scholarly journals Effect of Low-Dose Gamma Radiation and Lipoic Acid on High- Radiation-Dose Induced Rat Brain Injuries

Dose-Response ◽  
2021 ◽  
Vol 19 (4) ◽  
pp. 155932582110448
Author(s):  
Nahed Abdel-Aziz ◽  
Ahmed A Elkady ◽  
Eman M Elgazzar
Keyword(s):  
Brain Injury ◽  
Lipoic Acid ◽  
Low Dose ◽  
Brain Injuries ◽  
Neuroprotective Activity ◽  
Whole Body ◽  
High Dose ◽  
Γ Irradiation ◽  
Experimental Conditions ◽  
Adaptive Mechanisms

Aim This work aims to investigate the possible radio-adaptive mechanisms induced by low-dose (LD) whole-body γ-irradiation alone or combined with alpha-lipoic acid (ALA) administration in modulating high-dose (HD) head irradiation–induced brain injury in rats. Materials and Methods Rats were irradiated with LD (.25 Gy) 24 hours prior HD (20 Gy), and subjected to ALA (100 mg/kg/day) 5 minutes after HD and continued for 10 days. At the end of the experiment, animals were sacrificed and brain samples were dissected for biochemical and histopathological examinations. Results HD irradiation-induced brain injury as manifested by elevation of oxidative stress, DNA damage, apoptotic, and inflammatory markers in brain tissue. Histological examination of brain sections showed marked alterations. However, LD alone or combined with ALA ameliorated the changes induced by HD. Conclusion Under the present experimental conditions, LD whole-body irradiation exhibited neuroprotective activity against detrimental effects of a subsequent HD head irradiation. This effect might be due to the adaptive response induced by LD that activated the anti-oxidative, anti-apoptotic, and anti-inflammatory mechanisms in the affected animals making them able to cope with the subsequent high-dose exposure. However, the combined LD exposure and ALA supplementation produced a further modulating effect in the HD-irradiated rats.

Low-Dose and High-Dose Synacthen Tests and the Hemodynamic Response to Hydrocortisone in Acute Traumatic Brain Injury

2009 ◽  
Vol 11 (2) ◽  
pp. 158-164 ◽  
Author(s):  
R. S. Wijesurendra ◽  
F. Bernard ◽  
J. Outtrim ◽  
B. Maiya ◽  
S. Joshi ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Low Dose ◽  
Hemodynamic Response ◽  
High Dose ◽  
Acute Traumatic Brain Injury

scholarly journals Selective regulation of cellular and secreted multimeric adiponectin by antidiabetic therapies in humans

2009 ◽  
Vol 297 (3) ◽  
pp. E767-E773 ◽  
Author(s):  
Susan A. Phillips ◽  
Jacqueline Kung ◽  
Theodore P. Ciaraldi ◽  
Charles Choe ◽  
Louis Christiansen ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Low Dose ◽  
Whole Body ◽  
Serum Adiponectin ◽  
High Dose ◽  
Hmw Adiponectin ◽  
Dose Combination ◽  
Cell Expression ◽  
The Impact

Adiponectin, an insulin-sensitizing factor secreted from adipose tissue, is decreased in individuals with type 2 diabetes (T2D) and increased in response to thiazolidinedione (TZD) therapy. Changes in its secretion and assembly into higher-order forms affect insulin sensitivity. To determine the relative potency of TZDs on intra-adipocyte multimerization and secretion of adiponectin, we assessed the impact of in vivo low- or high-dose rosiglitazone treatment alone or combined with metformin in subjects with T2D. T2D subjects received high-dose rosiglitazone (8 mg/day), high-dose metformin (2,000 mg/day), or low-dose combination rosiglitazone-metformin therapy (4 mg + 1,000 mg/day) for 4 mo. All subjects were then switched to high-dose rosiglitazone-metformin combination therapy (8 mg + 2,000 mg/day) for another 4 mo. Low-dose rosiglitazone increased serum adiponectin, whereas the high dose increased both adipocyte content and serum adiponectin levels. TZDs selectively increased the percentage of circulating adiponectin in the potent, high-molecular-weight (HMW) form. No TZD effects were evident on multimer distribution in the cell. Expression of the chaperone protein ERp44, which retains adiponectin within the cell, was decreased by TZD treatment. No changes occurred in Ero1-Lα expression. Metformin had no effect on any of these measures. Increases in adiponectin correlated with improvements in insulin sensitivity. In vivo, TZDs have apparent dose-dependent effects on cellular and secreted adiponectin. TZD-mediated improvements in whole body insulin sensitivity are associated with increases in circulating but not cellular levels of the HMW adiponectin multimer. Finally, TZDs promote the selective secretion of HMW adiponectin, potentially, in part, through decreasing the expression of the adiponectin-retaining protein ERp44.

Effects of acute ethanol intoxication on experimental brain injury in the rat: neurobehavioral and phosphorus-31 nuclear magnetic resonance spectroscopy studies

1995 ◽  
Vol 82 (5) ◽  
pp. 813-821 ◽  
Author(s):  
Iwao Yamakami ◽  
Robert Vink ◽  
Alan I. Faden ◽  
Thomas A. Gennarelli ◽  
Robert Lenkinski ◽  
...  
Keyword(s):  
Nuclear Magnetic Resonance ◽  
Brain Injury ◽  
Magnetic Resonance ◽  
Low Dose ◽  
Resonance Spectroscopy ◽  
High Dose ◽  
Severe Brain Injury ◽  
High Severity ◽  
Acute Ethanol ◽  
Free Magnesium

✓ Using the lateral fluid-percussion model of experimental brain injury in the rat, the authors investigated the effect of acute ethanol (EtOH) intoxication on cardiovascular changes, neurological motor deficits, brain bioenergetics, and mortality associated with traumatic brain injury. Two hours after gastric administration of EtOH (low dose in 20 animals, 1.5 g/kg; high dose in 28, 3.0 g/kg) or saline (equal volume), animals were subjected to a fluid-percussion brain injury centered over the left parietal cortex. These injuries were of either moderate (X = 2.2 atm; 10 animals/treatment) or high severity (X = 3.0 atm; 18 animals/saline, 10 animals/low-dose EtOH, and 18 animals/high-dose EtOH). Neurological motor function was evaluated daily over a 1-week period, while a subset of eight animals receiving high-dose EtOH and subjected to brain injury of high severity were monitored for 4 hours using phosphorus-31 nuclear magnetic resonance spectroscopy to determine intracellular pH, free magnesium, and brain cytosolic phosphorylation potential. A significant (p < 0.05) and prolonged (up to 1 hour) hypotension was observed in animals pretreated with either low- or high-dose EtOH. Neither low-dose (blood—EtOH concentration = 110 ± 40 mg/dl) nor high-dose (blood—EtOH = 340 ± 70 mg/dl) EtOH had any effect on survival or neurological motor function after moderate brain injury. Following severe brain injury, animals pretreated with high-dose (blood—EtOH concentration = 352 ± 65 mg/dl) EtOH showed a significantly increased mortality and markedly worsened neurological deficits at 24 hours postinjury. Following injury, free magnesium and cytosolic phosphorylation potential declined in both groups by approximately 50% to 60%, with no significant differences between groups with respect to these variables. In contrast, brain intracellular pH in the EtOH-treated animals was consistently higher than in the control group after injury. These data suggest that prior exposure to EtOH, particularly at high concentrations, may have detrimental effects on neurobehavioral function and survival in the acute period (up to 24 hours) after severe brain injury, and may be associated with posttraumatic cerebral alkalosis.

scholarly journals Temporal patterns of microglial activation in white matter following experimental mild traumatic brain injury: a systematic literature review

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Prashanth S. Velayudhan ◽  
Nicole Schwab ◽  
Lili-Naz Hazrati ◽  
Anne L. Wheeler
Keyword(s):  
Brain Injury ◽  
White Matter ◽  
Microglial Activation ◽  
Brain Injuries ◽  
Experimental Studies ◽  
Current Understanding ◽  
Future Research ◽  
Cell Integrity ◽  
Experimental Conditions ◽  
Wide Range

AbstractMild traumatic brain injuries (mTBIs) are a prevalent form of injury that can result in persistent neurological impairments. Microglial activation has become increasingly recognized as a key process regulating the pathology of white matter in a wide range of brain injury and disease contexts. As white matter damage is known to be a major contributor to the impairments that follow mTBI, microglia have rightfully become a common target of investigation for the development of mTBI therapies and biomarkers. Recent work has demonstrated that the efficacy of microglial manipulation as a therapeutic intervention following injury or disease is highly time-sensitive, emphasizing the importance of advancing our understanding of the dynamics of post-mTBI microglial activation from onset to resolution. Current reporting of microglial activation in experimental studies of mTBI is non-standardized, which has limited our ability to identify concrete patterns of post-mTBI microglial activation over time. In this review, we examine preclinical studies of mTBI that report on microglial activation in white matter regions to summarize our current understanding of these patterns. Specifically, we summarize timecourses of post-mTBI microglial activation in white matter regions of the brain, identify factors that influence this activation, examine the temporal relationship between microglial activation and other post-mTBI assessments, and compare the relative sensitivities of various methods for detecting microglial activation. While the lack of replicated experimental conditions has limited the extent of conclusions that can confidently be drawn, we find that microglia are activated over a wide range of timecourses following mTBI and that microglial activation is a long-lasting outcome of mTBI that may resolve after most typical post-mTBI assessments, with the exception of those measuring oligodendrocyte lineage cell integrity. We identify several understudied parameters of post-mTBI microglial activation in white matter, such as the inclusion of female subjects. This review summarizes our current understanding of the progression of microglial activation in white matter structures following experimental mTBI and offers suggestions for important future research directions.

scholarly journals Morphological changes of rat jejunum after whole body γ-irradiation and their impact in biodosimetry

2008 ◽  
pp. 475-479
Author(s):  
D Driák ◽  
J Österreicher ◽  
J Vávrová ◽  
Z Řeháková ◽  
Z Vilasová
Keyword(s):  
Morphological Changes ◽  
Absorbed Dose ◽  
Whole Body ◽  
Control Group ◽  
Specific Marker ◽  
Rat Jejunum ◽  
Γ Irradiation ◽  
Experimental Conditions ◽  
The North ◽  
Causal Therapy

Gastrointestinal form is the second stage of the Acute Radiation Syndrome (ARS) with a threshold dose of 8 Gy. It represents an absolutely lethal clinical-pathological unit, enteritis necrohemorrhagica (duodenitis, jejunitis, ileitis, respectively) with unknown causal therapy. The purpose of our study has been to evaluate the morphological changes in a model of radiationinduced enteritis in rats and estimate the significance of changes in biodosimetry. Wistar rats were randomly divided into 21 groups, 10 animals per group. Samples of the jejunum were taken 24, 48, 72, and 96 h after the whole-body γ-irradiation with the doses of 1, 5, 10, 15, and 20 Gy, and routinely stained with hematoxylin and eosin. Five morphometric markers – intercryptal distance, enterocytal height on the top and base of villus, length of basal lamina of 10 enterocytes and enterocytal width – in irradiated rat jejunum were examined. The results were compared with sham-irradiated control group. After lethal doses of irradiation, all morphometric parameters of jejunum significantly changed. With the exception of intercryptal distance, they might be considered as suitable biodosimetric markers under these experimental conditions. Our morphometry results in radiation-induced jejunitis are in accordance with those in other studies. We were the first who quantified morphological postirradiation changes in animal jejunum. Some of them might be used under experimental conditions. This experimental study is a predecessor of the clinical assessment of a specific marker. Under clinical practice, the sensitive biodosimetric parameter could serve as one of the guidance for evaluation of the absorbed dose in irradiated troops as well as rescue workers. This is in accordance with tasks and Standardization Agreement of the North Atlantic Treaty Organization.

Unimpaired thermogenic response to noradrenaline in genetic (ob/ob) and hypothalamic (MSG) obese mice

1984 ◽  
Vol 4 (4) ◽  
pp. 343-349 ◽  
Author(s):  
A. G. Duloo ◽  
D. S. Miller
Keyword(s):  
Metabolic Rate ◽  
Room Temperature ◽  
Low Dose ◽  
Monosodium Glutamate ◽  
Whole Body ◽  
High Dose ◽  
Obese Mice ◽  
Subcutaneous Injections ◽  
Noradrenaline Administration ◽  
Thermogenic Response

The thermogenic response to noradrenaline administration was investigated at 25° in two models of obese mice (genetic ob/ob obesity of the ‘QEC’ strain and monosodium-glutamate-induced obesity) and in their respective lean littermates. Subcutaneous injections of a low dose of noradrenaline (I00 μg/kg body wt.) eJevated metabolic rate by about 3096 in both obese models but not in their respective lean counterparts. In contrast, the increase in metabolic rate after injections of a high dose of noradrenaline (600 μg/kg body wt.) was of a similar magnitude in both lean and obese animals: metabolic rate was increased by 70–80%. These results indicate that the overall whole body thermogenic capacity is unimpaired at room temperature in this ‘QEC’ strain of ob/ob mice and in the hypothalamic damaged obese mice. Obesity in these models is therefore not associated with a reduced ability to respond to noradrenaline but could rather be due to a failure to release noradrenaline.

Sign in / Sign up

Export Citation Format

Share Document