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Mechanisms of distal axonal degeneration in peripheral neuropathies

NEUROSCIENCE LETTERS 2015年 596卷 33-50页

作者： Cashman, Christopher R. Hoeke, Ahmet Dept Neurosci Sacramento CA USA Dept Neurol Sacramento CA USA Johns Hopkins Univ MSTP MD PhD Program Baltimore MD 21205 USA

Peripheral neuropathy is a common complication of a variety of diseases and treatments, including diabetes, cancer chemotherapy, and infectious causes (HIV, hepatitis C, and Campylobacter jejuni). Despite the fundamental difference between these insults, peripheral neuropathy develops as a combination of just six primary mechanisms: altered metabolism, covalent modification, altered organelle function and reactive oxygen species formation, altered intracellular and inflammatory signaling, slowed axonal transport, and altered ion channel dynamics and expression. All of these pathways converge to lead to axon dysfunction and symptoms of neuropathy. The detailed mechanisms of axon degeneration itself have begun to be elucidated with studies of animal models with altered degeneration kinetics, including the slowed Wallerian degeneration (Wld(s)) and Sarm knockout animal models. These studies have shown axonal degeneration to occur through a programmed pathway of injury signaling and cytoskeletal degradation. Insights into the common disease insults that converge on the axonal degeneration pathway promise to facilitate the development of therapeutics that may be effective against other mechanisms of neurodegeneration. (C) 2015 Elsevier Ireland Ltd. All rights reserved.

关键词： Peripheral neuropathy Guillain-Barre syndrome Diabetes HIV neuropathy Mitochondrial aging Campylobacter jejuni Chemotherapy induced peripheral neuropathy Wld(s) Mechanisms of neuropathy Post-infectious neuropathy

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Grafted lineage-restricted precursors differentiate exclusively into neurons in the adult spinal cord

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EXPERIMENTAL NEUROLOGY 2002年第2期177卷 360-375页

作者： Han, SSW Kang, DY Mujtaba, T Rao, MS Fischer, I Drexel Univ Coll Dept Neurobiol & Anat MD PHD Program Philadelphia PA 19129 USA NIA Neurosci Lab GRC Baltimore MD 21224 USA

Multipotent neural stem cells (NSCs) have the potential to differentiate into neuronal and glial cells and are therefore candidates for cell replacement after CNS injury. Their phenotypic fate in vivo is dependent on the engraftment site, suggesting that the environment exerts differential effects on neuronal and glial lineages.. In particular, when grafted into the adult spinal cord, NSCs are restricted to the glial lineage, indicating that the host spinal cord environment is not permissive for neuronal differentiation. To identify the stage at which neuronal differentiation is inhibited we examined the survival, differentiation, and integration of neuronal restricted precursor (NRP) cells, derived from the embryonic spinal cord of transgenic alkaline phosphatase rats, after transplantation into the adult spinal cord. We found that grafted NRP cells differentiate into mature neurons, survive for at least 1 month, appear to integrate within the host spinal cord, and extend processes in both the gray and white matter. Conversely, grafted glial restricted precursor cells did not differentiate into neurons. We did not observe glial differentiation from the grafted NRP cells, indicating that they retained their neuronal restricted properties in vivo. We conclude that the adult nonneurogenic CNS environment does not support the transition of multipotential NSCs to the neuronal commitment stage, but does allow the survival, maturation, and integration of NRP cells. (C) 2002 Elsevier Science (USA) .

关键词： neuronal precursors glial precursors spinal cord stem cells neuronal differentiation transplantation transgenic rats neurogenesis neuronal replacement

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A mechanism for Tn5 inhibition -: Carboxyl-terminal dimerization

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第1期274卷 86-92页

作者： Braam, LAM Goryshin, IY Reznikoff, WS Univ Wisconsin Dept Biochem Madison WI 53706 USA Univ Wisconsin MD PHD Program Madison WI 53706 USA

Tn5 is unique among prokaryotic transposable elements in that it encodes a special inhibitor protein identical to the Tn5 transposase except lacking a short NH2-terminal DNA binding sequence. This protein regulates transposition through nonproductive protein-protein interactions with transposase, We have studied the mechanism of Tn5 inhibition in vitro and find that a heterodimeric complex between the inhibitor and transposase is critical for inhibition, probably via a DNA-bound form of transposase. Two dimerization domains are known in the inhibitor/transposase shared sequence, and we show that the COOH-terminal domain is necessary for inhibition, correlating with the ability of the inhibitor protein to homodimerize via this domain. This regulatory complex may provide clues to the structures of functional synaptic complexes. Additionally, we find that NH2- and COOH-terminal regions of transposase or inhibitor are in functional contact. The NH2 terminus appears to occlude transposase homodimerization (hypothetically mediated by the COOH terminus), an effect that might contribute to productive transposition. Conversely, a deletion of the COOH terminus uncovers a secondary DNA binding region in the inhibitor protein which is probably located near the NH2 terminus.

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Functional characterization of the Tn5 transposase by limited proteolysis

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JOURNAL OF BIOLOGICAL CHEMISTRY 1998年第18期273卷 10908-10913页

作者： Braam, LAM Reznikoff, WS Univ Wisconsin Dept Biochem Madison WI 53706 USA Univ Wisconsin MD PHD Program Madison WI 53706 USA

The 476 amino acid Tn5 transposase catalyzes DNA cutting and joining reactions that cleave the Tn5 transposon from donor DNA and integrate it into a target site. Protein-DNA and protein-protein interactions are important for this tranposition process. A truncated transposase variant, the inhibitor, decreases transposition rates via the formation of nonproductive complexes with transposase. Here, the inhibitor and the transposase are shown to have similar secondary and tertiary folding. Using limited proteolysis, the transposase has been examined structurally and functionally. A DNA binding region was localized to the N-terminal 113 amino acids. Generally, the N terminus of transposase is sensitive to proteolysis but can be protected by DNA. Two regions are predicted to contain determinants for protein-protein interactions, encompassing residues 114-314 and 441-476. The dimerization regions appear to be distinct and may have separate functions, one involved in synaptic complex formation and one involved in nonproductive multimerization. Furthermore, predicted catalytic regions are shown to lie between major areas of proteolysis.

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PulsePoint dispatch associated patient characteristics and prehospital outcomes in a mid-sized metropolitan area

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RESUSCITATION 2022年 170卷 36-43页

作者： Smida, Tanner Salerno, Jessica Weiss, Leonard Martin-Gill, Christian Salcido, David D. Univ Pittsburgh Sch Med Pittsburgh PA USA West Virginia Univ MD PhD Program Morgantown WV 26506 USA

Background: Mobile phone-based dispatch of volunteers to out-of-hospital cardiac arrests (OHCA) has been shown to increase the likelihood of early CPR and AED application. In the United States, limited characterization of patients encountered as a result of such systems exists. Aims: Examine prehospital case characteristics and outcomes from a multi-year deployment of PulsePoint Respond in Pittsburgh, Pennsylvania. Methods: PulsePoint event timing, location, and associated prehospital electronic health records (ePCRs) were obtained for EMS-encountered OHCA cases that did and did not generate PulsePoint alerts within the service area of Pittsburgh EMS from July 2016 to October 2020. ePCRs were reviewed and OHCA case characteristics were extracted according to the Utstein template. PulsePoint-associated OHCA and nonPulsePoint-associated OHCA were compared. Results: Of 840 total PulsePoint dispatches, 64 (7.6%) were for OHCA associated with a resuscitation attempt. Forty-one (64.1%) were witnessed, 38 (59.4%) received bystander CPR, and 13 (20.0%) of these patients had an AED applied prior to EMS arrival. Twenty-seven (39.7%) had an initial shockable rhythm, and 31 (48.4%) patients achieved ROSC in the field. In the city of Pittsburgh, there were 1229 total OHCA during the study period, with an estimated 29.6% occurring in public. When PulsePoint-associated and publicly occurring non-PulsePoint-associated OHCA were compared, baseline characteristics (age, sex, witnessed status) were similar, but PulsePoint-associated OHCA received more bystander CPR (p = 0.008). Conclusions: A minority of PulsePoint dispatches in Pittsburgh were triggered by true OHCA. The majority of OHCA during the study period occurred within private residences where PulsePoint responders are not currently dispatched. PulsePoint dispatches were associated with prognostically favorable OHCA characteristics and increased bystander CPR performance.

关键词： PulsePoint PulsePoint Respond CPR Bystander CPR Bystander defibrillation AED Automated external defibrillator Public access AED Out-of-hospital cardiac arrest Cardiac arrest OHCA Bystander CPR recruitment Bystander Crowdsourcing Crowdsourcing CPR BLS Bystander intervention Smartphone Smartphone app Smartphone application

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Antidepressant Psychopharmacology and the Social Brain

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PSYCHIATRY-INTERPERSONAL AND BIOLOGICAL PROCESSES 2011年第1期74卷 72-86页

作者： Novick, Andrew M. Univ S Dakota Sanford Sch Med Dept Basic Biomed Sci MD PhD Program Vermillion SD 57069 USA

Antidepressant drugs are a mainstay in psychiatric treatment and have the ability to influence neural substrates related to social bonding and interaction. This article explores the potential neurobiological overlap between social attachment and antidepressant mechanisms and reviews work related to the effects of antidepressants on separation distress, social affiliation, dominance hierarchies, romantic love, and socio-emotional processing. It is proposed that similarities between antidepressant pharmacology and the neurobiological effects of an effective care-giver may help create a sense of safety that in turn promotes changes in behavior and mood.

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Genomic data processing with GenomeFlow

arXiv

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arXiv 2025年

作者： Park, Junseok Maury, Eduardo A. Oh, Changhoon Shin, Donghoon Denisko, Danielle Lee, Eunjung Alice Division of Genetics and Genomics Boston Children’s Hospital 3 Blackfan Circle BostonMA United States Department of Pediatrics Harvard Medical School 25 Shattuck St BostonMA United States Bioinformatics Integrative Genomics Program Harvard/MIT MD-PHD Program Harvard Medical School BostonMA United States Program in Medical and Population Genetics Broad Institute of MIT and Harvard CambridgeMA United States Graduate School of Information Yonsei University 50 Yonsei-ro Seodaemun-gu Seoul Korea Republic of Department of Human Centered Design and Engineering University of Washington SeattleWA United States Department of Biomedical Informatics Harvard Medical School BostonMA United States

Advances in genome sequencing technologies generate massive amounts of sequence data that are increasingly analyzed and shared through public repositories. On-demand infrastructure services on cloud computing platforms enable the processing of such large-scale genomic sequence data in distributed processing environments with a significant reduction in analysis time. However, parallel processing on cloud computing platforms presents many challenges to researchers, even skillful bioinformaticians. In particular, it is difficult to design a computing architecture optimized to reduce the cost of computing and disk storage as genomic data analysis pipelines often employ many heterogeneous tools with different resource requirements. To address these issues, we developed GenomeFlow, a tool for automated development of computing architecture and resource optimization on Google Cloud Platform, which allows users to process a large number of samples at minimal cost. We outline multiple use cases of GenomeFlow demonstrating its utility to significantly reduce computing time and cost associated with analyzing genomic and transcriptomic data from hundreds to tens of thousands of samples from several consortia. Here, we describe a step-by-step protocol on how to use GenomeFlow for a common genomic data processing task. We introduce this example protocol geared toward a bioinformatician with little experience in cloud computing. © 2025, CC BY.

关键词： Cloud platforms

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From Heart to Eye: Central Retinal Artery Occlusion Secondary to Endocarditis: Septic Embolism

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JACC: Case Reports 2025年第6P2期30卷 103299-103299页

作者： Santa-Ana-Bayona, Maria Jose Acosta-Gutiérrez, Gilberto H. Martinez-Dominguez, Pavel Landeros-Magdaleno, Rosslet Garcia-Gutierrez, Alejandro Ponce-Acosta, Camila Berarducci, Joaquin Guerra, Enrique C. Dominguez-Luna, Ximena Espinola-Zavaleta, Nilda Department of Nuclear Cardiology National Institute of Cardiology Ignacio Chavez Mexico City Mexico Mexican Faculty of Medicine La Salle University Mexico City Mexico MD–PHD (PECEM) Program School of Medicine National Autonomous University of Mexico Mexico City Mexico Asociación Para Evitar la Ceguera (APEC) Mexico City Mexico Department of Echocardiography ABC Medical Center Mexico City Mexico

Infective endocarditis (IE) remains a medical challenge. Potential complications such as heart failure and septic embolization may arise, prompting early recognition and treatment. We present the case of a 78-year-old woman with sudden, painless monocular vision loss in the left eye, without other accompanying symptoms. Ophthalmologic evaluation revealed central retinal artery occlusion. A holosystolic murmur was heard at the apex. Further echocardiography confirmed IE. Despite efforts, prognosis of IE is poor, with an in-hospital mortality of 25% in our country, with high risk of embolism (20% to 50%). According to epidemiology, central retinal artery occlusion is a rare complication, resulting from valvular vegetation, occurring in <1% of patients. Unfortunately, there is no accepted treatment to reverse retinal damage caused by central retinal artery occlusion. © 2025 The Authors

关键词： central retinal artery occlusion embolism infective endocarditis

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Effects of oxidative and alkylating damage on microsatellite instability in nontumorigenic human cells

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MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS 2004年第1-2期546卷 29-38页

作者： Maneval, ML Eckert, KA Penn State Univ Coll Med Jake Gittlen Canc Res Inst MD PhD Training Program Hershey PA 17033 USA

Microsatellite instability is a phenomenon that is well characterized in mismatch repair-deficient tumor cell lines, including the potential etiological role of endogenous DNA damage. However, our understanding of microsatellite mutational mechanisms in repair-proficient, nontumorigenic cells is limited. We determined microsatellite mutation frequencies for human lymphoblastoid cells using an episomal DNA shuttle vector in which a (TTCC/AAGG)(9) microsatellite is inserted in-frame within the herpes simplex virus thymidine kinase (HSV-tk) gene. The responses of plasmid-bearing cells to reactive oxygen species or alkylating agents were compared after treatment with hydrogen peroxide (H2O2) and N-ethyl-N-nitrosourea (ENU). H2O2 treatment induced a statistically significant increase in overall HSV-tk mutation frequency relative to controls, with catalase reducing the effect. H2O2 treatment increased the mutation frequency within the microsatellite and the HSV-tk coding region to a similar extent (five and six-fold, respectively, relative to the control). Mutational specificity analyses demonstrated that the proportion of mutations within the microsatellite is not statistically different among the H2O2, catalase, and PBS treatment groups. In contrast, treatment of cells bearing the microsatellite vector with ENU altered the mutational spectrum, relative to solvent control. ENU induced the expected base substitutions within the HSV-tk coding region, but did not increase the microsatellite mutation frequency. The low level of microsatellite mutagenesis observed after reactive oxygen species (ROS) insult likely reflects the normal repair processes of these nontumorigenic, repair-competent cells. Our ex vivo experiments demonstrate the manner in which repetitive DNA in normal human cells might respond to endogenous mutagens. (C) 2003 Elsevier B.V All rights reserved.

关键词： herpes simplex virus thymidine kinase microsatellite instability oxidative damage hydrogen peroxide

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Simultaneous Photoacoustic Detection of Red Blood Cell Aggregation and Oxygenation

Simultaneous Photoacoustic Detection of Red Blood Cell Aggre...

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IEEE International Ultrasonics Symposium (IUS)

作者： Hysi, Eno Saha, Ratan K. Kolios, Michael C. Louisiana State Univ Sch Med MD PhD Program New Orleans LA 70112 USA

ISBN: (纸本)9781467345620;9781467345613

Red blood cell (RBC) aggregation is a reversible process which occurs in the presence of increased plasma fibrinogen concentration and low flow conditions. It results in the RBCs forming structures that resemble "stacks of coins" and/or clusters impairing blood flow and the ability of oxygen to diffuse to surrounding tissues. We investigate the use of photoacoustics (PA) to detect and monitor RBC aggregation and the effect of aggregation on the sample oxygenation level. In this study, porcine RBCs were illuminated at 750nm and 1064 nm and the oxygen saturation of each sample was estimated. Aggregation was induced by varying the concentration of Dextran-70. Changes in the photoacoustic signal strength suggest that in the presence of RBC aggregates, the release of oxygen into the surroundings is impaired. A 30% increase in oxygen saturation was measured based on changes in the PA signal when comparing the non-aggregated and aggregated blood samples. This work demonstrates that PA imaging has the potential to detect changes due to RBC aggregation and monitor oxygenation level.

关键词： Photoacoustics Red Blood Cell Aggregation Oxygen Saturation

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