Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0262471 (ENT)
5,307 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Doppler ultrasound examination is an easy and non-invasive examination technique to image the anatomical and functional situation of cervical vessels. An increasing number of ENT-specialists has been using Doppler sonography in the diagnosis of cochlear and vestibular disorders. We analysed the frequency of pathological Doppler examination results of 150 patients with vertigo, hearing loss and tinnitus. Especially patients with vertigo bear a greater risk for stenosis of the extracranial arteries (28%) compared to an asymptomatical population (1%). Patients with hearing loss and tinnitus showed a different degree of artery disorders (23% of the patients with hearing loss; 18% of the patients with tinnitus). Patients bearing no risk for atherosclerosis showed in 13% (vertigo) and 8% (hearing loss and tinnitus) stenosis of the cervical arteries. Thus we found by Doppler ultrasound examination more stenoses in patients with cochlear or vestibular symptoms than in an asymptomatical population. The early attribution of stenosis to a malfunction of the inner ear helps to avoid invasive examinations of cervical vessels. In addition to this, imminent cerebral ischaemia can be revealed at an early stage.
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PMID:[Incidence of Doppler ultrasound detectable stenoses of cervical arteries in patients with cochlear-vestibular symptoms]. 826 28

Tinnitus is a frequent symptom but a tinnitus that is rhythmic and synchronous with the patient's heartbeat is rare. The symptom "pulsating noise in the ear" may be due to various cause but most frequently, by glomus tumors, intracranial hypertension and atherosclerosis of the carotid arteries. Pulsatile tinnitus can often present a serious diagnostic problem. The diagnostic evaluation includes physical examination, audiologic assessment and imaging techniques (ultrasonic examination of cervical vessels, high-resolution computed tomography of the temporal bones, nuclear magnetic resonance, angiography of the carotid arteries and magnetic resonance angiography). Evaluation should be individualized but must include a thorough ENT work up. The evaluation of the patient includes otomicroscopy, palpation and auscultation of ears and cervical region and the head positioning test. The cause of pulsatile tinnitus may be even identified on otoscopic examination. Further investigations by other specialities (neurology, internal medicine, ophthalmology) may become necessary. Life-threatening causes such as arteriovenous shunts or carotid artery stenosis must be ruled out. Nevertheless, in several cases it will not be possible to determine the etiology of tinnitus. Finally, therapeutic options which occasionally can include surgical techniques or interventional radiology are discussed.
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PMID:[Pulsating tinnitus]. 1070 57

The etiology of the atherosclerosis that occurs in diabetes mellitus is unclear. Adenosine has been shown to inhibit growth of rat aortic smooth muscle cells. Nucleoside transporters play an integral role in adenosine function by regulating adenosine levels in the vicinity of adenosine receptors. Therefore, we studied the effect of 25 mM d-glucose, which mimics hyperglycemia of diabetes, on adenosine transport in cultured human aortic smooth muscle cells (HASMCs). Although RT-PCR demonstrated the presence of equilibrative nucleoside transporter-1 (ENT-1) and ENT-2 mRNA, functional studies revealed that adenosine transport in HASMCs was predominantly mediated by ENT-1 and inhibited by nitrobenzylmercaptopurine riboside (NBMPR, IC(50) = 0.69 +/- 0.05 nM). Adenosine transport in HASMCs was increased by >30% after treatment for 48 h with 25 mM d-glucose, but not with equimolar d-mannitol and l-glucose. Kinetic studies showed that d-glucose increased V(max) of adenosine transport without affecting K(m). Similarly, d-glucose increased B(max) of high-affinity [(3)H]NBMPR binding, while the dissociation constant (K(d)) was not changed. Consistent with these observations, 25 mM d-glucose increased mRNA and protein expression of ENT-1. Treatment of serum-starved cells with the selective inhibitors of MAPK/ERK, PD-98059 (40 microM) and U-0126 (10 microM), abolished the effect of d-glucose on ENT-1. We conclude that d-glucose upregulates the protein and message expression and functional activity of ENT-1 in HASMCs, possibly via MAPK/ERK-dependent pathways. Pathologically, the increase in ENT-1 activity in diabetes may affect the availability of adenosine in the vicinity of adenosine receptors and, thus, alter vascular functions in diabetes.
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PMID:D-Glucose upregulates adenosine transport in cultured human aortic smooth muscle cells. 1569 55

A 49-year old employee of a drug store with neck pain, painful thyroid gland, and elevated erythrocyte sedimentation rate (38 mm/h) was diagnosed as subacute thyreoiditis (de Quervain). However, application of oral corticosteroids (prednisone 50 mg/d) during three days did not reduce pain as expected. Therefore, the patient was admitted for further evaluation. Clinical examination showed a female in a pain-relieving posture (forward neck flexion). Further examinations including ultrasound of the thyroid, computertomography of the neck, and ENT examination did not reveal etiology of the pain. Finally, electrocardiography showed subacute infero-posterior myocardial infarction, and coronary angiography revealed severe coronary two vessel disease. Tabacco smoking since the age of fourteen (35 pack years) was identified as the only major risk factor for premature atherosclerosis. Diagnosis of subacute thyreoiditis is made from clinical and laboratory findings. Treatment with nonsteroidal antiinflammatory drugs or corticosteroids usually relieves pain within two or three days. Otherwise, etiology of the disease must be re-evaluated considering any disease localized in neck or thorax region. Antiinflammatory treatment of subacute thyreoiditis has to be continued for weeks or months.
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PMID:["Subacute thyreoiditis" without response on corticosteroid therapy]. 1594 Sep 11