Annals of the New York Academy of Sciences

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Brain Circuits Involved in Corticotropin‐Releasing Factor‐Norepinephrine Interactions during Stress
Annals of the New York Academy of Sciences - Tập 1018 Số 1 - Trang 25-34 - 2004
Adrian J. Dunn, Artur H. Świergiel, Vitaly Palamarchouk
Abstract: Corticotropin‐releasing factor (CRF)‐ and norepinephrine (NE)‐containing neurons in the brain are activated during stress, and both have been implicated in the behavioral responses. NE neurons in the brain stem can stimulate CRF neurons in the hypothalamic paraventricular nucleus (PVN) to activate the hypothalamic‐pituitary‐adrenocortical axis and may affect other CRF neurons. CRF‐containing neurons in the PVN, the amygdala, and other brain areas project to the area of the locus coeruleus (LC), and CRF injected into the LC alters the electrophysiologic activity of LC‐NE neurons. Neurochemical studies have indicated that CRF applied intracerebroventricularly or locally activates the LC‐NE system, and microdialysis and chronoamperometric measurements indicate increased NE release in LC‐NE terminal fields. However, chronoamperometric studies indicated a significant delay in the increase in NE release, suggesting that the CRF input to LC‐NE neurons is indirect. The reciprocal interactions between cerebral NE and CRF systems have been proposed to create a “feed‐forward” loop. It has been postulated that a sensitization of such a feed‐forward loop may underlie clinical depression. However, in the majority of studies, repeated or chronic stress has been shown to decrease the behavioral and the neurochemical responsivity to acute stressors. Repeated stress also seems to decrease the responsivity of LC neurons to CRF. These results do not provide support for a feed‐forward hypothesis. However, a few studies using certain tasks have indicated sensitization, and some other studies have suggested that the effect of CRF may be dose dependent. Further investigations are necessary to establish the validity or otherwise of the feed‐forward hypothesis.
Rationale for the clinical guidelines for myasthenia gravis in Japan
Annals of the New York Academy of Sciences - Tập 1413 Số 1 - Trang 35-40 - 2018
Hiroyuki Murai, Kimiaki Utsugisawa, Yuriko Nagane, Shigeaki Suzuki, Tomihiro Imai, Masakatsu Motomura
AbstractAccording to the 2014 Japanese clinical guidelines for myasthenia gravis, the most important priority in treatment is maintaining patients’ health‐related quality of life. Therefore, the initial treatment goal is defined as maintaining a postintervention status of minimal manifestations or better (according to the Myasthenia Gravis Foundation of America classification) with an oral prednisolone dose of 5 mg/day or less. Every effort should be made to attain this level as rapidly as possible. To achieve this goal, the guidelines recommend minimizing the oral prednisolone dose, starting calcineurin inhibitors early in the course of treatment, using intravenous methylprednisolone infusion judiciously (often combined with plasma exchange/plasmapheresis or intravenous immunoglobulin), and effectively treating patients with an early, fast‐acting treatment strategy. The early, fast‐acting treatment strategy enables more frequent and earlier attainment of the initial goal than other strategies. Thymectomy is considered an option for treating nonthymomatous early‐onset myasthenia gravis in patients with antiacetylcholine receptor antibodies and thymic hyperplasia in the early stages of the disease.
<i>Extraocular Muscle Susceptibility to Myasthenia Gravis</i>
Annals of the New York Academy of Sciences - Tập 1132 Số 1 - Trang 220-224 - 2008
Jindřich Šoltýs, Bendi Gong, Henry J. Kaminski, Yuefang Zhou, Linda L. Kusner
Extraocular muscle (EOM) is susceptible to neuromuscular junction disorders, in particular, myasthenia gravis (MG). While EOM physiological characteristics and the ocular motor system requirements contribute to the propensity of ocular motor deficits observed among patients with MG, the authors propose that EOM have immunological features that place the muscles at risk for immune attack. Genomic profiling studies have demonstrated that genes associated with the immune response are differentially expressed in EOM, with particular differences in both classical and alternative complement‐mediated immune response pathways. Intrinsic complement regulators are expressed at lower levels at rodent EOM neuromuscular junctions, which would put them at risk for the complement‐mediated injury that occurs in MG. In fact, systemic C inhibition in experimental autoimmune MG (EAMG) induced by administration of acetylcholine receptor (AChR) antibodies or immunization with AChR will eliminate complement deposition at junctions of other skeletal muscle, but not EOM. Also, EOM junctions have greater injury in active and passive EAMG by several measures, suggesting that the lack of complement inhibition puts the EOM at risk. Among ocular myasthenia patients, serum AChR antibody levels are low, which would support the concept that EOM junctions are more susceptible to antibody injury than are other junctions. These observations suggest that complement inhibitory therapies may prove to be particularly effective in treatment of ocular myasthenia.
MORPHOLOGICAL SIMILARITIES BETWEEN THE DOG KIDNEY CELL LINE MDCK AND THE MAMMALIAN CORTICAL COLLECTING TUBULE*
Annals of the New York Academy of Sciences - Tập 372 Số 1 - Trang 384-405 - 1981
J. D. Valentich
A PERSPECTIVE ON THE APPLICATION OF GENETIC ENGINEERING: STABILITY OF RECOMBINANT PLASMID
Annals of the New York Academy of Sciences - Tập 369 Số 1 - Trang 1-14 - 1981
Tadayuki Imanaka, Setsuya Aiba
THIAMIN AS A CATALYST OF CHEMTOSMOTIC ENERGY TRANSDUCTIONS
Annals of the New York Academy of Sciences - Tập 378 Số 1 - Trang 442-448 - 1982
Robert D. Brown
Prefrontal Cortical Networks Related to Visceral Function and Mood
Annals of the New York Academy of Sciences - Tập 877 Số 1 - Trang 383-396 - 1999
Joseph L. Price
ABSTRACT: At least twenty‐two architectonic areas can be distinguished within the orbital and medial prefrontal cortex (OMPFC). Although each of these areas has a distinct structure and connections, they can be grouped into two “networks,” defined by cortico‐cortical connections that primarily interconnect areas within each network. The networks also have different connections to the striatum, medial thalamus, and other brain regions. The orbital network consists of most of the areas in the orbital cortex. It receives several sensory inputs (olfactory, gustatory, visceral afferent, somatic sensory, and visual) that appear to be related to feeding. It also receives many limbic inputs from the amygdala, entorhinal and perirhinal cortex, and subiculum, including a specific projection from the ventrolateral part of the basal amygdaloid nucleus. The orbital network may therefore serve as a substrate to integrate viscerosensory information with affective signals. The medial network consists of areas on the medial frontal surface together with a few select areas in the orbital cortex. These areas have few direct sensory inputs, and their limbic inputs are somewhat different than those to the orbital network (e.g., from the ventromedial part of the basal amygdaloid nucleus). However, they provide the major output from the OMPFC to the hypothalamus and brain stem (especially the periaqueductal gray). The medial network may therefore serve as a visceromotor system to provide frontal cortical influence over autonomic and endocrine function. Connections between the networks presumably allow information flow from viscerosensory to visceromotor systems. In addition to a probable role in eating behavior, this system appears to be involved in guiding behavior and regulation of mood. Lesions of the ventromedial prefrontal cortex result in sociopathic behavior and difficulty in making appropriate choices, whereas functional imaging studies indicate that subjects with unipolar and bipolar depression have abnormal activity in medial and orbital prefrontal areas. Many of these areas also show volume changes and decreased glial number and density in mood‐disordered subjects.
Annexin II and Regulation of Cell Surface Fibrinolysis
Annals of the New York Academy of Sciences - Tập 902 Số 1 - Trang 265-271 - 2000
Katherine A. Hajjar, Suchitra S. Acharya
Abstract: The regulated function of the fibrinolytic system is fundamental to the solubilization of fibrin‐containing thrombi and to a number of other biologic processes. In recent years, several receptors, which serve to localize proteolytic activity on the cell surface, have been identified on endothelial cells, blood cells, neuronal cells, and tumor cells. One such receptor is annexin II, a calcium‐ and phospholipid‐binding protein that serves as a profibrinolytic coreceptor for tissue plasminogen activator and plasminogen on endothelial cells. Accumulating evidence suggests that impaired cell surface fibrinolytic assembly could lead to progressive atherothrombotic disease. In addition, dysregulation of annexin II expression in acute promyelocytic leukemia is an important mechanism for the bleeding diathesis associated with this malignancy.
CANCER AMONG BENZOYL CHLORIDE MANUFACTURING WORKERS
Annals of the New York Academy of Sciences - Tập 271 Số 1 - Trang 67-70 - 1976
H. Sakabe, Hidetsuru Matsushita, Shigezi Koshi
RENAL EXTRACTION OF PARA‐AMINOHIPPURATE AND CREATININE MEASURED BY CONTINUOUS <i>IN VIVO</i> SAMPLING OF ARTERIAL AND RENAL‐VEIN BLOOD
Annals of the New York Academy of Sciences - Tập 102 Số 1 - Trang 46-54 - 1962
Rodney B. Harvey, Ann Janice Brothers
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