Publications by authors named "Jonathan Toot"

Objective: To determine headache diagnosis and treatment patterns in the outpatient setting, focusing on documentation of the International Classification of Headache Disorders (ICHD) criteria.

Design, Setting, And Participants: Retrospective cohort data were collected from electronic medical records of adults aged 18-35 who presented to resident-staffed family medicine outpatient clinics in the Midwest, USA, for a new or worsening headache between 2015 and 2016. Diagnosis codes were used to summarize the overall nature and prevalence of headaches.

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The immune system of the rat undergoes substantial functional and morphological development during the postnatal period. Some aspects of this development are genetically predetermined, while other aspects depend on environmental influences. Detailed information on postnatal development is important in the interpretation of histopathologic findings in juvenile toxicology and pubertal assay studies, as well as other studies conducted in juvenile rats.

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The etiology of preeclampsia remains unknown. However, a contributing factor to this hypertensive disease of pregnancy is a reduction in uterine perfusion pressure resulting in placental ischemia. Uterine arteries may be a major regulator of this process through changes in vascular reactivity and localized blood flow.

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The SHR Y chromosome has loci which are involved with behavioral, endocrine and brain phenotypes and respond to acute stress to a different degree than that of the WKY Y chromosome. The objectives were to determine if WKY males with an SHR Y chromosome (SHR/y) when compared to males with a WKY Y chromosome would have: 1. a greater increase in systolic and diastolic blood pressures (BP), heart rate (HR), and locomotor activity when placed in an open field environment and during an acute stress procedure; 2.

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Background: Testosterone (T) and the sympathetic nervous system each contribute to the pathology of hypertension. Altered blood vessel reactivity is also associated with the pathology of high blood pressure. The purpose of this study was to examine the effects of T manipulation in the regulation of resistance-sized blood vessel reactivity.

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Background: Testosterone (T) and the androgen receptor (AR) are involved in mechanisms associated with hypertension and vessel reactivity.

Objective: To investigate T and the AR on blood vessel reactivity, testicular feminized male (TFM; AR deficient males) and normal androgen receptor (NAR) male rats were used. Therefore, if the functional AR is necessary for plasma T to regulate vessel responsiveness, TFM males will exhibit altered vessel function compared to NAR males.

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Androgens interact with catecholamines in the central nervous system (CNS) to regulate many physiological processes including blood pressure (BP). To test the hypothesis that testosterone (T) and 5a-dihydrotestosterone (DHT) modulate CNS catecholamines and BP through androgen receptor (AR)-dependent and independent mechanisms, we used the testicular feminized male (Tfm) rat. Females that carry the AR mutation (Tfm mutation) on the X chromosome were bred with spontaneously hypertensive rat (SHR) males.

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Increased sympathetic nervous system (SNS) activity, testosterone, and spontaneously hypertensive rat Y chromosome (SHR Yc) play a role in a genetic model of hypertension. Male rats with the SHR Yc and Wistar-Kyoto (WKY) autosomes (denoted SHR/y) exhibit these characteristics when compared to rats with the WKY Yc and WKY autosomes (denoted WKY). We hypothesized that chronic social stress will increase blood pressure and SNS activity more in SHR/y males compared to WKY males, resulting in increased myogenic reactivity along with decreased vasoconstriction of small mesenteric arteries.

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Background: The Y-chromosome (Yc) and testosterone (T) increase blood pressure and may also influence renal electrolyte excretion. Therefore, the goal of this study was to determine if the Yc combined with T manipulation could influence renal Na and K excretion.

Methods: To investigate the role of the Yc and T, consomic borderline hypertensive (SHR/y) and normotensive Wistar-Kyoto (WKY) rat strains were used (15 weeks) in three T treatment groups: castrate, castrate with T implant and gonadally intact males.

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Background: We have developed a rat cell model for studying collagen type I production in coronary artery adventitial fibroblasts. Increased deposition of adventitial collagen type I leads to stiffening of the blood vessel, increased blood pressure, arteriosclerosis and coronary heart disease. Although the source and mechanism of collagen deposition is yet unknown, the adventitia appears to play a significant role.

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The Spontaneously Hypertensive Rat (SHR) model was used to test the hypothesis that a locus on the SHR Y-chromosome is responsible for increased aggression resulting from increased serum testosterone and decreased amygdala serotonin content compared to the WKY Y-chromosome. To examine the Y-chromosome in SHR and WKY males, consomic Y-chromosome strains were used (WKY.SHR-Y and SHR.

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