Molecular and Cellular Changes in the Pathogenesis of Endometriosis

Osmolarity of a fixative vehicle has long been known to have an effect on the tissue preservation. An increase in tissue osmolarity occurs in ischemia-damaged tissue and affects the morphology. In this study, we examined cellular changes in ischemic rat myocardium induced by varying fixative toxicity.Rats were sacrificed by decapitation and the hearts immediately removed and retrogradily perfused through the aorta with anoxic Kurbs-Henseleit medium. Hearts were then placed in a bag with a small amount of medium at 37°C for 90 minutes. Hearts were perfusion-fixed using 2% glutaraldehyde in 0.1 M cacodylate buffer pH -7.3 at three osmolarities. The isotonic buffer was adjusted to 311 mOsm/kg using D-manitol. Hypertonic buffers were adjusted to 375 and 400 mOsm/kg. One-half hour after perfusion fixation, the hearts were sliced and cut into small blocks and allowed to fix overnight at 4°C. Blocks were post fixed in osmium, en bloc stained in uranyl acetate, dehydrated in ethanol and embedded in Spurr medium.

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Immune Actions on the Peripheral Nervous System in Pain

International Journal of Molecular Sciences ◽

10.3390/ijms22031448 ◽

2021 ◽

Vol 22 (3) ◽

pp. 1448

Author(s):

Jessica Aijia Liu ◽

Jing Yu ◽

Chi Wai Cheung

Keyword(s):

Chronic Pain ◽

Nervous System ◽

Peripheral Nervous System ◽

Immune Cells ◽

Molecular Mechanisms ◽

Process Integration ◽

Current Knowledge ◽

Therapeutic Strategies ◽

Lipid Mediators ◽

Cellular Changes

Pain can be induced by tissue injuries, diseases and infections. The interactions between the peripheral nervous system (PNS) and immune system are primary actions in pain sensitizations. In response to stimuli, nociceptors release various mediators from their terminals that potently activate and recruit immune cells, whereas infiltrated immune cells further promote sensitization of nociceptors and the transition from acute to chronic pain by producing cytokines, chemokines, lipid mediators and growth factors. Immune cells not only play roles in pain production but also contribute to PNS repair and pain resolution by secreting anti-inflammatory or analgesic effectors. Here, we discuss the distinct roles of four major types of immune cells (monocyte/macrophage, neutrophil, mast cell, and T cell) acting on the PNS during pain process. Integration of this current knowledge will enhance our understanding of cellular changes and molecular mechanisms underlying pain pathogenies, providing insights for developing new therapeutic strategies.

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Cyclic Guanosine Monophosphate Modulates Locomotor Acceleration Induced by Nitric Oxide but not Serotonin in Clione limacina Central Pattern Generator Swim Interneurons

Integrative Organismal Biology ◽

10.1093/iob/obaa045 ◽

2020 ◽

Author(s):

Thomas J Pirtle ◽

Richard A Satterlie

Keyword(s):

Nitric Oxide ◽

Central Pattern Generator ◽

Guanylyl Cyclase ◽

Signal Transduction Pathway ◽

Soluble Guanylyl Cyclase ◽

Cyclic Guanosine Monophosphate ◽

Pattern Generator ◽

Guanosine Monophosphate ◽

Cellular Changes ◽

Clione Limacina

Abstract Typically, the marine mollusk, Clione limacina, exhibits a slow, hovering locomotor gait to maintain its position in the water column. However, the animal exhibits behaviorally relevant locomotor swim acceleration during escape response and feeding behavior. Both nitric oxide and serotonin mediate this behavioral swim acceleration. In this study, we examine the role that the second messenger, cGMP, plays in mediating nitric oxide and serotonin-induced swim acceleration. We observed that the application of an analog of cGMP or an activator of soluble guanylyl cyclase increased fictive locomotor speed recorded from Pd-7 interneurons of the animal’s locomotor central pattern generator. Moreover, inhibition of soluble guanylyl cyclase decreased fictive locomotor speed. These results suggest that basal levels of cGMP are important for slow swimming and that increased production of cGMP mediates swim acceleration in Clione. Because nitric oxide has its effect through cGMP signaling and because we show herein that cGMP produces cellular changes in Clione swim interneurons that are consistent with cellular changes produced by serotonin application, we hypothesize that both nitric oxide and serotonin function via a common signal transduction pathway that involves cGMP. Our results show that cGMP mediates nitric oxide-induced but not serotonin-induced swim acceleration in Clione.

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Stress tolerance phenotype of industrial yeast: industrial cases, cellular changes, and improvement strategies

Applied Microbiology and Biotechnology ◽

10.1007/s00253-019-09993-8 ◽

2019 ◽

Vol 103 (16) ◽

pp. 6449-6462 ◽

Cited By ~ 5

Author(s):

Xueliang Qiu ◽

Juan Zhang ◽

Jingwen Zhou ◽

Zhen Fang ◽

Zhengming Zhu ◽

...

Keyword(s):

Stress Tolerance ◽

Industrial Yeast ◽

Cellular Changes ◽

Improvement Strategies

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MORPHOLOGICAL STUDIES IN EXPERIMENTAL CRETINISM

Journal of Experimental Medicine ◽

10.1084/jem.17.6.636 ◽

1913 ◽

Vol 17 (6) ◽

pp. 636-652 ◽

Cited By ~ 33

Author(s):

Arthur L. Tatum

Keyword(s):

Adrenal Glands ◽

The Body ◽

The Other ◽

Degenerative Changes ◽

Morphological Studies ◽

Cellular Changes ◽

Anatomical Basis ◽

Parenchymatous Organ ◽

Islands Of Langerhans

In summarizing the findings of this paper it may be said that degenerative changes have been noted in practically every parenchymatous organ. Among these the most striking has been that of serous imbibition by the most active cells of these organs. In regard to the changes in the glands of internal secretion, the findings corroborate the statements of Cushing in regard to hypophysectomy, that removal of one gland of internal secretion results in changes in all the other glands. In this case, degenerative changes predominate in the hypophysis, thymus, ovary, and testis, while hyperplasia is seen in the islands of Langerhans and the medullas of the adrenal glands. Finally, in the rabbit athyroidism is responsible for grave degenerative changes in practically all organs and tissues of the body, and many of the symptoms of cretinism have an anatomical basis in organic cellular changes.

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