Therapeutic irradiation of the brain is associated with a number of adverse effects, including cognitive impairment. Although the pathogenesis of radiation-induced cognitive injury is unknown, it may involve loss of neural precursor cells from the subgranular zone (SGZ) of the hippocampal dentate gyrus and alterations in new cell production (neurogenesis). Young adult male C57BL mice received whole brain irradiation, and 6-48 h later, hippocampal tissue was assessed using immunohistochemistry for detection of apoptosis and numbers of proliferating cells and immature neurons. Apoptosis peaked 12 h after irradiation, and its extent was dose dependent. Forty-eight h after irradiation, proliferating SGZ cells were reduced by 93-96%; immature neurons were decreased from 40 to 60% in a dose-dependent fashion. To determine whether acute cell sensitivity translated into long-term changes, we quantified neurogenesis 2 months after irradiation with 0, 2, 5, or 10 Gy. Multiple injections of BrdUrd were given to label proliferating cells, and 3 weeks later, confocal microscopy was used to determine the percentage of BrdUrd-labeled cells that showed mature cell phenotypes. The production of new neurons was significantly reduced by X-rays; that change was dose dependent. In contrast, there were no apparent effects on the production of new astrocytes or oligodendrocytes. Measures of activated microglia indicated that changes in neurogenesis were associated with a significant inflammatory response. Given the known effects of radiation on cognitive function and the relationship between hippocampal neurogenesis and associated memory formation, our data suggest that precursor cell radiation response and altered neurogenesis may play a contributory if not causative role in radiation-induced cognitive impairment.

3. Demand Response ProgramsMany utility companies are using cutting edge technology to learn how customers heat or cool their homes and businesses in order to prevent brownouts or the need for rolling blackouts during extreme weather events.


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Gluten sensitivity is sometimes referred to as gluten intolerance. Gluten sensitivity is a medically more accurate way to refer to the condition. To learn more about the current definitions for conditions related to celiac disease, visit our glossary.

Gluten sensitivity has been clinically recognized as less severe than celiac disease because people with gluten sensitivity do not test positive for celiac disease based on blood testing, and do not have damage to their small intestines found in individuals with celiac disease.

Research has also shown that gluten sensitivity does not result in the increased intestinal permeability, also known as leaky gut, that is characteristic of celiac disease. Leaky gut permits toxins, bacteria and undigested food proteins to seep through the GI barrier and into the bloodstream, and research suggests that it is an early biological change that comes before the onset of several autoimmune diseases.

Gluten sensitivity shares many symptoms with celiac disease. However, individuals with non-celiac gluten sensitivity have more extraintestinal or non-GI symptoms, such as headache, brain fog, joint pain, and numbness in the legs, arms or fingers. Symptoms typically appear hours or days after gluten has been consumed.

Currently, there are no recommended methods to test for non-celiac gluten sensitivity. It is a diagnosis of exclusion, which means that other causes, including celiac disease and wheat allergy, need to be ruled out and the patient needs to feel better on the gluten-free diet. Some doctors offer saliva, blood or stool testing. However, these tests have not been validated and are therefore not accepted.

Experiencing the different dimensions of life can be interesting when all your senses are working correctly. But sometimes, one or more of your senses can go into overdrive, and you may develop extreme sensitivity to stimuli such as touch, light, sound, taste, smell, or temperature. This heightened sensitivity may even cause pain. If you experience this kind of extreme sensitivity, your doctor may diagnose you with hyperesthesia.

Light sensitivity is a common symptom of migraine (as is sensitivity to sounds or smells), but not everyone who has the disease will experience it. Identify other symptoms of migraine and find answers to Frequently Asked Questions to help you start the conversation about migraine with your primary care provider.

While migraine is a common disease that affects 39 million Americans, no two migraine experiences are the same. Symptoms can vary from light sensitivity and dizziness to food cravings or body chills. Explore these Frequently Asked Questions about migraine symptoms to see if you might be experiencing migraine.

A study in the American Journal of Dentistry reported that dentin hypersensitivity affects between 15% and 20% of the general population, increasing to 57% for those who have undergone a dental procedure.

Liu XX, Tenenbaum HC, Wilder RS, Quock R, Hewlett ER, Renn YF. Pathogenesis, diagnosis and management of dentin hypersensitivity: an evidence-based overview for dental practitioners. BMC Oral Health. 2020;20:220. doi:10.1186/s12903-020-01199-z

Ayad F, Ayad N, Vazquez J, Zhang YP, Mateo LR, Cummins D. Use of a toothpaste containing 8% arginine and calcium carbonate for immediate and lasting relief of dentin hypersensitivity: A simple and effective in-office procedure. Am J Dent. 2018;31(3):135-140.

The American Academy of Endodontists (AAE) describes tooth sensitivity as a brief sensation caused by a stimulus, such as heat or cold, to exposed dentin, the layer beneath the hard, white enamel of the teeth. When dentin loses its protective covering, the nerves within the teeth lose their buffer.

With so many possible causes, working with your dentist to address sensitive teeth is essential, both to find the cause and create a treatment plan. Possible solutions include an over-the-counter or prescription desensitizing toothpaste or a fluoride treatment, among other office procedures, according to the ADA.

My mouse sensitivity is very high in all menus, but is completely normal in game. I've reinstalled Skyrim 2 times, deleted all my mods, done everything I've found online but nothing has worked. Any help would be very appreciated.

Such findings, and the lack of uniform biologic explanations for the disorder, have led some to conclude that all MCS cases are likely psychogenic. Regardless, it remains a matter of debate as to whether the psychological symptoms are a causative factor or a consequence of the disorder. Labarge and McCaffrey [16] have suggested that, in most cases, a previous history of mental disease (e.g., anxiety, depression, mood disorders) exists prior the diagnosis of MCS (see also [124,135,136,137]). In contrast, others have suggested that the environmental sensitivity pathology is more likely the cause of the psychological disturbances, predating the psychological symptoms [2,18,138,139]. Such symptoms strongly impact the whole life of MCS patients, including their social relationships, personal concerns, jobs, and quality of life [140,141].

Immunogenic dysregulation has also been observed following cytokine release due to exposure to xenobiotics [198,199]. Jalava et al. [200] found that fine particulate matter in urban air are triggers for inflammatory and cytotoxic effects. Moreover, Belpomme, Campagnac and Irigaray [201] observed that MCS and Electro-Hypersensitivity (EHS) patients exhibited higher levels of histamine, inflammatory processes affecting thalamus and limbic system, and oxidative stress compared to controls (for a consensus report on specific markers in electrohypersensitivity, see [202]). The authors considered these as reliable and objective etiopathogenic biomarkers for diagnosis, suggesting a common pathological mechanism in the two disorders [see De Luca et al. [34] for an interesting review on dependable biological markers of MCS and Hoover at al. [203] regarding the relationship between reliability of some immunological tests and MCS].

Perhaps the best evidence for a role of NO and PN as underlying biochemical mechanisms of MCS comes from a series of studies of Pall. According to Pall [209,210,211,212,213], hypersensitivity reported by MCS patients is likely due to a cascade of biochemical factors, which begins with an increase in N-methyl-d-aspartate (NMDA) receptor activation (e.g., due to organic solvents) which, in turn, give rise to an increase in NO and the oxidative product of PN (ONOO). Notably, environmental stressors that stimulate NMDA receptors also act on limbic kindling/neural sensitization and/or neurogenic inflammation processes. These provoke, as a final step, progressive extreme sensitivity to organic solvents and increased blood barrier permeability which increase the access of chemicals to the CNS and decrease natural detoxification processes.

The QEESI is comprised of five sections, each of which contains 10 questions. The sections are: Chemical Exposures, Other Exposures, Symptoms, Masking Index, and Impact of Sensitivities. With the exception of the Masking Index, which requires yes or no answers, each section asks the subject to rate the degree to which they experience functional disability. In the case of Chemical Exposures, this relates to a series of different chemicals, whereas Other Exposures relates to exposures to various foods, drugs, fabrics, etc. Symptoms relates to various body parts, e.g., muscles, joints, stomach, heart, as well as mood and other psychological factors, whereas Impact of Sensitivities addresses how the symptoms influence everyday life (e.g., social relationships, travel, choice of clothing, use of personal care products). The Masking Index poses questions about personal habits, such as smoking, drinking, use of caffeinated beverages, exposures to chemicals in the home or workplace, etc. Separate scores are determined for each of the five QEESI sections, with normative data implying low, medium, and high chemical sensitivities. ff782bc1db

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