Effect of Insulin-Induced Hypoglycaemia on the Central Nervous System: Evidence from Experimental Studies

2014 ◽  
Vol 26 (3) ◽  
pp. 123-150 ◽  
Author(s):  
V. F. H. Jensen ◽  
I. B. Bøgh ◽  
J. Lykkesfeldt
2020 ◽  
Author(s):  
Florian MICHAUD ◽  
Mario Lamas ◽  
Urbano Lugrís ◽  
Javier Cuadrado

Abstract Experimental studies and EMG collections suggest that a specific strategy of muscle coordination is chosen by the central nervous system to perform a given motor task. A popular mathematical approach for solving the muscle recruitment problem is optimization. Optimization-based methods minimize or maximize some criterion (objective function or cost function) which reflects the mechanism used by the central nervous system to recruit muscles for the movement considered. The proper cost function is not known a priori, so the adequacy of the chosen function must be validated according to the obtained results. In addition of the many criteria proposed, several physiological representations of the musculotendon actuator dynamics along with different musculoskeletal models can be found in the literature, which hinders the selection of the best neuromusculotendon model for each application. Seeking to provide a fair base for comparison, this study measures the efficiency and accuracy of: i) four different criteria; ii) one static and three physiological representations of the musculotendon actuator dynamics; iii) a synergy-based method; all of them within the framework of inverse-dynamics based optimization. Motion/force/EMG gait analyses were performed on ten healthy subjects. A musculoskeletal model of the right leg actuated by 43 Hill-type muscles was scaled to each subject and used to calculate joint moments, musculotendon kinematics and moment arms. Muscle activations were then estimated using the different approaches, and these estimates were compared with EMG measurements. Although similar results were obtained with all the methods, it must be pointed out that a higher complexity of the method does not guarantee better results, as the best correlations with experimental values were obtained with two simplified approaches.


1939 ◽  
Vol 70 (6) ◽  
pp. 565-582 ◽  
Author(s):  
Peter K. Olitsky

The results of investigations thus far carried out on experimental avian encephalomyelitis indicate that the virus of this newly described disease conforms to the group of definitely established viruses. It was essential to determine its taxonomy since the only prior record of its study (1) defines the infective agent as a virus because the usual cultural attempts failed to reveal a visible microorganism to be identified with it, and because the transmissible agent passed through Seitz and Berkefeld N filters. At the present time such determinants fail completely to satisfy the criteria for defining a virus and their acceptance would lead to the inclusion of certain filtrable microbic agents, difficult to reveal except by special cultural procedures, as viruses (10). The virus of avian encephalomyelitis is distinct from that of equine encephalomyelitis and is clearly a virus sui generis. The striking feature of its properties is its narrow range of host susceptibility—only the avian species are responsive to inoculation; ordinary laboratory animals are apparently resistant, even to large numbers of chicken cerebral infective doses. In addition, it is probable that its size is in the range of that of the equine virus. Studies also reveal that the virus is not easily sedimented by centrifugation (that is, at 5400 R.P.M. for one hour in the angle centrifuge and at 12,000 R.P.M. for one hour in the open air centrifuge) and is resistant to the action of glycerol and to drying. It is readily filtrable through Seitz one and two disc filters, through Berkefeld V and N candles, and is active in dilutions in broth up to 10–6. It passes through gradocol membranes of 73 mµ average pore diameter at least (the end-point has not as yet been definitely determined). An attack of the experimental disease leads to development of resistance to reinoculation and of antibodies in the serum. Old birds are reported as being refractory to infection, both in nature and in the laboratory (1, 2). Whether this resistance in mature animals is due to earlier exposure to infection, or to the development of structural or physiological barriers to invasion by the virus, remains still to be determined. Under experimental conditions, the route by which the virus acts uniformly to induce disease is the intracerebral. Yet in certain instances other peripheral ways of inoculation such as the intraperitoneal, subcutaneous, intradermal, intravenous, intramuscular, intrasciatic, may also be effective. Thus far, in limited experiments, feeding, or instilling nasally, or injecting into the vitreous body the infective agent has been ineffective. Whether the viral progression is axonal from peripheral sites is still to be determined; as should be also the question whether it multiplies in any of the organs other than the central nervous tissues. The virus was not detected in the blood during the period of incubation or during the acute phases of the experimental disease. So that unless it is found that other animals harbor the virus, or that still other sources of it exist as yet not disclosed, it is not likely that the disease is disseminated by a blood-sucking insect. The actual portal of entry and the factor in the spread of the disease in nature is still obscure, since the evidence here presented is still too incomplete to elucidate these problems. The pathological lesions induced are of interest. The neuronal reaction resembles that brought about by axonal disturbance (axon reaction, Nissl's or retrograde degeneration). The question may well be asked whether there may not be here an initial injury by the virus to the axonal process of the neuron, which in turn induces the retrograde changes in the cell body. This has as yet to be studied, as well as the possibility of viral progression along an axonal route with or without concurrent multiplication. The significance of the second major lesion in the central nervous system, namely, the generally marked perivascular reaction, is also still to be determined. Finally, the only observable and histopathological change in organs other than the central nervous tissues (in which we have not as yet noted the change) is in the hyperplasia of the normally present lymphoid islands. One is impressed by the prodigious numbers of lymphoid elements surrounding the vessels of the central nervous system and the question here is whether these hyperplastic areas serve as depots to supply the cells for this perivascular reaction.


2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Rodolfo Pinto-Almazán ◽  
Julia J. Segura-Uribe ◽  
Eunice D. Farfán-García ◽  
Christian Guerra-Araiza

Hormone replacement therapy (HRT) increases the risk of endometrial and breast cancer. A strategy to reduce this incidence is the use of tibolone (TIB). The aim of this paper was to address the effects of TIB on the central nervous system (CNS). For the present review, MEDLINE (via PubMed), LILACS (via BIREME), Ovid Global Health, SCOPUS, Scielo, and PsycINFO (ProQuest Research Library) electronic databases were searched for the results of controlled clinical trials on peri- and postmenopausal women published from 1990 to September 2016. Also, this paper reviews experimental studies performed to analyze neuroprotective effects, cognitive deficits, neuroplasticity, oxidative stress, and stroke using TIB. Although there are few studies on the effect of this hormone in the CNS, it has been reported that TIB decreases lipid peroxidation levels and improves memory and learning. TIB has important neuroprotective effects that could prevent the risk of neurodegenerative diseases in postmenopausal women as well as the benefits of HRT in counteracting hot flashes, improving mood, and libido. Some reports have found that TIB delays cognitive impairment in various models of neuronal damage. It also modifies brain plasticity since it acts as an endocrine modulator regulating neurotransmitters, Tau phosphorylation, and decreasing neuronal death. Finally, its antioxidant effects have also been reported in different animal models.


1995 ◽  
Vol 41 (1) ◽  
pp. 39-45
Author(s):  
H. A. Shvyrkova

After the publication of data on the detection of insulin in brain tissue, interest in studying the role of insulin in the central nervous system (CNS) and changes in the central nervous system in diabetes mellitus increased sharply. In patients with diabetes, a high frequency of mental disorders has been established. Complications of the nervous system in children whose mothers were pregnant with diabetes during pregnancy are described in literature. The role of insulin in the development and differentiation of neurons, potentiation of synaptic activity, the exchange of catecholamines, transcription of genes in nerve cells has been identified, which allows a better understanding of the mechanism of diabetic encephalopathy. This review analyzes the results of experimental studies of the central nervous system in diabetes.


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