Iowa Commission on the Status of African-Americans Annual Report, 2002

Annual report for the Iowa Commission on the Status of African-Americans.

Iowa Commission on the Status of African-Americans Annual Report, 2003

Annual report for the Iowa Commission on the Status of African-Americans.

Iowa Commission on the Status of African-Americans Annual Report, 2001

Annual report for the Iowa Commission on the Status of African-Americans.

The Iowa African-American Journal, July 1999, Vol. 5, no. 3

Newsletter for the Iowa Commission on the Status of African-Americans

The Iowa African-American Journal, January 2000, Vol. 6, no. 1

Newsletter for the Iowa Commission on the Status of African-Americans

The Iowa African-American Journal, July 2000, Vol. 6, no. 2

Newsletter for the Iowa Commission on the Status of African-Americans

The Iowa African-American Journal, November 2000, Vol. 6, no. 3

Newsletter for the Iowa Commission on the Status of African-Americans

The Iowa African-American Journal, Spring/Fall 2001, Vol. 7, no. 1

Newsletter for the Iowa Commission on the Status of African-Americans

The Iowa African-American Journal, Spring/Fall 2002, Vol. 8, no. 1

Newsletter for the Iowa Commission on the Status of African-Americans

The Iowa African-American Journal, Winter 2002/Spring 2003, Vol. 8, no. 2

Newsletter for the Iowa Commission on the Status of African-Americans

The Iowa African-American Journal, October 1999, Vol. 5, no. 4

Newsletter for the Iowa Commission on the Status of African-Americans

Iowa Commission on the Status of African-Americans, Strategic Plan, 2004

Strategic Plan for the Iowa Commission on the Status of African-Americans

African tick-bite fever: a new entity in the differential diagnosis of multiple eschars in travelers. Description of five cases imported from South Africa to Switzerland.

African tick-bite fever (ATBF) is a newly described spotted fever rickettsiosis that frequently presents with multiple eschars in travelers returning from sub-Saharan Africa and, to a lesser extent, from the West Indies. It is caused by the bite of an infected Amblyomma tick, whose hunting habits explain the typical presence of multiple inoculation skin lesions and the occurrence of clustered cases. The etiological agent of ATBF is Rickettsia africae, an emerging tick-borne pathogenic bacterium. We describe herein a cluster of five cases of ATBF occurring in Swiss travelers returning from South Africa. The co-incidental infections in these five patients and the presence of multiple inoculation eschars, two features pathognomonic of this rickettsial disease, suggested the diagnosis of ATBF. Indeed, the presence of at least one inoculation eschar is observed in 53-100% of cases and multiple eschars in 21-54%. Two patients presented regional lymphadenitis and one a mild local lymphangitis. Though a cutaneous rash is described in 15-46% of cases, no rash was observed in our series. ATBF was confirmed by serology. Thus, ATBF has recently emerged as one of the most important causes of flu-like illness in travelers returning from Southern Africa. The presence of one or multiple eschars of inoculation is an important clinical clue to the diagnosis. It can be confirmed by serology or by PCR of a biopsy of the eschar. Culture can also be done in reference laboratories. Dermatologists and primary care physicians should know this clinical entity, since an inexpensive and efficient treatment is available.

Neuron-to-neuron wild-type Tau protein transfer through a trans-synaptic mechanism: relevance to sporadic tauopathies.

BACKGROUND: In sporadic Tauopathies, neurofibrillary degeneration (NFD) is characterised by the intraneuronal aggregation of wild-type Tau proteins. In the human brain, the hierarchical pathways of this neurodegeneration have been well established in Alzheimer's disease (AD) and other sporadic tauopathies such as argyrophilic grain disorder and progressive supranuclear palsy but the molecular and cellular mechanisms supporting this progression are yet not known. These pathways appear to be associated with the intercellular transmission of pathology, as recently suggested in Tau transgenic mice. However, these conclusions remain ill-defined due to a lack of toxicity data and difficulties associated with the use of mutant Tau. RESULTS: Using a lentiviral-mediated rat model of hippocampal NFD, we demonstrated that wild-type human Tau protein is axonally transferred from ventral hippocampus neurons to connected secondary neurons even at distant brain areas such as olfactory and limbic systems indicating a trans-synaptic protein transfer. Using different immunological tools to follow phospho-Tau species, it was clear that Tau pathology generated using mutated Tau remains near the IS whereas it spreads much further using the wild-type one. CONCLUSION: Taken together, these results support a novel mechanism for Tau protein transfer compared to previous reports based on transgenic models with mutant cDNA. It also demonstrates that mutant Tau proteins are not suitable for the development of experimental models helpful to validate therapeutic intervention interfering with Tau spreading.

The Governor’s Task Force on African-Americans in Prison, 2001

Report produced by the Department of Corrections