhir Richard Zheng Christopher W Schultz Dongwei Zhang Courtney L Thomas Xuchen Zhang Jinping Lai michael schild Xuefeng Zhang Xiuli Liu Department of Pathology and Anatomical Sciences University of MissouriColumbiaMO 65212United States Department of Pathology Indiana UniversityIndianapolisIN 46202United States Division of Medical Oncology Mayo ClinicRochesterMN 55905United States Department of Pathology Dartmouth-Hitchcock Medical CenterLebanonPA 03766United States Department of Pathology Pennsylvania State Health Milton S.Hershey Medical CenterHersheyPA 17033United States Department of Pathology Thomas Jefferson University HospitalPhiladelphiaPA 19107United States Department of Pathology and Lab Medicine University of Rochester Medical CenterRochesterNY 14642United States Department of Pathology Yale UniversityNew HavenCT 06510United States Department of Pathology and Laboratory Medicine Kaiser Permanente Sacramento Medical CenterSacramentoCA 95825United States Department of Pathology Duke UniversityDurhamNC 27710United States Department of Pathology Cleveland ClinicClevelandOH 44195United States Department of Pathology Immunology and Lab MedicineUniversity of FloridaGainesvilleFL 32610United States

BACKGROUND In order to improve risk stratification and clinical management of the pancreatic ductal adenocarcinoma(PDAC),the American Joint Committee on Cancer(AJCC)has published its eighth edition staging *** major changes have been introduced in the new staging system for both T and N *** the rarity of resectable disease,distal pancreatic cancer is likely underrepresented in the published clinical studies,and how the impact of the staging system actually reflects on to clinical outcomes remain *** To validate the AJCC 8th edition of TNM staging in distal *** A retrospective cohort study was performed in seven academic medical centers in the United *** prognostic factors associated with progression-free survival(PFS)and overall survival(OS)were evaluated through univariate and multivariate *** Overall,454 patients were enrolled in the study,and were divided into 2 subgroups:Invasive intraductal papillary mucinous neoplasms(IPMN)(115 cases)and non-IPMN associated adenocarcinoma(339 cases).Compared to invasive IPMN,non-IPMN associated adenocarcinomas are more common in relatively younger patients,have larger tumor size,are more likely to have positive lymph nodes,and are associated with a higher tumor(T)stage and nodal(N)stage,lymphovascular invasion,perineural invasion,tumor recurrence,and a worse PFS and *** cohort was predominantly categorized as stage 3 per AJCC 7th edition staging manual,and it’s more evenly distributed based on 8th edition staging manual.T and N staging of both 7th and 8th edition sufficiently stratify PFS and OS in the entire cohort,although dividing into N1 and N2 according to the 8th edition does not show additional *** PDAC arising in IPMN,T staging of the 7th edition and N1/N2 staging of the 8th edition appear to further stratify PFS and *** PDAC without an IPMN component,T staging from both versions fails to stratify PFS and *** The AJ

关键词： Pancreatic cancer Pancreatic ductal adenocarcinoma Prognosis Intraductal papillary mucinous neoplasms Survival American Joint Committee on Cancer

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NECAB family of neuronal calcium-binding proteins in health and disease

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Neural Regeneration Research 2025年第5期20卷 1236-1243页

作者： Diones Bueno michael K.E.Schafer Sudena Wang michael J.Schmeisser Axel Methner Institute for Molecular Medicine University Medical Center of the Johannes Gutenberg-UniversityMainzGermany Department of Anesthesiology University Medical Center of the Johannes Gutenberg-UniversityMainzGermany Institute of Anatomy University Medical Center of the Johannes Gutenberg-UniversityMainzGermany

The N-terminal EF-hand calcium-binding proteins 1–3(NECAB1–3) constitute a family of predominantly neuronal proteins characterized by the presence of at least one EF-hand calcium-binding domain and a functionally less well characterized C-terminal antibiotic biosynthesis monooxygenase domain. All three family members were initially discovered due to their interactions with other proteins. NECAB1 associates with synaptotagmin-1, a critical neuronal protein involved in membrane trafficking and synaptic vesicle exocytosis. NECAB2 interacts with predominantly striatal G-protein-coupled receptors, while NECAB3 partners with amyloid-β A4 precursor protein-binding family A members 2 and 3, key regulators of amyloid-β production. This demonstrates the capacity of the family for interactions with various classes of proteins. NECAB proteins exhibit distinct subcellular localizations: NECAB1 is found in the nucleus and cytosol, NECAB2 resides in endosomes and the plasma membrane, and NECAB3 is present in the endoplasmic reticulum and Golgi apparatus. The antibiotic biosynthesis monooxygenase domain, an evolutionarily ancient component, is akin to atypical heme oxygenases in prokaryotes but is not wellcharacterized in vertebrates. Prokaryotic antibiotic biosynthesis monooxygenase domains typically form dimers, suggesting that calcium-mediated conformational changes in NECAB proteins may induce antibiotic biosynthesis monooxygenase domain dimerization, potentially activating some enzymatic properties. However, the substrate for this enzymatic activity remains uncertain. Alternatively, calcium-mediated conformational changes might influence protein interactions or the subcellular localization of NECAB proteins by controlling the availability of protein–protein interaction domains situated between the EF hands and the antibiotic biosynthesis monooxygenase domain. This review summarizes what is known about genomic organization, tissue expression, intracellular localization, interac

关键词： calcium EF hand mitochondria nervous system signal transduction

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Small extracellular vesicles derived from cerebral endothelial cells with elevated microRNA 27a promote ischemic stroke recovery

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Neural Regeneration Research 2025年第1期20卷 224-233页

作者： Yi Zhang Zhongwu Liu michael Chopp michael Millman Yanfeng Li Pasquale Cepparulo Amy Kemper Chao Li Li Zhang Zheng Gang Zhang Department of Neurology Henry Ford HospitalDetroitMIUSA Department of Physics Oakland UniversityRochesterMIUSA Department of Pathology Henry Ford HospitalDetroitMIUSA Division of Pharmacology Department of NeuroscienceReproductive and Dentistry SciencesSchool of MedicineUniversity of Naples“Federico Ⅱ”NaplesItaly

Axonal remodeling is a critical aspect of ischemic brain repair processes and contributes to spontaneous functional *** previous in vitro study demonstrated that exosomes/small extracellular vesicles(sEVs)isolated from cerebral endothelial cells(CEC-sEVs)of ischemic brain promote axonal growth of embryonic cortical neurons and that microRNA 27a(miR-27a)is an elevated miRNA in ischemic *** the present study,we investigated whether normal CEC-sEVs engineered to enrich their levels of miR-27a(27a-sEVs)further enhance axonal growth and improve neurological outcomes after ischemic stroke when compared with treatment with non-engineered CEC-sEVs.27a-sEVs were isolated from the conditioned medium of healthy mouse CECs transfected with a lentiviral miR-27a expression *** EVs isolated from CECs transfected with a scramble vector(Scra-sEVs)were used as a *** male mice were subjected to permanent middle cerebral artery occlusion and then were randomly treated with 27a-sEVs or *** array of behavior assays was used to measure neurological *** with treatment of ischemic stroke with Scra-sEVs,treatment with 27a-sEVs significantly augmented axons and spines in the peri-infarct zone and in the corticospinal tract of the spinal grey matter of the denervated side,and significantly improved neurological *** vitro studies demonstrated that CEC-sEVs carrying reduced miR-27a abolished 27a-sEV-augmented axonal *** analysis revealed that 27a-sEVs systemically administered preferentially localized to the pre-synaptic active zone,while quantitative reverse transcription-polymerase chain reaction and Western Blot analysis showed elevated miR-27a,and reduced axonal inhibitory proteins Semaphorin 6A and Ras Homolog Family Member A in the peri-infarct *** of the Clathrin-dependent endocytosis pathway substantially reduced neuronal internalization of *** data provide evidence that 27a-sEVs have

关键词： axonal remodeling cerebral endothelial cells exosomes miR-27a mitochondria Semaphorin 6A small extracellular vesicles stroke

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Acute and chronic excitotoxicity in ischemic stroke and late-onset Alzheimer's disease

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Neural Regeneration Research 2025年第7期20卷 1981-1988页

作者： Shan Ping Yu Emily Choi michael QJiang Ling Wei Department of Anesthesiology Emory University School of MedicineAtlantaGAUSA Center for Visual and Neurocognitive Rehabilitation Atlanta Veterans Affairs Medical CenterDecaturGAUSA

Stroke and Alzheimer's disease are common neurological disorders and often occur in the same *** comorbidity of the two neurological disorders represents a grave health threat to older *** review presents a brief background of the development of novel concepts and their clinical *** activity of glutamatergic N-methyl-D-aspartate receptors and N-methyl-D-aspartate receptor-mediated Ca^(2+)influx is critical for neuronal *** ischemic insult induces prompt and excessive glutamate release and drastic increases of intracellular Ca^(2+)mainly via N-methyl-D-aspartate receptors,particularly of those at the extrasynaptic *** Ca^(2+)-evoked neuronal cell death in the ischemic core is dominated by necrosis within a few hours and days known as acute ***,mild but sustained Ca^(2+)increases under neurodegenerative conditions such as in the distant penumbra of the ischemic brain and early stages of Alzheimer's disease are not immediately toxic,but gradually set off deteriorating Ca^(2+)-dependent signals and neuronal cell loss mostly because of activation of programmed cell death *** on the Ca^(2+)hypothesis of Alzheimer's disease and recent advances,this Ca^(2+)-activated“silent”degenerative excitotoxicity evolves from years to decades and is recognized as a unique slow and chronic *** N-methyl-D-aspartate receptor subunit GluN3A,primarily at the extrasynaptic site,serves as a gatekeeper for the N-methyl-D-aspartate receptor activity and is neuroprotective against both acute and chronic *** stroke and Alzheimer's disease,therefore,share an N-methyl-D-aspartate receptor-and Ca^(2+)-mediated mechanism,although with much different time *** is thus proposed that early interventions to control Ca^(2+)homeostasis at the preclinical stage are pivotal for individuals who are susceptible to sporadic late-onset Alzheimer's disease and Alzheimer's disease-related

关键词： Ca^(2+)hypothesis cognitive deficits hyperactivity late-onset Alzheimer's disease neurodegeneration N-methyl-D-aspartate receptors N-methyl-D-aspartate receptor subunits pathogenesis preventive treatment

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Scalable Ir‑Doped NiFe_(2)O_(4)/TiO_(2)Heterojunction Anode for Decentralized Saline Wastewater Treatment and H_(2)Production

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Nano-Micro Letters 2025年第3期17卷 1-18页

作者： Sukhwa Hong Jiseon Kim Jaebeom Park Sunmi Im michael R.Hoffmann Kangwoo Cho Division of Environmental Science and Engineering Pohang University of Science and Technology(POSTECH)Pohang 790−784Korea Linde Laboratory California Institute of TechnologyPasadenaCA 91125USA Institute for Convergence Research and Education in Advanced Technology(I‑CREATE) Yonsei University International CampusIncheon 21983Republic of Korea

Wastewater electrolysis cells(WECs)for decentralized wastewater treatment/reuse coupled with H_(2)production can reduce the carbon footprint associated with transportation of water,waste,and energy *** study reports Ir-doped NiFe_(2)O_(4)(NFI,~5 at%Ir)spinel layer with TiO_(2)overlayer(NFI/TiO_(2)),as a scalable heterojunction anode for direct electrolysis of wastewater with circumneutral pH in a single-compartment *** dilute(0.1 M)NaCl solutions,the NFI/TiO_(2)marks superior activity and selectivity for chlorine evolution reaction,outperforming the benchmark IrO_(2).Robust operation in near-neutral pH was *** including operando X-ray absorption spectroscopy unveiled crucial roles of TiO_(2) which serves both as the primary site for Cl−chemisorption and a protective layer for NFI as an ohmic *** electrolysis of NH4+-laden synthetic wastewater demonstrated that NFI/TiO_(2)not only achieves quasi-stoichiometric NH_(4)^(+)-to-N_(2)conversion,but also enhances H_(2)generation efficiency with minimal competing reactions such as reduction of dissolved oxygen and reactive *** scaled-up WEC with NFI/TiO_(2)was demonstrated for electrolysis of toilet wastewater.

关键词： Wastewater electrolysis cell Ir-doped NiFe_(2)O_(4) Reactive chlorine species Decentralized H_(2)production On-site wastewater treatment

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A spotlight on dosage and subject selection for effective neuroprotection: exploring the central role of mitochondria

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Neural Regeneration Research 2025年第4期20卷 1081-1082页

作者： John Mitrofanis Jonathan Stone michael R.Hamblin Pierre Magistretti Alim-Louis Benabid Glen Jeffery Fonds Clinatec UniversitéGrenoble AlpesGrenobleFrance School of Medical Science University of SydneySydneyAustralia Faculty of Health Sciences University of JohannesburgJohannesburgSouth Africa King Abdullah University of Science and Technology ThuwalSaudi Arabia Institute of Ophthalmology University College LondonLondonUK

Neurons are notoriously vulnerable cell *** the slightest change in their internal and/or external environments will cause much distress and dysfunction,leading often to their death.A range of pathological conditions,including stroke,head trauma,and neurodegenerative disease,can generate stress in neurons,affecting their survival and proper *** most neural pathologies,mitochondria become dysfunctional and this plays a pivotal role in the process of cell *** challenge over the last few decades has been to develop effective interventions that improve neuronal homeostasis under pathological *** interventions,often referred to as disease-modifying or neuroprotective,have,however,proved frustratingly elusive,at both preclinical and,in particular,clinical *** this perspective,we highlight two factors that we feel are key to the development of effective neuroprotective *** are:firstly,the choice of dose of intervention and method of application,and secondly,the selection of subjects,whether they be patients or the animal model.

关键词： protective dosage distress

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