109,673 research outputs found
[Letter from H. T. Staiti to N. J. McLeod - December 27, 1905]
No full textLetter from H. T. Staiti to N. J. McLeod, discussing a matter which Staiti says he will be able to handle in "ten or fifteen days"
Mcleod, H S, NX18566
No full textThis record was harvested from a previous catalogue system and will be withdrawn in 2025. Information in this record may be superseded or incomplete. Visit this record in UMA's new catalogue at: https://archives.library.unimelb.edu.au/nodes/view/404058Surname: MCLEOD. Given Name(s) or Initials: H S. Military Service Number or Last Known Location: NX18566. Missing, Wounded and Prisoner of War Enquiry Card Index Number: 21534.240198
Item: [2016.0049.36350] "Mcleod, H S, NX18566
Mcleod, H C, 22815
No full textThis record was harvested from a previous catalogue system and will be withdrawn in 2025. Information in this record may be superseded or incomplete. Visit this record in UMA's new catalogue at: https://archives.library.unimelb.edu.au/nodes/view/404030Surname: MCLEOD. Given Name(s) or Initials: H C. Military Service Number or Last Known Location: 22815. Missing, Wounded and Prisoner of War Enquiry Card Index Number: 32497.240143
Item: [2016.0049.36322] "Mcleod, H C, 22815
Mcleod, K H, QX4550
No full textThis record was harvested from a previous catalogue system and will be withdrawn in 2025. Information in this record may be superseded or incomplete. Visit this record in UMA's new catalogue at: https://archives.library.unimelb.edu.au/nodes/view/404071Surname: MCLEOD. Given Name(s) or Initials: K H. Military Service Number or Last Known Location: QX4550. Missing, Wounded and Prisoner of War Enquiry Card Index Number: 1612.240224
Item: [2016.0049.36363] "Mcleod, K H, QX4550
Neuroacanthocytosis Syndromes
No full textNeuroacanthocytosis (NA) syndromes are a group of genetically defined diseases characterized by the association of red blood cell acanthocytosis and progressive degeneration of the basal ganglia. NA syndromes are exceptionally rare with an estimated prevalence of less than 1 to 5 per 1'000'000 inhabitants for each disorder. The core NA syndromes include autosomal recessive chorea-acanthocytosis and X-linked McLeod syndrome which have a Huntington's disease-like phenotype consisting of a choreatic movement disorder, psychiatric manifestations and cognitive decline, and additional multi-system features including myopathy and axonal neuropathy. In addition, cardiomyopathy may occur in McLeod syndrome. Acanthocytes are also found in a proportion of patients with autosomal dominant Huntington's disease-like 2, autosomal recessive pantothenate kinase-associated neurodegeneration and several inherited disorders of lipoprotein metabolism, namely abetalipoproteinemia (Bassen-Kornzweig syndrome) and hypobetalipoproteinemia leading to vitamin E malabsorption. The latter disorders are characterized by a peripheral neuropathy and sensory ataxia due to dorsal column degeneration, but movement disorders and cognitive impairment are not present. NA syndromes are caused by disease-specific genetic mutations. The mechanism by which these mutations cause neurodegeneration is not known. The association of the acanthocytic membrane abnormality with selective degeneration of the basal ganglia, however, suggests a common pathogenetic pathway. Laboratory tests include blood smears to detect acanthocytosis and determination of serum creatine kinase. Cerebral magnetic resonance imaging may demonstrate striatal atrophy. Kell and Kx blood group antigens are reduced or absent in McLeod syndrome. Western blot for chorein demonstrates absence of this protein in red blood cells of chorea-acanthocytosis patients. Specific genetic testing is possible in all NA syndromes. Differential diagnoses include Huntington disease and other causes of progressive hyperkinetic movement disorders. There are no curative therapies for NA syndromes. Regular cardiologic studies and avoidance of transfusion complications are mandatory in McLeod syndrome. The hyperkinetic movement disorder may be treated as in Huntington disease. Other symptoms including psychiatric manifestations should be managed in a symptom-oriented manner. NA syndromes have a relentlessly progressive course usually over two to three decades
McLeod myopathy revisited: more neurogenic and less benign
No full textThe X-linked McLeod neuroacanthocytosis syndrome (MLS) has originally been denoted as ‘benign' McLeod myopathy. We assessed the clinical findings and the muscle pathology in the eponymous index patient, Hugh McLeod, and in nine additional MLS patients. Only one patient had manifested with neuromuscular symptoms. During a mean follow-up of 15 years, however, eight patients including the initial index patient showed elevated skeletal muscle creatine kinase levels ranging from 300 to 3000 U/L, and had developed muscle weakness and atrophy. Two patients had disabling leg weakness. Muscle histology was abnormal in all 10 patients. Clear but unspecific myopathic changes were found in only four patients. All patients, however, had neurogenic changes of variable degree. Post-mortem motor and sensory nerve examinations support the view that muscle atrophy and weakness are predominantly due to an axonal motor neuropathy rather than to a primary myopathy. Multisystem manifestations developed in eight patients at a mean age of 39 years. Three patients manifested with psychiatric features comprising schizophrenia-like psychosis and personality disorder, two presented with generalized seizures and one with chorea. During follow-up, seven patients developed chorea, six had psychiatric disorders, five had cognitive decline and three had generalized seizures. Five patients died because of MLS-related complications including sudden cardiac death, chronic heart failure and pneumonia between 55 and 69 years. In conclusion, our findings confirm that MLS is not a benign condition but rather a progressive multisystem disorder sharing many features with Huntington's diseas
Guide to the microfilm edition of Mary McLeod Bethune papers
No full textBib id: 4775167 "Black studies research sources."; "pt. 1. Writings, diaries, scrapbooks, biographical materials and files on the National Youth Administration and women's organization, 1918-1955 / editorial adviser, Elaine M. Smith ; project coordinator and guide compiled by Randolph H. Boehm -- pt. 2. Correspondence files, 1914-1955 -- pt. 3. Subject files, 1939-1955 -- pt. 4. Administration of Bethune-Cookman College and the Mary Mcleod Bethune Foundation, 1915-1955.
Law Library, University of Idaho. Dean Menard and Walter H. McLeod shelving. [202-13]
No full text1974 photograph of the Law Library. Dean Menard and Walter H. McLeod shelve books in the new library. [PG1_202-13
Letter to Alexander Hamilton, Queenston, from Alexander McLeod, Sherriff’s Office, Niagara, 18 July 1837
No full textLetter to Alexander Hamilton, Queenston, from Alexander McLeod, Sherriff’s Office,
Niagara. The letter states that he has no doubt the youth will get bail, and he has
enclosed a bond. He notes that the prisoners almost killed Wheeler yesterday, and six
of the criminals escaped, but were all retaken. The locks in their door, which opens into
the debtors ward, were picked by some of the debtors. When the old man was going in,
they shoved open the door and made a rush on him, beating him unmercifully with
sticks. He was able to defend himself and delayed them in their progress until the alarm
was raised and they were eventually secured. He notes that the debtors would not
assist Wheeler. He also states that Morrison is at present boarding with Mr. H.
Thompson, July 18, 1837. Postmarked Niagara U.C. 18 July 1837 (date handwritten)
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