Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studied were mass disease outbreaks on eight farms in calves intensively fed concentrate mixtures that were rich in phosphorus compounds. Clinically, there were selling and deformations of the joints with pains. The tarsal and carpal joints were chiefly involved. Kyphosis of the backbone, spastic paresis of the posterior part of the body as well as tetaniform spasms in the initial stage of the disease were also observed. Morphologically, the diseased animals manifested erosions and thinning of the joint cartilage, tearing of the Achilles tendon, and increased amounts of the joint fluid. The histologic study revealed edema of the cartilage cells, disorders in the structure of the hyalin cartilage, formation of cavities, and broadening of the lumen of the Haversian canals. In most cases the blood serum presented hyperphosphatemia (up to 15.67 mg% inorganic P) and relative or absolute hypocalcemia (up to 4.47 mg% Ca). On the farm both hypocalcemia and hypophosphatemia were observed. Good prophylactic results were obtained through correct Ca:P ratios in the diet that contained calcium additives as well as by the injection of vitamin D solutions, etc. It is believed that these cases should be referred to a distinctive form of rickets of a characteristic clinical course' the inadequate Ca:P ratios in the rations playing the main etiologic role. Subsidiary causes are probably vitamin D deficiency, restricted movement of the animals, and mechanical traumata caused by the animal's own bodyweight.
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PMID:[Study of disorders in calcium and phosphorus metabolism in the intensive fattening of young cattle]. 125 54

Chronic compressive myelopathy was induced in domestic rabbits by implanting bone morphogenetic protein on the ligamentum flavum of the lumbar spine, and the resulting spinal cord lesion was studied histopathologically. In addition, morphometry of myelinated nerve fibers of the white matter in the pathologic specimens was performed to elucidate the mechanisms of cord injury. No loss of white matter nerve fibers was seen when the cord compression ratio (sagittal diameter/transverse diameter) was > 45%, although 6 months later myelin thinning was present throughout the white matter. When the cord compression ratio was < or = 45%, loss of fibers, particularly of large fibers, was seen in the superficial layer of the white matter, with the nerve fibers remaining after 6 months showing decreased diameters. No motor paresis was evident in any animal. These histologic changes represent the early pathologic condition induced by chronic cord compression.
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PMID:Histopathologic and morphometric study of spinal cord lesion in a chronic cord compression model using bone morphogenetic protein in rabbits. 146 13

Cleidocranial dysostosis (CCD) is a rare congenital disorder characterized by the heredity, the disturbance of the ossification of the skull and clavicles, and dental anomaly. The entity of CCD was established by Marie and Sainton in 1898. In Japan about 150 cases have been reported since Haneda's first report in 1933. Recently we experienced a rare case of CCD associated with the temporal arachnoid cyst. The patient was a 61-year-old male who had suffered from mild spastic paresis of the left upper extremity since his childhood. One morning he suddenly noticed motor weakness of the left upper and lower extremities and was transferred to our hospital. On admission we observed the left hemiparesis (MMT 3/5), the left central type facial palsy, and the left long tract signs. Physical examination disclosed frontal bossing, depression of the forehead, sloped shoulders, cone-shaped thorax, and thoracic scoliosis. Plain skull radiograph showed persistent metopic suture and frontal fontanelle, many wormian bones around coronal and lambdoid sutures. Plain radiographs of the systemic bones also showed typical features of CCD such as dysplasia of the lateral third of the bilateral clavicles, deformities of the cervical vertebral bodies, thoracic scoliosis, and wide symphysis. CT scan disclosed the right putaminal hemorrhage, the right temporal arachnoid cyst, enlargement of the right middle fossa, thinning of the temporal bone adjacent to the arachnoid cyst. It also showed the atrophy of the right cerebral peduncle and midbrain. Surgical treatment was performed to remove the hematoma and release the cyst. Several neurological disorders associated with CCD have been reported such as epilepsy, mental retardation, spastic paresis etc.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of cleidocranial dysostosis associated with arachnoid cyst]. 343 33

The clinical and radiological findings in six extradural and nine intradural arachnoid cysts are discussed in relation to previous reports. Only two cysts failed to opacify during positive contrast myelography; in both cases Myodil was used and in one of them contrast medium had entered the cyst on delayed films taken at 24 h. Pain was always improved and generally cured by operation, only two patients having some residual backache. There was permanent improvement of neurological function in only eight cases. The factors associated with poor permanent recovery after surgical treatment were: 1) very marked thinning of the spinal cord by the cyst, and 2) relatively longer duration of paresis--only one case had paresis for under 2 years (mean 4.8 years) compared with only two cases for over 1 year (mean 2 years) in those with good recovery.
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PMID:Spinal arachnoid cysts: clinical and radiological correlation with prognosis. 706 14

The effects of high toxic doses of the anticancer drugs, etoposide and its phosphate derivative, BMY-40481, on the nervous system of female CD-1 mice were examined by light microscopy (LM) and transmission electron microscopy. Mice were euthanatized 4 wk following a single iv injection of either 0, 50, 100, or 150 mg/kg of BMY-40481 or 44 or 88 mg/kg of etoposide. Mice treated with 100 or 150 mg/kg of BMY-40481 or 88 mg/kg of etoposide had clinical symptomology of progressive ataxia, impaired righting reflex, and splaying and paresis of fore- and hindlimbs at day 8. Similar, dose-related LM changes were observed with both drugs at all doses and consisted of degeneration of dorsal root ganglion cells and axonal degeneration of their distal and proximal processes in peripheral nerves, dorsal spinal roots, and dorsal funiculi of spinal cord. Axonal degeneration was characterized by LM as shrinkage, swelling, and fragmentation of axon cylinders accompanied by secondary demyelination. Degenerative changes in ganglion cell bodies included eccentric nuclei, cytoplasmic vacuolation, central chromatolysis, and peripheral clumping of Nissl's bodies. Ultrastructurally, ganglion cell bodies had focally extensive dilation of the rough endoplasmic reticulum, mitochondrial swelling, increased numbers of phagolysosomes and prominent aggregations of microfilaments (globular filamentous bodies). Ultrastructural axonal changes occurred primarily in large, myelinated fibers and consisted of axonal swelling or loss, thinning of myelin sheaths, and a decrease in the number of organelles. This is the first report of etoposide-related sensory neuropathy in laboratory rats, a model that my be useful for the study of etoposide-related peripheral neuropathy in humans.
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PMID:Etoposide- and BMY-40481-induced sensory neuropathy in mice. 789 82

Gnotobiotic mice inoculated with an enterohemorrhagic Escherichia coli (EHEC) O157:H7 strain developed a flaccid paresis, usually culminating in death. The bacteria colonized feces at 10(9) to 10(10) CFU per g (inoculum size: 2.0 x 10(9) CFU/mouse), and Shiga-like toxins (SLTs) were detected in the feces. A microscopic examination of colons showed mild inflammatory cell infiltration, thinning of the intestinal wall, or necrotic foci. Necrosis of tubular cells was noted in these symptomatic mice. Microhemorrhage, thrombosis, and edematous changes of the brain were also seen. Inflammatory cytokines, tumor necrosis factor alpha (TNF-alpha), interleukin 1alpha (IL-1alpha), and IL-6, were detected in the kidney after EHEC infection, but not in the serum. In the brain, only TNF-alpha was detected. When 2.0 x 10(2) CFU of EHEC O157:H7 was fed to germ-free mice, the number of bacteria began to rise rapidly on day 1 and was maintained at 10(8)to 10(9) CFU/g of feces. SLTs were detected in the feces of the mice. However, the mice showed no histological changes and no cytokine responses, similar to what was found for controls. Treatment with TNF-alpha modified the clinical neural signs, histopathological changes, and cytokine responses; mice treated with TNF-alpha developed severe neurotoxic symptoms and had higher frequencies of systemic symptoms and glomerular pathology. Strong cytokine responses were seen in the kidney and brain. Serum cytokines were also detected in this group. In contrast, a TNF-alpha inhibitor (protease inhibitor) inhibited these responses, especially in the brain. However, local synthesis of the cytokines was observed in the kidney. Thus, TNF-alpha and the other proinflammatory cytokines could be important in modifying the disease caused by EHEC.
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PMID:Role of tumor necrosis factor alpha in gnotobiotic mice infected with an Escherichia coli O157:H7 strain. 942 58

After atraumatic birth, three neonates presented with muscle hypotonia and weakness. Flaccid paresis of the upper extremities, spasticity of the lower extremities, dissociate sensory loss and autonomic dysfunction developed later. This ruled out the initial, tentative diagnoses of cerebral palsy, spinal muscular atrophy or hereditary neuropathy. Diagnostic imaging revealed marked thinning of the cervical spinal cord in all patients. The possible aetiology of these lesions is considered. In all cases, an antenatal or perinatal infarction is thought to be the most probable cause. Different clinical pictures following intrauterine spinal cord ischemia are discussed. Spinal cord lesion must be considered even after atraumatic birth.
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PMID:Cervical spinal cord atrophy in the atraumatically born neonate: one form of prenatal or perinatal ischaemic insult? 1269 May 68

Silent sinus syndrome is an insidious maxillary sinus inflammatory disease causing a lowering, thinning, or even absorption of the orbital floor. Patients usually present with progressive enophthalmos and hypoglobus. We report a 41-year-old man with silent sinus syndrome who presented with cyclovertical diplopia masquerading as superior oblique muscle paresis in the fellow eye. Inferior oblique myectomy in the fellow eye resulted in excellent alignment.
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PMID:Silent sinus syndrome causing cyclovertical diplopia masquerading as superior oblique paresis in the fellow eye. 2103 75

Churge-Strauss Syndrome belongs to systematic, necrotic inflammation of medium and small vessels diseases. In this paper it is presented a case of 63 years old man with benign asthma, recognized six month earlier. Later occurs fever, difficulties with breathing, cough, fast progressing paresis of tree limbs, thinning and nephrotic syndrome with fast growing renal failure. Base for recognition was clinical picture and laboratory tests which showed elevetion of inflammation parameters (CRP, ESR), eosinophilia (18%) and p-ANCA antibodies. Treatment with glucocorticosteroids and cyclophosphamide was started. After six month proteinuria decreased. Paresis regressed and patient's movement abilities were improved. Renal failure stayed in fourth stadium of chronic renal disease. The aim of this paper is presentation diagnostic difficulties of Churge-Strauss Syndrome of atypical course with fast growing renal failure with neurological complications.
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PMID:[Rapid course of Churge-Strauss syndrome--since appearance of asthma till development of renal failure and neurological complication]. 2256 82

An 8-day-old female Holstein Friesian calf was examined because of congenital spastic paresis of the hind limbs. Myelography revealed deviation and thinning of subarachnoid contrast medium columns in the lumbar segment. Upon magnetic resonance imaging, the 'hour-glass' subdural compression appeared as a T1-hypointense, T2-hyperintense ovoidal area suggestive of cerebral spinal fluid collection, compatible with hydrosyringomyelia. The calf was euthanized and the necropsy confirmed the diagnosis of segmental spinal cord hypoplasia of the lumbar tract associated to hydromyelic and syringomyelic cavities.
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PMID:Segmental spinal cord hypoplasia in a Holstein Friesian calf. 2309 95


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