Evaluation of Temperature Transients at Various Body Temperature Measuring Sites Using a Fast Response Thermistor Bead Sensor

2013 ◽  
Author(s):  
Oleg Vesnovsky ◽  
L. D. Timmie Topoleski ◽  
Laurence W. Grossman ◽  
Jon P. Casamento ◽  
Liang Zhu
Keyword(s):  
Immune System ◽  
Body Temperature ◽  
Pulmonary Artery ◽  
Temperature Control ◽  
Surgical Procedures ◽  
Fast Response ◽  
The Body ◽  
Control Center ◽  
Post Surgery ◽  
The Brain

Body temperature monitoring of humans has been an important tool for helping clinicians diagnose infections, detect fever, monitor thermoregulation functions during surgical procedures, and assess post-surgery recovery.1–3 Fever itself is typically not considered a disease. It is a response of the body to a disease, which is often inflammatory in nature. Elevation of the set point at the body temperature control center, the brain hypothalamus, is caused by circulating pyrogens produced by the immune system responding to diseases. Since the brain hypothalamus is not easily accessed by thermometers, other body locations have been identified as alternative measuring sites. Those sites include the pulmonary artery, rectum, bladder, distal esophagus and nasopharynx, sublingual surface of the tongue, under the armpit, tympanic membrane, and forehead.

The Ouroboros of Inflammatory Signaling to the Brain for the Control of Neuroendocrine Function

2021 ◽  
Author(s):  
Georgia E. Hodes
Keyword(s):  
Nervous System ◽  
Immune System ◽  
Immune Regulation ◽  
The Body ◽  
Immune Disorders ◽  
Inflammatory Signaling ◽  
Late 20Th Century ◽  
Immune Systems ◽  
Neuroendocrine Function ◽  
The Brain

In the late 20th century, the discovery that the immune system and central nervous system were not autonomous revolutionized exploration of the mechanisms by which stress contributes to immune disorders and immune regulation contributes to mental illness. There is increasing evidence of stress as integrated across the brain and body. The immune system acts in concert with the peripheral nervous system to shape the brain’s perception of the environment. The brain in turn communicates with the endocrine and immune systems to guide their responses to that environment. Examining the groundwork of mechanisms governing communication between the body and brain will hopefully provide a better understanding of the ontogeny and symptomology of some mood disorders.

scholarly journals The Legacy of Sickness Behaviors

2020 ◽  
Vol 11 ◽  
Author(s):  
Keith W. Kelley ◽  
Stephen Kent
Keyword(s):  
Immune System ◽  
Body Temperature ◽  
Communication Systems ◽  
Memory Deficits ◽  
Sleep Disruption ◽  
Sickness Behaviors ◽  
Systemic Infections ◽  
The Brain ◽  
Conceptual Advance

Systemic infections of all types lead to a syndrome known as sickness behaviors. Changes in the behavior of febrile humans and animals formed the original basis for this concept. Body temperature is behaviorally regulated in both endotherms and ectotherms. However, infections cause other changes in body functions, including sleep disruption, anorexia, cognitive and memory deficits and disorientation. The brain mediates this entire cluster of symptoms, even though most major infections occur outside the brain. The true importance of sickness behaviors is not the numerous discoveries of symptoms that affect all of us when we get sick. Instead, the legacy of 30 years of research in sickness behaviors is that it established the physiologic importance of reciprocal communication systems between the immune system and the brain. This conceptual advance remains in its infancy.

scholarly journals Pathways of neuro-immune communication: past and present time, clinical application

2020 ◽  
Vol 22 (3) ◽  
pp. 405-418
Author(s):  
E. A. Korneva
Keyword(s):  
Immune System ◽  
Autoimmune Diseases ◽  
Vagus Nerve ◽  
Inflammatory Diseases ◽  
Sympathetic Nerves ◽  
The Body ◽  
Autonomic Nerves ◽  
Neural Pathways ◽  
Pulsed Ultrasound ◽  
The Brain

Fundamental studies in neuroimmunophysiology are the keystone for development of new therapeutic approaches to the treatment of infectious, allergic, oncologic and autoimmune diseases. The achievements in this field allowed approving new treatment methods based on irritation of afferent and efferent fibers of autonomic nerves. That became possible due to numerous studies of pathways between the immune and nervous systems performed over last two decades. The milestones in the history of neuroimmune communication research are represented here. The immune system organs – bone marrow, thymus and spleen are coupled to central nervous system (CNS) via sympathetic nerves. Information about LPS and bacteria emergence in peritoneum, intestine and parenchymal organs reaches the brain via parasympathetic pathways. After vagotomy, the brain neurons do not respond to this kind of antigens. The pattern of brain responses to different applied antigens (the EEG changes and the quantity of c-Fos-positive neurons) is specific for definite antigen, like as algorithms of electroneurogram after exposure to different cytokines. Activation of parasympathetic nerves causes the inhibition of inflammation. The entry of any antigens into the body initiates production of cytokines (IL-1, TNFα, IL-6, IFNγ etc.), via specific receptors which are present on peripheral neurons and terminals of vagus nerve, i.e. the vagal afferent terminals and neurons respond to cytokine action, and these signals are transmitted to CNS neurons. The afferent vagal fibers end on the dorsal vagal complex neurons in the caudal part of medulla oblongata. The information about bacterial antigens, LPS and inflammation is transmitted to the brain via afferent autonomic neural pathways. The speed of this process is high and significantly depends on the rates of cytokine production that are transmitters of signals upon the antigen exposure. It is important to emphasize that this events occur within minutes, and the response to the received information proceeds by reflex mechanisms, i.e., within fraction of a second, as exemplified by inflammation (“inflammation reflex”). This is a fundamentally new and revolutionary discovery in the functional studies of immune system regulation. Clinical efficiency of n. vagus stimulation by pulsed ultrasound was shown, being used for the treatment of inflammatory, allergic and autoimmune diseases, e.g., multiple sclerosis, rheumatoid arthritis, renal inflammatory diseases. Electrical stimulation of the vagus nerve reduces the death of animals in septic shock by 80%. The mentioned data have made a revolution in understanding the functional arrangement of immune system in the body. A hypothesis is represented, which suggests how the information on the antigen exposure is transmitted to the brain.

CONGENITAL TOXOPLASMOSIS

PEDIATRICS ◽  
1949 ◽  
Vol 4 (4) ◽  
pp. 432-442
Author(s):  
SVEN GARD ◽  
J. HENNING MAGNUSSON ◽  
F. WAHLGREN ◽  
GUNNAR GILLE
Keyword(s):  
Spinal Cord ◽  
Cerebrospinal Fluid ◽  
Body Temperature ◽  
Liver Biopsy ◽  
Neutralization Test ◽  
High Titer ◽  
Congenital Toxoplasmosis ◽  
The Body ◽  
The Brain

An account is given of congenital toxoplasmosis in a child who died at the age of 43 days. The patient, who was somnolent from birth, showed the following symptoms: bilateral microphthalmia and chronic bilateral uveitis; considerable hydrocephalus internus, mainly symmetric, cerebral calcifications and pronounced typical changes in the cerebrospinal fluid, hypoprothrombinemia and eosinophilia; enlargement of the liver and spleen; marked lability of the body temperature with wide variations. The postmortem findings, both macroscopic and microscopic, were typical in every respect, with pronounced necrotic encephalitis in the cerebrum and characteristic foci of granulomata in the brainstem and the spinal cord. Toxoplasma in the form of pseudocysts were demonstrated in the affected parts of the brain. Typical Toxoplasma were isolated from the spinal fluid on three occasions, from material obtained by liver biopsy and from pieces of brain and spleen removed at autopsy. Serum from the patient as well as from the mother gave a positive neutralization test in rabbits. The in vitro dye test according to Sabin and Feldman yielded a positive result with a high titer value. The strain of Toxoplasma isolated ("G. L.") seems to be serologically identical with the American strains "RH" and "LM."

The expression of the cold shock protein RNA binding motif protein 3 is transcriptionally responsive to organ temperature in mice

2020 ◽  
Vol 27 ◽  
Author(s):  
Ayako Ushio ◽  
Ko Eto
Keyword(s):  
Gene Expression ◽  
Body Temperature ◽  
Rna Binding ◽  
Mild Hypothermia ◽  
Reproductive Organs ◽  
The Body ◽  
Cold Shock Protein ◽  
Binding Motif ◽  
Liver And Kidney ◽  
The Brain

Background: Mild hypothermia, i.e. maintenance of organ temperature by up to 8°C lower than body temperature, is a critical strategy for exerting some functions of the cells and organs normally, and is an useful therapy for recovering properly from some diseases, including myocardial infarction, cardiac arrest, brain injury, and ischemic stroke. Nevertheless, there were no focusses so far on organ temperature and potential responses of gene expression to organ temperature in organs of homeothermic animals that survive under normal conditions. Objective: The present study aimed to assess organ temperature in homeothermic animals and evaluate the effect of their organ temperature on the expression of the cold shock protein RNA binding motif protein 3 (RBM3), and to gain insights into the organ temperature-mediated regulation of RBM3 gene transcription via Nuclear factor β-light-chain-enhancer of activated B cells (NF-κB) p65, which had been identified as a transcription factor that is activated by undergoing the Ser276 phosphorylation and promotes the RBM3 gene expression during mild hypothermia. Methods: We measured the temperature of several organs, where RBM3 expression was examined, in female and male mice. Next, in male mice, we tested NF-κB p65 expression and its Ser276 phosphorylation in organs that have their lower temperature than body temperature and compared them with those in organs that have their temperature near body temperature. Results: Organ temperature was around 32°C in the brain and reproductive organs, which is lower than the body temperature, and around 37°C in the heart, liver, and kidney, which is comparable to the body temperature. The expression of RBM3 was detected greatly in the brain and reproductive organs with their organ temperature of around 32°C, and poorly in the heart, liver, and kidney with their organ temperature of around 37°C. In accordance with the changes in the RBM3 expression, the NF-κB p65 Ser276 phosphorylation was detected more greatly in the testis and brain with their organ temperature of around 32°C, than in the heart, liver, and kidney with their organ temperature of around 37°C, although the NF-κB p65 expression was unchanged among all the organs tested. Discussion: Our data suggested that organ temperature lower than body temperature causes the expression of RBM3 in the brain and reproductive organs of mice, and that lower organ temperature causes the NF-κB p65 activation through the Ser276 phosphorylation, resulting in an increase in the RBM3 gene transcription, in the brain and reproductive organs of mice. Conclusion: The study may present the possibility that organ temperature-induced alterations in gene expression are organ specific in homeotherms and the possibility that organ temperature-induced alterations in gene expression are transcriptionally regulated in some organs of homeotherms.

scholarly journals Formation of the “setting” level of body temperature regulation during endotoxin fever

2020 ◽  
Vol 17 (1) ◽  
pp. 28-37
Author(s):  
F. I. Vismont ◽  
A. F. Vismont
Keyword(s):  
Body Temperature ◽  
Blood Plasma ◽  
Temperature Regulation ◽  
Brain Temperature ◽  
The Body ◽  
Body Temperature Regulation ◽  
Norepinephrine Turnover ◽  
Arginine Hydrochloride ◽  
Biochemical Research ◽  
The Brain

The experiments on rats and rabbits using modern physiological, biochemical research methods and the pharmacological approach established that in the body, the action of bacterial endotoxin, accompanied by fever, leads to a significant decrease in blood plasma and in CSF of the arginine content. In rabbits after 30 min intravenous administration of carbon-labeled arginine hydrochloride (25 μCi/kg) at the endotoxin fever peak (after the 60 min injection of endotoxine E. coli), the radioactivity level in the blood plasma decreases and significantly increases in the cerebrospinal fluid and the hypothalamus tissue. It was revealed that although the content and speed of norepinephrine turnover in the hypothalamus after the introduction of L-arginine hydrochloride (100 μg) into the ventricles of the rats does not change in comparison with control animals, however, the chemoreactive properties of the thermoregulatory structures of the brain have changed, which manifests itself in the change in the expression and duration of thermoregulatory effects of the central action of norepinephrine and acetylcholine. It was established that the administration of L-arginine hydrochloride into the brain ventricles at a dose of 100 μg per animal or in the blood flow at a dose of 20 mg/kg caused the pronounced antipyretic effect. It was found that L-arginine hydrochloride (100 μg), after it has been introduced into the ventricles of the brain, increases the impulse activity of heat-sensitive neurons of the medial preoptic region of the anterior hypothalamus in rabbits due to a brain temperature growth when the animal’s body is overheated. Apparently, CSF arginine can be considered as an important factor in the changes in the excitability thresholds of cold and heat-sensitive neurons in the hypothalamus and in the formation of the “setpoint” of body temperature regulation during endotoxin fever.

scholarly journals The Influence of Mild Body and Brain Hypothermia on Ischemic Brain Damage

1990 ◽  
Vol 10 (3) ◽  
pp. 365-374 ◽  
Author(s):  
Hiroaki Minamisawa ◽  
Carl-Henrik Nordström ◽  
Maj-Lis Smith ◽  
Bo K. Siesjö
Keyword(s):  
Body Temperature ◽  
Brain Damage ◽  
The Body ◽  
Reticular Nucleus ◽  
Temperature Sensitive ◽  
Ischemic Brain Damage ◽  
Neuronal Necrosis ◽  
Ischemic Brain ◽  
Selective Neuronal Vulnerability ◽  
The Brain

The influence of brain and body temperature on ischemic brain damage, notably on the density and distribution of selective neuronal vulnerability, was studied in SPF-Wistar rats subjected to 15 min of forebrain ischemia induced by bilateral occlusion of the common carotid arteries combined with arterial hypotension (50 mm Hg) in a room air environment. In one group of animals, the body temperature was maintained at 37°C but no attempt was made to prevent heat losses from the ischemic brain; i.e., the head was not heated during ischemia. Under those conditions the temperature of the caudoputamen and at a subcutaneous site over the skull bone spontaneously fell to ∼32°C. In four other groups, both the rectal and the subcutaneous skull temperatures were maintained at 38, 37, 35, and 33°C during the ischemia. Our results confirm those recently reported when brain temperature was varied during 20 min of ischemia, with body temperature kept constant. Thus, the histopathological outcome of the brain damage, as assessed after 7 days of recovery, was strongly temperature dependent. Whereas ischemia at 37–38°C consistently caused neuronal necrosis in the hippocampus, neocortex, and caudoputamen, spontaneous cooling of the brain during ischemia at a rectal temperature of 37°C significantly reduced the ischemic damage. Intentional lowering of temperature to 35°C markedly reduced and to 33°C virtually prevented neuronal necrosis in some but not all of the regions studied. While damage to the caudoputamen was extremely temperature sensitive, that affecting the CA1 sector of the hippocampus, and particularly the lateral reticular nucleus of the thalamus, was less so. Our results suggest that whatever biochemical events are responsible for selective neuronal vulnerability, they are temperature sensitive; however, since there are differences in sensitivity between different parts of the brain, more than one mechanism may be involved.

scholarly journals Are anti-CTL4 and anti-PD-1 an effective biomarker in immunotherapy?

2022 ◽  
Vol 3 (1) ◽  
pp. 01-04
Author(s):  
Hasibe Vural
Keyword(s):  
Immune System ◽  
Cancer Therapy ◽  
The Body ◽  
Self Knowledge ◽  
The Individual ◽  
The Brain

The task of the immune system is to prevent foreign organisms from entering the body, if microbes have entered the body, to destroy them, to prevent or delay their spread. One of the most important features of the immune system is that it has the ability to recognize and distinguish millions of different microbes that are foreign to it. The immune system, like the brain, evaluates and synthesizes the situation, which is this breeding organ, and produces different training and special responses to microbes, cancer. This is a feature that does not exist in any system or organ except the brain and immune system. In summary, the task of the immune system is to protect the essence of the individual. For this reason, he knows himself first and does not harm the essence. In this context, it can be said that the immune system spends as much effort on self-knowledge as it does on fighting the enemy. This rewiev article is intended to provide an overview of the CTLA-4 and PD-1 pathways and the description of their efficacy in cancer therapy or immunotherapy.

Basic concepts of immunology and neuroimmunology

2000 ◽  
Vol 9 (6) ◽  
pp. 1-6 ◽  
Author(s):  
Anil Sehgal ◽  
Mitchel S. Berger
Keyword(s):  
T Cells ◽  
Immune System ◽  
Current Knowledge ◽  
Effective Means ◽  
Lymphatic Vessels ◽  
The Body ◽  
Activated T Cells ◽  
The Central Nervous System ◽  
System Review ◽  
The Brain

The immune system is a complex network of specialized cells and organs that defends the human body against attack from foreign pathogens. The major lymphocytes involved in protecting the body against potential infections are B and T cells, which also play an important role in combating tumor growth. The cells of the immune system patrol the tissues and organs through both blood and lymphatic vessels, but some organs—including cornea, testes, and brain—are usually not patrolled by these cells. The brain has been thought to be an immune-privileged site because of the tight blood–brain barrier (BBB) that protects it. Few cells migrate to the brain under normal circumstances, because the BBB permits only certain molecules to cross into brain tissue. Recently, however, studies have shown that activated T cells exposed to antigen can cross the intact BBB and migrate into brain. This finding opens the path to developing effective means of immunotherapy for lesions of the central nervous system. The authors discuss basic facets of the immune system, review the current knowledge about human neuroimmunology, and survey current strategies for developing immunotherapy-based treatments for human brain tumors.

scholarly journals ATIM-44. A PHASE I FIRST-IN-HUMAN TRIAL OF TWO ADENOVIRAL VECTORS EXPRESSING HSV1-TK AND FLT3L FOR TREATING NEWLY DIAGNOSED RESECTABLE MALIGNANT GLIOMA: THERAPEUTIC REPROGRAMMING OF THE BRAIN IMMUNE SYSTEM

2019 ◽  
Vol 21 (Supplement_6) ◽  
pp. vi11-vi11
Author(s):  
Pedro Lowenstein ◽  
Daniel A Orringer ◽  
Oren Sagher ◽  
Jason Heth ◽  
Shawn Hervey-Jumper ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Immune System ◽  
Phase I ◽  
Median Survival ◽  
Dose Escalation ◽  
Adenoviral Vectors ◽  
Secondary Outcome ◽  
Newly Diagnosed ◽  
Post Surgery ◽  
The Brain

Abstract This is an interim report on a first in human Phase I dose escalation trial of the combination of two adenoviral vectors expressing HSV1-TK or Flt3L for the treatment of newly diagnosed, resectable malignant gliomas. Lack of dendritic cells from the brain precludes anti-glioma immune responses. We combined tumor cytotoxicity (Ad-HSV1TK) with recruitment of dendritic cells to gliomas (Ad-Flt3L) to induce anti-glioma immunity. In experimental models this treatment induces powerful cytotoxic CD8 and CD4 T-dependent anti-glioma immunity, immunological memory, and the capacity to recognize neo-antigens. The trial was approved through a FDA-IND, and all institutional cttees. Treatment was administered intraoperatively following complete glioma resection in newly diagnosed tumors. The trial consisted of vector dose escalation, starting at 1x10^9 v.p., and increasing to 1x10^11 v.p. of each vector, through 6 cohorts of 3 patients each. Two cycles of 14 days of valacyclovir were administered to activate HSV1-TK cytotoxicity. Cycle 1 starts on Day 1–3 post surgery for 14 days, and Cycle 2 on Week 8–12. Standard radiation, i.e., 60 Gy in 2 Gy fractions over 6 weeks, with concurrent temozolomide, was followed by cyclic temozolomide. Examination of tumor samples at primary resection and first recurrence show an increase in the infiltration of inflammatory cells. The experimental treatment was well tolerated. An MTD was not reached. There were approx. 248 AEs, and 26 SAEs; these were not linked to treatment. As secondary outcome, median survival of contemporary controls was 604 days, and median survival of trial patients was 742 days. Our results show for the first time that reprogramming of the host’s brain immune system to recognize gliomas reveals a new approach for the treatment of highly malignant brain tumors. Clinical trial information: NCT01811992.

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