The Legacy of Jonathan A. Ship

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/71579/1/j.1754-4505.2008.00031.x.pd

Integration of oral health care into geriatric primary care: proposal for collaboration

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/91312/1/j.1754-4505.2012.00255.x.pd

The development of the Coalition for Oral Health for the Aging

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/86896/1/j.1754-4505.2011.00206.x.pd

Oral healthcare systems for an ageing population: concepts and challenges

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/138847/1/idj12343_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/138847/2/idj12343.pd

Oral healthcare access and adequacy in alternative long-term care facilities

This study was undertaken to determine practices and perceived barriers to access related to oral health by surveying administrators in Michigan alternative long-term care facilities (ALTCF). A 24-item questionnaire was mailed to all 2,275 Michigan ALTCF serving residents aged 60+. Facility response rate was 22% (n = 508). Eleven percent of facilities had a written dental care plan; 18% stated a dentist examined new residents; and 19% of facilities had an agreement with a dentist to come to the facility, with 52% of those being for emergency care only. The greatest perceived barriers were willingness of general and specialty dentists to treat residents at the nursing facility and/or private offices as well as financial concerns. Substantial barriers to care were uniformly perceived.Oral health policies and practices within Michigan ALTCF vary, as measured by resources, attitudes, and the availability of professional care. There is limited involvement by dental professionals in creating policy and providing consultation and service.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/79086/1/j.1754-4505.2010.00132.x.pd

Heterogeneity of Signal Transducer and Activator of Transcription Binding Sites in the Long-Terminal Repeats of Distinct HIV-1 Subtypes

HIV-1 can be subdivided into distinct subtypes; the consequences of such a genomic variability remain largely speculative. The long terminal repeats (LTR) control HIV transcription and reflect the major differences of distinct viral subtypes. Three regions in the HIV-1 subtype B LTR are close matches to the Signal Transducer and Activator of Transcription (STAT) consensus sequence. Here, we show heterogeneity in these putative STAT binding sites among HIV-1 LTR subtypes A through G. Transfection of constitutively activated STAT5 lead to transcriptional activation of HIV-1 expression in 293T cells transfected with a reporter assay driven by HIV-1 LTR subtype B. Constitutively activated STAT5 transactivated the LTR of various subtypes in U937 cells with different potency. These findings support and expand the potential relevance of STAT5 activation in HIV infection and may bear relevance for a differential regulation of latency and expression of different subtypes of HIV-1

Digenic Leigh syndrome on the background of the m.11778G>A Leber hereditary optic neuropathy variant

Leigh syndrome spectrum (LSS) is a primary mitochondrial disorder defined neuropathologically by a subacute necrotizing encephalomyelopathy and characterized by bilateral basal ganglia and/or brainstem lesions. LSS is associated with variants in several mitochondrial DNA genes and more than 100 nuclear genes, most often related to mitochondrial complex I (CI) dysfunction. Rarely, LSS has been reported in association with primary Leber hereditary optic neuropathy (LHON) variants of the mitochondrial DNA, coding for CI subunits (m.3460G>A in MT-ND1, m.11778G>A in MT-ND4 and m.14484T>C in MT-ND6). The underlying mechanism by which these variants manifest as LSS, a severe neurodegenerative disease, as opposed to the LHON phenotype of isolated optic neuropathy, remains an open question. Here, we analyse the exome sequencing of six probands with LSS carrying primary LHON variants, and report digenic co-occurrence of the m.11778G > A variant with damaging heterozygous variants in nuclear disease genes encoding CI subunits as a plausible explanation. Our findings suggest a digenic mechanism of disease for m.11778G>A-associated LSS, consistent with recent reports of digenic disease in individuals manifesting with LSS due to biallelic variants in the recessive LHON-associated disease gene DNAJC30 in combination with heterozygous variants in CI subunits

Progranulin Gene Variability and Plasma Levels in Bipolar Disorder and Schizophrenia

Basing on the assumption that frontotemporal lobar degeneration (FTLD), schizophrenia and bipolar disorder (BPD) might share common aetiological mechanisms, we analyzed genetic variation in the FTLD risk gene progranulin (GRN) in a German population of patients with schizophrenia (n = 271) or BPD (n = 237) as compared with 574 age-, gender- and ethnicity-matched controls. Furthermore, we measured plasma progranulin levels in 26 German BPD patients as well as in 61 Italian BPD patients and 29 matched controls

A General Strategy to Endow Natural Fusion-protein-Derived Peptides with Potent Antiviral Activity

Fusion between the viral and target cell membranes is an obligatory step for the infectivity of all enveloped virus, and blocking this process is a clinically validated therapeutic strategy

Clinical, biochemical and genetic spectrum of 70 patients with ACAD9 deficiency: Is riboflavin supplementation effective?

Background: Mitochondrial acyl-CoA dehydrogenase family member 9 (ACAD9) is essential for the assembly of mitochondrial respiratory chain complex I. Disease causing biallelic variants in ACAD9 have been reported in individuals presenting with lactic acidosis and cardiomyopathy. Results: We describe the genetic, clinical and biochemical findings in a cohort of 70 patients, of whom 29 previously unpublished. We found 34 known and 18 previously unreported variants in ACAD9. No patients harbored biallelic loss of function mutations, indicating that this combination is unlikely to be compatible with life. Causal pathogenic variants were distributed throughout the entire gene, and there was no obvious genotype-phenotype correlation. Most of the patients presented in the first year of life. For this subgroup the survival was poor (50% not surviving the first 2 years) comparing to patients with a later presentation (more than 90% surviving 10 years). The most common clinical findings were cardiomyopathy (85%), muscular weakness (75%) and exercise intolerance (72%). Interestingly, severe intellectual deficits were only reported in one patient and