Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.27.1 (RNase)
16,360 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The method of intraductal administration of ribonuclease as a therapeutic measure was developed on an experimental model of acute pancreatitis in albino rats. Morphological and biochemical examination showed that intraductal administration of ribonuclease in a dose of 0.5 mg produces a positive therapeutic effect, which allowed the method to be applied in complex treatment of 33 patients with various forms of acute pancreatitis. Administration of ribonuclease into the pancreatic duct relieved the attack of pain and reduced the level of lipo- and proteolytic enzymes in blood. No complications were encountered in endoscopic cannulation of the main pancreatic duct and subsequent administration of ribonuclease.
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PMID:[Use of ribonuclease in multimodal treatment of acute pancreatitis]. 204 54

We have described a spectrum of pancreatic surgery after cardiopulmonary bypass. At one end is a subclinical lesion which was manifested only by elevations in serum isoamylase levels (27 percent of patients) and increased ribonuclease levels (13 percent of patients) in asymptomatic patients followed after cardiac surgery. At the other end is a severe and often lethal necrotizing pancreatitis. Acute necrotizing pancreatitis was found at autopsy in 25 percent of 138 patients who died after cardiac surgery, and it correlated strongly with low output, acute tubular necrosis, and infarction of the liver, spleen, or bowel. It was the principal cause of death in 4 percent of these patients. In addition, 24 percent of 38 nonsurgical patients who died from cardiac failure and hypoperfusion had acute pancreatitis at autopsy, whereas acute pancreatitis was not observed in 55 nonsurgical patients who died without a significant period of low output. Acute pancreatitis was recognized postoperatively in 12 patients (0.2 percent). Three had mild pancreatitis, and all responded well to conservative therapy. In nine patients, fulminant necrotizing pancreatitis developed. Their courses were characterized by significant early postoperative hemodynamic compromise, abdominal distention, ileus, fever, and episodes of late vascular instability associated with hypocalcemia. The diagnosis of pancreatitis was usually missed because of the absence of pain, tenderness and hyperamylasemia. The diagnosis was confirmed at laparotomy in eight patients and at autopsy in one. The only two survivors among the nine with severe cases had aggressive mobilization, debridement, and wide drainage of the necrotic pancreas. We suggest that a mild subclinical injury to the pancreas may occur as a consequence of cardiopulmonary bypass and may progress to severe ischemic necrosis if hypoperfusion follows in the postoperative period, the presentation of necrotizing pancreatitis may be atypical in the cardiac surgical patient and should be considered if nonspecific abdominal symptoms are present, and aggressive debridement and drainage may be the optimal treatment for aggressive forms of this disease.
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PMID:Acute pancreatitis after cardiopulmonary bypass. 258 Apr 53

Fibronectin, a large extracellular glycoprotein, mediates the interaction of cells with the extracellular matrix. Heterogeneity in the structure of fibronectin is largely due to the alternative splicing of three exons (IIIB, IIIA and V) during processing of the fibronectin primary transcript. Osteoarthritis, a degenerative disease of synovial joints, is characterized by a progressive loss of the articular cartilage eventually resulting in pain and loss of joint function. In contrast to the loss of most cartilage matrix proteins accompanying this process, osteoarthritic cartilage contains more fibronectin than disease-free cartilage. We examined the splicing patterns of fibronectin mRNA from adult human articular cartilage of normal and osteoarthritic joints by RNase protection (exon IIIA and exon IIIB) and reversed transcription-polymerase chain reaction (exon V) assays to determine whether or not the increased fibronectin content in osteoarthritic cartilage is also associated with differences in the splicing patterns of these three alternatively spliced exons. The results revealed no gross differences in splicing of these exons between the fibronectin mRNA isolated from adult human articular normal and osteoarthritic cartilage. Thus alterations in the structure of cartilage fibronectin do not appear to correlate with the increased level of fibronectin protein associated with osteoarthritis.
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PMID:Splicing patterns of fibronectin mRNA from normal and osteoarthritic human articular cartilage. 858 48

Mammalian sensory neurons express a voltage-gated sodium channel named SNS. Here we report the identification of an SNS transcript (SNS-A) that contains an exact repeat of exons 12, 13 and 14 encoding a partial repeat of domain II. Because the exons 12-14 are present in single copies in genomic DNA, the SNS-A transcript must arise by trans-splicing. Nerve growth factor, which regulates pain thresholds, and the functional expression of voltage-gated sodium channels increases the levels of the SNS-A transcript several-fold both in vivo and in vitro as measured by RNase protection methods, as well as RT-PCR. These data demonstrate a novel regulatory role for the nerve growth factor and are the first example of trans-splicing in the vertebrate nervous system.
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PMID:Trans-splicing of a voltage-gated sodium channel is regulated by nerve growth factor. 1006 96

1. The effect of endogenous glucocorticoid hormones on the expression of rat B(1) receptors was examined by means of molecular and pharmacological functional approaches. 2. Rats were adrenalectomized (ADX), and 7 days after this procedure the intradermal injection of B(1) receptor agonist des-Arg(9)-BK produced a significant increase in the paw volume, while only a weak effect was observed in sham-operated animals. A similar increase in the contractile responses mediated by B(1) agonist des-Arg(9)-BK was also observed in the rat portal vein in vitro. 3. Chemical ADX performed with mitotane (a drug that reduces corticosteroid synthesis) produced essentially the same up-regulation of B(1) receptors as that observed in ADX rats. 4. The modulation of B(1) receptor expression was evaluated by ribonuclease protection assay, employing mRNA obtained from the lungs and paw of ADX rats. 5. Additionally, both paw oedema and contraction of portal vein mediated by B(1) agonist des-Arg(9)-BK in ADX rats, were markedly inhibited by treatment with dexamethasone, or COX-2 inhibitor meloxican, or with the NF-kappaB inhibitor PDTC. Interestingly, the same degree of inhibition was achieved when the animals were treated with a combination of submaximal doses of dexamethasone and PDTC. 6. The involvement of NF-kappaB pathway was further confirmed by mobility shift assay using nuclear extracts from lung, paw and heart of ADX rats. It was also confirmed that the treatment of ADX rats with dexamethasone, PDTC or dexamethasone plus PDTC completely inhibit NF-kappaB activation caused by absence of endogenous glucucorticoid. 7. Together, the results of the present study provide, for the first time, molecular and pharmacological evidence showing that B(1) kinin receptor expression can be regulated through endogenous glucocorticoids by a mechanism dependent on NF-kappaB pathway. Clinical significance of the present findings stem from evidence showing the importance of B(1) kinin receptors in the mediation of inflammatory and pain related responses.
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PMID:Molecular and pharmacological evidence for modulation of kinin B(1) receptor expression by endogenous glucocorticoids hormones in rats. 1115 7

Peripheral nerve injury can lead to a persistent neuropathic pain state in which innocuous tactile stimulation elicits pain behavior (tactile allodynia). Spinal administration of the anticonvulsant gabapentin suppresses allodynia by an unknown mechanism. In vitro studies indicate that gabapentin binds to the alpha(2)delta-1 (hereafter referred to as alpha(2)delta) subunit of voltage-gated calcium channels. We hypothesized that nerve injury may result in altered alpha(2)delta subunit expression in spinal cord and dorsal root ganglia (DRGs) and that this change may play a role in neuropathic pain processing. Using a rat neuropathic pain model in which gabapentin-sensitive tactile allodynia develops after tight ligation of the left fifth and sixth lumbar spinal nerves, we found a >17-fold, time-dependent increase in alpha(2)delta subunit expression in DRGs ipsilateral to the nerve injury. Marked alpha(2)delta subunit upregulation was also evident in rats with unilateral sciatic nerve crush, but not dorsal rhizotomy, indicating a peripheral origin of the expression regulation. The increased alpha(2)delta subunit expression preceded the allodynia onset and diminished in rats recovering from tactile allodynia. RNase protection experiments indicated that the DRG alpha(2)delta regulation was at the mRNA level. In contrast, calcium channel alpha(1B) and beta(3) subunit expression was not co-upregulated with the alpha(2)delta subunit after nerve injury. These data suggest that DRG alpha(2)delta regulation may play an unique role in neuroplasticity after peripheral nerve injury that may contribute to allodynia development.
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PMID:Upregulation of dorsal root ganglion (alpha)2(delta) calcium channel subunit and its correlation with allodynia in spinal nerve-injured rats. 1124 71

In spinal nerve ligated Lewis strain neuropathic rats, pain behaviors and the rate of ectopic discharges of injured sensory neurons were significantly reduced by systemic injection of phentolamine. A pharmacological study indicated that this adrenergic dependency was mediated by alpha(1)-adrenoceptors (alpha(1)-AR). The development of adrenergic sensitivity in injured sensory neurons might have resulted from changes in adrenoceptor expression as a consequence of changed expression of adrenoceptor genes. This possibility was examined by determining the changes in the mRNA expression of 3 subtypes of alpha(1)-ARs, alpha(1a)-, alpha(1b)-, and alpha(1d)-ARs, in the dorsal root ganglia (DRG) after spinal nerve ligation. The L4 and L5 spinal nerves were tightly ligated in Lewis rats. One week later, the L4 and L5 DRG were collected and RNase protection assay (RPA) and in situ hybridization were performed. In the DRG of unoperated rats, a moderate amount of alpha(1a)-AR mRNA was present while the amount of either alpha(1b)-AR or alpha(1d)-AR mRNA was small. After spinal nerve ligation, there was a significant increase in the amount of alpha(1b)-AR mRNA in the nerve ligated DRG as measured by RPA. The amount of alpha(1a)-AR mRNA was decreased to 20% of the normal level while that of alpha(1d)-AR mRNA did not change. The in situ hybridization study showed that the number of alpha(1b)-AR mRNA positive neurons increased in spinal nerve ligated DRG, confirming the results of RPA study. These data suggest that the up-regulated expression of alpha(1b)-AR mRNA in axotomized DRG neurons may play an important role in the development of adrenergic sensitivity in injured sensory neurons and thus contribute to the sympathetically maintained pain in spinal nerve ligated neuropathic Lewis rats.
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PMID:Differential expression of alpha1-adrenoceptor subtype mRNAs in the dorsal root ganglion after spinal nerve ligation. 1158 93

Our previous studies showed that the ectopic discharges in injured sensory neurons and mechanical allodynia that developed after spinal nerve ligation were significantly reduced by application of a low concentration of tetrodotoxin (TTX) to the corresponding dorsal root ganglion (DRG) of the ligated spinal nerve. Based on these data, we hypothesized that expression of TTX-sensitive sodium channels is up-regulated in the injured sensory neurons and that such up-regulation plays an important role in the generation of ectopic discharges and thus pain behaviors in spinal nerve ligated neuropathic rats. To test this hypothesis, the present study examined the changes in three subtypes of TTX-sensitive sodium channels in the DRG after spinal nerve ligation. The changes in the total amount of mRNA for alpha-subunits of sodium channel brain type I (type I), brain type II (type II) and brain type III (type III) were determined by RNase protection assays (RPA). The population of DRG neurons expressing type III sodium channel protein was examined by an immunohistochemical method with antibodies to type III sodium channels. In the normal DRG, the level of mRNA for the type I sodium channel is high while that for type II and type III is very low. After spinal nerve ligation, the expression of type III mRNA was significantly increased at 16-h postoperatively (PO), doubled by 3 days PO and then was maintained at this high level until the end of the experiment (7 days PO). By contrast, the amount of mRNA for type I and type II sodium channels started to decrease at 1 day PO and were reduced to 25-50% of the normal control levels by 7 days after nerve ligation. Neurons showing positive immunostaining for type III sodium channels were rare ( approximately 3.2% of total population) in the normal DRG but increased after nerve ligation to 21% and 15% of the total neuronal population by 1 day and 7 days PO, respectively. Type III immunoreactivity was found preferentially in medium to large sized neurons. Thus the majority of neurons with cell bodies having diameters > or =40 microm became type III-positive after nerve ligation. The data indicate that the increased expression of type III sodium channels in axotomized sensory neurons may be the critical factor for the TTX sensitivity of ectopic discharges in injured sensory neurons and thus the generation of ectopic discharges and neuropathic pain behaviors in spinal nerve ligated rats.
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PMID:The changes in expression of three subtypes of TTX sensitive sodium channels in sensory neurons after spinal nerve ligation. 1168 87

Alcohol misusers frequently have difficulties in gait, and various muscle symptoms such as cramps, local pain and reduced muscle mass. These symptoms are common in alcoholic patients and have previously been ascribed as neuropathological in origin. However, biochemical lesions and/or the presence of a defined myopathy occur in alcoholics as a direct consequence of alcohol misuse. The myopathy occurs independently of peripheral neuropathy, malnutrition and overt liver disease. Chronic alcoholic myopathy is characterized by selective atrophy of Type II fibres and the entire muscle mass may be reduced by up to 30%. This myopathy is arguably the most prevalent skeletal muscle disorder in the Western Hemisphere and occurs in approximately 50% of alcohol misusers. Alcohol and acetaldehyde are potent inhibitors of muscle protein synthesis, and both contractile and non-contractile proteins are affected by acute and chronic alcohol dosage. Muscle RNA is also reduced by mechanisms involving increased RNase activities. In general, muscle protease activities are either reduced or unaltered, although markers of muscle membrane damage are increased which may be related to injury by reactive oxygen species. This supposition is supported by the observation that in the UK, alpha-tocopherol status is poor in myopathic alcoholics. Reduced alpha-tocopherol may pre-dispose the muscle to metabolic injury. However, experimental alpha-tocopherol supplementation is ineffective in preventing ethanol-induced lesions in muscle as defined by reduced rates of protein synthesis and in Spanish alcoholics with myopathy, there is no evidence of impaired alpha-tocopherol status. In conclusion, by a complex series of mechanisms, alcohol adversely affects skeletal muscle. In addition to the mechanical changes to muscle, there are important metabolic consequences, by virtue of the fact that skeletal muscle is 40% of body mass and an important contributor to whole-body protein turnover.
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PMID:Alcoholic skeletal muscle myopathy: definitions, features, contribution of neuropathy, impact and diagnosis. 1178 53

Increased purinergic sensitivity of injured sensory neurons suggests the possible involvement of purinoceptors for the generation of pain after nerve injury. To identify the purinoceptors that are involved, the changes in mRNA levels of 6 subtype purinoceptors were examined in the dorsal root ganglia (DRG) of the normal rat and after spinal nerve ligation, using RNase protection assay (RPA). In addition, the P2X(2) containing neurons were examined in the L5 DRG, using an immunohistochemical method. The relative amounts of mRNAs for the six purinoceptor subtypes were in the order of P2X(3)>>P2X(4)>P2X(6)>P2X(5) approximately P2X(2)>P2X(1) in the normal lumbar DRG. After nerve injury, the mRNA of P2X(5) was increased, those of P2X(3) and P2X(6) were decreased, and those of P2X(2) and P2X(4) were unchanged. Immunohistochemical studies, however, showed 23% of the total DRG neurons are P2X(2) positive in the normal L5 DRG, but that increased to 73% after nerve ligation. These data suggest that not only transcriptional but also posttranscriptional changes of multiple purinoceptors might be involved in the enhancement of purinergic sensitivity in injured sensory neurons.
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PMID:Changes in the gene expression of six subtypes of P2X receptors in rat dorsal root ganglion after spinal nerve ligation. 1252 93


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