Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seasonal Affective Disorder (SAD) has received formal research attention only within the last eight years. Diagnostic criteria for SAD include many characteristics typical of depression: sadness, low self-esteem, lack of energy, social withdrawal, and suicide ideation, and features of atypical depression: carbohydrate craving, overeating, weight gain, and hypersomnia. Differential diagnosis of the disorder depends on an onset in fall/winter and remission in spring/summer. It was hypothesized that spinal cord injury (SCI) patients would have a higher incidence of the disorder in the northern latitudes because of decreased outdoor activities in winter and because of such light-depriving winter survival tactics as installing opaque plastic for storm windows. SCI patient responded to a postal survey which included Rosenthal's Seasonal Pattern Assessment Questionnaire (SPAQ) and the Beck Depression Inventory (BDI). Results showed a substantially higher rate of SAD among SCI patients than in the normative sample.
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PMID:Seasonal affective disorder in a spinal cord injury population. 158 5

Seasonal changes in behavior und physiology have been recognized in humans since ancient times. Their relevance to psychiatry was described in further detail at least as early as in the middle of the last century. However, it was only in the past six years that clinical studies were undertaken systematically to describe the profile of a syndrome that was called seasonal affective disorder (SAD) by Rosenthal et al. It emerged, that this condition is characterized by changes in affect with depressed mood, anxiety and irritability and decreased energy. In contrast to major affective disorder these patients exhibit increased appetite with carbohydrate craving, weight gain and an increased duration of sleep. Seasonality of mood and behavior appears to be a dimension affecting many different people including normal individuals and those with conditions other than SAD. In vulnerable individuals these changes may reach symptomatic levels whereas in normals they may be regarded as acceptable fluctuations.
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PMID:[Season-related forms of depression. I. Principles and clinical description of the syndrome]. 329 Jun 93

Seasonal changes in human behavior have been recognized since ancient times. Starting in 1980 systematic research has been carried out by Rosenthal et al. (1984), who described and characterized a psychopathological and clinical syndrome which is linked to fall/winter and shows remission in spring/summer and which was termed seasonal affective disorder (SAD). The symptomatology includes depressed mood, decreased energy, hypersomnia, increased appetite and subsequently weight gain and frequently carbohydrate craving. The efficacy of light therapy with bright, fluorescent, full-spectrum light has been widely demonstrated for treatment of fall/winter SAD. In addition, treatment with selective serotonin reuptake inhibitors appears to be successful in this condition.
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PMID:[Fall/winter depression and its therapy]. 781 Jan 51

Numerous investigators have shown a strong association between the seasons and the incidence of depression, mania and suicides. However, little has been known about patients who reveal affective episodes in association with the changing seasons year after year. Lewy and Rosenthal established the concept of Seasonal Affective Disorder (SAD). SAD is characterized by recurring cycles of fall-winter depression and spring-summer hypomania (or euthymia). Depressive symptoms often include hypersomnia, anergia, fatigue, carbohydrate craving and weight gain. The syndrome occurs predominantly in women and begins in late twenties. Lewy, Rosenthal and other investigators found that exposure of the SAD patients to bright artificial light improved depressive symptoms. Some hypotheses of light therapy are proposed, however, each of them has not well explained the mechanisms.
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PMID:[Light therapy of patients with seasonal affective disorder]. 800 95

Seasonal affective disorder (SAD) is a condition characterized by annually occurring major depressive episodes which was described by Rosenthal et al. in 1984. It occurs most commonly in women and the onset usually being in early adulthood. These episodes are regularly occurring in fall and winter with full remission during the following spring and summer. The patient's mood is a combination of depression and mild anxiety accompanied by fatigue, loss of libido, and a profound reduction of socialisation. During winter depression, most of these patients complain of atypical vegetative symptoms accompanied by hypersomnia, hyperphagia, carbohydrate craving, and weight gain. Hypotheses on the underlying mechanisms of these behavioral and neurovegetative disorders indicate that environmental variables, e.g., climate, latitude, light, and changes in neurotransmitter fraction that naturally occur with the seasons may be important. Phototherapy is being increasingly used for the treatment of seasonal affective disorder. The antidepressant effect of light therapy in the treatment of SAD has been widely shown. The response in patients with SAD is contingent on the exposure of the patients' eyes to light. Further important factors are the duration of daily treatment and light intensity. However, the role of timing of phototherapy remains controversial. The biological basis of the diverse psychological and biological changes in SAD and the underlying mechanisms of action of phototherapy are still unclear and require further study.
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PMID:[Seasonal depression]. 945 88

A 16-year-old male presented to an emergency room after falling on his head while inebriated. The patient had only a history of recent fatigue and demonstrated no focal neurological deficit. MRI revealed a cystic and solid, enhancing midline cerebellar lesion. A suboccipital craniotomy was performed. Histologically, the mass showed large bizarre cells arranged in sheets with admixed small lymphocytes. The pleomorphic population had ample glassy eosinophilic cytoplasm and intranuclear inclusions. An infiltrating component resembling diffuse astrocytoma could be found in areas. Rosenthal fibers were particularly abundant in the areas of infiltrating glioma. Mitotic activity was very low, and necrosis was absent. Reticulin fibers between individual cells were focally abundant. Glial fibrillary acidic protein and vimentin were strongly expressed in many cells, while synaptophysin and neurofilament protein were not. Ki-67 showed a very low proliferation index. The pathologic diagnosis was pleomorphic xanthoastrocytoma (PXA) of the cerebellum. PXA is a diagnosis typically regarded as a superficial meningocerebral neoplasm. This case is one of sixteen cerebellar PXAs reported in the literature.
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PMID:A 16-year-old male with a cerebellar mass. 1907 85

Glucocorticoids such as dexamethasone are widely used as comedication in the treatment of head and neck cancer, e.g., to improve appetite and decrease weight loss and fatigue in patients with advanced disease or as antiallergic and antiemetic prophylaxis during anti-EGFR therapy. However, the literature suggests that dexamethasone induces resistance to antineoplastic agents in many solid tumor models in vitro and in vivo. Since this phenomenon has never been investigated in head and neck cancer, the present study was conducted to investigate the effect of dexamethasone on the antiproliferative activity of cetuximab in vitro in squamous cell carcinoma of the head and neck (SCCHN) cell lines. The antiproliferative effect of the anti-EGFR agent cetuximab alone and in combination with increasing concentrations of dexamethasone was examined in eight SCCHN cell lines at three different time-points (24, 48 and 72 h). Cell growth inhibition and viability were measured quantitatively using WST and LDH assays. Absolute tumor cell numbers were determined by cell counting in a Rosenthal chamber. Cetuximab alone inhibited the growth of all eight SCCHN cell lines significantly (p=0.008). In some cases the addition of dexamethasone reduced the antiproliferative activity of cetuximab (p<or=0.038) but remained significant in all of the eight SCCHN cell lines compared with untreated controls (p<or=0.028) at each drug concentration and each time-point. In contrast to the results reported for other tumor models, in our study dexamethasone showed in the majority of the evaluated dexamethasone drug concentrations and time-points no inhibition of the cytotoxic activity of cetuximab. The reasons for these discrepant findings are unclear but may be related to the degree of tumor cell differentiation or proliferation rate. Thus, further studies are required to elucidate the molecular mechanisms underlying the interaction between dexamethasone and cetuximab in different tumors.
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PMID:Does dexamethasone inhibit anticancer activity of cetuximab in squamous cell carcinoma cell lines of the head and neck? 1951 20