Cell Degeneration in the Larval Ventral Horn of Xenopus laevis (Daudin)

Development ◽  
1961 ◽  
Vol 9 (2) ◽  
pp. 269-284
Author(s):  
Arthur Hughes
Keyword(s):  
Regional Differences ◽  
Balance Sheet ◽  
Ventral Horn ◽  
Spinal Ganglia ◽  
Cell Degeneration ◽  
Mammalian Embryos ◽  
A Cell ◽  
Vertebrate Embryos ◽  
Cell Balance ◽  
Developing Nervous System

Cell death accompanies a variety of developmental processes in many tissues and systems of organs. A comprehensive review by Glücksmann (1951) has revealed how widespread is the occurrence of degenerating cells in vertebrate embryos. Within the developing nervous system, the earliest descriptions of cellular degeneration are due to Barbieri (1905) in Amphibia, and to Collin (1906) in the chick embryo. Since that time, destruction of cells has been observed in the morphogenesis of the neural tube, most recently by Boyd (1955) and by Källén (1955) in early mammalian embryos; in the establishment of regional differences between limb and non limb-levels in spinal ganglia of the chick (Hamburger & Levi-Montalcini, 1949), and also in the histogenesis of Anuran ventral horn cells (Xenopus, Hughes & Tschumi, 1958; Eleutherodactylus, Hughes, 1959). The present study is also concerned with ventral horn cells in Xenopus. Here the aim has been to draw up a cell balance-sheet during development based both on counts of numbers of ventral horn neuroblasts throughout their differentiation, and also of the number of degenerating cells among them at each stage.

Cell turnover in the spinal ganglia of Xenopus laevis tadpoles

Development ◽  
1965 ◽  
Vol 13 (1) ◽  
pp. 63-72
Author(s):  
M. C. Prestige
Keyword(s):  
Balance Sheet ◽  
Ventral Horn ◽  
Spinal Ganglia ◽  
Sensory Cells ◽  
Cell Turnover ◽  
Hind Limbs ◽  
Time Graph ◽  
Relationship Of ◽  
The Relationship ◽  
Developing Spinal Cord

Hughes (1961) has drawn up a balance-sheet of the lumbar ventral horn cells during the development of Xenopus, based both on counts of numbers of ventral horn cells throughout differentiation and of the number of degenerating cells among them at each stage. In this way, he showed that the total number of ventral horn cells is reduced from between 3000 and 4000 at differentiation to 1200 at the end of metamorphosis; that the most rapid period of decline in cell numbers is accompanied by a peak in the time graph of the number of degenerations; and concluded that for every neurone which finally differentiates, some eight or nine neuroblasts undergo degeneration. This is an example of histogenetic degeneration (Glücksmann, 1951), that is, cell death relating to the differentiation of functioning organs. In order to investigate further the relationship of the limb to the developing spinal cord, a similar balance-sheet has been drawn up for the sensory cells of the hind-limbs which are in dorsal ganglia 8–10

scholarly journals Impact of Global Transcriptional Silencing on Cell Cycle Regulation and Chromosome Segregation in Early Mammalian Embryos

2021 ◽  
Vol 22 (16) ◽  
pp. 9073
Author(s):  
Martin Anger ◽  
Lenka Radonova ◽  
Adela Horakova ◽  
Diana Sekach ◽  
Marketa Charousova
Keyword(s):  
Cell Cycle ◽  
Chromosome Segregation ◽  
Significant Proportion ◽  
Transcriptional Silencing ◽  
Early Embryo ◽  
Global Changes ◽  
Embryonic Genome ◽  
Mammalian Embryos ◽  
A Cell ◽  
And Behavior

The onset of an early development is, in mammals, characterized by profound changes of multiple aspects of cellular morphology and behavior. These are including, but not limited to, fertilization and the merging of parental genomes with a subsequent transition from the meiotic into the mitotic cycle, followed by global changes of chromatin epigenetic modifications, a gradual decrease in cell size and the initiation of gene expression from the newly formed embryonic genome. Some of these important, and sometimes also dramatic, changes are executed within the period during which the gene transcription is globally silenced or not progressed, and the regulation of most cellular activities, including those mentioned above, relies on controlled translation. It is known that the blastomeres within an early embryo are prone to chromosome segregation errors, which might, when affecting a significant proportion of a cell within the embryo, compromise its further development. In this review, we discuss how the absence of transcription affects the transition from the oocyte to the embryo and what impact global transcriptional silencing might have on the basic cell cycle and chromosome segregation controlling mechanisms.

The response of the brachial ventral horn of Xenopus laevis to forelimb amputation during development

Development ◽  
1976 ◽  
Vol 36 (3) ◽  
pp. 453-468
Author(s):  
Joanne E. Fortune ◽  
Antonie W. Blackler
Keyword(s):  
Xenopus Laevis ◽  
Normal Development ◽  
Developmental Stages ◽  
Neuronal Degeneration ◽  
Neuronal Loss ◽  
Cell Loss ◽  
Cell Number ◽  
Ventral Horn ◽  
Cell Degeneration ◽  
Cell Numbers

The normal development of the brachial ventral horn of the frog Xenopus laevis and the response of the brachial ventral horn to complete forelimb extirpation at five developmental stages were assessed histologically. Differentiation of brachial ventral horn neurons occurred in pre-metamorphic tadpoles between stages 52/53 and 57. Mean cell number in the brachial ventral horn reached a peak of 2576 (S.E.M. = ±269, n = 2) per side of the spinal cord at stage 55 and decreased to 1070 (S.E.M. = ± 35, n =7) by the end of metamorphosis. Cell degeneration was presumed to be the mode of cell loss since it was most prevalent during the period of rapid decrease in cell numbers. The response of the ventral horn to forelimb removal varied with the stage of the animal at amputation. Following amputation at stage 52/53 or 54 the ipsilateral ventral horn neurons appeared less differentiated than those on the controlside and a rapid cell loss of about 80 % occurred on the operated side. These effects occurred more rapidly after ablation at stage 54 than at stage 52/53. Amputation at stage 58, 61, or 66 caused chromatolysis in the ventral horn, a period of relative cell excess on the operated side, and a delayed neuronal loss of 32–66%. It was concluded that excess cell degeneration accounted for cell loss and that suppression of normal neuronal degeneration caused the relative cell excess on the operated side. The data indicate that the brachial ventral horn was indifferent to the periphery before stage 54, was quickly affected by limb removal between stages 54 and 58, and by stage 58 had entered a phase in which a delay preceded cell death. No forelimb regeneration occurred.

Risk management with a duration gap approach

2020 ◽  
Vol 11 (6) ◽  
pp. 1257-1300 ◽  
Author(s):  
Jamshaid Anwar Chattha ◽  
Syed Musa Alhabshi ◽  
Ahamed Kameel Mydin Meera
Keyword(s):  
Commercial Banks ◽  
Regional Differences ◽  
Balance Sheet ◽  
Gap Model ◽  
Asset Liability Management ◽  
Content Type ◽  
Banking Systems ◽  
Liability Management ◽  
Duration Gap ◽  
The Impact

Purpose In line with the IFSB and BCBS methodology, the purpose of this study is to undertake a comparative analysis of dual banking systems for asset-liability management (ALM) practices with the duration gap, in Islamic Commercial Banks (ICBs) and Conventional Commercial Banks (CCBs). Based on the research objective, two research questions are developed: How do the duration gaps of ICBs compare with those of similar sized CCBs? Are there any country-specific and regional differences among ICBs in terms of managing their duration gaps? Design/methodology/approach The research methodology comprises two-stages: stage one uses a duration gap model to calculate the duration gaps of ICBs and CCBs; stage two applies parametric tests. In terms of the duration gap model, the study determines the duration gap with a four-step process. The study selected a sample of 100 banks (50 ICBs and 50 CCBs) from 13 countries for the period 2009-2015. Findings The paper provides empirical insights into the duration gap and ALM of ICBs and CCBs. The ICBs have more variations in their mean duration gap compared to the CCBs, and they have a tendency for a higher (more) mean duration gap (28.37 years) in comparison to the CCBs (11.79 years). The study found ICBs as having 2.41 times more duration gap compared to the CCBs, and they are exposed to increasing rate of return (ROR) risk due to their larger duration gaps and severe liquidity mismatches. There are significant regional differences in terms of the duration gap and asset-liability management. Research limitations/implications Future studies also consider “Off-Balance Sheet” activities of the ICBs, with multi-term duration measures. A larger sample size of 100 ICBs with 10 years’ data after the GFC would be more beneficial to the industry. In addition, the impact of an increasing benchmark rate (e.g. 100, 200 and 300 bps) on the ICBs as per the IFSB 20 per cent threshold can also be established with the duration gap approach to identify the vulnerabilities of the ICBs. Practical implications The study makes profound contributions to the literature and suggests various policy recommendations for Islamic banks, regulators, and standard setters of the ICBs, for identifying and measuring the significance of the duration gaps; and management of the ROR risk under Pillar 2 of the BCBS and IFSB, for financial soundness and stability purposes. Originality/value To the best of the authors’ knowledge, this is a pioneer study in Islamic banking involving a sample of 100 banks (50 ICBs and 50 CCBs) from 13 countries. The results of the study provide original empirical evidence regarding the estimation of duration gap, and variations across jurisdictions in terms of vulnerability of ICBs and CCBs in dual banking systems.

scholarly journals 0363 : Development of a cell isolation method in large mammals: regional differences in calcium signaling across left atrium from sheep

2015 ◽  
Vol 7 (2) ◽  
pp. 164-165
Author(s):  
Caroline Cros ◽  
Caroline Pascarel-Auclerc ◽  
David Benoist ◽  
Olivier Bernus ◽  
Pierre Jais ◽  
...  
Keyword(s):  
Calcium Signaling ◽  
Left Atrium ◽  
Regional Differences ◽  
Cell Isolation ◽  
Large Mammals ◽  
Isolation Method ◽  
A Cell

1. What are stem cells?

2021 ◽  
pp. 1-18
Author(s):  
Jonathan Slack
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Structural Unit ◽  
Embryonic Stem ◽  
Cell Types ◽  
The Body ◽  
Differentiated Cells ◽  
Mammalian Embryos ◽  
A Cell

‘What are stem cells?’ explains that a stem cell is a cell that can both reproduce itself and generate offspring of different functional cell types and begins by considering the nature of cells in general, wherein cells are understood to be the ultimate structural unit of an animal or plant body. Stem cells in the body persist long term, usually for the lifetime of the organism. Good examples of differentiated cells arising from stem cells are those of the skin, the blood, and the lining of the intestine. Embryonic stem cells are grown in culture from early mammalian embryos. The reason that stem cell research is seen as the source for new cures is largely because this technology offers a route to cell therapy.

scholarly journals STUDIES ON PSEUDORABIES (INFECTIOUS BULBAR PARALYSIS, MAD ITCH)

1933 ◽  
Vol 58 (4) ◽  
pp. 415-433 ◽  
Author(s):  
E. Weston Hurst
Keyword(s):  
Nerve Cell ◽  
Glial Cells ◽  
Nerve Cells ◽  
Spinal Ganglia ◽  
Cell Degeneration ◽  
Intracerebral Inoculation ◽  
Bulbar Paralysis ◽  
Nuclear Alterations ◽  
Cardinal Symptom ◽  
In Cells

The histology of pseudorabies differs materially in various animal species. In the rabbit, subcutaneous, intradermal or intramuscular inoculation leads to local inflammation and necrosis. The infection ascends the peripheral nerve (possibly both interstitially and by the axis-cylinders) to the corresponding spinal ganglia and segments of the spinal cord, where primary degeneration of nerve and glial cells takes place. The nerve cell changes are probably responsible for the cardinal symptom of the disease, itching. Death ensues soon after virus reaches the medulla, before visible changes have been produced here. Intracerebral inoculation is followed by characteristic lesions in the meninges, in subpial glial cells and in superficially placed nerve cells. Morbid changes in the lungs are not necessarily related to the presence of virus, but specific lesions may be present. Intranuclear inclusions bearing some resemblance to those in herpetic encephalitis, yellow fever, etc., occur in cells derived from all embryonic layers. The disease in the guinea pig resembles closely that in the rabbit and is modified only by the slightly greater resistance of the animal. In the monkey after intracerebral inoculation, widespread degeneration and necrosis of cortical nerve cells are accompanied by the appearance of specific nuclear alterations in nerve and glial cells, but not in cells of mesodermal origin. No lesions are found in other viscera. In the spontaneous disease in the cow lesions approximate more closely to those in the monkey than to those in the rabbit. In the pig vascular and interstitial lesions predominate, nerve cell degeneration is relatively slight and typical inclusions are not observed. These differences probably explain the benign course of the malady following subcutaneous inoculation in this animal. The lymphatic system, too, participates in the reaction to the virus.

A Familial Peripheral Neuropathy and Glomerulopathy in Gelbvieh Calves

2003 ◽  
Vol 40 (1) ◽  
pp. 63-70 ◽  
Author(s):  
R. J. Panciera ◽  
K. E. Washburn ◽  
R. N. Streeter ◽  
J. G. Kirkpatrick
Keyword(s):  
Peripheral Neuropathy ◽  
Peripheral Nerves ◽  
Pedigree Analysis ◽  
Spinal Nerve ◽  
Ventral Horn ◽  
Spinal Ganglia ◽  
Limb Ataxia ◽  
Familial Relationship ◽  
Spinal Cord Cell ◽  
Glomerular Lesions

Nine Gelbvieh calves originating in four herds and clinically presenting with rear limb ataxia/ paresis had histopathologically confirmed peripheral neuropathy and a proliferative glomerulopathy. Degenerative lesions were severe in peripheral nerves, dorsal and ventral spinal nerve roots, and less marked in dorsal fasciculi of the spinal cord. Cell bodies of spinal ganglia were minimally diseased; ventral horn neurons occasionally had central chromatolysis and nuclear displacement. Glomerular lesions ranged from mild mesangial hypercellularity to glomerulosclerosis. Pedigree analysis of affected animals from one herd indicated a strong familial relationship and probable hereditary basis for the syndrome.

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