Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunoreactive calcitonin and calcium concentrations were determined on 581 plasma samples collected during 23 studies on 20 cows. Sample collections in each study was begun approximately 1 month prior to parturition and continued for about 1 month after parturition. The cows were grouped according to the degree of hypocalcemia encountered at parturition. The parturient paresis group consisted of 10 cows which developed severe hypocalcemia (3.91 plus or minus 0.22 mg/100 ml, mean plus or minus se) accompanied by paresis; the nonparetic hypocalcemic group consisted of 5 cows which developed severe hypocalcemia (5.70 plus or minus 0.03 mg/100 ml) but not paresis; and the control group consisted of 8 cows which experienced only a mild hypocalcemia (8.50 plus or minus 0.27 mg/100 ml) at parturition. In the prepartal period prior to the onset of hypocalcemia, the respective mean plasma calcium concentrations (plus or minus se) of the 3 groups were 10.1 plus or minus 0.11, 9.95 plus or minus 0.20, and 10.2 plus or minus 0.17 mg/100 ml. The development of severe hypocalcemia in the parturient paresis and nonparetic hypocalcemic groups was not accompanied by an increase in plasma calcitonin concentration. Furthermore, plasma calcitonin concentraion of these 2 groups was less than that of control cows during the parturient period as well as during the month before and the month after parturition. The plasma calcium nadir at parturition was positively related to the mean prepartal (encompassing the period from 30 days until 60 h before parturition) plasma calcitonin concentration (r = 0.57, t= 3.14, p less than 0.005); i.e., the lower the prepartal plasma calcitonin concentration the more severe the hypocalcemia at parturtion. These observations suggest that the development of hypocalcemia at parturition is not due to an increased secretion of calcitonin, but instead they suggest that parturient hypocalcemia may be associated with a diminished prepartal secretion of calcitonin.
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PMID:Diminished prepartal plasma calcitonin concentration on cows developing parturient hypocalcemia. 112 17

A comparative assessment was made of the hormonal control of calcium homeostasis in eight dairy cows which developed parturient paresis and in seven normal animals from the same herd. Plasma levels of calcium, phosphorus, magnesium, free hydroxyproline, 25-hydroxycholecalciferol (25-OHD), 1,25-dihydroxycholecalciferol (1,25-(OH)2D), parathyroid hormone, calcitonin, prolactin and oestrogen were monitored from 30 days prepartum to 15 days post partum. Prepartum levels of plasma calcium, hydroxyproline and calcitonin were depressed in the paretic animals, and plasma levels of phosphorus and oestrogen were elevated. Plasma levels of 25-OHD remained stable in both groups, whereas levels of 1,25-(OH)2D, parathyroid hormone and prolactin rose sharply at parturition. Plasma hydroxyproline, an index of bone resorption, began to rise 2 days prepartum in the control cows but not until 2 days post partum in the paretic cows. The data indicate that bone resorption was inhibited in the paretic group at the onset of lactation, and that a decreased capacity for bone resorption is a major factor in the susceptibility of some cows to this disease. The failure of the paretic animals to resorb bone was not associated with an inability to synthesize the calcium-mobilizing hormones parathyroid hormone or 1,25-(OH)2D, or to regulate the production of calcitonin. However, hypocalcaemia in the affected animals was associated with a significantly higher plasma level of oestrogen (a known inhibitor of bone resorption) in the immediate prepartum period. Following parturition, plasma levels of oestrogen fell rapidly and active bone resorption ensued in the paretic animals.
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PMID:A hormonal assessment of bovine parturient paresis: evidence for a role of oestrogen. 690 89

Botulinum toxin is widely used for the treatment of focal movement disorders, where chemodenervation is used to decrease hyperactivity in selected muscles. Beside a focal paresis, widespread effects on neuromuscular synaptic function have been demonstrated. However, reactions of motoneurons after neuromuscular chemodenervation without gross morphological lesions are largely unknown. Peripheral axotomy, in contrast, leads to profound changes in the expression of several genes, including those encoding neurotransmitters, in motoneurons. We therefore examined the expression of neurotransmitter genes in rat motoneurons six days after intramuscular botulinum toxin application in the right gastrocnemius muscle. Similar doses of botulinum toxin as used in human where injected. A focal bilateral increase in expression of the choline acetyltransferase gene and a widespread bilateral increase of the beta-calcitonin-gene-related peptide and the enkephalin genes was measured in motoneurons after botulinum toxin injection. Cholecystokinin had a lower expression after botulinum toxin injections. Growth-associated protein 43, nitric oxide synthase, somatostatin and proopiomelanocortin messenger RNA were not found in motoneurons of both groups. Our results demonstrate that changes in the expression of neurotransmitter genes in motoneurons also occur after chemodenervation but with different patterns to those found after mechanical nerve lesioning. These changes reflect focal and widespread modulative events. The knowledge of these events should lead to a better understanding of the focal paralysis and of the more widespread effects found in human after intramuscular injection of botulinum toxin.
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PMID:Expression of neurotransmitter genes in rat spinal motoneurons after chemodenervation with botulinum toxin. 914 3

Calcium (Ca) is essential for life in higher animals. It is involved in the normal functioning of a wide variety of tissues and physiologic processes which include bone formation, muscle contraction, nerve transmission, blood clotting and as a second messenger regulating the actions of many hormones. In order for these functions to be carried out properly, blood Ca concentrations must be monitored and regulated within strict limitations. The discovery of the vitamin D endocrine system has resulted in the realization that Ca regulation in mammals and birds involves a coordinated effort between the hormones parathyroid hormone (PTH), calcitonin and the hormonally-active form of vitamin D3, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3]. Failure of this system to maintain normal blood Ca concentrations at parturition is a common occurrence in ruminants leading to clinical (periparturient paresis, milk fever) and subclinical hypocalcemia. Vitamin D sterols have played a significant role in efforts to avoid parturient hypocalcemia and this report will summarize advantages and disadvantages associated with their use.
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PMID:Role of vitamin D in calcium homeostasis and its use in prevention of bovine periparturient paresis. 1462 94

Botulinum toxin (BT) has been perceived as a lethal threat for many centuries. In the early 1980s, this perception completely changed when BT's therapeutic potential suddenly became apparent. We wish to give an overview over BT's mechanisms of action relevant for understanding its therapeutic use. BT's molecular mode of action includes extracellular binding to glycoprotein structures on cholinergic nerve terminals and intracellular blockade of the acetylcholine secretion. BT affects the spinal stretch reflex by blockade of intrafusal muscle fibres with consecutive reduction of Ia/II afferent signals and muscle tone without affecting muscle strength (reflex inhibition). This mechanism allows for antidystonic effects not only caused by target muscle paresis. BT also blocks efferent autonomic fibres to smooth muscles and to exocrine glands. Direct central nervous system effects are not observed, since BT does not cross the blood-brain barrier and since it is inactivated during its retrograde axonal transport. Indirect central nervous system effects include reflex inhibition, normalisation of reciprocal inhibition, intracortical inhibition and somatosensory evoked potentials. Reduction of formalin-induced pain suggests direct analgesic BT effects possibly mediated by blockade of substance P, glutamate and calcitonin gene-related peptide.
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PMID:Botulinum toxin: mechanisms of action. 1565 Mar 6

This review describes therapeutically relevant mechanisms of action of botulinum toxin (BT). BT's molecular mode of action includes extracellular binding to glycoproteine structures on cholinergic nerve terminals and intracellular blockade of the acetylcholine secretion. BT affects the spinal stretch reflex by blockade of intrafusal muscle fibres with consecutive reduction of Ia/II afferent signals and muscle tone without affecting muscle strength (reflex inhibition). This mechanism allows for antidystonic effects not only caused by target muscle paresis. BT also blocks efferent autonomic fibres to smooth muscles and to exocrine glands. Direct central nervous system effects are not observed, since BT does not cross the blood-brain-barrier and since it is inactivated during its retrograde axonal transport. Indirect central nervous system effects include reflex inhibition, normalisation of reciprocal inhibition, intracortical inhibition and somatosensory evoked potentials. Reduction of formalin-induced pain suggests direct analgesic BT effects possibly mediated through blockade of substance P, glutamate and calcitonin gene related peptide.
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PMID:Botulinum toxin: mechanisms of action. 1583 90

An interaction between blood levels of parathyroid hormone, calcitonin, 1.25-dihydroxycholecalciferol and levels of calcium, phosphorus and magnesium was examined in 85 cows, which included healthy cows and cows with ostemalacia, mastitis and paresis. Levels of parathyroid hormone (PTH) and calcitonin were determined in vitro using IMMULITE analyser (Diagnostic Products Corporation, USA), by means of immunometric assay. Levels of vitamin D were measured using the enzyme linked immunosorbent assay (ELISA). Levels of calcium, phosphorus and magnesium were determined using the automated Eos-Bravo analyser (Hospitex Diagnostics, Italy) with HOSPITEX reagents. The lowest blood levels of calcium (1.38 +/- 0.18 mmol/L) and phosphorus (0.65 +/- 0.12 mmol/L) were found in cows with parturient paresis. Decreased blood levels of phosphorus and magnesium were also determined in cows with osteomalacia. For cows with parturient paresis, which received a mineral supplement, the average serum level of calcium was by 20.7% higher than the level found in those which did not receive a supplement, and the level of phosphorus was by 23.6% higher, however, these levels remained low. The blood level of parathyroid hormone ranged from 3.47 to 5.20 pmol/L in healthy cows and from 3.95 to 15.21 pmol/L in sick cows. The highest and statistically significant increase in blood PTH level (up to 18.31 +/- 1.88 pmol/L) was found in cows with parturient paresis. The blood level of PTH correlated inversely with the level of calcium in cows with osteomaliacia (r = -0.89) and in cows with parturient paresis (r = -0.49 and r = -0.61, respectively). The serum level of calcitonin ranged from 1.46 pmol/L to 2.40 pmol/L in healthy and sick cows and the difference was not statistically significant. Lower serum levels of vitamin D were found in heifers-in-calf and in cows with mastitis. A clear correlation between levels of calcitonin, vitamin D and macronutrients was not found.
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PMID:Interaction between the levels of hormones and minerals in sera of healthy and sick cows. 1638 50

Complex-regional pain syndromes (CRPS), formerly known as Sudeck's dystrophy and causalgia, belong to the neuropathic pain syndromes. CRPS may develop following fractures, limb trauma or lesions of the peripheral or central (CNS) nervous system. Occasionally, CRPS may also develop spontaneously. The clinical picture comprises a characteristic clinical triade of symptoms including autonomic (disturbances of skin temperature, colour, presence of sweating abnormalities), sensory (pain and hyperalgesia) and motor (paresis, tremor, dystonia) disturbances. Diagnosis is mainly based on clinical signs. However, additional laboratory, neurophysiological and radiological examinations may help to corroborate correct diagnosis. Several pathophysiological concepts have been proposed to explain the complex symptoms of CRPS: 1, facilitated neurogenic inflammation; 2, pathological sympatho-afferent coupling; 3, neuroplastic changes within the CNS. Furthermore, there is accumulating evidence that genetic factors may predispose for CRPS. Therapy is based on a multidisciplinary approach. Non-pharmacological approaches include physiotherapy and occupational therapy. Pharmacotherapy is based on individual symptoms and includes steroids, free radical scavengers, treatment of neuropathic pain, and finally agents interfering with bone metabolism (calcitonin, biphosphonates). Sympathetic blocks are useful for the treatment of sympathetically maintained pain. Invasive therapeutic concepts include implantation of spinal cord stimulators. This review covers new aspects of pathophysiology and therapy of CRPS.
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PMID:[Complex regional pain syndromes: new aspects on pathophysiology and therapy]. 1744 40

Complex regional pain syndrome (CRPS), formerly known as Sudeck's dystrophy and causalgia, is a disabling and distressing pain syndrome. We here provide a review based on the current literature concerning the epidemiology, etiology, pathophysiology, diagnosis, and therapy of CRPS. CRPS may develop following fractures, limb trauma or lesions of the peripheral or CNS. The clinical picture comprises a characteristic clinical triad of symptoms including autonomic (disturbances of skin temperature, color, presence of sweating abnormalities), sensory (pain and hyperalgesia), and motor (paresis, tremor, dystonia) disturbances. Diagnosis is mainly based on clinical signs. Several pathophysiological concepts have been proposed to explain the complex symptoms of CRPS: (i) facilitated neurogenic inflammation; (ii) pathological sympatho-afferent coupling; and (iii) neuroplastic changes within the CNS. Furthermore, there is accumulating evidence that genetic factors may predispose for CRPS. Therapy is based on a multidisciplinary approach. Non-pharmacological approaches include physiotherapy and occupational therapy. Pharmacotherapy is based on individual symptoms and includes steroids, free radical scavengers, treatment of neuropathic pain, and finally agents interfering with bone metabolism (calcitonin, biphosphonates). Invasive therapeutic concepts include implantation of spinal cord stimulators. This review covers new aspects of pathophysiology and therapy of CRPS.
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PMID:Complex regional pain syndromes: new pathophysiological concepts and therapies. 2018 Aug 38