Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Advantages of CAPD in diabetic uremic patients may offer better control of visual and neurological disease. There remain some undesired side effects, i.e: obesity, blood lipid imbalance and loss of appetite due to glucose absorption. In February 1988 four diabetic uremic CAPD patients (2 males and 2 females with an average age of 62.25 +/- 11.32, range 52-76) began treatment substituting one of the usual glucose exchanges with 1% aminoacid solution. Treatment time averaged 52 months (range 9-17). Each month the patients were examined clinically and via blood chemistries. Every 3 months clearances, residual renal function, ocular fundus and motor nerve conductance velocity were measured. Plasma nitrogen increased, while triglycerides, cholesterol and total protein remained unchanged; bicarbonate decreased causing slight acidosis. There were no significant variations of either clearances or ultrafiltration and the quantity of insulin administered decreased. Results confirm that a 1% aminoacid solution can be used as an osmotic agent in peritoneal dialysis to prevent some of the complications such as blood lipid imbalance. The slight acidosis can be corrected by increasing the buffer content of the bag.
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PMID:CAPD in diabetics: use of aminoacids. 198 40

Central sleep apnea is a disorder characterized by apneic episodes during sleep with no associated ventilatory effort. More commonly than not these apneas are seen in patients who also have obstructive and mixed events. Although patients with this disorder frequently complain of insomnia and depression, frank hypersomnolence is rarely encountered. As these complaints are common ones seen in numerous clinical situations, and since sleep studies are rarely conducted to investigate their etiology, the true incidence of central sleep apnea has not been determined. The etiology of central apnea remains unknown, although the association between these breathing events and a number of other disease processes has increased our understanding of the disorder. Central apneas during sleep commonly occur after hyperventilation with the associated hypocapnic alkalosis. This occurs at high altitude when hyperventilation is induced by hypoxia and at sea level when spontaneous nocturnal hyperventilation occurs. This suggests that PCO2 is the primary stimulus to ventilation during sleep and that loss of this drive, as occurs with hypocapnia, may produce dysrhythmic breathing. Patients with complete absence of ventilatory chemosensitivity such as occurs with Ondine's curse (central alveolar hypoventilation) or the obesity-hypoventilation syndrome may also have central apneas. For reasons that remain unexplained, central sleep apnea is commonly seen in patients with congestive heart failure, nasal obstruction, and certain neurologic disorders. However, in most patients with central sleep apnea no obvious cause or association can be found. The treatment of this disorder is not entirely satisfactory. If it is severe, mechanical ventilation during sleep can be provided by any one of a number of techniques. However, for the patient who simply complains of insomnia and is found to have a moderate number of central apneas, the treatment choices are limited. Acetazolamide has been shown to decrease central apneas during short-term use, but results have been variable with prolonged administration. Other ventilatory stimulants seem to have little efficacy. Interestingly, oxygen administration has been shown to reduce central apneas considerably in a number of studies, although the explanation for its success is unknown. Central sleep apnea therefore remains a relatively rare disorder whose etiology is not fully understood and whose treatment is not completely satisfactory.
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PMID:Central sleep apnea. 393 82

Uterine procidentia and pelvic-floor hernia are quite common among postmenopausal multiparous Caucasian women. Predisposing factors are age, obesity, childbirth trauma, neurologic disorders, and musculo-fascia weaknesses. Hysterectomy and pelvic floor repair constitute the definitive therapy for pelvic floor hernia and uterine prolapse, but vaginal pessaries made of rubber or plastic can also be of therapeutic value. Pessaries also facilitate preoperative healing of the vaginal or cervical ulcerations which are quite common in longstanding cases of uterine procidentia (third degree prolapse). Common complications of pessary use are vaginal irritation, allergic reactions, leukorrhea and bleeding. Hard pessaries have fewer associated complications. Proper fitting and continued post insertion care are necessary. Unless contraindicated, acid douches and or creams and estrogenic creams should be used with the pessaries. Pessaries should be removed every 6 weeks for cleansing; otherwise, ulceration, superimposed infections, and fistulas could develop. In cases of incarcerated pessaries, the use of estrogenic creams (which improve the condition of the vagina) will easily help remove the pessaries. 3 case reports are briefly discussed to illustrate the management of incarcerated pessaries in elderly women. The patients reported in these cases did not have follow-up care after insertion of the pessary, thus requiring intervention years later. Patients with bleeding problems despite normal cytologic findings should undergo fractional curettage later to rule out malignancy. Although incarcerated pessaries rarely occur, application of estrogenic creams will easily remove them.
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PMID:Management of incarcerated vaginal pessaries. 724 Jun 22

Natural BD is a nonpurulent acute/subacute encephalitis of horses and sheep with a propensity to involve the olfactory and limbic systems, and the brain stem. The inflammation is concentrated primarily in the gray matter, but subcortical white matter may also be affected. Experimental BD can be produced in a series of animals from birds to primates. The neuropathology after experimental infection is similar to that in natural disease but the inflammatory changes are more diffuse. In the rat and mouse, a persistent/tolerant infection can also be induced, in which inflammatory changes are conspicuously absent. In the course of persistent infection of the rat, an elective, focal degeneration ensues that involves the dentate gyrus, retina, and, less frequently, the magnocellular part of the hippocampus. The cytopathic destruction of the dentate gyrus is the likely anatomical substrate of learning deficiencies and behavioral changes, prominent features of chronic infection. Later in infection, more diffuse and random degeneration of neurons can be found. In all species infected, viral antigens are produced in excess and fill all neuronal processes. Beside neurons, glial cells are infected as well. The agent spreads in the nervous system axonally and transsynaptically (transneuronally). The type of neurotransmitter receptors in the synapse and their interaction with viral proteins may modulate the spread of infection (Gosztonyi et al. 1994). Virus particles have not been visualized in the brain in any phase of the disease. During persistent infection of the rat, production of viral proteins has a phasic character. Some rats survive acute infection and develop an obesity syndrome. The anatomical basis of this syndrome is not fully clarified; inflammatory destruction of the infundibular region, vacuolar degeneration of the paraventricular nucleus of the hypothalamus and severe, progressive involution of the hippocampal formation most probably play an important role in the production of this neuroendocrine syndrome. In the acute disease, inflammatory reaction can severely aggravate virus-induced cytopathology, but cannot be the sole cause of the neurological disease, since infection with high passage virus can lead to a similarly severe disease in the absence of inflammatory changes.
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PMID:Borna disease--neuropathology and pathogenesis. 778 50

Alexithymia is a concept created by Sifneos and characterized by an inability to find words to describe feelings or emotions. The phenomenon seems to be also related to a poverty of cognitive and symbolic processes (de Bonis, 1986). Alexithymia was first studied in psychosomatic disorders, then in several other somatic disorders as chronic bronchitis, chronic pain, obesity, abuse disorders. It also appears in non medically ill subjects. The french validation of the Toronto alexithymia Scale (TAS) in general population (n = 786) has shown 8.14% alexithymia frequency. The TAS is a 26-items self-report measure rated on a five-point likert scale. In the study we use the TAS and we refer to a visual test: the Parallel Visual Information Processing Test (PVIPT), involving the connexionist theory in the neuropsychological approach of alexithymia. The neuropsychological model is based on cerebral hemispheric specialization: emotions are localized in the right hemisphere and verbal expression depends on the left hemisphere in right-handed persons. The model posits that alexithymia is related to a lack of connection between the two cerebral hemispheres. It explains the deficit to verbally articulate emotions. The aim of our study is to compare the quality of cognitive and symbolic process (PVIPT) in alexithymic and non alexithymic subjects in general population. 773 students are tested with the TAS. We find 47 alexithymic subjects (6.08%). 22 alexithymic subjects and the control group (35 non alexithymic subjects) are evaluated with the PVIPT. Results are coherent with our previous studies on alexithymia in somatic disorders on one hand and alexithymia in neurological disease on the other hand. Theorical model, clinical observation and experimental results tend to define congruent hypothesis relative to the anxious pathology, supporting the reflexion and the research in the domain of the emotional disorders.
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PMID:[Parallel visual processing characteristics in healthy alexithymic subjects. Administration of the Toronto Alexithymia Scale and the parallel visual information test]. 868 78

A 32-year-old woman was hospitalized with recurrent left-sided chest pain and dyspnea on exertion, which had progressed for approximately 10 years. Since age 18 she had been spending more than twelve hours per day in a predominantly seated position on a floor mat, engaged in Japanese dressmaking. A chest roentgenogram showed marked dilation of the main pulmonary arteries, bilateral oligemia in the upper lung fields and a peripheral infiltration in the middle field of the left lung. The (99m)Tc-MAA perfusion lung scan showed multiple defects in both lungs, but no abnormal findings were detected on a 133Xe ventilation scan. A pulmonary angiogram showed multiple occlusions of pulmonary arteries in both lungs. Because recurrent chest pain and dyspnea had been present for a long time, and because ultrasonic cardiography revealed pulmonary hypertension repeatedly for several years, pulmonary thromboembolism was considered to be chronic and recurrent. The patient had none of the following risk factors for pulmonary emboli: malignancy, neurological disease, heart disease, obesity, pregnancy, or a congenital coagulative abnormality such as deficiency of AT-III, protein C, protein S, or plasminogen. Because no other cause could be found, the chronic recurrent pulmonary thromboembolism most likely resulted from extensive sedentary work that caused stagnation of venous return and deep vein thrombosis.
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PMID:[Chronic recurrent pulmonary thromboembolism associated with sedentary work]. 862 76

Diabetic complications constitute the principal clinical and economic burdens of diabetes. Available evidence indicates that sustained reduction in hyperglycemia (as measured by HbA1c) reduces the incidence of diabetic complications, including microvascular and neurological disease, and will likely reduce the risk of macrovascular disease. In the U.S., targeting interventions to aged and ethnic subpopulations, which are currently receiving suboptimal care, and increasing efforts to lower the average HbA1c concentrations one or two percentage points in people with diabetes would be a more cost-effective goal than aiming for a theoretical HbA1c threshold below which the risk of complications is negligible. Other risk factors for diabetic complications, such as obesity, hypertension, cigarette smoking, and hypercholesterolemia, must also be addressed to reduce the burden of diabetes.
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PMID:The burden of chronic hyperglycemia. 985 Apr 86

Viruses can induce progressive neurologic disorders associated with diverse pathological manifestations, and therefore, viral infection of the brain can impair differentiated neural functions, depending on the initial viral tropism. We have previously reported that canine distemper virus (CDV) targets certain mouse brain structures, including the hypothalamus, early and selectively. Infected mice exhibit acute encephalitis, with late disease, characterized by motor impairment or obesity syndrome, appearing in some of the surviving mice several months after the initial viral replication. In the present study, we show viral persistence in the hypothalami of obese mice, as demonstrated by low, but still significant, levels of CDV nucleoprotein transcripts, associated with a dramatic decrease in F gene mRNAs. Given the pivotal role of the hypothalamus in obesity (eating behavior, energy consumption, and neuroendocrine function) and that of leptin, the adipose tissue-derived satiety factor acting through hypothalamic receptors, we analyzed the leptin networks in both obese and nonobese mice. The discrepancy found between the chronic and dramatic increase in blood leptin levels and the occurrence of obesity may be due to leptin resistance in the brain. In fact, expression of the long leptin receptor isoform, representing the functional leptin receptor, was specifically downregulated in the hypothalami of obese mice, explaining their inability to generate an adequate response to leptin in the brain. Intriguingly, during the acute phase of infection, its expression was increased in CDV-targeted structures in all infected mice and remained high in obese mice in all CDV-targeted structures, except for the hypothalamus. The biphasic change in hypothalamic leptin receptor expression seen during the progression of CDV-induced obesity provides a new paradigm for understanding mechanisms of neuroendocrinological, virus-induced abnormalities.
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PMID:Alteration of the leptin network in late morbid obesity induced in mice by brain infection with canine distemper virus. 1043 20

Stearoyl-CoA desaturase (SCD) (EC 1.14.99.5) is an endoplasmic reticulum-bound enzyme that catalyzes the delta9-cis desaturation of saturated fatty acyl-CoAs, the preferred substrates being palmitoyl- and stearoyl-CoA, which are converted to palmitoleoyl- and oleoyl-CoA, respectively. These monounsaturated fatty acids are used as substrates for the synthesis of triglycerides, wax esters, cholesteryl esters and membrane phospholipids. The saturated to monounsaturated fatty acid ratio affects membrane phospholipid composition and alteration in this ratio has been implicated in a variety of disease states including cardiovascular disease, obesity, diabetes, neurological disease, skin disorders and cancer. Thus, the expression of SCD is of physiological importance in normal and disease states. Several mammalian SCD genes have been cloned. A single human, three mouse and two rat are the best characterized SCD genes. The physiological role of each SCD isoform and the reason for having three or more SCD gene isoforms in the rodent genome are currently unknown. A clue as to the physiological role of the SCD, at least SCD1 gene and its endogenous products came from recent studies of asebia mouse strains that have a natural mutation in the SCD1 gene and a mouse model with a targeted disruption of the SCD1 gene. In this review we discuss our current understanding of the physiological role of SCD in lipid synthesis and metabolism.
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PMID:Role of stearoyl-coenzyme A desaturase in lipid metabolism. 1253 75

Stearoyl-CoA desaturase (SCD) is the rate-limiting enzyme catalyzing the synthesis of monounsaturated fatty acids, mainly oleate (18:1) and palmitoleate (16:1). These represent the major monounsaturated fatty acids of membrane phospholipids, triglycerides, wax esters and cholesterol esters. The ratio of saturated to monounsaturated fatty acids affects phospholipid composition and alteration in this ratio has been implicated in a variety of disease states including cardiovascular disease, obesity, diabetes, neurological disease, and cancer. For this reason, the expression of SCD is of physiological significance in both normal and disease states. Several SCD gene isoforms (SCD1, SCD2, SCD3) exist in the mouse and one SCD isoform that is highly homologous to the mouse SCD1 is well characterized in human. The physiological role of each SCD isoform and the reason for having three or more SCD gene isoforms in the rodent genome are currently unknown but could be related the substrate specificities of the isomers and their regulation through tissue-specific expression. The recent studies of asebia mouse strains that have a natural mutation in the SCD1 gene and a mouse model with a targeted disruption of the SCD1 gene have provided clues concerning the role that SCD1 and its endogenous products play in the regulation of metabolism.
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PMID:Regulation of stearoyl-CoA desaturases and role in metabolism. 1465 89


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