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The Journal of Visualized Experiments (JoVE) is a peer reviewed, PubMed-indexed video journal. Our mission is to increase the productivity of scientific research.

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In JoVE (29)

Other Publications (4)

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Articles by Aaron Kolski-Andreaco in JoVE

 JoVE General

Мышь надпочечников сотовый хромаффинных Изоляция


JoVE 129 1/05/2007

1, 2,3, 4, 1, 2,3

1Department of Physiology and Biophysics, University of California, Irvine (UCI), 2Department of Physiology and Biophysics, University of Southern California, Keck School of Medicine, 3Zilkha Neurogenetic Institute, University of Southern California, Keck School of Medicine, 4Department of Developmental and Cell Biology, University of California, Irvine (UCI)

Надпочечников медуллярного хромаффинных системах клеточных культур являются чрезвычайно полезными для изучения возбуждения секреции связи в в создании пробирке. Этот протокол иллюстрирует метод, используемый для рассекать надпочечников, а затем изолировать медуллярного регионе избавлением от коры надпочечников. Переваривание мозга в одиночных камерах хромаффинных затем продемонстрирована.

 JoVE General

Фактор Роста покрытием из бисера Размещение на Спинной эксплантов переднего мозга


JoVE 134 1/30/2007

1, 2, 3

1Department of Developmental and Cell Biology, University of California, Irvine (UCI), 2Department of Physiology and Biophysics, University of California, Irvine (UCI), 3Department of Pathology, University of California, Irvine (UCI)

Это видео демонстрирует два способа приготовления и укладки бусы, которые были покрыты фактора роста, на эксплантатов развивающихся коры головного мозга. Эти шарики могут быть использованы, чтобы вызвать пространственно ограниченных экспрессии генов на развитие нервной ткани, такие как передний мозг эксплантов. Методы даны для использования как Affi-Gel бисером и гепарин acryllic бисером.

 JoVE General

Мышь Спинной изоляции эксплантов переднего мозга


JoVE 135 1/30/2007

1, 2, 3

1Department of Developmental and Cell Biology, University of California, Irvine (UCI), 2Department of Physiology and Biophysics, University of California, Irvine (UCI), 3Department of Pathology, University of California, Irvine (UCI)

Это видео демонстрирует протокола для выделения и культивирования эксплантатов мыши переднего мозга от embyonic день 12 мышей. Процедуры по удалению матки, эмбрионов из матки, и рассечение эмбриона даны. Кроме того методологии для передачи этих эксплантов на специализированные мембраны, на которых они культивируются демонстрируется. Развитие переднего мозга могут быть изучены в лабораторных использованием этого препараты, а также изменения в экспрессии генов.

 JoVE General

Культура Мышь нейронных стволовых клеток прекурсоров


JoVE 152 2/25/2007

1, 2, 3, 2

1Department of Developmental and Cell Biology, University of California, Irvine (UCI), 2Department of Pathology, University of California, Irvine (UCI), 3Department of Physiology and Biophysics, University of California, Irvine (UCI)

Это видео описывает метод, используемый для изоляции neuroprecursors из развивающихся коры эмбриональных мышей. Процедура снятия эмбрионов из матки, рассекая корковой ткани, и перевариванием изолированных кора головного мозга показано на рисунке.

 JoVE Editorial

В мае этого года в Юпитер


JoVE 3449 5/04/2011

Основных моментов для нашего майском номере включают методы измерения познания в невесомости, изолируя комаров клетки иммунной системы, инженерные рекомбинантные вакцины атипичной пневмонии, и выявление опухоли с тепловидения. Кроме того, процедуры выделения нервных стволовых клеток из человеческих эмбриональных мозга и культивирования антиген-представляющих клеток печени также будут освобождены.

 JoVE Editorial

Июль 2012: В этом месяце в Юпитер


JoVE 5010 7/01/2012

1, 2

1JoVE Content Production, 2Department of Ophthalmology, Massachusetts Eye and Ear

Исторически сложилось так, черт возьми, журнал Визуализированные экспериментов, была сосредоточена в основном на биомедицинские исследования и разработаны подразделы для биоинженерии, клинических и трансляционных медицины, иммунологии и инфекции, и Neuroscience. В июле этого года, Юпитер запускает прикладной физики раздел, который включает в себя ряд контент из физики плазмы для материаловедения. Мы начинаем новый раздел с заметным статьи из Purdue University, где исследователи в Центре лазерной основе производства изучают.

 JoVE Editorial

Август 2012: В этом месяце в Юпитер


JoVE 5016 8/01/2012

1, 2

1Department of Ophthalmology, Massachusetts Eye and Ear, 2JoVE Content Production

Традиционные микроскопия требует объективы для увеличения образцов, а также может включать в себя многочисленные оптические компоненты, такие как дополнительные цели, фильтров и зеркал преломляют свет и направляют на оптических датчиков. Август 2012 вопрос Юпитера (журнал Визуализированные эксперименты) отмечена третья публикация из Озджан Lab (Университет Калифорнии, Лос-Анджелес) на линзу объектива бесплатно бесплатно "на чипе" микроскопия платформа, которую они впервые.

 JoVE Editorial

2012: год в обзоре


JoVE 5049 1/03/2013

1, 2

1Department of Ophthalmology, Massachusetts Eye and Ear, 2JoVE Content Production

Вот посмотрите на некоторые этапы и основные моменты 2012 года в журнале Визуализированные Эксперименты (Юпитера).

Other articles by Aaron Kolski-Andreaco on PubMed

SK3-1C, a Dominant-negative Suppressor of SKCa and IKCa Channels

The Journal of Biological Chemistry. Feb, 2004  |  Pubmed ID: 14638680

Small conductance Ca2+-activated K+ channels, products of the SK1-SK3 genes, regulate membrane excitability both within and outside the nervous system. We report the characterization of a SK3 variant (SK3-1C) that differs from SK3 by utilizing an alternative first exon (exon 1C) in place of exon 1A used by SK3, but is otherwise identical to SK3. Quantitative RT-PCR detected abundant expression of SK3-1C transcripts in human lymphoid tissues, skeletal muscle, trachea, and salivary gland but not the nervous system. SK3-1C did not produce functional channels when expressed alone in mammalian cells, but suppressed SK1, SK2, SK3, and IKCa1 channels, but not BKCa or KV channels. Confocal microscopy revealed that SK3-1C sequestered SK3 protein intracellularly. Dominant-inhibitory activity of SK3-1C was not due to a nonspecific calmodulin sponge effect since overexpression of calmodulin did not reverse SK3-1C-mediated intracellular trapping of SK3 protein, and calmodulin-Ca2+-dependent inactivation of CaV channels was not affected by SK3-1C overexpression. Deletion analysis identified a dominant-inhibitory segment in the SK3-1C C terminus that resembles tetramerization-coiled-coiled domains reported to enhance tetramer stability and selectivity of multimerization of many K+ channels. SK3-1C may therefore suppress calmodulin-gated SKCa/IKCa channels by trapping these channel proteins intracellularly via subunit interactions mediated by the dominant-inhibitory segment and thereby reduce functional channel expression on the cell surface. Such family-wide dominant-negative suppression by SK3-1C provides a powerful mechanism to titrate membrane excitability and is a useful approach to define the functional in vivo role of these channels in diverse tissues by their targeted silencing.

A Drosophila Protein Specific to Pheromone-sensing Gustatory Hairs Delays Males' Copulation Attempts

Current Biology : CB. Jun, 2006  |  Pubmed ID: 16753571

In insects, increasing evidence suggests that small secreted pheromone binding proteins (PBPs) and odorant binding proteins (OBPs) are important for normal olfactory detection of airborne pheromones and odorants far from their source. In contrast, it is unknown whether extracellular ligand binding proteins participate in perception of less volatile chemicals, including many pheromones, that are detected by direct contact with chemosensory organs. CheB42a, a small Drosophila melanogaster protein unrelated to known PBPs or OBPs, is expressed and likely secreted in only a small subset of gustatory sensilla on males' front legs, the site of gustatory perception of contact pheromones. Here we show that CheB42a is expressed specifically in the sheath cells surrounding the taste neurons expressing Gr68a, a putative gustatory pheromone receptor for female cuticular hydrocarbons that stimulate male courtship. Surprisingly, however, CheB42a mutant males attempt to copulate with females earlier and more frequently than control males. Furthermore, CheB42a mutant males also attempt to copulate more frequently with other males that secrete female-specific cuticular hydrocarbon pheromones, but not with females lacking cuticular hydrocarbons. Together, these data indicate that CheB42a is required for a normal gustatory response to female cuticular hydrocarbon pheromones that modulate male courtship.

Kv1.3 Channels Are a Therapeutic Target for T Cell-mediated Autoimmune Diseases

Proceedings of the National Academy of Sciences of the United States of America. Nov, 2006  |  Pubmed ID: 17088564

Autoreactive memory T lymphocytes are implicated in the pathogenesis of autoimmune diseases. Here we demonstrate that disease-associated autoreactive T cells from patients with type-1 diabetes mellitus or rheumatoid arthritis (RA) are mainly CD4+ CCR7- CD45RA- effector memory T cells (T(EM) cells) with elevated Kv1.3 potassium channel expression. In contrast, T cells with other antigen specificities from these patients, or autoreactive T cells from healthy individuals and disease controls, express low levels of Kv1.3 and are predominantly naïve or central-memory (T(CM)) cells. In T(EM) cells, Kv1.3 traffics to the immunological synapse during antigen presentation where it colocalizes with Kvbeta2, SAP97, ZIP, p56(lck), and CD4. Although Kv1.3 inhibitors [ShK(L5)-amide (SL5) and PAP1] do not prevent immunological synapse formation, they suppress Ca2+-signaling, cytokine production, and proliferation of autoantigen-specific T(EM) cells at pharmacologically relevant concentrations while sparing other classes of T cells. Kv1.3 inhibitors ameliorate pristane-induced arthritis in rats and reduce the incidence of experimental autoimmune diabetes in diabetes-prone (DP-BB/W) rats. Repeated dosing with Kv1.3 inhibitors in rats has not revealed systemic toxicity. Further development of Kv1.3 blockers for autoimmune disease therapy is warranted.

Modulators of Small- and Intermediate-conductance Calcium-activated Potassium Channels and Their Therapeutic Indications

Current Medicinal Chemistry. 2007  |  Pubmed ID: 17584055

Calcium-activated potassium channels modulate calcium signaling cascades and membrane potential in both excitable and non-excitable cells. In this article we will review the physiological properties, the structure activity relationships of the existing peptide and small molecule modulators and the therapeutic importance of the three small-conductance channels KCa2.1-KCa2.3 (a.k.a. SK1-SK3) and the intermediate-conductance channel KCa3.1 (a.k.a. IKCa1). The apamin-sensitive KCa2 channels contribute to the medium afterhyperpolarization and are crucial regulators of neuronal excitability. Based on behavioral studies with apamin and on observations made in several transgenic mouse models, KCa2 channels have been proposed as targets for the treatment of ataxia, epilepsy, memory disorders and possibly schizophrenia and Parkinson's disease. In contrast, KCa3.1 channels are found in lymphocytes, erythrocytes, fibroblasts, proliferating vascular smooth muscle cells, vascular endothelium and intestinal and airway epithelia and are therefore regarded as targets for various diseases involving these tissues. Since two classes of potent and selective small molecule KCa3.1 blocker, triarylmethanes and cyclohexadienes, have been identified, several of these postulates have already been validated in animal models. The triarylmethane ICA-17043 is currently in phase III clinical trials for sickle cell anemia while another triarylmethane, TRAM-34, has been shown to prevent vascular restenosis in rats and experimental autoimmune encephalomyelitis in mice. Experiments showing that a cyclohexadiene KCa3.1 blocker reduces infarct volume in a rat subdural hematoma model further suggest KCa3.1 as a target for the treatment of traumatic and possibly ischemic brain injury. Taken together KCa2 and KCa3.1 channels constitute attractive new targets for several diseases that currently have no effective therapies.

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