scholarly journals Induced loss in cerebral tissues of respiratory response to electrical impulses, and its partial restoration by additional substrates

1953 ◽  
Vol 54 (2) ◽  
pp. 305-312 ◽  
Author(s):  
H. McIlwain ◽  
Marion B. R. Gore
1968 ◽  
Vol 46 (6) ◽  
pp. 543-548 ◽  
Author(s):  
S. Nakazawa ◽  
J. H. Quastel

Ammonium ions cause a suppression of the respiratory response of rat brain cortex slices to electrical stimulation and this is partly reversed by the addition of DL-methionine sulfoxide or L-glutamine but not by addition of L-glutamate or DL-α-methylglutamate. Other basic ions, e.g. tetramethylammonium, pyridine, or pyrimidine, at equivalent concentrations are without effect. Ammonium ions have less inhibitory effect on the respiratory response to high potassium ion concentrations than on that due to application of electrical impulses. They also bring about a marked suppression of the rate of glycine uptake into rat brain cortex slices, the effect being much greater with electrically stimulated brain than with unstimulated brain. Methionine sulfoxide diminishes this suppressive effect. They exercise relatively small inhibitory effects on the depressed rate of glycine uptake obtained in the presence of high potassium ion concentrations. The effect of ammonium ions is considered to be partly due to the fall in cell ATP brought about by the operation of glutamine synthetase. The results are consistent with the view that the extent of stimulation of brain respiration due to electrical impulses or to increased concentration of potassium ions is dependent on the cell level of ATP. L-Glutamate, L-glutamine, or γ-aminobutyrate diminishes the suppressive effects of ammonium ions on glycine influx into brain. L-Glutamate, moreover, diminishes the stimulatory effects of electrical stimulation on brain respiration, lesser effects being produced by L-glutamine or γ-aminobutyrate.


2017 ◽  
Vol 10 (1) ◽  
pp. 32-37
Author(s):  
Hyeokjoon NA ◽  
Taeyun KANG ◽  
Yongbeom PYEON ◽  
Kyounghoon LEE
Keyword(s):  

2021 ◽  
Vol 8 (4) ◽  
pp. 40
Author(s):  
Marietta Easterling ◽  
Simone Rossi ◽  
Anthony J Mazzella ◽  
Michael Bressan

Cardiac pacemaker cells located in the sinoatrial node initiate the electrical impulses that drive rhythmic contraction of the heart. The sinoatrial node accounts for only a small proportion of the total mass of the heart yet must produce a stimulus of sufficient strength to stimulate the entire volume of downstream cardiac tissue. This requires balancing a delicate set of electrical interactions both within the sinoatrial node and with the downstream working myocardium. Understanding the fundamental features of these interactions is critical for defining vulnerabilities that arise in human arrhythmic disease and may provide insight towards the design and implementation of the next generation of potential cellular-based cardiac therapeutics. Here, we discuss physiological conditions that influence electrical impulse generation and propagation in the sinoatrial node and describe developmental events that construct the tissue-level architecture that appears necessary for sinoatrial node function.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Qing Xia ◽  
Xiangtian Ling ◽  
Zhonghao Wang ◽  
Tao Shen ◽  
Minghao Chen ◽  
...  

Abstract Purpose and background Recently, we found that maximal medial rectus recession and lateral rectus resection in patients with complete lateral rectus paralysis resulted in a partial restoration of abduction. In an attempt to understand some of the mechanisms involved with this effect we examined gene expression profiles of lateral recti from these patients, with our focus being directed to genes related to myogenesis. Materials and methods Lateral recti resected from patients with complete lateral rectus paralysis and those from concomitant esotropia (controls) were collected. Differences in gene expression profiles between these two groups were examined using microarray analysis and quantitative Reverse-transcription PCR (qRT-PCR). Results A total of 3056 differentially expressed genes (DEGs) were identified between these two groups. Within the paralytic esotropia group, 2081 genes were up-regulated and 975 down-regulated. The results of RT-PCR revealed that PAX7, MYOG, PITX1, SIX1 and SIX4 showed higher levels of expression, while that of MYOD a lower level of expression within the paralytic esotropia group as compared with that in the control group (p < 0.05). Conclusion The decreased expression of MYOD in the paralytic esotropia group suggested that extraocular muscle satellite cell (EOMSCs) differentiation processes were inhibited. Whereas the high expression levels of PAX7, SIX1/4 and MYOG, suggested that the EOMSCs were showing an effective potential for differentiation. The stimulation resulting from muscle surgery may induce EOMSCs to differentiate and thus restore abduction function.


Author(s):  
Tanvi Khera ◽  
Yanqin Du ◽  
Daniel Todt ◽  
Katja Deterding ◽  
Benedikt Strunz ◽  
...  

Abstract Background Treatment with direct acting antivirals (DAAs) in patients with chronic hepatitis C infection leads to partial restoration of soluble inflammatory mediators (SIMs). In contrast, we hypothesized that early DAA treatment of acute hepatitis C with DAAs may normalize most SIMs. Methods In this study, we made use of a unique cohort of acute symptomatic hepatitis C who cleared HCV with a 6-week course of ledipasvir/sofosbuvir. Plasma samples were used for proximity extension assay (PEA) measuring 92 proteins. Results Profound SIM alterations were observed in acute HCV patients, with marked upregulation of IL-6 and CXCL10 while certain mediators were down-regulated (e.g. MCP-4, IL-7). During treatment and follow-up, the majority of SIMs decreased but not all normalized (e.g. CDCP1, IL-18). Of note, SIMs that were down-regulated before DAA treatment remained suppressed while others that were initially unchanged, declined to lower values during treatment and follow-up (e.g.CD244). Conclusions Acute hepatitis C was associated with marked changes in the soluble inflammatory milieu as compared to both chronic hepatitis patients and healthy controls. Whereas early DAA treatment partly normalized this altered signature, long-lasting imprints of HCV remained. Thus, acute HCV-induced changes in the immune system may persist even after a short duration of viremia.


2021 ◽  
pp. 1869415
Author(s):  
Andrey Khlopkov ◽  
Oksana Sherstneva ◽  
Maria Ladeynova ◽  
Marina Grinberg ◽  
Lyubov Yudina ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Laura Sanchis-Artero ◽  
Juan Francisco Martínez-Blanch ◽  
Sergio Manresa-Vera ◽  
Ernesto Cortés-Castell ◽  
Marina Valls-Gandia ◽  
...  

AbstractIntestinal dysbiosis is key in the onset and development of Crohn’s disease (CD). We evaluated the microbiota changes in CD patients before and after a six-month anti-TNF treatment, comparing these changes with the microbiota of healthy subjects. This prospective multicenter observational study involved 27 CD patients initiating anti-TNF treatment and 16 healthy individuals. Inflammatory activity was determined at baseline, 3 and 6 months, classifying patients into responders and non-responders. Fecal microbiota was analyzed by massive genomic sequencing thought 16S rRNA amplicon sequencing before and after six months of anti-TNF treatment. The CD cohort showed a decrease in genera of the class Clostridia, short-chain fatty acid producers, and an increase in the phylum Proteobacteria (p < 0.01) versus the healthy cohort. After anti-TNF treatment, the phylum Proteobacteria also increased in non-responders versus responders (13/27) (p < 0.005), with the class Clostridia increasing. In addition, alpha diversity increased in responders versus non-responders (p < 0.01), tending towards eubiosis. An association was found (p < 0.001) in the F.prausnitzii/E.coli ratio between responders and non-responders. The F/E ratio was the most accurate biomarker of anti-TNF response (area under the curve 0.87). Thus, anti-TNF treatment allows partial restoration of intestinal microbiota in responders and the F.prausnitzii/E.coli ratio can provide a reliable indicator of response to anti-TNF in CD.


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