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)

Previous studies have shown that the concentrations of 3', 5' cyclic adenosine monophosphate (cAMP) and 3', 5' cyclic guanosine monophosphate (cGMP) in cerebrospinal fluid (CSF), brain, or both, are increased by melanotropic peptides and catechol amines, and by cholinergic agents. The present study measured the concentrations of cAMP, cGMP, and melanotropic activity in the CSF of normal patients and in 136 subjects with various neurologic diseases. In normal lumbar CSF, concentrations (ave +/- SD) were: cAMP, 21 +/- 8 mM; cGMP, 2.4 +/- 0.5 mM; melanotropic activity, 17 +/- 6 units/100 ml. Concentrations of cAMP, cGMP, and melanotropic activity did not differ significantly (P is less than .05) from normal in the following categories of adult and pediatric patients: back pain due to vertigo of unknown cause; cerebral atrophy; cerebral vascular disease; and brain tumor subdural hematoma not causing increased ventricular pressure. Nine children with retarded psychomotor development caused by diffuse brain disease (infection, trauma, hemorrhage, degenerative process, long-standing hydrocephalus with thinning of the cerebral mantle) had subnormal levels of cAMP and melanotropic activity. These two variables were significantly correlated in the entire series of CSF samples (r=+0.55, P is less than .005). cGMP was elevated in the ventricular fluid of adult and pediatric patients when the ventricular pressure was abnormally elevated. The nucleotide's level rose as high as 50 X normal when ventricular pressure exceeded 300 mm H2O. The concentration of ventricular cGMP was proportional to that of ventricular pressure (r=+0.76, P is less than .005). The correlation was similar regardless of the type of hydrocephalus (congenital or acquired, communicating or obstructive), the age of the patient, or the nature of the underlying disease.
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PMID:Observations on the cyclic nucleotide concentrations in human cerebrospinal fluid. 18 45

A series of six cases of cerebral tumor with ipsilateral cerebral hemiatrophy, including four cases admitted at our institute, were studied. Various common clinical features were noted in these six cases. The mechanism whereby ipsilateral hemiatrophy of the cerebrum arises from brain tumor has been discussed on the basis of symptomatologic and clinicopathologic findings noted in these 6 cases. 1) The onset of the disease was between 8 and 14 years of age with a mean of 11 years and 8 months; thus all the 6 patients being juvenile. 2) Presenting symptoms developed from 1 year and 2 months to 4 years before admission, with an average of 2 years and 1 month. The clinical course was therefore relatively chronic in every case. 3) Presenting symptoms were: decline of school work, hemiparesis and loss of consciousness. These symptoms were all progressive throughout the course. The principal symptoms were hemiparesis, hemihypoesthesia, character and emotional changes, deterioration of mental faculties and behavioral abnormalities. No sign or symptom of significant increase of intracranial pressure were observed in any case. 4) Ipsilateral cerebral hemiatrophy on the tumor side was evidenced by carotid angiography and by pneumoencephalography. 5) The common site of tumor in this series was the thalamus and its surrounding areas. 6) The tumor was invariably a pinealoma which seemed to be ectopic in every case. 7) The obtained histopathological findings suggest that the ipsilateral cerebral hemiatrophy was due to thinning of the cerebral cortex with degeneration and disappearance of ganglion cells, demyelination in the subcortex and destruction of axons. Our speculated mechanism of ipsilateral cerebral hemiatrophy due to thalamic tumor is that thalamic tumor causes the degeneration and disappearance of thalamic ganglion cells and nerve fibers, consequently occurring secondary Waller's degeneration of afferent and projecting fibers from the thalamus as well as retrograde degeneration of efferent fibers, thus resulting in an extensive atrophy of the cerebral cortex and subcortical tissue.
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PMID:Brain tumor with ipsilateral cerebral hemiatrophy in children. 52 47

Early imaging or blood biomarkers of tumor response are desperately needed to customize antiangiogenic therapy for cancer patients. Anti-vascular endothelial growth factor (VEGF) therapy can "normalize" brain tumor vasculature by decreasing vessel diameter and permeability, and thinning the abnormally thick basement membrane. We hypothesized that the extent of vascular normalization will be predictive of outcome of anti-VEGF therapy in glioblastoma. We used advanced magnetic resonance imaging methods to monitor vascular parameters and treatment response in 31 recurrent glioblastoma patients enrolled in a phase II trial of cediranib, an oral pan-VEGF receptor tyrosine kinase inhibitor. We evaluated the correlation between clinical outcome and magnetic resonance imaging-measured changes in vascular permeability/flow (i.e., K(trans)) and in microvessel volume, and the change of circulating collagen IV levels, all after a single dose of cediranib. Here, we show that evaluation of biomarkers as early as after one day of anti-VEGF therapy with cediranib is predictive of response in patients with recurrent glioblastoma. Changes in K(trans), microvessel volume, and circulating collagen IV correlated with duration of overall survival and/or progression-free survival (P < 0.05). When we combined these three parameters into a "vascular normalization index," we found that it closely associated with overall survival (rho = 0.54; P = 0.004) and progression-free survival (rho = 0.6; P = 0.001). The vascular normalization index described here should be validated in randomized clinical trials.
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PMID:A "vascular normalization index" as potential mechanistic biomarker to predict survival after a single dose of cediranib in recurrent glioblastoma patients. 1954 89

To describe the morphologic magnetic resonance imaging (MRI) findings in histologically proven therapy-induced cerebral necrosis. We retrospectively reviewed the morphologic MRI findings in patients with therapy-induced cerebral necrosis. Images were reviewed for size, location, and characteristics of signal intensity abnormalities and T1-contrast enhancement. Images were also assessed for mass effect, necrosis, cyst, atrophy, cortical thinning, and leukoencephalopathy. The individual imaging characteristics were correlated with clinical and treatment variables. There were 44 patients. Seventy percent had a glioma, all patients had received radiation, and 57% had received chemotherapy in close proximity to radiation. All images demonstrated contrast enhancement, predominantly in the white matter. Enhancement was present in the periventricular/subependymal region in 50% of cases and the corpus callosum in 27%. The most common pattern of lesion peripheral enhancement was "spreading wavefront" and of interior enhancement was "Swiss cheese/soap bubble." The enhancing lesion was single in 60% of cases. Mass effect was present in 93% of patients. Location and patterns of enhancement were significantly associated with the interval from brain radiation to the diagnosis of therapy-induced cerebral necrosis, tumor histology, patient age, type of radiation, and administration of systemic chemotherapy. This is the largest study of the morphologic conventional MRI findings in pathologically confirmed therapy-induced cerebral necrosis. We characterized the imaging findings in a variety of tumor types following a variety of radiation treatments and other antineoplastic therapy. These findings may be of value in identifying therapy-induced cerebral necrosis in patients treated for a brain tumor.
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PMID:Morphologic magnetic resonance imaging features of therapy-induced cerebral necrosis. 2049 Jun 12