Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pre-treatment by neuraminidase of lymphocytes obtained from peripheral blood of normal donors significantly enhanced E- and EAC-rosette formation. Of other lymphoid cells only spleen cells showed significant enhancement of E-rosettes. The EAC-rosettes slightly increased when the peripheral blood lymphocytes from patients with acute lymphoblastic leukemia or chronic lymphocytic leukemia and MOLT-4 lymphoid cells were pre-treated with this enzyme. The EAC-rosettes were not increased by neuraminidase treatment of phytohemagglutinin-induced blasts, thymus cells or spleen cells. Pre-treatment of peripheral blood lymphocytes with neuraminidase also increased the proportion of stable E-rosettes resistant to incubation at 37 degrees C and to vigorous shaking. Various concentrations of neuraminidase (1-100 U/ml) produced enhancement of E- and EAC-rosettes with the highest activity at 25 and 50 U/ml. Neuraminidase treatment of sheep red blood cells failed to increase the proportion of E-rosettes of peripheral blood lymphocytes. The increased rosette forming capacity induced by neuraminidase is probably related to changes in lymphocyte surface properties.
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PMID:Enhanced E- and EAC-rosette formation by neuraminidase. 96 28

In 37 patients with some hereditary diseases of the nervous system (deforming muscular dystonia, hepatocerebral dystrophy, essential tremor, etc.), as well as in 22 healthy subjects (donors), the percentage and the absolute content of the T- and B-lymphocytes in the blood were determined. Use was made of the reactions of spontaneous, active, and complementary rosette formation and determination of the B-cells from superficial immunoglobulins. In all the hereditary diseases listed a drop of the content of thymus-dependent lymphocytes and an increase of the capacity of lymphocytes for complementary rosette formation were revealed. The data obtained can be, probably, interpreted as evidences of a secondary immunodeficient state, possibly, caused by metabolic disturbances which are known to play an essential role in the pathogenesis of hereditary diseases of the nervous system.
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PMID:[Quantitative evaluation of the T- and B-systems of immunity in various hereditary diseases of the nervous system]. 697 36

Repeated restraint stress induces an atrophy of apical dendrites of CA3c pyramidal neurons in the hippocampus, but the relationship between stress and adrenocortical activation has not been thoroughly investigated. In order to better understand the relationship between neural and non-neural indices of the severity of stress, we investigated the temporal relationship between CA3c dendritic atrophy and indices of adrenal steroid stress responsiveness. For this purpose, we used two different stress regimens: repeated restraint stress (6 h/day) and a chronic multiple stress paradigm (shaking, restraint and swimming, each day), differing in the degree of adrenal activation produced over 14 and 21 days. Atrophy of dendrites of CA3c neurons was found after 21 days of stress, but not after 14 days, and was of a similar magnitude for both stressors. However, non-neural measures differed between the two stress paradigms: (i) chronic restraint stress caused a significant habituation by day 21 in the corticosterone response to acute restraint, whereas chronic multiple stress exposure was not accompanied by habituation of the corticosterone response to restraint; (ii) chronic restraint stress caused neither adrenal hypertrophy nor thymus atrophy, but did reduce the rate of body weight gain throughout the 21 days, whereas chronic multiple stress caused a transient adrenal hypertrophy (on day 14), delayed suppression of thymus weight (on day 21) and transient reduction of body weight gain (on days 7 and 14, but not on day 21). Thus the non-neural indices of response to stress--although complex in their time course--suggest that the multiple stress regimen is a somewhat more potent chronic stressor for corticosterone and adrenal responses. Yet both stress regimens produced the same degree of apical dendritic atrophy in CA3c pyramidal neurons. These results are consistent with a model in which adrenocortical secretion plays a permissive role in enabling another agent, namely, excitatory amino acids, to produce the final effect.
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PMID:Stress-induced atrophy of apical dendrites of hippocampal CA3c neurons: comparison of stressors. 863 35

A study of the effect of montirelin hydrate (NS-3), a new drug for the treatment of disturbance of consciousness, during the period of organogenesis was conducted in Sprague-Dawley rats. Female rats were given the drug intravenously at dose levels of 0 (control), 0.02, 1 and 50 mg/kg from day 7 to day 17 of pregnancy. Twenty-three or twenty-five female rats per dose level were sacrificed on day 20 of pregnancy for examination of their fetuses, and the pregnant rats (13-15 per dose levels) were allowed to deliver naturally for postnatal examination of their offspring. In the 1 or 50 mg/kg group, water consumption and the weights of adrenals of the dams increased and the weights of the thymus of the dams decreased. In addition, tremor, disappeared within some minutes, was observed from day 7 to day 16 of pregnancy in all dams given 50 mg/kg. Moreover, food consumption increased and the weights of the submaxillary glands of the dams given 50 mg/kg increased. The drug had no effect on the number of corpora lutea and implantations, on fetal mortality, on fetal body weights, on sex ratio, or on external, visceral and skeletal development of the fetuses. The drug also did not affect delivery. The drug did not have any adverse effects on the newborn such as the number of live newborns, birth index and body weights of live newborn, or on the postnatal development of the first generation offspring (F1) such as differentiation, functional development, emotionality, motor ability, learning ability or reproductive performance. The drug also had no adverse effects of the second generation offspring (F2). These results show that the NOAEL of montirelin hydrate are 0.02 mg/kg for general toxicity in mother animals, 50 mg/kg for pregnancy and delivery of mother animals and 50 mg/kg for development of their offspring.
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PMID:[Reproductive and developmental toxicity studies of montirelin hydrate (2)--Teratogenicity and postnatal study in rats by intravenous administration]. 901 62

A study of the effect of montirelin hydrate (NS-3), a new drug for the treatment of disturbance of consciousness, during the perinatal and lactation periods was conducted in Sprague-Dawley rats. Female rats were given the drug intravenously at dose levels of 0 (control), 0.02, 1 and 50 mg/kg from day 17 of pregnancy to day 21 after delivery. All pregnant rats were allowed to deliver naturally for postnatal examination of their offspring. In the 1 and 50 mg/kg groups, food and water consumptions decreased after delivery and the weights of adrenals of the dams increased. In addition, tremor, disappeared within some minutes, was observed during administration period in all dams given 50 mg/kg. Moreover, body weight gain was suppressed after delivery, and the weights of submaxillary glands increased, and the weights of thymus and liver decreased in the dams given 50 mg/kg. The drug did not affect delivery. The drug did not have any adverse effects on the newborn including the number of live newborns, birth index and body weights of live newborn. In the 1 or 50 mg/kg group, body weight gains were suppressed and food consumption decreased in the offspring. The drug did not have any adverse effects on the postnatal development of the offspring such as differentiation, functional development, emotionality, motor ability, learning ability or reproductive performance. These results show that the NOAEL of montirelin hydrate are 0.02 mg/kg for general toxicity in mother animals, 50 mg/kg for reproductive function in mother animals and 0.02 mg/kg for their offspring.
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PMID:[Reproductive and developmental toxicity studies of montirelin hydrate (4)--Perinatal and postnatal study in rats by intravenous administration]. 901 64

The results of the first global grafting of the thymus and a thymus-sternum block are given. The grafting of immunocompetent organs in children with the Louis-Bar syndrome is shown to cause to a partial and in some cases significant recovery of immunological parameters. Thus, blast-cell transformation showed 10-40% increases, the titers of antibodies to Staphylococcus and Escherichia coli rose, and immunoglobulin A that was generally absent in these children before surgery appeared. The clinical effect of grafting was noticeably observed 20-30 days after surgery. The most significant parameters were as follows: cessation of sinusitis, rhinitis, bronchitis, and purulent skin lesions. Neurological syndromes improved: tremor and staggering gait diminished, ocular convergence normalized. Thereafter such operations were made in 27 patients with Bruton's disease and in 3 patients with lymphogranulomatosis. The grafting of immunocompetent organs led to the design of agents derived from the thyroid gland (Tactivin) and bone marrow (myelopid). The immunobiological and clinical effects of Tactivin in the past 15-20 years are given in detail. The basic principles in immunomodulating therapy with thymic agents are presented.
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PMID:[From transplantation of the thymus to molecular reconstruction of the immune system]. 1039 94

AlphaMUPA is a line of transgenic mice that, compared with their wild type (WT) counterparts, spontaneously eat less (approximately 20%) and live longer (average approximately 20%), thus resembling dietary-restricted (DR) mice. Here, we show that body temperature was significantly reduced in alphaMUPA compared with WT throughout a wide range of ages. Plasma corticosterone was significantly higher in young alphaMUPA compared to young WT; however, it significantly declined in aged alphaMUPA, but not in aged WT. In addition, age-associated thymus involution occurred in alphaMUPA as it did in WT. Thus alphaMUPA mice appear to largely resemble, but also to somewhat differ from diet-restricted animals. We also report on four new transgenic lines that, like alphaMUPA, produced in the brain the mRNA that encodes the extracellular protease urokinase (uPA); however, transgenic uPA expression was most extensive and widespread in the alphaMUPA brain, where it also occurred in the hypothalamus. AlphaMUPA was also the only line that ate less, but also showed another characteristic, high frequency leg muscle tremor seen only at unstable body states. We hypothesize that transgenic uPA in the brain could have caused the alphaMUPA phenotypic alterations. Thus alphaMUPA offers a unique transgenic model of inherently reduced eating to investigate the homeostatic state of delayed aging at the systemic and single-cell levels.
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PMID:AlphaMUPA mice: a transgenic model for increased life span. 1063 29