Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Elucidation of the process of degeneration of injured axons is important for the development of therapeutic modules for the treatment of spinal cord injuries. The aim of this study was to establish a method for time-lapse observation of injured axons in living animals after spinal cord contusion injury. YFP (yellow fluorescent protein)-H transgenic mice, which we used in this study, express fluorescence in their nerve fibers. Contusion damage to the spinal cord at the 11th vertebra was performed by IH (Infinite Horizon) impactor, which applied a pressure of 50 kdyn. The damaged spinal cords were re-exposed during the observation period under anesthesia, and then observed by two-photon excited fluorescence microscopy, which can observe deep regions of tissues including spinal cord axons. No significant morphological change of injured axons was observed immediately after injury. Three days after injury, the number of axons decreased, and residual axons were fragmented. Seven days after injury, only fragments were present in the damaged tissue. No hind-limb movement was observed during the observation period after injury. Despite the immediate paresis of hind-limbs following the contusion injury, the morphological degeneration of injured axons was delayed. This method may help clarification of pathophysiology of axon degeneration and development of therapeutic modules for the treatment of spinal cord injury.
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PMID:Evaluation of Injured Axons Using Two-Photon Excited Fluorescence Microscopy after Spinal Cord Contusion Injury in YFP-H Line Mice. 2618 75

Kahlbaum was the first to propose catatonia as a separate disease following the example of general paresis of the insane, which served as a model for establishing a nosological entity. However, Kahlbaum was uncertain about the nosological position of catatonia and considered it a syndrome, or "a temporary stage or a part of a complex picture of various disease forms". Until recently, the issue of catatonia as a separate diagnostic category was not entertained, mainly due to a misinterpretation of Kraepelin's influential views on catatonia as a subtype of schizophrenia. Kraepelin concluded that patients presenting with persistent catatonic symptoms, which he called "genuine catatonic morbid symptoms", particularly including negativism, bizarre mannerisms, and stereotypes, had a poor prognosis similar to those of paranoid and hebephrenic presentations. Accordingly, catatonia was classified as a subtype of dementia praecox/schizophrenia. Despite Kraepelin's influence on psychiatric nosology throughout the 20th century, there have only been isolated attempts to describe and classify catatonia outside of the Kraepelinian system. For example, the Wernicke-Kleist-Leonhard school attempted to comprehensively elucidate the complexities of psychomotor disturbances associated with major psychoses. However, the Leonhardian categories have never been subjected to the scrutiny of modern investigations. The first three editions of the DSM included the narrow and simplified version of Kraepelin's catatonia concept. Recent developments in catatonia research are reflected in DSM-5, which includes three diagnostic categories: Catatonic Disorder due to Another Medical Condition, Catatonia Associated with another Mental Disorder (Catatonia Specifier), and Unspecified Catatonia. Additionally, the traditional category of catatonic schizophrenia has been deleted. The Unspecified Catatonia category could encourage research exploring catatonia as an independent diagnostic entity.
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PMID:Catatonia as a putative nosological entity: A historical sketch. 2904 55