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)

Conditions for the production of microbial L-serine hydroxymethyltransferase and for the conversion of glycine to L-serine were studied. A number of microorganisms were screened for their abilities to form and accululate L-serine from glycine, and Sarcina albida was selected as the best organism. Enzyme activity in this organism as high as 0.12 U/ml could be produced in shaken cultures at 30 degrees C in a medium containing glucose, ammonium sulfate, glycine, yeast extract, and inorganic salts. L-Serine was produced most efficiently by shaking cells at 30 degrees C in a reaction mixture containing 20% glycine, 5 X 10(-3) M formaldehyde, and 3 X 10(-4) M pyridoxal phosphate in yields of 22 mg of broth in 5 days. L-Serine was easily isolated in 84% yields by ion-exchange resin.
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PMID:Production of L-serine by Sarcina albida. 3 97

The behavioural response of rat pups, 1-20 days of age, to subcutaneous injection of formalin in a rear paw is described. Formalin-injected pups were compared to handled controls and to pups that received an injection of normal saline. Ongoing behaviour was recorded every 2 min for 60 min after injection. Injection of normal saline produced little disorganization of behaviour, although day-1, -3 and -6 pups did frequently flex the limb on the injected side early in the session. Injection of 10 microliters of 1% formalin depressed active and quiet sleep in pups 10 days old and younger. Much less disruption of sleep was observed in day-15 pups, and in day-20 pups it was necessary to increase the concentration of formalin to 2.5% to produce a consistent behavioural response. The specific responses of pups to formalin injection were flexion of the limb, shaking the limb, and licking the injected paw. Pups of all ages displayed all of these responses, but in pups younger than 10 days, only limb flexion was consistent. Shaking became a consistent response in day-10 pups and licking in day-15 and -20 pups. Non-specific behaviours (squirming, vigorous rear kicks with both hind limbs and convulsive whole body jerks) were markedly increased by formalin in younger pups with a developmental pattern: squirming and kicking in day-1 pups, kicking and jerking in day-3 to -15 pups. Non-specific behaviours decreased and specific behaviours increased with age. In addition, the overall intensity and duration of the response decreased with age. The biphasic time course of the response of adult rats to formalin injection did not appear until 15 days of age.
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PMID:The behavioral response to formalin in preweanling rats. 145 9

Administration of 5% formalin into the rat or guinea pig hind paw evokes two spontaneous responses: flinching/shaking and licking/biting of the injected paw. The temporal and behavioral characteristics of these objective endpoints are described. Additionally, several practical suggestions aimed at standardizing this test for the evaluation of analgesics are presented. The early/acute and late/tonic (0-10 and 20-35 min post-formalin, respectively) phases of flinching were used to quantitate antinociception in the rat. PD 117302, the kappa selective agonist, was three times more potent than morphine against tonic flinching after SC administration. Formalin may therefore be a noxious stimulus of choice in the evaluation of kappa agonists. Morphine was only twice as potent against tonic flinching as against acute flinching or the tail-dip reflex to water (50 degrees C). In contrast, PD 117302 was 27 times less potent on early phase and was inactive in the tail-dip test. Thus, while morphine is essentially equipotent across tests, PD 117302 shows a spectrum of activity with impressive potency and efficacy being obtained against tonic pain. Kappa receptors may therefore be prominently involved in tonic pain states. Aspirin given orally was not consistently antinociceptive in either phase of the formalin test. Spinal transection completely abolished late phase responding but only partly attenuated flinching in the early phase. This suggests that the relative involvement of spinal (as opposed to supraspinal) processing of noxious inputs may, at least in part, be a function of stimulus intensity and underlie the differences in antinociceptive potency observed in this work.
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PMID:Standardization of the rat paw formalin test for the evaluation of analgesics. 188 2

A comparison was made of the spontaneous nociceptive behaviors elicited by s.c. injection into the rat hind paw of the following 8 irritants: acetic acid, carrageenan, formalin, kaolin, platelet-activating factor, mustard oil (given topically), serotonin, and yeast. Two distinct quantifiable behaviors indicative of pain were identified: flinching/shaking of the paw and hindquarters and licking/biting of the injected paw. These behaviors were prolonged and intense after formalin and acetic acid. Formalin-induced flinching was biphasic across time, a finding potentially useful for the study of both acute and tonic pain. Of the remaining test agents, only yeast caused significant spontaneous behavioral activity, which was of low intensity but long duration. Different time-courses for nociceptive behavior and development of edema were demonstrated for formalin, acetic acid and yeast. It is therefore unlikely that these endpoints are causally related. Overall, the present data strongly support the use of formalin as a noxious stimulus in tonic pain research.
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PMID:The rat paw formalin test: comparison of noxious agents. 230 68

The extraction of fish muscle protein using SDS containing solubilization buffers was studied varying the time and the temperature of solubilization, as well as pH and SDS concentration of the buffer. At pH less than 6 the myofibrillar proteins were incompletely solubilized; temperatures of 80-100 degrees C resulted in protein degradation observable in the SDS-PAGE. Samples of fish muscle containing high amounts of formaldehyde (50 mmoles FA/kg wet weight) could only be solubilised at 100 degrees C; on the other hand it was possible to solubilize cooked and/or canned products under mild conditions (2% SDS, 1% 2-ME, pH 8.9, shaking for 2 h at 60 degrees C).
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PMID:Solubilization of fish muscle proteins with buffers containing sodium dodecyl sulfate. 401 19

Formalin which was said to produce prolonged pain and inflammation was injected subcutaneously into the back of guinea pigs, and minor tremor pain response (MTP-response) was measured using the MT-pick up, integrator and digital volt meter. The MTP-response curve showed a biphasic pattern. Immediately after injection, the MTP-response curve showed a significant peak which lasted for about 2 min (the first phase) and subsequently dipped rapidly, and after 5 min, it began to rise slowly again and had a peak at 30 min (the second phase). Morphine (6 mg/kg, s.c.) inhibited completely the first and second phases. Levallorphan (1.2 mg/kg), however, reversed the inhibitory effect of morphine at the first phase, but not at the second phase. Aspirin (200 mg/kg, i.p.), aminopyrine (100 mg/kg, s.c.) and pentazocine (5 mg-10 mg/kg, s.c.) inhibited significantly the formalin-induced MTP-response at both phases. Pyridinol carbamate (200 mg/kg, i.p.) and hydrocortisone (25 mg/kg, i.p.) had no effect on the MTP-response at the first phase, but inhibited it at the second phase. There was a parallelism between the time course of the vascular permeability induced by formalin and that of the second phase of MTP-response. From these results, it is suggested that the first phase of MTP-response is derived from the direct effect of formalin on free nerve endings, while the second phase is derived from the inflammation. Since two kinds of pain features were differentiated in this method, the relationships with so-called "immediate pain" and "delayed pain" were discussed. Furthermore, this method can be utilized to assess pain and the action of analgesics objectively and quantitatively.
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PMID:[Formalin-induced minor tremor response as an indicator of pain]. 651 Aug 42

Straight and branched chain aliphatic monoamines, which are not normal tissue constituents, are deaminated selectively by type B monoamine oxidase (MAO-B). They exhibit a high affinity towards the active site of MAO-B and this made them very useful pharmacologically. An anticonvulsant prodrug, Milacemide [2-(N-pentyl)glycinamide] is deaminated by MAO-B and this facilitates a mechanism of delivering glycine into the CNS. We have found that 2-propyl-pentylamine (2-propyl-1-aminopentane) and N-(2-propylpentyl)glycinamide are also converted by MAO-B to valproic acid and glycine both in vitro and in vivo; these compounds, however, cause severe tremor. By attaching a propargylamine group the resultant series of aliphatic propargylamine derivatives have been shown to be very potent selective MAO-B inhibitors. They are chemically quite different from most other MAO-B inhibitors, since they do not possess any aromatic structures. The relatively short chain aliphatic propargylamines, i.e. N-2-pentyl-N-methylpropargylamine and N-2-hexyl-N-methylpropargylamine, are 4 to 5 times more potent and more selective than selegiline (1-deprenyl) with respect to the inhibition of MAO-B in brain following oral administration. Semicarbazide-sensitive amine oxidase (SSAO) catalyzes the deamination of not only longer chain aliphatic amines but also short chain aliphatic amines including methylamine. Formaldehyde is produced from methylamine by SSAO. Increased methylamine deamination may cause cellular damage in some pathological conditions, such as uraemia and diabetes. We have observed that cultured human endothelial cells are damaged by methylamine in the presence of SSAO. Inhibition of the SSAO activity completely protects these cells from the methylamine-SSAO induced damage.
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PMID:Deamination of aliphatic amines by type B monoamine oxidase and semicarbazide-sensitive amine oxidase; pharmacological implications. 793 Dec 56

5 cases of allergic contact dermatitis from rubber footwear were investigated by a combination of patch testing in patients and chemical analysis of causative rubber products. Our studies revealed 2-mercaptobenzothiazole (MBT) and benzothiazyl disulfide (MBTS) (typical allergenic accelerators) as causative chemicals in 3 cases from children's rubber shoes, ladies' rubber boots and ladies' canvas shoes. These 3 patients reacted to mercaptobenzothiazole-type accelerators including MBT and MBTS. MBT and MBTS were determined in each item of causative footwear by chemical analysis, including extraction by shaking with acetone-chloroform (1:1) mixture at room temperature and determination using reversed-phase high-performance liquid chromatography (RP-HPLC). Subsequently, we identified styrenated phenol (SP), a newly found allergenic antioxidant, as a causative chemical in a case from ladies' canvas shoes. The patient reacted to SP but not to MBT and MBTS, though SP, MBT and MBTS were determined in the causative shoes by gas chromatography (GC), GC-mass spectrometry (GC-MS) and HPLC. We also identified p-tert-butylphenol-formaldehyde resin (PTBP-F-R), (a known allergenic adhesive ingredient) as a causative chemical in a case from ladies' sneakers. The patient reacted to PTBP-F-R but not to p-tert-butylphenol (PTBP), MBT and MBTS. These 4 compounds were determined in the causative sneakers by GC, GC-MS and HPLC. Thus, our studies revealed that not only known allergens, such as MBT, MBTS and PTBP-F-R, but also a newly found one, such as SP, were important causes of allergic contact dermatitis from rubber footwear.
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PMID:Identification of causative chemicals of allergic contact dermatitis using a combination of patch testing in patients and chemical analysis. Application to cases from rubber footwear. 815 59

Patients reporting sensitivity to multiple chemicals at levels usually tolerated by the healthy population were administered standardized questionnaires to evaluate their symptoms and the exposures that aggravated these symptoms. Many patients were referred for medical tests. It is thought that patients with chemical sensitivity have organ abnormalities involving the liver, nervous system (brain, including limbic, peripheral, autonomic), immune system, and porphyrin metabolism, probably reflecting chemical injury to these systems. Laboratory results are not consistent with a psychologic origin of chemical sensitivity. Substantial overlap between chemical sensitivity, fibromyalgia, and chronic fatigue syndrome exists: the latter two conditions often involve chemical sensitivity and may even be the same disorder. Other disorders commonly seen in chemical sensitivity patients include headache (often migraine), chronic fatigue, musculoskeletal aching, chronic respiratory inflammation (rhinitis, sinusitis, laryngitis, asthma), attention deficit, and hyperactivity (affected younger children). Less common disorders include tremor, seizures, and mitral valve prolapse. Patients with these overlapping disorders should be evaluated for chemical sensitivity and excluded from control groups in future research. Agents whose exposures are associated with symptoms and suspected of causing onset of chemical sensitivity with chronic illness include gasoline, kerosene, natural gas, pesticides (especially chlordane and chlorpyrifos), solvents, new carpet and other renovation materials, adhesives/glues, fiberglass, carbonless copy paper, fabric softener, formaldehyde and glutaraldehyde, carpet shampoos (lauryl sulfate) and other cleaning agents, isocyanates, combustion products (poorly vented gas heaters, overheated batteries), and medications (dinitrochlorobenzene for warts, intranasally packed neosynephrine, prolonged antibiotics, and general anesthesia with petrochemicals). Multiple mechanisms of chemical injury that magnify response to exposures in chemically sensitive patients can include neurogenic inflammation (respiratory, gastrointestinal, genitourinary), kindling and time-dependent sensitization (neurologic), impaired porphyrin metabolism (multiple organs), and immune activation.
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PMID:Profile of patients with chemical injury and sensitivity. 916 75

An antibody-direct epifluorescent filter technique (Ab-DEFT) detected 100% of the raw ground beef samples inoculated with Escherichia coli O157:H7 cells (0.15 cells g-1) and incubated in a prewarmed, modified buffered peptone water (mBPW) non-selective enrichment broth for 5 h at 42 degrees C in an orbital shaking water bath (200 rev min-1). Over 50% of the microscopic fields viewed were positive (1-10 fluorescent cells field-1) in the Ab-DEFT. All positive screening results were confirmed within 24 h by subjecting 1 ml of the mBPW to the Dynabeads anti-E. coli O157 immunomagnetic separation procedure, followed by plating on MacConkey sorbitol agar containing 5-bromo-4-chloro-3-indolyl-beta-D-glucuronide. At this cell concentration, 41.7% of the inoculated samples were detected by the conventional method involving a 24-h selective enrichment. Exposure to viable cells before filtration was minimized by using a 0.58% formaldehyde concentration for 5 min at 50 degrees C (killed > 4.00 logs of E. coli O157:H7 cells) without affecting cell fluorescence.
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PMID:A 5-h screening and 24-h confirmation procedure for detecting Escherichia coli O157:H7 in beef using direct epifluorescent microscopy and immunomagnetic separation. 917 47


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