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)

A 40-year-old man who was resected ascending colon and terminal ileum (10 cm) in Aug. 1978, with the diagnosis of Crohn's disease, was admitted to our hospital with general fatigue, paresthesia and tremor in May. 1984. A peripheral blood examination on admission revealed Hb 10.1 g/dl, RBC 234 X 10(4)/mm3, MCV 131.4 fl, MCH 43.2 pg. A bone marrow specimen showed marked erythroid hyperplasia (W/E 1.44) with megaloblastic change. While serum folate level was normal, serum vitamin B12 value was low and Schilling test showed vitamin B12 malabsorption. Roentgenologic and endoscopic examinations revealed diffuse cobblestone appearances in small intestine (from anastomosis part to duodenal bulb). These examinations suggested vitamin B12 malabsorption with diffuse Crohn's disease caused megaloblastic anemia. The patient had been treated with vitamin B12 1,000 micrograms/day injection and, in Sep. 1984, he recovered from megaloblastic anemia (Hb 13.4 g/dl, RBC 440 X 10(4)/mm3, MCV 90.7 fl, MCH 30.4 pg).
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PMID:[Megaloblastic anemia associated with diffuse intestinal Crohn's disease]. 271 98

Clinical, hematologic and hemoglobin composition data on the first case of Hb 0-Arab in association with beta 0-thalassemia in Yugoslavia are reported here. The propositus was a 26-years-old female from Strumica who was admitted to the hospital for several times because of anemia, hepatosplenomegaly, occasional abdominal pains, malaise and fatigue. Laboratory results presented: Hb 10.0 g/dl, RBC 3.84.10(12)/L, PCV 0.260 l/l, MCV 68 fl, MCH 26 pg, reticulocyte count 1.8%, anisopoikilocytosis, polychromasis, numerous target cells, total bilirubin 2.1 mg/dl, (indirect 1.7 mg/dl), serum-Fe 32.3 microM/L. A starch gel electrophoresis of hemolysate provided evidence for the presence of abnormal hemoglobin (approximately 85%) and Hb F (approximately 15%); the Hb A was absent. Familial screening showed her father was heterozygous for the abnormal hemoglobin, whereas the mother was heterozygous for beta-thalassemia. In vitro biosynthesis disclosed a total absence of beta globin and reduced synthesis of beta x x and gamma globin. The alpha/beta x + gamma-globin ratio was 1.77 (normal, 1.0 + 0.1). Amino acid analysis revealed that lysine substituted for glutamic acid at the position one hundred twenty-one of the beta chain (= Hb 0-Arab or beta 121 Glu----Lys).
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PMID:[Hemoglobin O Arab in interaction with beta 0-thalassemia]. 273 98

Brown adipose tissue-deficient [uncoupling protein (UCP)-promoter-driven diphtheria toxin A (DTA)] mice develop obesity as a result of both decreased energy expenditure and hyperphagia. The hyperphagia occurs despite high serum leptin levels. Hence, this is a model of leptin-resistant obesity in which the mechanism driving hyperphagia is unknown. Leptin is a regulator of a number of hypothalamic neuropeptides involved in energy homeostasis. In ob/ob mice, leptin deficiency results in increased expression of neuropeptide Y (NPY), agouti-related protein (AGRP), and melanin-concentrating hormone (MCH), and decreased expression of POMC. We have previously shown that NPY is reduced in the UCP-DTA mouse, suggesting a normal NPY response to leptin. To define other potential sites of leptin resistance, we used in situ hybridization to evaluate the expression of messenger RNAs (mRNAs) encoding a number of peptides, including NPY, AGRP, MCH, and POMC. We confirmed that the decrease in NPY expression previously detected by Northern blots reflects a decrease in NPY expression in the arcuate nucleus. AGRP mRNA was also decreased, whereas POMC mRNA levels in the arcuate nucleus were the same as control. MCH mRNA levels in the lateral hypothalamic area were also decreased. In contrast, there was induction of NPY expression in the dorsomedial hypothalamic nucleus in the UCP-DTA animals but not in the controls. The results indicate that these neuropeptides generally respond to leptin and that the hyperphagia seen in the UCP-DTA mice is likely the result of dysregulated expression of other, as yet unexamined, hypothalamic peptides, or lies at sites distal to the hypothalamus.
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PMID:Characterization of expression of hypothalamic appetite-regulating peptides in obese hyperleptinemic brown adipose tissue-deficient (uncoupling protein-promoter-driven diphtheria toxin A) mice. 979 75

The neural circuitry that mediates mood under normal and abnormal conditions remains incompletely understood. Most attention in the field has focused on hippocampal and frontal cortical regions for their role in depression and antidepressant action. While these regions no doubt play important roles in these phenomena, there is compelling evidence that other brain regions are also involved. Here we focus on the potential role of the nucleus accumbens (NAc; ventral striatum) and its dopaminergic input from the ventral tegmental area (VTA), which form the mesolimbic dopamine system, in depression. The mesolimbic dopamine system is most often associated with the rewarding effects of food, sex, and drugs of abuse. Given the prominence of anhedonia, reduced motivation, and decreased energy level in most individuals with depression, we propose that the NAc and VTA contribute importantly to the pathophysiology and symptomatology of depression and may even be involved in its etiology. We review recent studies showing that manipulations of key proteins (e.g. CREB, dynorphin, BDNF, MCH, or Clock) within the VTA-NAc circuit of rodents produce unique behavioral phenotypes, some of which are directly relevant to depression. Studies of these and other proteins in the mesolimbic dopamine system have established novel approaches to modeling key symptoms of depression in animals, and could enable the development of antidepressant medications with fundamentally new mechanisms of action.
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PMID:The mesolimbic dopamine reward circuit in depression. 1656 99

Ovariectomy (OVX) leads to hyperphagia and weight gain in rats, which can be prevented by estradiol (E2) replacement; however, the role of endogenous E2 on feeding and energy homeostasis in female mice has not been well characterized. The primary goal of this study was to assess the relative contribution of increased energy intake and decreased energy expenditure to OVX-induced weight gain in female rats and mice. OVX led to hyperphagia in rats, but did not produce daily, nor cumulative, hyperphagia in mice. OVX decreased mass-specific metabolic rate in mice, but not in rats. OVX decreased home cage locomotor activity in both species. Pair-feeding attenuated OVX-induced weight gain in rats and produced both short- and long-term changes in expression of key hypothalamic genes involved in food intake and energy homeostasis, i.e., the anorexigenic neuropeptide pro-opiomelanocortin (POMC) and the orexigenic neuropeptides: melanin-concentrating hormone (MCH) and agouti-related peptide (AgRP). No differences in hypothalamic gene expression were observed between OVX'd and sham mice. The results suggest that OVX-induced weight gain is mediated by hyperphagia and reduced locomotor activity in rats, but that in mice, it is primarily mediated by reduced locomotor activity and metabolic rate.
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PMID:Female mice and rats exhibit species-specific metabolic and behavioral responses to ovariectomy. 2006 98

A 39-year-old woman was admitted to our hospital with an eight-month history of dyspnea on exertion, weakness and increasing fatigue. She reported repeated episodes of menometrorrhagia and underwent a myomectomy. She is not a vegetarian. Her menstrual bleeding: 3-5 days per month. Two months ago, she complained of burning sensation of the tongue upon swallowing food and noted brittle nails. She tolerated soft foods. On physical examination, she was pale; her nails were very thin, fragile and somewhat concave. Her oral examination showed angular stomatitis, depapillated tongue and glossitis. The clinical diagnosis was anemia and dysphagia. Laboratory tests were: Hb: 7.0g/dL, MCV: 57.42fL, MCH: 15.82 pg; leukocytes: 4,980; reticulocytes: 2.18%, reticulocyte index: 0.1%, serum iron: 21ug/dl, total iron binding capacity (TIBC): 286, transferrin saturation: 7% and serum ferritin: 27ng/ml. The peripheral blood smear showed anisocytosis and hypochromic microcytic cells. Thevenon test was negative. Abdominal ultrasound: uterine myoma. A barium swallow X-ray showed a 2-mm linear filling defect between the 4th and 5th cervical vertebrae in the anteroposterior and lateral view; it protruded from the anterior wall and reduced esophageal lumen by 60%. In the endoscopy, we found a fibrous web in the cricopharyngeal area. Serial dilatations were performed over a guidewire using Savary-Gilliard dilators with diameter up to 14 mm, improving dysphagia. She was treated with transfusional therapy and parenteral iron. She was discharged with ferrous sulfate and folic acid. The Plummer-Vinson syndrome, Paterson-Brown-Kelly or sideropenic dysphagia is characterized by dysphagia, irondeficiency anemia and upper esophageal web. The syndrome is described as very rare.
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PMID:[Plummer-Vinson syndrome: report of a case and review of literature]. 2302 85

The common nutritional deficiency, iron deficiency, causes Iron Deficiency Anemia (IDA) throughout the world especially in the developing countries. In Ayurveda, different herbal, mineral or herbomineral drugs have been emphasized to combat anemia (Panduroga). Trikatrayadi Lauha and Fersolate-CM (a modern medicine taken as standard control) were administered to the patients to evaluate their role in Panduroga. A simple random sampling method was followed for the clinical study. The 56 iron deficiency anemic patients of both sexes and age group between 16 to 70 years divided into two groups - Group-A (n=34) and Group-C (n=22) were treated with Trikatrayadi lauha and Fersolate-CM, respectively. Both drugs provided significant effect on the signs and symptoms of Shrama (fatigue), Shwasa (dyspnea on exertion), Daurbalya (weakness), Pandu Varna (pallor/yellowish-whitish), Hridspandana (palpitation), Hatanala (diminished digestive capacity), Bhrama (giddiness), Aruchi (anorexia), Arohana Ayasa (exhaustion during climbing), Shiroruja (headache) and Shotha (edema). Trikatrayadi Lauha provided significant results on Hb gm%, RBC, PCV, MCV, serum iron, percent transferrin saturation and TIBC where as insignificant changes were found in MCH and MCHC. Fersolate-CM provided significant results on Hb gm%, RBC, PCV, MCV, MCH, serum iron, percent transferrin saturation and TIBC whereas insignificant change was found in MCHC. Trikatrayadi Lauha showed significant results on Panduroga and Iron Deficiency Anaemia (IDA).
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PMID:Efficacy of Trikatrayadi Lauha in Panduroga with reference to Iron Deficiency Anemia. 2304 86