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822 citation(s) found for "Kaiser, U B".

Albuminuria and the risk of incident stroke and stroke types in older adults
Aguilar, M.I., O’Meara, Ellen S. , Longstreth, W.T. , Hart, R. G., Katz, Ronit , Sarnak, Mark J. , Rifkin, Dena E. , Seliger, Stephen L. , Pérgola, Pablo E. , Shlipak, Michael G.

Neurology | September 2, 2010 | Volume: 75 | Issue: 15 | Pages: 1343-1350

10.1212/wnl.0b013e3181f73638 | PMID 20810996 Get It

Moesin1 and Ve-cadherin are required in endothelial cells during in vivo tubulogenesis
Kaiser, Mark S., Nasevicius, Aidas, Clark, Karl J. , Wadman, Shannon A., Roberg-Perez, Sharon E., Ekker, Stephen C. , Hackett, Perry B., McGrail, Maura , Essner, Jeffrey J. , Wang, Ying , Larson, Jon D. , Ekker, Stephen C , Clark, Karl J , McGrail, Maura , Essner, Jeffrey

Development | August 24, 2010 | Volume: 137 | Issue: 18 | Pages: 3119-3128

10.1242/dev.048785 | PMID 20736288 Get It

Endothelial tubulogenesis is a crucial step in the formation of functional blood vessels during angiogenesis and vasculogenesis. Here, we use in vivo imaging of living zebrafish embryos expressing fluorescent fusion proteins of β-Actin, α-Catenin, and the ERM family member Moesin1 (Moesin a), to define a novel cord hollowing process that occurs during the initial stages of tubulogenesis in intersegmental vessels (ISVs) in the embryo. We show that the primary lumen elongates along cell junctions between at least two endothelial cells during embryonic angiogenesis. Moesin1-EGFP is enriched around structures that resemble intracellular vacuoles, which fuse with the luminal membrane during expansion of the primary lumen. Analysis of silent heart mutant embryos shows that initial lumen formation in the ISVs is not dependent on blood flow; however, stabilization of a newly formed lumen is dependent upon blood flow. Zebrafish moesin1 knockdown and cell transplantation experiments demonstrate that Moesin1 is required in the endothelial cells of the ISVs for in vivo lumen formation. Our analyses suggest that Moesin1 contributes to the maintenance of apical/basal cell polarity of the ISVs as defined by adherens junctions. Knockdown of the adherens junction protein Ve-cadherin disrupts formation of the apical membrane and lumen in a cell-autonomous manner. We suggest that Ve-cadherin and Moesin1 function to establish and maintain apical/basal polarity during multicellular lumen formation in the ISVs.
Using temporal cycles in spontaneous speech to quantify linguistic impairments in patients with neurodegenerative disorders.
Kaiser, Eden, Pakhomov, Serguei , Boley, Daniel , Birnbaum, Angela K. , Knopman, David S.

The Journal of the Acoustical Society of America | March 23, 2010 | Volume: 127 | Issue: 3_Supplement | Pages: 1996-1996

10.1121/1.3385172 Get It

Fronto-temporal lobar degeneration (FTLD) is a form of dementia which may manifest through symptoms similar to Alzheimer’s, including language-specific impairment. Linguistic manifestations of the disorder are often described in subjective assessments of the disorder, but not always easily quantifiable using objective tests. This paper investigates a speech characteristic not yet assessed in FTLD patients, that of “temporal cycles” [Henderson et al. (1966); Butterworth and Goldman-Eisler (1979)]. Temporal cycles in the speech of healthy adults consist of alternating and roughly equal periods of fluent and hesitant speech [Roberts and Kirsner (2000)]. A time series analysis of temporal cycles was conducted using spontaneous speech from 45 adults diagnosed with FTLD. Patients’ cognitive functioning was assessed using the language-specific clinical dementia rating (CDR) scale by board-certified neurologists. Periodicity of temporal cycles was quantified using the proportion of the energy in the highest peak to the total energy in the power spectrum. It was found that this measure was correlated with independent CDR assessments. The results of this study indicate that temporal cycles may be used to characterize the effects of neurodegenerative disorders on speech communication. [Work supported by US NIA Grants Nos. R01-AG023195, P50-AG16574, P30-AG19610, and NIH NIA-1R01AG026390, and Univ. of MN Academic Health Center.]
Dyspnea and Wheezing after Adenosine Injection in a Patient with Eosinophilic Bronchitis
Cartin‐Ceba, Rodrigo , Aubry, Marie Christine, Lim, Kaiser G.

Case Reports in Medicine | November 8, 2009 | Volume: 2009 | Issue: No issue available | Pages: 1-4

10.1155/2009/356462 | PMID 19902011 Get It

A 58-year-old nonsmoker female was referred for evaluation of chronic cough of 13 months duration. After an initial work-up, the patient was diagnosed to have chronic cough due to eosinophilic bronchitis. The diagnostic work-up for eosinophilic bronchitis and bronchial biopsy is discussed. Eosinophilic bronchitis is differentiated from asthma. In addition, the patient developed dyspnea, flushing, and wheezing after the administration of adenosine during a cardiac stress test in spite of a negative methacholine challenge. This indirect stimulus of airway hyperresponsiveness suggests the possible involvement of mast cells in eosinophilic bronchitis.
Methods for Analysis in Pharmacogenomics: Lessons from the Pharmacogenetics Research Network Analysis Group
Srinivasan, Balaji S., Conti, David V. , Gu, Xiangjun, Haines, Jonathan L., Jorgenson, Eric , Kraja, Aldi T., Lasky‐Su, Jessica , Li, Lang , Rodin, Andréi S. , Province, Mike, Ritchie, Marylyn D. , Province, Michael A. , Chen, Jinbo , Cheng, Cheng , Duan, Shiwei , Fridley, Brooke L. , Wang, Dai , Conti, David V , Lasky-Su, Jessica , Province, Mike

Pharmacogenomics | February 10, 2009 | Volume: 10 | Issue: 2 | Pages: 243-251

10.2217/14622416.10.2.243 | PMID 19207025 Get It

Phase III Randomized, Placebo-Controlled, Double-Blind Trial of Risedronate for the Prevention of Bone Loss in Premenopausal Women Undergoing Chemotherapy for Primary Breast Cancer
Hines, Stephanie L., Mincey, Betty A., Sloan, Jeff A. , Thomas, Sachdev , Chottiner, Elaine G., Loprinzi, Charles L. , Carlson, Mark D., Atherton, Pamela J., Salim, Muhammad , Perez, Edith A. , Atherton, Philip J. , Atherton, Pamela J., Atherton, Philip J.

Journal of Clinical Oncology | December 16, 2008 | Volume: 27 | Issue: 7 | Pages: 1047-1053

10.1200/jco.2008.19.1783 | PMID 19075260 Get It

Purpose Risedronate prevents bone loss in postmenopausal women. The purpose of this study was to determine whether risedronate prevents bone loss in premenopausal women undergoing chemotherapy for breast cancer. Patients and Methods Premenopausal women undergoing chemotherapy for breast cancer were treated with oral calcium 600 mg and vitamin D 400 U daily and randomly assigned to receive oral risedronate 35 mg weekly or placebo, with all these therapies beginning within a month of the start of chemotherapy. Most chemotherapy regimens included anthracyclines, taxanes, or cyclophosphamide. Bone mineral density (BMD) was measured at baseline and 1 year. The primary end point was the change in lumbar spine (LS) BMD from baseline to 1 year. Results A total of 216 women enrolled; 170 women provided BMD data at 1 year. There was no difference in the mean change or percent change in LS BMD between groups, with a loss of 4.3% in the risedronate arm and 5.4% for placebo at 1 year (P = .18). Loss of BMD at the femoral neck and total hip were also similar between treatment groups. Risedronate was well tolerated, with no significant differences in adverse events compared with placebo, except that arthralgias and chest pain were worse in those receiving the placebos. Conclusion Risedronate did not prevent bone loss in premenopausal women undergoing adjuvant chemotherapy for breast cancer.
HYPERMANGANESEMIA, HEREDITARY HEMORRHAGIC TELANGIECTASIA, BRAIN ABSCESS: THE HEPATIC CONNECTION
Boeve, B. F., Cowl, Clayton T. , Ellison, Jay W., Kamath, Priyatham, Swanson, Karen L., Kumar, Naveen

Neurology | September 29, 2008 | Volume: 71 | Issue: 14 | Pages: 1118-1119

10.1212/01.wnl.0000326959.44088.e0 | PMID 18824676 Get It

Meeting Report: Consensus Statement—Parkinson’s Disease and the Environment: Collaborative on Health and the Environment and Parkinson’s Action Network (CHE PAN) Conference 26–28 June 2007
Bronstein, Jeff M. , Carvey, Paul M., Chen, Honglei , Cory‐Slechta, Deborah A. , Monte, Donato A. Di , Duda, John E. , English, Paul , Goldman, Samuel M. , Grate, Stephen J., Hoppin, Jane A. , Jewell, Sarah A. , Kamel, Freya , Langston, J. William, Logroscino, Giancarlo , Nelson, Lorene M. , Ravina, Bernard, Rocca, Walter A. , Ross, G. Webster, Schettler, Ted, Schwarzschild, Michael A. , Scott, Bill, Seegal, Richard F., Singleton, Andrew , Steenland, Kyle , Eeden, Stephen Van Den, Weisskopf, Marc G. , Hansen, Johnni , Koroshetz, Walter J. , Tanner, Caroline M. , Logroscino, Giancarlo

Environmental Health Perspectives | August 25, 2008 | Volume: 117 | Issue: 1 | Pages: 117-121

10.1289/ehp.11702 | PMID 19165397 Get It

Abstract Background Parkinson’s disease (PD) is the second most common neurodegenerative disorder. People with PD, their families, scientists, health care providers, and the general public are increasingly interested in identifying environmental contributors to PD risk. Methods In June 2007, a multidisciplinary group of experts gathered in Sunnyvale, California, USA, to assess what is known about the contribution of environmental factors to PD. Results We describe the conclusions around which they came to consensus with respect to environmental contributors to PD risk. We conclude with a brief summary of research needs. Conclusions PD is a complex disorder, and multiple different pathogenic pathways and mechanisms can ultimately lead to PD. Within the individual there are many determinants of PD risk, and within populations, the causes of PD are heterogeneous. Although rare recognized genetic mutations are sufficient to cause PD, these account for < 10% of PD in the U.S. population, and incomplete penetrance suggests that environmental factors may be involved. Indeed, interplay among environmental factors and genetic makeup likely influences the risk of developing PD. There is a need for further understanding of how risk factors interact, and studying PD is likely to increase understanding of other neurodegenerative disorders.
Early Experience with the Bioabsorbable Anal Fistula Plug
Lawes, Daniel, Efron, J., Abbas, Maher A. , Heppell, Jacques, Young‐Fadok, Tonia M.

World Journal of Surgery | March 28, 2008 | Volume: 32 | Issue: 6 | Pages: 1157-1159

10.1007/s00268-008-9504-1 | PMID 18373120 Get It

AbstractPurposeManagement of anal fistula represents a balance between curing the condition and maintaining anal continence. Recent reports of the results of the porcine anal fistula plug have demonstrated excellent fistula healing rates without reporting significant complications.MethodsThe outcome of patients who underwent treatment for anal fistula with the Surgisis® anal plug was retrospectively reviewed.ResultsTwenty patients were treated; three underwent concomitant anal advancement flap at the time of plug placement. Seventeen patients had a trans‐sphincteric fistula, and three had an anoperineal fistula. Ten patients had previously undergone failed surgical therapy to cure their fistula, including anal advancement flap in four, muscle interposition flap in two, fistulotomy in two, and cutting seton placement in two. Mean follow‐up was 7.4 months. Only 4 of 17 (24%) patients treated with the plug alone had closure of their fistula. Acute postoperative sepsis was seen in 5 of 17 (29%) patients treated with the plug alone. Four developed perianal abscesses that required incision and drainage, and one intersphincteric abscess was treated with antibiotics. Two of the patients who underwent concomitant anal advancement flaps and plug placement healed successfully.ConclusionsContrary to other published series, the use of the Surgisis® anal plug was associated with a low rate of fistula healing and a high incidence of perianal sepsis. The addition of a transanal advancement flap to the procedure may improve success rates.
Identification of Prognostic Biomarkers for Prostate Cancer
Kosari, Farhad , Munz, Jan Marie A., Savci‐Heijink, C. Dilara , Spiro, Craig, Klee, Eric W. , Kube, Dagmar Marie, Tillmans, Lori S. , Karnes, R. Jeffrey , Cheville, John C. , Vasmatzis, George , Slezak, Jeff M.

Clinical Cancer Research | March 17, 2008 | Volume: 14 | Issue: 6 | Pages: 1734-1743

10.1158/1078-0432.ccr-07-1494 | PMID 18347174 Get It

Abstract Purpose: This paper describes a process for the identification of genes that can report on the aggressiveness of prostate tumors and thereby add to the information provided by current pathologic analysis. Materials and Methods: Expression profiling data from over 100 laser capture microdissection derived samples from nonneoplastic epithelium; Gleason patterns 3, 4, and 5 and node metastasis prostate cancer were used to identify genes at abnormally high levels in only some tumors. These variably overexpressed genes were stratified by their association with aggressive phenotypes and were subsequently filtered to exclude genes with redundant expression patterns. Selected genes were validated in a case-control study in which cases (systemic progression within 5 years) and controls (no systemic progression at 7 years of follow-up) were matched for all clinical and pathologic criteria from time of prostatectomy (n = 175). Both cases and controls, therefore, could have nodal invasion or seminal vesicle involvement at the time of initial treatment. Results: A number of candidate variably overexpressed genes selected for their association with aggressive prostate cancer phenotype were evaluated in the case control study. The most prominent candidates were SSTR1 and genes related to proliferation, including TOP2A. Conclusions: The process described here identified genes that add information not available from current clinical measures and can improve the prognosis of prostate cancer.