Subject(s)
Levodopa/therapeutic use , Parkinsonian Disorders/diagnosis , Parkinsonian Disorders/drug therapy , Spastic Paraplegia, Hereditary/diagnosis , Spastic Paraplegia, Hereditary/drug therapy , Adult , Humans , Male , Parkinsonian Disorders/complications , Pedigree , Spastic Paraplegia, Hereditary/complicationsSubject(s)
Autoantibodies/blood , Brain/pathology , Lupus Vasculitis, Central Nervous System/diagnosis , Anticonvulsants/therapeutic use , Azathioprine/therapeutic use , Brain/physiopathology , Cyclophosphamide/therapeutic use , Electroencephalography , Female , Humans , Immunosuppressive Agents/therapeutic use , Injections, Intravenous , Lupus Vasculitis, Central Nervous System/drug therapy , Lupus Vasculitis, Central Nervous System/immunology , Magnetic Resonance Imaging , Methylprednisolone/therapeutic use , Neuroprotective Agents/therapeutic use , Phenytoin/therapeutic use , Seizures/diagnosis , Seizures/etiology , Serologic Tests , Treatment OutcomeSubject(s)
Hypertensive Encephalopathy/diagnosis , Renin/metabolism , Adult , Amlodipine/therapeutic use , Antihypertensive Agents/therapeutic use , Doxazosin/therapeutic use , Drug Therapy, Combination , Female , Humans , Hypertensive Encephalopathy/drug therapy , Magnetic Resonance Imaging , Renin-Angiotensin System/physiology , Seizures/etiology , Syndrome , Treatment OutcomeSubject(s)
Copper/deficiency , Peripheral Nervous System Diseases/etiology , Postgastrectomy Syndromes/diagnosis , Anemia, Macrocytic/drug therapy , Anemia, Macrocytic/etiology , Ceruloplasmin/deficiency , Copper Sulfate/therapeutic use , Diagnostic Errors , Evoked Potentials , Female , Gait Disorders, Neurologic/diagnosis , Gluconates/therapeutic use , Humans , Iron Deficiencies , Magnetic Resonance Imaging , Middle Aged , Pain/etiology , Paresthesia/drug therapy , Paresthesia/etiology , Peripheral Nervous System Diseases/diagnosis , Postgastrectomy Syndromes/drug therapy , Spinal Cord/pathology , Time Factors , Vitamin B 12 Deficiency/etiology , Zinc/deficiencySubject(s)
Brain Diseases/microbiology , Brain Diseases/pathology , Immunocompromised Host , Nocardia Infections/immunology , Adult , Anemia, Hemolytic, Autoimmune/drug therapy , Anti-Bacterial Agents/therapeutic use , Anti-Inflammatory Agents/therapeutic use , Brain Diseases/drug therapy , Brain Neoplasms/pathology , Diagnosis, Differential , Female , Humans , Immunoglobulins, Intravenous/therapeutic use , Magnetic Resonance Imaging , Methylprednisolone/therapeutic use , Nocardia Infections/drug therapyABSTRACT
Major insights have been attained into the molecular pathology of the trinucleotide repeat neurodegenerative diseases over the past decade. Genetic definition has allowed subclassification into translated polyglutamine diseases, which are due to CAG repeat expansions, and a more heterogeneous group in which the trinucleotide repeat remains untranslated. The polyglutamine disorders are due to a toxic gain of function of mutant expanded proteins. Neuronal intranuclear inclusions (NIIs) characteristically occur. Protein misfolding, interference with DNA transcription and RNA processing, activation of apoptosis and dysfunction of cytoplasmic elements have all been invoked in the toxic process. The end result is apoptotic cell death with many aspects of neuronal function being perturbed. Promising progress has been made into arresting and reversing neurodegeneration in both cellular and animal models. The molecular mechanisms underlying the untranslated group remain less clear. Impedance of gene transcription secondary to abnormal DNA structures formed by repeats, modification of chromatin gene packaging and dysfunction at the RNA level have all been suggested as possible pathological mechanisms. These diseases remain irreversible. It is hoped that clarification of the molecular pathogenic mechanisms will provide the tools for future therapeutic intervention.
Subject(s)
Neurodegenerative Diseases/genetics , Trinucleotide Repeats , Animals , Humans , Huntington Disease/genetics , Intranuclear Inclusion Bodies/pathology , Mutation , Neurodegenerative Diseases/pathology , Peptides/geneticsSubject(s)
Adenocarcinoma/diagnosis , Adenocarcinoma/secondary , Brain Neoplasms/diagnosis , Brain Neoplasms/secondary , Prostatic Neoplasms/diagnosis , Headache/etiology , Horner Syndrome/etiology , Humans , Magnetic Resonance Imaging , Male , Mesencephalon/pathology , Middle Aged , Occipital Lobe , Pons/pathologyABSTRACT
Bradykinin contracts both the pig and rabbit iris sphincter preparations. In the pig, the bradykinin antagonists Lys,Lys-[Hyp3, Thi5,8,D-Phe7]-BK and D-Arg-[Hyp3,Thi5,D-Tic7,Oic8]-BK (HOE140) inhibited responses with pKB estimates of 6.0 and 8.4, respectively. These affinities are markedly lower than in the rabbit preparation, suggesting that different receptors are present in each of the two species.
