RESUMEN
OBJECTIVE: To investigate olfactory function in elderly subjects requiring nursing care to clarify its association with appetite and nutritional status. SETTING: Facility for the elderly requiring nursing care. PARTICIPANTS: The subjects were 158 elderly people requiring nursing care and 37 elderly people not requiring nursing care. MEASUREMENTS: Experiment I: Olfactory function and factors (cognitive function, appetite, and nutritional status) that may be associated with it were compared between the elderly subjects requiring nursing care and those not requiring nursing care using covariance analysis in consideration of age. For evaluation, the OSIT-J was used for olfactory function, the HDS-R for cognitive function, the CNAQ for appetite, and BMI for nutritional status. Experiment II: The subjects were the same elderly subjects requiring nursing care in Experiment I, and food intake was surveyed in addition to the OSIT-J, HDS-R, CNAQ, and BMI. A univariate linear regression analysis was performed with OSIT-J as the response variable, and age, HDS-R, CNAQ, BMI, and food intake as the explanatory variables. RESULTS: Experiment I: On covariance analysis, the OSIT-J score was significantly lower for the elderly subjects requiring nursing care than for those not requiring nursing care (p<0.01). The mean score was 8 or lower in both groups, demonstrating lower olfactory function in both groups. Regarding factors that may be associated with olfactory function, a significant difference was noted in the HDS-R (p<0.01), confirming significantly lower cognitive function in the elderly subjects requiring nursing care. No significant difference was noted in the CNAQ or BMI. Experiment II: On a univariate linear regression analysis, an association with the OSIT-J was noted for age and HDS-R. Age was inversely correlated and the HDS-R was positively correlated. Factors associated with lower olfactory function in the elderly subjects requiring nursing were age and cognitive function, whereas appetite, nutritional status, and food intake were not associated. CONCLUSION: Olfactory function in elderly subjects requiring nursing care was poorer than that in those not requiring nursing care, suggesting that aging and cognitive decline are associated with lower olfactory function. In addition, no association of lower olfactory function with appetite, nutritional status, or food intake was noted in the elderly subjects requiring nursing care.
Asunto(s)
Apetito/fisiología , Enfermería Geriátrica/normas , Estado Nutricional/fisiología , Olfato/fisiología , Anciano , Anciano de 80 o más Años , Femenino , Humanos , MasculinoRESUMEN
The objectives of the present study were to investigate the effects of the stage of the estrous cycle at the start of an estradiol benzoate (EB) and progesterone (P) based treatment protocol on new follicular wave emergence, subsequent estrus and ovulation. The experiment was conducted using a crossover design with each cow (five cross-bred cows) being assigned to one of three groups at 3-month intervals within a 1-year period. Estrous cycle stage in individual cows was initially synchronized with prostaglandin F(2)alpha. After detection of estrus, each cow was injected intramuscularly (i.m.) with 2 mg EB and 200 mg P (EB/P) on day 5, 12 or 17 of the estrous cycle (estrus=day 0), followed by 1 mg EB i.m. 12 days after the EB/P treatment. Ovarian ultrasonographic examinations showed that the emergence of a new follicular wave occurred after EB/P treatment in all groups and the mean interval from EB/P treatment to wave emergence did not differ among the groups (3.2-3.8 days). All cows in each group exhibited behavioral estrus and ovulated the newly formed dominant follicle. However, cows in the day-17 group exhibited estrus 1-3 days before the second EB injection. The concentrations of progesterone showed faster reduction, during the treatment period, in the day-12 and -17 groups compared to the day-5 group. These results indicate that the EB/P treatment induces an emergence of a new follicular wave, irrespective of the estrous cycle stage at the start of treatment, but the effect of EB/P protocol on estrous/ovulation synchronization is influenced by the stage of the estrous cycle.
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Bovinos/fisiología , Cuerpo Lúteo/efectos de los fármacos , Estro/efectos de los fármacos , Folículo Ovárico/efectos de los fármacos , Ovulación/efectos de los fármacos , Progesterona/sangre , Animales , Estudios Cruzados , Estradiol/análogos & derivados , Estradiol/farmacología , Ciclo Estral/efectos de los fármacos , Sincronización del Estro/efectos de los fármacos , Femenino , Fármacos para la Fertilidad Femenina/farmacología , Progesterona/farmacologíaRESUMEN
To investigate the role of thromboxane A(2) in the development of hypertension in the fructose-fed rat, we treated male fructose-fed rats with dazmegrel (a thromboxane synthase inhibitor) and monitored blood pressure, fasting plasma parameters, and insulin sensitivity for 7 weeks. Systolic blood pressure was measured each week using tail plethysmography, and an oral glucose tolerance test was performed at the end of the study to assess insulin sensitivity. Treatment with a 60% fructose diet and dazmegrel (100 mg. kg(-1). d(-1) via oral gavage) was initiated on the same day. Plasma triglyceride levels increased 2-fold in both fructose- and fructose/dazmegrel-treated groups, and plasma insulin levels tended to be higher in these groups, although not significantly. Systolic blood pressure increased significantly throughout the study in the fructose-fed group only (132+/-3 versus 112+/-4 mm Hg in control rats, 118+/-2 mm Hg in control-treated rats, 116+/-2 mm Hg in fructose-treated rats). Both fructose groups demonstrated a higher peak insulin response to oral glucose challenge and had 40% to 60% lower insulin sensitivity index values. The results of this study show that treatment with a thromboxane synthase inhibitor, dazmegrel, can prevent the development of hypertension but does not improve insulin sensitivity or other fructose-induced metabolic impairments. Based on these data, we conclude that the potent vasoconstrictor thromboxane is involved in the link between hyperinsulinemia/insulin resistance and hypertension.
Asunto(s)
Inhibidores Enzimáticos/farmacología , Fructosa/administración & dosificación , Hipertensión/prevención & control , Imidazoles/farmacología , Tromboxano-A Sintasa/antagonistas & inhibidores , 6-Cetoprostaglandina F1 alfa/sangre , 6-Cetoprostaglandina F1 alfa/metabolismo , Animales , Aorta/efectos de los fármacos , Aorta/metabolismo , Glucemia/efectos de los fármacos , Glucemia/metabolismo , Presión Sanguínea/efectos de los fármacos , Epoprostenol/sangre , Hipertensión/sangre , Hipertensión/inducido químicamente , Insulina/sangre , Ratas , Ratas Wistar , Tromboxano B2/sangre , Tromboxano B2/metabolismo , Tromboxanos/sangre , Triglicéridos/sangreRESUMEN
To evaluate the potential contribution of endothelin-1 (ET-1) toward the cardiovascular complications of diabetes, the present study examined the effects of chronic ET receptor blockade with bosentan on heart function and vascular reactivity in streptozotocin (STZ)-induced diabetic rats. Wistar rats were divided into four groups: control, control bosentan-treated, diabetic, and diabetic bosentan-treated. After chronic bosentan treatment, cardiac function and vascular reactivity were assessed. Exvivo working heart function was determined in terms of rate of contraction (+dP/dt), rate of relaxation (-dP/dt), and left ventricular developed pressure (LVDP). Contractile responses to ET-1 were determined in isolated superior mesenteric arteries. In addition, ET-1-like immunoreactivity was determined in ventricular and vascular tissues by immunohistochemistry. Cardiac function was depressed in the untreated-diabetic group. Bosentan treatment improved working heart function; hearts from the diabetic bosentan-treated group exhibited improved LVDP and -dP/dt. The contractile responses of mesenteric arteries to ET-1 were exaggerated in the untreated-diabetic group. Long-term bosentan treatment normalized these responses. Immunohistochemical analyses revealed increased ET-1-like immunoreactivity in ventricular and vascular tissues from untreated diabetic rats. These data show the beneficial effects of ET(A/B) receptor blockade on cardiovascular function in STZ-diabetic rats. An altered ET-1 system may contribute toward the pathogenesis of cardiovascular dysfunction in diabetes.
Asunto(s)
Antihipertensivos/farmacología , Diabetes Mellitus Experimental/tratamiento farmacológico , Antagonistas de los Receptores de Endotelina , Sulfonamidas/farmacología , Animales , Función del Atrio Izquierdo/efectos de los fármacos , Bosentán , Endotelina-1/análisis , Endotelina-1/sangre , Masculino , Arterias Mesentéricas/fisiología , Contracción Miocárdica/efectos de los fármacos , Ratas , Ratas Wistar , Vasoconstricción/efectos de los fármacosRESUMEN
OBJECTIVE: Endothelin-1 (ET-1) has been suggested to play an important role in the pathogenesis of diabetes-induced vascular complications. The primary purpose of the present study was to examine the potential beneficial effects of chronic ET receptor blockade (with bosentan) on vascular function in renal arteries from streptozotocin (STZ)-induced diabetic rats. DESIGN: Wistar rats were divided into four groups: control (C), control bosentan-treated (CB), diabetic (D) and diabetic bosentan-treated (DB). Following 10 weeks of bosentan treatment, vascular responses to norepinephrine (NE), ET-1, acetylcholine (ACh) were determined in vascular segments of renal arteries, both with and without the endothelium denuded, according to the following protocol: (1) a cumulative dose-response curve (DRC) to NE in the absence and presence of the nitric oxide synthase (NOS) inhibitor L-NAME (2) cumulative DRC to ET-1 and (3) cumulative DRC to ACh in precontracted arteries. In addition, plasma ET-1 was assayed and ET-1-like immunoreactivity was determined in vascular tissues by immunohistochemistry. RESULTS: The maximum contractile responses to NE and ET-1 were markedly exaggerated in endothelium-intact renal arteries from untreated D rats while ACh responses were preserved. Arteries denuded of endothelium did not exhibit exaggerated responses to NE or ET-1. L-NAME treatment did not affect responses to NE in arteries with or without endothelium. Strikingly, responses to NE and ET-1 (in arteries with endothelium) were completely normalized following long-term bosentan treatment. In addition, plasma ET-1 levels did not differ between C and D groups. However, renal arteries isolated from the D group exhibited increased ET-1-like immunoreactivity (local ET-1 content). CONCLUSION: These data uncover, for the first time, beneficial effects of mixed ETA/ETB receptor blockade on renal artery vascular function in diabetes. Alterations in the production and/or action of ET-1 may have important implications in the development of vascular dysfunction in experimental diabetes.
Asunto(s)
Antihipertensivos/farmacología , Diabetes Mellitus Experimental/fisiopatología , Arteria Renal/efectos de los fármacos , Arteria Renal/fisiopatología , Sulfonamidas/farmacología , Acetilcolina/farmacología , Animales , Bosentán , Relación Dosis-Respuesta a Droga , Endotelina-1/sangre , Endotelina-1/metabolismo , Endotelio Vascular/fisiopatología , Inhibidores Enzimáticos/farmacología , Técnicas In Vitro , Masculino , NG-Nitroarginina Metil Éster/farmacología , Norepinefrina/farmacología , Ratas , Ratas Wistar , Factores de Tiempo , Vasoconstricción , Vasoconstrictores/farmacologíaRESUMEN
Insulin has been shown to elicit vasodilation through increases in nitric oxide (NO) production. To examine whether insulin may modulate the availability of tetrahydrobiopterin (BH4) (an absolute cofactor requirement for NO synthase activation), we studied the effects of insulin (150 nmol/L) on femoral arterial reactivity (to norepinephrine [NE]) in the presence and absence of 2,4-diamino-6-hydroxypyrimidine (DAHP), a specific inhibitor of BH4 production. Our data indicate that inhibition of BH4 synthesis results in an attenuation in the vasodepressor effect of insulin. One possibility is that insulin may regulate NO production by increasing cofactor (BH4) availability for activation of NO synthase.
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Biopterinas/análogos & derivados , Insulina/farmacología , Vasodilatación/efectos de los fármacos , Animales , Biopterinas/biosíntesis , GTP Ciclohidrolasa/biosíntesis , Hipoxantinas/farmacología , Masculino , Óxido Nítrico/fisiología , Norepinefrina/farmacología , Ratas , Ratas Sprague-DawleyRESUMEN
Effects of pioglitazone on plasma insulin levels, systolic blood pressure and arterial reactivity were studied in spontaneously hypertensive (SH) rats. Chronic treatment of SH rats with pioglitazone decreased plasma insulin levels and blood pressure. Direct effects of pioglitazone on vascular reactivity were also studied in aortae and superior mesenteric arteries from SH rats. Pioglitazone markedly inhibited arginine vasopressin (AVP) and norepinephrine (NE) responses without affecting responses to potassium chloride (KCl). These data suggest that (a) antihypertensive effects of pioglitazone in SH rats may be mediated via a direct vasodepressor effect, and (b) vasodilation may be coupled to insulin sensitivity in SH rats.
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Hiperinsulinismo/tratamiento farmacológico , Hipertensión/tratamiento farmacológico , Hipoglucemiantes/uso terapéutico , Tiazoles/uso terapéutico , Tiazolidinedionas , Vasodilatadores/uso terapéutico , Animales , Arginina Vasopresina/farmacología , Evaluación Preclínica de Medicamentos , Insulina/sangre , Masculino , Norepinefrina/farmacología , Pioglitazona , Cloruro de Potasio/farmacología , Ratas , Ratas Endogámicas SHRRESUMEN
To better define limb-girdle muscular dystrophy (LGMD), we examined 58 patients clinically and pathologically who fulfilled the criteria for LGMD and had normal dystrophin expression in their muscle biopsies. Only 27.6% of patients had evidence of inheritance. The onset of disease varied from 2 to 58 years of age, averaging 17.2 years. The disease progression also differed from patient to patient. In addition to evidence of muscle fiber necrosis and regeneration, in all muscle biopsies there were fibers with architectural changes of disorganized intermyofibrillar networks including moth-eaten (100%), lobulated (40%), whorled (17%) and targetoid (8%) fibers. The lobulated fibers which have never been reported in Duchenne muscular dystrophy (DMD) were seen in the advanced stages of LGMD, although the significance of such fibers remains unknown. On immunohistochemical examination, dystrophin-associated proteins (DAPs) and laminin were normally expressed along the surface membrane of muscle fibers, including the lobulated fibers.
Asunto(s)
Extremidades/fisiopatología , Proteínas de la Membrana , Distrofias Musculares/patología , Distrofias Musculares/fisiopatología , Adulto , Proteínas del Citoesqueleto/metabolismo , Distrofina/metabolismo , Histocitoquímica , Humanos , Inmunohistoquímica , Glicoproteínas de Membrana/metabolismo , Persona de Mediana Edad , Músculos/metabolismo , Músculos/patología , Músculos/fisiopatología , Necrosis , Regeneración , UtrofinaRESUMEN
Late adult onset distal myopathies usually show vacuolar degeneration as a characteristic feature in muscle pathology. In this study vacuolar degeneration was not present in 12 patients with late adult onset distal myopathy. All patients were members of a large kindred, with 26 patients showing this new form of distal leg myopathy. Additionally, a severely disabling proximal muscular dystrophy appeared in eight other members of the large consanguineous kindred. Muscle biopsies were obtained from clinically affected muscles, and from clinically unaffected muscles in patients with distal myopathy. For comparison specimens from various muscles of patients with severe proximal dystrophy were also studied. Histopathological changes correlating to muscular dystrophy were extensive in all muscles studied in patients with proximal dystrophy, and in tibial anterior muscles in patients with distal myopathy. Mild myopathic changes, mainly increased internal nuclei in muscle fibers, were detected in clinically unaffected muscles in the distal myopathy. The spectrum of findings is compatible with the hypothesis of previous clinical and genetic studies, indicating that the severe proximal dystrophy could be a homozygous manifestation of the dominantly inherited gene of the distal tibial muscle dystrophy.
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Distrofias Musculares/genética , Enfermedades Neuromusculares/genética , Adulto , Anciano , Femenino , Humanos , Inmunohistoquímica , Masculino , Persona de Mediana Edad , Músculos/química , Distrofias Musculares/metabolismo , Distrofias Musculares/patología , Enfermedades Neuromusculares/metabolismo , Enfermedades Neuromusculares/patología , Linaje , Fenotipo , Factores de Tiempo , VacuolasRESUMEN
Abnormalities of dystrophin, a cytoskeletal protein of muscle and nerve, are generally considered specific for Duchenne and Becker muscular dystrophy. However, several patients have recently been identified with dystrophin deficiency who, before dystrophin testing, were considered to have Fukuyama congenital muscular dystrophy (FCMD) on the basis of clinical findings. Epidemiologic data suggest that only 1/3500 males with autosomal recessive FCMD should have abnormal dystrophin. To explain the observation of 3/23 FCMD males with abnormal dystrophin, we propose that dystrophin and the FCMD gene product interact and that the earlier onset and greater severity of these patients' phenotype (relative to Duchenne muscular dystrophy) are due to their being heterozygous for the FCMD mutation in addition to being hemizygous for Duchenne muscular dystrophy, a genotype that is predicted to occur in 1/175,000 Japanese males. This model may help explain the genetic basis for some of the clinical and pathological variability seen among patients with FCMD, and it has potential implications for understanding the inheritance of other autosomal recessive disorders in general. For example, sex ratios for rare autosomal recessive disorders caused by mutations in proteins that interact with X chromosome-linked gene products may display predictable deviation from 1:1.
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Distrofina/genética , Distrofias Musculares/genética , Anomalías Múltiples/genética , Western Blotting , Deleción Cromosómica , Expresión Génica , Genes , Genes Recesivos , Ligamiento Genético , Heterocigoto , Humanos , Masculino , Distrofias Musculares/patología , Fenotipo , Cromosoma XRESUMEN
Using immunocytochemical methods, we examined the intensity and distribution of dystrophin and spectrin immunostaining of skeletal muscles from 51 congenital muscular dystrophy (CMD) patients including 36 Fukuyama congenital muscular dystrophy (FCMD) and 15 non-FCMD (other CMD). 17 age-matched spinal muscular atrophy (SMA) and 5 Duchenne muscular dystrophy (DMD) patient biopsies were studied as controls. All 15 non-FCMD and SMA patients showed normal localization of dystrophin at the surface membrane of each muscle fiber which was undetectable in DMD. In contrast, 34 of 36 FCMD patients exhibited an unusual immunostaining pattern with occasional (17-43%; mean = 28) negative or abnormally immunoreacted (partially deficient, fluffy or intense) fibers for dystrophin. Dystrophin was absent in 2 of 36 patients having a clinical diagnosis of FCMD, and intragenic deletion of the DMD gene was detected in one. Spectrin, a membrane cytoskeletal protein related to dystrophin, also showed an increased number of abnormally immunostained fibers in FCMD (25%), but not so high in age-matched DMD (9%) or SMA patient muscle (0%). Thus, our results suggested the presence of intrinsic factor(s) that produce abnormality of the plasma membrane of FCMD muscle.
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Distrofina/análisis , Músculos/patología , Distrofias Musculares/patología , Adolescente , Biopsia , Niño , Preescolar , Creatina Quinasa/análisis , Femenino , Humanos , Inmunohistoquímica , Lactante , Masculino , Atrofia Muscular/patología , Distrofias Musculares/congénito , Espectrina/análisisRESUMEN
Of the 3,048 diagnostic muscle biopsies processed by the National Institute of Neuroscience, Tokyo, over 12 years, 41 cases carried the clinical diagnosis of limb-girdle muscular dystrophy. We have analyzed all 41 cases for dystrophin content in muscle by both immunofluorescence and immunoblot. We identified five male patients with an abnormal dystrophin pattern diagnostic of Becker muscular dystrophy, and two female patients with dystrophin patterns consistent with a manifesting carrier of Duchenne muscular dystrophy diagnosis. Thus, 17% of our limb-girdle patients showed a dystrophinopathy, indicating that they in fact had a disorder related to Duchenne/Becker muscular dystrophy. Misclassification of isolated male limb-girdle patients was 31% (4/13), while misclassification of isolated female limb-girdle patients was 13% (2/15). Using multiplex polymerase chain reaction analyses of small amounts of muscle biopsy DNA confirmed a dystrophin gene deletion in all five male Becker dystrophy patients identified. This study emphasizes the clinical overlap between limb-girdle muscular dystrophy and dystrophinopathies, and reinforces the necessity of dystrophin protein and gene studies for the accurate clinical diagnosis of isolated cases of muscular dystrophy.
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Distrofina/química , Distrofias Musculares/metabolismo , Adolescente , Adulto , Niño , Preescolar , Distrofina/genética , Distrofina/metabolismo , Femenino , Técnica del Anticuerpo Fluorescente , Amplificación de Genes , Humanos , Immunoblotting , Masculino , Persona de Mediana Edad , Distrofias Musculares/genética , Distrofias Musculares/patología , Pelvis , Reacción en Cadena de la Polimerasa , HombroRESUMEN
Duchenne muscular dystrophy (DMD) is a fatal X-linked recessive disorder of muscle in children. The DMD gene product, "dystrophin", is absent from DMD, while the allelic disease, Becker muscular dystrophy (BMD), exhibits dystrophin of abnormal size and/or quantity. But we are still uncertain about the scenario that internally deleted (or duplicated) dystrophin in BMD possesses its carboxy (C)-terminal region, and severely truncated dystrophin in DMD does not. Here we use a new monoclonal antibody directed against an peptide in the C-terminal end of the dystrophin molecule to show that the C-terminus is preserved in 30 BMD and 24 control skeletal muscles but not in 21 DMD specimens. This result, taken together with data on deletions of the dystrophin gene, emphasizes both the diagnostic and biological importance of the C-terminal domain which is required for proper function and stability of dystrophin, and substantiates the validity of the reading frame hypothesis for DMD versus BMD deletions on a biochemical level.
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Anticuerpos Monoclonales , Distrofina/química , Músculos/química , Distrofias Musculares/metabolismo , Secuencia de Aminoácidos , Anticuerpos Monoclonales/inmunología , Especificidad de Anticuerpos , Deleción Cromosómica , Distrofina/deficiencia , Distrofina/genética , Distrofina/inmunología , Exones , Mutación del Sistema de Lectura , Genes , Humanos , Masculino , Modelos Genéticos , Datos de Secuencia Molecular , Músculos/patología , Distrofias Musculares/genética , Distrofias Musculares/patologíaRESUMEN
A 23-year-old male patient with Becker muscular dystrophy (BMD) who showed schizophrenic symptoms was reported. He tumbled easily and was poor at running since age at 8 years. He had difficulty in climbing stairs and was idle away all day long since age at 21 years. Although his premorbid personality was not schizoid, he showed auditory hallucinations and delusions without any psychogenetic moment at the age of 23. At first, he seemed to be schizophrenic, but after the treatment with antipsychotics, he always had an insight into his disease and exhibited natural emotional communication. He showed no autism and character changes. According to the Wechsler Adult Intelligence Scale (WAIS), intellectual impairment was notified (total IQ58). Neurological examinations revealed weakness and atrophy of muscles in the proximal part of his lower extremities, and pseudohypertrophy of calves. In the serum enzyme, serum creatine kinase (CK) level was elevated (700 U/L). Abnormal Q waves appeared in the leads, II, III, aVF, V5, V6 on the electrocardiogram (ECG), and the finding of the echocardiography suggested dilated cardiomyopathy. The electroencephalogram (EEG) revealed the basic rhythm of 9-10 Hz with 0 activities of 6-7 Hz which were predominant in frontparietal and central leads. The electromyogram (EMG) revealed a myopathic pattern with low voltage and short duration. A muscle biopsy from right biceps brachii disclosed the abnormal immunofluorescent staining pattern of dystrophin which is consistent with BMD patient, i.e., "patchy," discontinuous and faint immunoreaction at surface membrane of the fiber. Both molecular weight (380 kd: n = 400) and amount (30%; n = 100) of dystrophin were reduced.(ABSTRACT TRUNCATED AT 250 WORDS)
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Distrofias Musculares/psicología , Esquizofrenia/etiología , Adulto , Atrofia , Corteza Cerebral/patología , Distrofina/análisis , Humanos , Imagen por Resonancia Magnética , Masculino , Músculos/química , Músculos/patología , Distrofias Musculares/complicaciones , Distrofias Musculares/patologíaRESUMEN
We examined dystrophin, the protein product of the Duchenne muscular dystrophy gene, in muscle biopsy specimens from 4 male patients with quadriceps myopathy, all of whom showed a mild and slowly progressive myopathy confined to the quadriceps muscles. All 4 patients had clear abnormalities of dystrophin, and were diagnosed as having Becker muscular dystrophy by both immunofluorescence and immunoblot examinations; that is, dystrophin of an abnormal molecular mass was visualized in muscle cryosections as "patchy" or discontinuous immunostaining at the surface membrane of the muscle fibers. One patient had a brother who showed widespread myopathic changes consistent with typical Becker muscular dystrophy. We conclude that the syndrome called quadriceps myopathy includes a group of forme fruste Becker muscular dystrophy.
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Distrofina/análisis , Distrofias Musculares/patología , Adulto , Anciano , Electromiografía , Técnica del Anticuerpo Fluorescente , Humanos , Hipertrofia , Immunoblotting , Pierna , Masculino , Músculos/patología , Músculos/fisiopatología , Distrofias Musculares/genética , Distrofias Musculares/fisiopatología , Linaje , MusloRESUMEN
In vitro immunoglobulin (Ig) synthesis was studied using peripheral blood mononuclear cells (PBM) from 12 patients with myasthenia gravis (MG). In cultured PBM, levels of secreted IgG, IgM and IgA measured by ELISA, as well as the number of IgG-, IgM-, and IgA-secreting cells determined by reversed plaque assay, were higher in MG than in controls; this was not dependent upon the stimulation of PBM with pokeweed mitogen (PWM). PBM from 9 of 12 MG patients synthesized anti-acetylcholine receptor (AChR) antibodies in vitro in the presence of PWM, while PBM from 7 controls did not. Patients whose PBM secreted lower levels of each Ig class also secreted fewer or no anti-AChR antibodies. Levels of anti-AChR antibodies secreted in vitro showed a high degree of correlation with titers of sera from patients (r = 0.86). The results suggest that the process of anti-AChR antibody synthesis by PBM in vitro is related to that of Ig synthesis, and that PBM plays, at least in part, an important role in the production of anti-AChR antibodies in MG.