scholarly journals Effects of acute and chronic sleep loss on immune modulation of rats

2007 ◽  
Vol 293 (1) ◽  
pp. R504-R509 ◽  
Author(s):  
A. Zager ◽  
M. L. Andersen ◽  
F. S. Ruiz ◽  
I. B. Antunes ◽  
S. Tufik
Keyword(s):  
Sleep Deprivation ◽  
Immune Function ◽  
Lymphocyte Count ◽  
Cellular Response ◽  
Complement C3 ◽  
Control Group ◽  
Spleen Weight ◽  
Axillary Lymph ◽  
Recovery Sleep ◽  
Cell Counts

Sleep deprivation is now recognized as an increasingly common condition inherent to modern society, and one that in many ways, is detrimental to certain physiological systems, namely, immune function. Although sleep is now viewed by a significant body of researchers as being essential for the proper working of a host of defense systems, the consequences of a lack of sleep on immune function remains to be fully comprehended. The aim of the current study was to investigate how paradoxical sleep deprivation (PSD) for 24 and 96 h and sleep restriction (SR) for 21 days by the modified multiple-platform method, and their respective 24-h recovery periods, affect immune activation in rats. To this end, we assessed circulating white blood cell counts, lymphocyte count within immune organs, as well as Ig and complement production. The data revealed that PSD for 96 h increased complement C3 and corticosterone concentration in relation to the control group. In contrast, the spleen weight, total leukocytes, and lymphocytes decreased during SR for 21 days when compared with the control group, although production of a certain class of immunoglobulin, the IgM, did increase. After recovery sleep, lymphocyte count in axillary lymph nodes grew when rats had rebound sleep after PSD for 24 h, neutrophils increased after PSD 96 h and lymphocytes numbers were higher after SR 21 days. Such alterations during sleep deprivation suggest only minor alterations of nonspecific immune parameters during acute PSD, and a significant impairment in cellular response during chronic SR.

Phagocytosis of Colloidal Carbon by the Fixed Tissue and Peritoneal Macrophages of New Zealand Mice

1972 ◽  
Vol 17 (12) ◽  
pp. 383-392 ◽  
Author(s):  
K. Whaley ◽  
H. Singh ◽  
J. Webb
Keyword(s):  
New Zealand ◽  
Cellular Response ◽  
Strain Differences ◽  
Peritoneal Macrophages ◽  
Spleen Weight ◽  
Fixed Tissue ◽  
Cell Counts ◽  
Colloidal Carbon ◽  
Carbon Clearance ◽  
Clearance Studies

The peritoneal cellular response to colloidal carbon has been studied in NZB, NZW, BWF1, BALB/c, CBA and C3Hf mice aged 8 to 10 weeks. The overall patterns of total and differential peritoneal cell counts was similar in all 6 strains of mice. No inter-strain differences were noted in either the removal of carbon from the peritoneal cavity or the distribution of carbon in the fixed tissue macrophages. The results show that phagocytosis of colloidal carbon, an inert particle, is normal in New Zealand mice. Intravenous carbon clearance studies performed on NZB, BALB/c and CBA mice showed that phagocytosis of carbon was identical in each strain when correction was made for variations in liver and spleen weight.

scholarly journals Recovery sleep after extended wakefulness restores elevated A1adenosine receptor availability in the human brain

2017 ◽  
Vol 114 (16) ◽  
pp. 4243-4248 ◽  
Author(s):  
David Elmenhorst ◽  
Eva-Maria Elmenhorst ◽  
Eva Hennecke ◽  
Tina Kroll ◽  
Andreas Matusch ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Human Brain ◽  
Cognitive Performance ◽  
Brain Regions ◽  
Sleep Loss ◽  
Control Group ◽  
Sleep Episode ◽  
Recovery Sleep ◽  
Positron Emission ◽  
Performance Impairment

Adenosine and functional A1adenosine receptor (A1AR) availability are supposed to mediate sleep–wake regulation and cognitive performance. We hypothesized that cerebral A1AR availability after an extended wake period decreases to a well-rested state after recovery sleep. [18F]CPFPX positron emission tomography was used to quantify A1AR availability in 15 healthy male adults after 52 h of sleep deprivation and following 14 h of recovery sleep. Data were additionally compared with A1AR values after 8 h of baseline sleep from an earlier dataset. Polysomnography, cognitive performance, and sleepiness were monitored. Recovery from sleep deprivation was associated with a decrease in A1AR availability in several brain regions, ranging from 11% (insula) to 14% (striatum). A1AR availabilities after recovery did not differ from baseline sleep in the control group. The degree of performance impairment, sleepiness, and homeostatic sleep-pressure response to sleep deprivation correlated negatively with the decrease in A1AR availability. Sleep deprivation resulted in a higher A1AR availability in the human brain. The increase that was observed after 52 h of wakefulness was restored to control levels during a 14-h recovery sleep episode. Individuals with a large increase in A1AR availability were more resilient to sleep-loss effects than those with a subtle increase. This pattern implies that differences in endogenous adenosine and A1AR availability might be causal for individual responses to sleep loss.

scholarly journals Salmonella Enteritidis detection and immunological cellular response to experimental inoculation in day-old turkeys

2018 ◽  
Vol 39 (1) ◽  
pp. 177
Author(s):  
Eliete Souza Santana ◽  
Thiago Souza Azeredo Bastos ◽  
José Henrique Stringhini ◽  
Regiane Nascimento Gagno Porto ◽  
Robson Rodrigues Santana ◽  
...  
Keyword(s):  
Lymphocyte Count ◽  
Cellular Response ◽  
Salmonella Enteritidis ◽  
Bursa Of Fabricius ◽  
Control Group ◽  
Post Inoculation ◽  
Gradual Reduction ◽  
Treatment Groups ◽  
Experimental Inoculation ◽  
Almost All

The purpose of this research is to clarify aspects of the pathogenesis of Salmonella Enteritidis in experimentally inoculated day-old turkeys. Three treatments were conducted among a total of 120 turkeys; one control group and two treatment groups in which 6 x 102 CFU mL-1 and 7 x 105 CFU mL-1, respectively, of Salmonella Enteritidis was inoculated in the crops. Two birds from each treatment were sacrificed and necropsied at 1, 3, 4, 12, 18, and 24 hours, and 3, 4, 38, and 49 days post-inoculation. We re-isolated Salmonella, measured lymphocytes, and conducted immunohistochemical tests. Six hours post-inoculation, Salmonella was found in the investigated organs (yolk sac, cecum, fragments of spleen, and bursa of Fabricius) with conventional bacteriology and immunohistochemistry, and was continuously detected in almost all analyzed organs until turkeys were four-days old. Further, Salmonella was detected after 38 days in cecum, when the concentration 7 x 105 CFU mL-1 was given. At both inoculation concentrations, the number of lymphocytes was similar; larger quantities were found in the first hour post-inoculation, followed by a gradual reduction, reaching the lowest levels at 24 hours after inoculation. Afterwards, lymphocytes increased discreetly, remaining at the same level until 49 days after inoculation. In conclusion, inoculation concentration influences mitigation, dissemination, elimination, and persistence of this pathogen in turkeys. Lower concentrations promote less invasion as well as lower cell stain and lower lymphocyte count.

scholarly journals The anterolateral projections of the medial basal hypothalamus affect sleep

2009 ◽  
Vol 296 (4) ◽  
pp. R1228-R1238 ◽  
Author(s):  
Zoltan Peterfi ◽  
Gábor B. Makara ◽  
Ferenc Obál ◽  
James M. Krueger
Keyword(s):  
Sleep Deprivation ◽  
Eye Movement ◽  
Brain Temperature ◽  
Control Group ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Sleep Regulation ◽  
Medial Basal Hypothalamus ◽  
Recovery Sleep ◽  
Delta Activity

The role of the medial basal hypothalamus (MBH) and the anterior hypothalamus/preoptic area (AH/POA) in sleep regulation was investigated using the Halász knife technique to sever MBH anterior and lateral projections in rats. If both lateral and anterior connections of the MBH were cut, rats spent less time in non-rapid eye movement sleep (NREMS) and rapid eye movement sleep (REMS). In contrast, if the lateral connections remained intact, the duration of NREMS and REMS was normal. The diurnal rhythm of NREMS and REMS was altered in all groups except the sham control group. Changes in NREMS or REMS duration were not detected in a group with pituitary stalk lesions. Water consumption was enhanced in three groups of rats, possibly due to the lesion of vasopressin fibers entering the pituitary. EEG delta power during NREMS and brain temperatures (Tbr) were not affected by the cuts during baseline or after sleep deprivation. In response to 4 h of sleep deprivation, only one group, that with the most anterior-to-posterior cuts, failed to increase its NREMS or REMS time during the recovery sleep. After deprivation, Tbr returned to baseline in most of the treatment groups. Collectively, results indicate that the lateral projections of the MBH are important determinants of duration of NREMS and REMS, while more anterior projections are concerned with the diurnal distribution of sleep. Further, the MBH projections involved in sleep regulation are distinct from those involved in EEG delta activity, water intake, and brain temperature.

scholarly journals The effects of sleep deprivation on the processing of emotional facial expressions in young adults with and without ADHD

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ami Cohen ◽  
Kfir Asraf ◽  
Ivgeny Saveliev ◽  
Orrie Dan ◽  
Iris Haimov
Keyword(s):  
Young Adults ◽  
Sleep Deprivation ◽  
Facial Expressions ◽  
Interactive Effect ◽  
Control Group ◽  
Experimental Session ◽  
Poor Sleep ◽  
Adhd Group ◽  
Emotional Facial Expressions ◽  
Oddball Task

AbstractThe ability to recognize emotions from facial expressions is essential to the development of complex social cognition behaviors, and impairments in this ability are associated with poor social competence. This study aimed to examine the effects of sleep deprivation on the processing of emotional facial expressions and nonfacial stimuli in young adults with and without attention-deficit/hyperactivity disorder (ADHD). Thirty-five men (mean age 25.4) with (n = 19) and without (n = 16) ADHD participated in the study. During the five days preceding the experimental session, the participants were required to sleep at least seven hours per night (23:00/24:00–7:00/9:00) and their sleep was monitored via actigraphy. On the morning of the experimental session, the participants completed a 4-stimulus visual oddball task combining facial and nonfacial stimuli, and repeated it after 25 h of sustained wakefulness. At baseline, both study groups had poorer performance in response to facial rather than non-facial target stimuli on all indices of the oddball task, with no differences between the groups. Following sleep deprivation, rates of omission errors, commission errors and reaction time variability increased significantly in the ADHD group but not in the control group. Time and target type (face/non-face) did not have an interactive effect on any indices of the oddball task. Young adults with ADHD are more sensitive to the negative effects of sleep deprivation on attentional processes, including those related to the processing of emotional facial expressions. As poor sleep and excessive daytime sleepiness are common in individuals with ADHD, it is feasible that poor sleep quality and quantity play an important role in cognitive functioning deficits, including the processing of emotional facial expressions that are associated with ADHD.

scholarly journals Residual, differential neurobehavioral deficits linger after multiple recovery nights following chronic sleep restriction or acute total sleep deprivation

SLEEP ◽  
2020 ◽  
Author(s):  
Erika M Yamazaki ◽  
Caroline A Antler ◽  
Charlotte R Lasek ◽  
Namni Goel
Keyword(s):  
Sleep Deprivation ◽  
Response Speed ◽  
Sleep Loss ◽  
Sleep Restriction ◽  
Total Sleep Deprivation ◽  
Psychomotor Vigilance Test ◽  
Recovery Sleep ◽  
Time In Bed ◽  
Neurobehavioral Deficits ◽  
Chronic Sleep

Abstract Study Objectives The amount of recovery sleep needed to fully restore well-established neurobehavioral deficits from sleep loss remains unknown, as does whether the recovery pattern differs across measures after total sleep deprivation (TSD) and chronic sleep restriction (SR). Methods In total, 83 adults received two baseline nights (10–12-hour time in bed [TIB]) followed by five 4-hour TIB SR nights or 36-hour TSD and four recovery nights (R1–R4; 12-hour TIB). Neurobehavioral tests were completed every 2 hours during wakefulness and a Maintenance of Wakefulness Test measured physiological sleepiness. Polysomnography was collected on B2, R1, and R4 nights. Results TSD and SR produced significant deficits in cognitive performance, increases in self-reported sleepiness and fatigue, decreases in vigor, and increases in physiological sleepiness. Neurobehavioral recovery from SR occurred after R1 and was maintained for all measures except Psychomotor Vigilance Test (PVT) lapses and response speed, which failed to completely recover. Neurobehavioral recovery from TSD occurred after R1 and was maintained for all cognitive and self-reported measures, except for vigor. After TSD and SR, R1 recovery sleep was longer and of higher efficiency and better quality than R4 recovery sleep. Conclusions PVT impairments from SR failed to reverse completely; by contrast, vigor did not recover after TSD; all other deficits were reversed after sleep loss. These results suggest that TSD and SR induce sustained, differential biological, physiological, and/or neural changes, which remarkably are not reversed with chronic, long-duration recovery sleep. Our findings have critical implications for the population at large and for military and health professionals.

scholarly journals Cellular Response against Oxidative Stress, a Novel Insight into Lupus Nephritis Pathogenesis

2021 ◽  
Vol 11 (8) ◽  
pp. 693
Author(s):  
Corina Daniela Ene ◽  
Simona Roxana Georgescu ◽  
Mircea Tampa ◽  
Clara Matei ◽  
Cristina Iulia Mitran ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lupus Nephritis ◽  
Cellular Response ◽  
Molecular Mechanisms ◽  
Control Group ◽  
Dna Repair Mechanisms ◽  
Glycation End Products ◽  
Repair Mechanisms ◽  
Low Levels ◽  
Defective Dna Repair

The interaction of reactive oxygen species (ROS) with lipids, proteins, nucleic acids and hydrocarbonates promotes acute and chronic tissue damage, mediates immunomodulation and triggers autoimmunity in systemic lupus erythematous (SLE) patients. The aim of the study was to determine the pathophysiological mechanisms of the oxidative stress-related damage and molecular mechanisms to counteract oxidative stimuli in lupus nephritis. Our study included 38 SLE patients with lupus nephritis (LN group), 44 SLE patients without renal impairment (non-LN group) and 40 healthy volunteers as control group. In the present paper, we evaluated serum lipid peroxidation, DNA oxidation, oxidized proteins, carbohydrate oxidation, and endogenous protective systems. We detected defective DNA repair mechanisms via 8-oxoguanine-DNA-glycosylase (OGG1), the reduced regulatory effect of soluble receptor for advanced glycation end products (sRAGE) in the activation of AGE-RAGE axis, low levels of thiols, disulphide bonds formation and high nitrotyrosination in lupus nephritis. All these data help us to identify more molecular mechanisms to counteract oxidative stress in LN that could permit a more precise assessment of disease prognosis, as well as developing new therapeutic targets.

scholarly journals Combination of umbilical cord mesenchymal stem cells and standard immunosuppressive regimen for pediatric patients with severe aplastic anemia

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yang Lan ◽  
Fang Liu ◽  
Lixian Chang ◽  
Lipeng Liu ◽  
Yingchi Zhang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Aplastic Anemia ◽  
Umbilical Cord ◽  
Pediatric Patients ◽  
Statistical Significance ◽  
Severe Aplastic Anemia ◽  
Control Group ◽  
Open Label ◽  
Cell Counts

Abstract Background Defects of bone marrow mesenchymal stem cells (BM-MSCs) in proliferation and differentiation are involved in the pathophysiology of aplastic anemia (AA). Infusion of umbilical cord mesenchymal stem cells (UC-MSCs) may improve the efficacy of immunosuppressive therapy (IST) in childhood severe aplastic anemia (SAA). Methods We conducted an investigator-initiated, open-label, and prospective phase IV trial to evaluate the safety and efficacy of combination of allogenic UC-MSCs and standard IST for pediatric patients with newly diagnosed SAA. In mesenchymal stem cells (MSC) group, UC-MSCs were injected intravenously at a dose of 1 × 106/kg per week starting on the 14th day after administration of rabbit antithymocyte globulin (ATG), for a total of 3 weeks. The clinical outcomes and adverse events of patients with UC-MSCs infusion were assessed when compared with a concurrent control group in which patients received standard IST alone. Results Nine patients with a median age of 4 years were enrolled as the group with MSC, while the data of another 9 childhood SAA were analysed as the controls. Four (44%) patients in MSC group developed anaphylactic reactions which were associated with rabbit ATG. When compared with the controls, neither the improvement of blood cell counts, nor the change of T-lymphocytes after IST reached statistical significance in MSC group (both p > 0.05) and there were one (11%) patient in MSC group and two (22%) patients in the controls achieved partial response (PR) at 90 days after IST. After a median follow-up of 48 months, there was no clone evolution occurring in both groups. The 4-year estimated overall survival (OS) rate in two groups were both 88.9% ± 10.5%, while the 4-year estimated failure-free survival (FFS) rate in MSC group was lower than that in the controls (38.1% ± 17.2% vs. 66.7% ± 15.7%, p = 0.153). Conclusions Concomitant use of IST and UC-MSCs in SAA children is safe but may not necessarily improve the early response rate and long-term outcomes. This clinical trial was registered at ClinicalTrials.gov, identifier: NCT02218437 (registered October 2013).

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