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)

Most of the previous literature concerning otologic problems in compressed gas environments has emphasized middle ear barotrauma. With recent increases in commercial, military, and sport diving to deeper depths, inner ear disturbances during these exposures have been noted more frequently. Studies of inner ear physiology and pathology during diving indicate that the causes and treatment of these problems differ depending upon the phase and type of diving. Humans exposed to simulated depths of up to 305 meters without barotrauma or decompression sickness develop transient, conductive hearing losses with no audiometric evidence of cochlear dysfunction. Transient vertigo and nystagmus during diving have been noted with caloric stimulation, resulting from the unequal entry of cold water into the external auditory canals, and with asymmetric middle ear pressure equilibration during ascent and descent (alternobaric vertigo). Equilibrium disturbances noted with nitrogen narcosis, oxygen toxicity, hypercarbia, or hypoxia appear primarily related to the effects of these conditions upon the central nervous system and not to specific vestibular end-organ dysfunction. Compression of humans in helium-oxygen at depths greater than 152.4 meters results in transient symptoms of tremor, dizziness, and nausea plus decrements in postural equilibrium and psychomotor performance, the high pressure nervous syndrome. Vestibular function studies during these conditions indicate that these problems are due to central dysfunction and not to vestibular end-organ dysfunction. Persistent inner ear injuries have been noted during several phases of diving: 1) Such injuries during compression (inner ear barotrauma) have been related to round window ruptures occurring with straining, or a Valsalva's maneuver during inadequate middle ear pressure equilibration. Divers who develop cochlear and/or vestibular symptoms during shallow diving in which decompression sickness is unlikely or during compression in deeper diving, should be placed on bed rest with head elevation and avoidance of maneuvers which result in increased cerebrospinal fluid and intralabyrinthine pressure. With no improvement in symptoms after 48 hours, exploratory tympanotomy and repair of a possible labyrinthine window fistula should be considered. Recompression therapy is contraindicated in these cases...
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PMID:Diving injuries to the inner ear. 40 82

Eighteen professional divers (age range 24-33 yr, mean 28.3) participated in one simulated dive to 360 meters of seawater (msw) in a helium-oxygen (heliox) atmosphere with equal compression and decompression profiles. All divers were given an extensive neurologic examination before diving. Clinical neurologic symptoms observed during the dives were equilibrium disorder, sleep disturbances, fatigue, nausea, loose stools, stomach pain, tremor, mental disturbances, reduced appetite, and headache. Symptoms were scored individually by each diver. The symptoms were analyzed statistically by factor analysis, which grouped them into four factors. These symptoms are presumably related to functional disturbances in the brain stem and the cerebellum. Factor 3 symptoms (tremor, mental disturbances, reduced appetite) correlated significantly to a history of predive decompression sickness (P = 0.006) and to cerebral concussion (P = 0.023). Three divers were periodically unable to work at bottom due to equilibrium disorder, diarrhea, or nausea. One diver with mild polyneuropathy and slight cerebral atrophy as seen by computerized tomography and another diver with abnormal electroencephalography were periodically unable to work due to equilibrium disorder and nausea, respectively. We advocate that divers with signs of central or peripheral nervous system dysfunction should not be selected for deep diving.
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PMID:Analysis of neurologic symptoms in deep diving: implications for selection of divers. 232 22

To determine how cerebellar activity influences motor co-ordination, a simple motor act of an electric fish, Eigenmannia spp, was studied. Whenever the fish encounters an object of conductivity different from water, it bends the caudal two-thirds of its body towards the object. This behavior, called "probing", was analysed in the normal fish and in fish with a small cerebellar lesion. Probing could be described as a wave travelling along the body very similar to what one observes when shaking a rope of moderate elasticity. In normal fish, the wave starts at the tipe of the tail and proceeds towards the head, dying out after about two-thirds of the body length. A lesion in the corpus cerebelli causes this wave to start at the head and move towards the tail, though it is otherwise the same as in normal fish, i.e. it has the same frequency components as revealed by Fourier analysis. In addition to the change in probing, the lesioned fish also undulates its body while swimming whereas it is normally kept straight. This undulating wave turns out to be the same as that during probing where it is executed whilst the fish keeps itself on the spot with its locomotory apparatus, the anal fin, which is driven by muscles independent of the trunk muscles used for probing.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebellar influence on the time structure of movement in the electric fish Eigenmannia. 649 85

Using cryo-transmission electron microscopy, we have obtained abundant and reproducible evidence for a superstructure of dioleoylphosphatidylcholine (DOPC) bilayers. Dispersions of vesicles were prepared by gentle shaking of a 2% suspension of DOPC in water followed in part by extrusion through a porous technical membrane. Sampling and cryofixation took place at various times within 3 weeks after the preparation. From the micrographs we infer that the small fraction of vesicles enclosing one another develop passages (connections) between the bilayers. In contrast, the superstructure is basically a feature of disconnected membranes. Among its modifications are isolated membrane bends or folds and a grainy membrane texture with a minimal grain spacing of 4-6 nm. In the extruded dispersions the passages and the superstructure seem to be formed mostly within the first day. The fraction of smooth and unilamellar vesicles is large at all times and in all dispersions.
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PMID:Cryo-transmission electron microscopy of a superstructure of fluid dioleoylphosphatidylcholine (DOPC) membranes. 941 16

Expansion of a CGG.CCG-repeat tract in the 5'-untranslated region of the FMR1 (Fragile X mental retardation 1) gene causes its aberrant transcription. This produces symptoms ranging from premature ovarian failure and Fragile X associated tremor and ataxia syndrome to FMR syndrome, depending on the size of the expansion. The promoter from normal alleles shows four protein-binding regions in vivo. We had previously shown that in mouse brain extracts two of these sites are bound by USF1/USF2 (upstream stimulatory factors 1 and 2) heterodimers and NRF-1 (nuclear respiratory factor-1). We also showed that these sites are involved in the positive regulation of FMR1 transcription in neuronally derived cells. In the present study, we show that Sp1 (specificity protein 1) and Sp3 are also strong positive regulators of FMR1 promoter activity. We also show that, like Sp1 and E-box-binding proteins such as USF1 and USF2, NRF-1 causes DNA bending, in this case producing a bend of 57 degrees towards the major groove. The combined effect of the four protein-induced bends on promoter geometry is the formation of a highly compact arch-like structure in which the 5' end of the promoter is brought in close proximity to the 3' end. We had previously shown that while point mutations in the GC-boxes decrease promoter activity, deletion of either one of them leads to an increase in promoter activity. We can reconcile these observations with the positive effect of Sp1 and Sp3 if protein-induced bending acts, at least in part, to bring together distally spaced factors important for transcription initiation.
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PMID:The roles of Sp1, Sp3, USF1/USF2 and NRF-1 in the regulation and three-dimensional structure of the Fragile X mental retardation gene promoter. 1547 57

Early stage Parkinson's disease (PD) shares certain symptoms with essential tremor (ET), which makes it difficult to differentiate between the two. We analyzed cyclical body bends to find kinematic parameters that are capable of differentiating among PD, ET and normal control (NC) subjects. A linear discriminant analysis of the joint angles showed a reliable distinction between NC and the two groups of patients, while differentiating reasonably well between PD and ET. PD patients showed difficulty performing hip segment rotation around the vertical axis, whereas ET patients demonstrated enlarged torso sway in the frontal plane. These findings suggest that kinematic parameters of body movement in the standing position are sensitive enough to serve as subclinical marks in the early diagnosis of PD and ET.
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PMID:A comparative kinematic analysis of cyclical bending in patients with early stages of Parkinson's disease and in patients with essential tremor. 2445 61