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PubMed2002

PKC-beta controls I kappa B kinase lipid raft recruitment and activation in response to BCR signaling.

NF-kappa B signaling is required for the maintenance of normal B lymphocytes, whereas dysregulated NF-kappa B activation contributes to B cell lymphomas. The events that regulate NF-kappa B signaling in B lymphocytes are poorly defined. Here, we demonstrate that PKC-beta is specifically required for B cell receptor (BCR)-mediated NF-kappa B activation. B cells from protein kinase C-beta (PKC-beta)-deficient mice failed to recruit the I kappa B kinase (IKK) complex into lipid rafts, activate IKK, degrade I kappa B or up-regulate NF-kappa B-dependent survival signals. Inhibition of PKC-beta promoted cell death in B lymphomas characterized by exaggerated NF-kappa B activity. Together, these data define an essential role for PKC-beta in BCR survival signaling and highlight PKC-beta as a key therapeutic target for B-lineage malignancies.

Animals↗

PubMed2005

Live attenuated recombinant vaccine protects nonhuman primates against Ebola and Marburg viruses.

Vaccines and therapies are urgently needed to address public health needs stemming from emerging pathogens and biological threat agents such as the filoviruses Ebola virus (EBOV) and Marburg virus (MARV). Here, we developed replication-competent vaccines against EBOV and MARV based on attenuated recombinant vesicular stomatitis virus vectors expressing either the EBOV glycoprotein or MARV glycoprotein. A single intramuscular injection of the EBOV or MARV vaccine elicited completely protective immune responses in nonhuman primates against lethal EBOV or MARV challenges. Notably, vaccine vector shedding was not detectable in the monkeys and none of the animals developed fever or other symptoms of illness associated with vaccination. The EBOV vaccine induced humoral and apparent cellular immune responses in all vaccinated monkeys, whereas the MARV vaccine induced a stronger humoral than cellular immune response. No evidence of EBOV or MARV replication was detected in any of the protected animals after challenge. Our data suggest that these vaccine candidates are safe and highly efficacious in a relevant animal model.

Animals↗

PubMed2024

Rare variant contribution to the heritability of coronary artery disease.

Whole genome sequences (WGS) enable discovery of rare variants which may contribute to missing heritability of coronary artery disease (CAD). To measure their contribution, we apply the GREML-LDMS-I approach to WGS of 4949 cases and 17,494 controls of European ancestry from the NHLBI TOPMed program. We estimate CAD heritability at 34.3% assuming a prevalence of 8.2%. Ultra-rare (minor allele frequency ≤ 0.1%) variants with low linkage disequilibrium (LD) score contribute ~50% of the heritability. We also investigate CAD heritability enrichment using a diverse set of functional annotations: i) constraint; ii) predicted protein-altering impact; iii) cis-regulatory elements from a cell-specific chromatin atlas of the human coronary; and iv) annotation principal components representing a wide range of functional processes. We observe marked enrichment of CAD heritability for most functional annotations. These results reveal the predominant role of ultra-rare variants in low LD on the heritability of CAD. Moreover, they highlight several functional processes including cell type-specific regulatory mechanisms as key drivers of CAD genetic risk.

Humans↗

PubMed2004

Failure to induce oral tolerance to a soluble protein in patients with inflammatory bowel disease.

BACKGROUND & AIMS: Defective suppressor/regulatory T-cell activation has been proposed as a mechanism to explain the uncontrolled inflammatory process seen in inflammatory bowel disease (IBD). Previous studies have suggested that inappropriate activation of CD4+ T cells may occur in the gastrointestinal tract in these patients. Because suppressor/regulatory T cells are thought to be one mechanism for the promotion of oral tolerance, we attempted to induce tolerance in normal controls (n = 21) and patients with either Crohn's disease (CD, n = 12) or ulcerative colitis (UC, n = 13). METHODS: Subjects were fed keyhole limpet hemocyanin (KLH) before subcutaneous immunization and booster immunization. Blood for KLH-induced T-cell proliferation and serum for anti-KLH antibody was obtained at baseline and after feeding, immunization, and booster. RESULTS: In the control group, KLH feeding (50 and 250 mg) before immunization and booster resulted in reduced KLH-specific T-cell proliferation compared with the group that was not fed KLH (P < 0.002). However, both CD and UC patients showed significantly enhanced proliferation, without tolerance induction, when compared with baseline values (P < 0.035 and 0.02, respectively). Serum antibody to KLH was present only after immunization in the control group; however, anti-KLH antibody was seen after oral administration in both the UC and CD groups. CONCLUSIONS: Taken together, these data suggest that oral antigen administration does not result in tolerance in CD and UC patients, and might actually result in active immunity. This may reflect an in vivo functional defect in mucosal suppression of immune responses in IBD.

Administration, Oral↗

PubMed2003

Effectiveness of pneumococcal polysaccharide vaccine in older adults.

BACKGROUND: Streptococcus pneumoniae is the chief cause of pneumonia in older adults, but it remains unclear whether use of the pneumococcal polysaccharide vaccine alters the overall risk of community-acquired pneumonia. In a large population of older adults, we assessed the effectiveness of the pneumococcal vaccine. METHODS: In this retrospective cohort study, 47,365 Group Health Cooperative members 65 years of age or older were assessed over a three-year period. The primary outcomes were hospitalization because of community-acquired pneumonia (validated by chart review), pneumonia in patients who were not hospitalized ("outpatient pneumonia," determined from administrative data sources), and pneumococcal bacteremia. The association between pneumococcal vaccination and the risk of each outcome was evaluated by means of multivariate Cox proportional-hazards models, with adjustment for age, sex, nursing-home residence or nonresidence, smoking status, medical conditions, and receipt or nonreceipt of influenza vaccine. RESULTS: During the study period, 1428 cohort members were hospitalized with community-acquired pneumonia, 3061 were assigned a diagnosis of outpatient pneumonia, and 61 had pneumococcal bacteremia. Receipt of the pneumococcal vaccine was associated with a significant reduction in the risk of pneumococcal bacteremia (hazard ratio, 0.56; 95 percent confidence interval, 0.33 to 0.93) but a slightly increased risk of hospitalization for pneumonia (hazard ratio, 1.14; 95 percent confidence interval, 1.02 to 1.28). Pneumococcal vaccination did not alter the risk of outpatient pneumonia (hazard ratio, 1.04; 95 percent confidence interval, 0.96 to 1.13) or of any case of community-acquired pneumonia, whether or not it required hospitalization (hazard ratio, 1.07; 95 percent confidence interval, 0.99 to 1.14). CONCLUSIONS: These findings support the effectiveness of the pneumococcal polysaccharide vaccine for the prevention of bacteremia, but they suggest that alternative strategies are needed to prevent nonbacteremic pneumonia, which is a more common manifestation of pneumococcal infection in elderly persons.

Age Factors↗

PubMed2005

Combined oral contraceptives in women with systemic lupus erythematosus.

BACKGROUND: Oral contraceptives are rarely prescribed for women with systemic lupus erythematosus, because of concern about potential negative side effects. In this double-blind, randomized, noninferiority trial, we prospectively evaluated the effect of oral contraceptives on lupus activity in premenopausal women with systemic lupus erythematosus. METHODS: A total of 183 women with inactive (76 percent) or stable active (24 percent) systemic lupus erythematosus at 15 U.S. sites were randomly assigned to receive either oral contraceptives (triphasic ethinyl estradiol at a dose of 35 microg plus norethindrone at a dose of 0.5 to 1 mg for 12 cycles of 28 days each; 91 women) or placebo (92 women) and were evaluated at months 1, 2, 3, 6, 9, and 12. Subjects were excluded if they had moderate or high levels of anticardiolipin antibodies, lupus anticoagulant, or a history of thrombosis. RESULTS: The primary end point, a severe lupus flare, occurred in 7 of 91 subjects receiving oral contraceptives (7.7 percent) as compared with 7 of 92 subjects receiving placebo (7.6 percent). The 12-month rates of severe flare were similar: 0.084 for the group receiving oral contraceptives and 0.087 for the placebo group (P=0.95; upper limit of the one-sided 95 percent confidence interval for this difference, 0.069, which is within the prespecified 9 percent margin for noninferiority). Rates of mild or moderate flares were 1.40 flares per person-year for subjects receiving oral contraceptives and 1.44 flares per person-year for subjects receiving placebo (relative risk, 0.98; P=0.86). In the group that was randomized to receive oral contraceptives, there was one deep venous thrombosis and one clotted graft; in the placebo group, there was one deep venous thrombosis, one ocular thrombosis, one superficial thrombophlebitis, and one death (after cessation of the trial). CONCLUSIONS: Our study indicates that oral contraceptives do not increase the risk of flare among women with systemic lupus erythematosus whose disease is stable.

Adolescent↗

PubMed2003

Infliximab monotherapy provides rapid and sustained benefit for plaque-type psoriasis.

BACKGROUND: Effective, rapid-acting, safe therapies are needed for the long-term treatment of psoriasis. OBJECTIVE: We sought to evaluate infliximab monotherapy in maintaining clinical benefit in psoriasis. METHODS: A total of 33 patients received 3 doses of 5 or 10 mg/kg of infliximab or placebo at weeks 0, 2, and 6 (double-blind phase). During the open-label phase (weeks 10-26), responding patients were evaluated for relapse (loss of at least half of the improvement in the Psoriasis Area Severity Index score at week 10) and retreated with open-label infliximab (5 or 10 mg/kg) as needed. Placebo nonresponders were treated with an induction regimen of infliximab (5 or 10 mg/kg) and followed up through week 26. RESULTS: In all, 29 patients received either 5 or 10 mg/kg of infliximab in the open-label extension. At week 26, psoriasis area severity index response was maintained in 40% and 73% of patients receiving 5 and 10 mg/kg of infliximab, respectively. CONCLUSION: Infliximab produced a rapid, effective, and sustainable (through week 26) effect in patients with moderate to severe psoriasis.

Adult↗

PubMed2005

A common haplotype in the complement regulatory gene factor H (HF1/CFH) predisposes individuals to age-related macular degeneration.

Age-related macular degeneration (AMD) is the most frequent cause of irreversible blindness in the elderly in developed countries. Our previous studies implicated activation of complement in the formation of drusen, the hallmark lesion of AMD. Here, we show that factor H (HF1), the major inhibitor of the alternative complement pathway, accumulates within drusen and is synthesized by the retinal pigmented epithelium. Because previous linkage analyses identified chromosome 1q25-32, which harbors the factor H gene (HF1/CFH), as an AMD susceptibility locus, we analyzed HF1 for genetic variation in two independent cohorts comprised of approximately 900 AMD cases and 400 matched controls. We found association of eight common HF1 SNPs with AMD; two common missense variants exhibit highly significant associations (I62V, chi2 = 26.1 and P = 3.2 x 10(-7) and Y402H, chi2 = 54.4 and P = 1.6 x 10(-13)). Haplotype analysis reveals that multiple HF1 variants confer elevated or reduced risk of AMD. One common at-risk haplotype is present at a frequency of 50% in AMD cases and 29% in controls [odds ratio (OR) = 2.46, 95% confidence interval (1.95-3.11)]. Homozygotes for this haplotype account for 24% of cases and 8% of controls [OR = 3.51, 95% confidence interval (2.13-5.78)]. Several protective haplotypes are also identified (OR = 0.44-0.55), further implicating HF1 function in the pathogenetic mechanisms underlying AMD. We propose that genetic variation in a regulator of the alternative complement pathway, when combined with a triggering event, such as infection, underlie a major proportion of AMD in the human population.

Aged↗

PubMed2004

Mechanistic analysis of the Saccharomyces cerevisiae kinesin Kar3.

Kar3 is a minus-end-directed microtubule motor that is implicated in meiotic and mitotic spindle function in Saccharomyces cerevisiae. To date, the only truncated protein of Kar3 that has been reported to promote unidirectional movement in vitro is GSTKar3. This motor contains an NH2-terminal glutathione S-transferase (GST) tag followed by the Kar3 sequence that is predicted to form an extended alpha-helical coiled-coil. The alpha-helical domain leads into the neck linker and COOH-terminal motor domain. Kar3 does not homodimerize with itself but forms a heterodimer with either Cik1 or Vik1, both of which are non-motor polypeptides. We evaluated the microtubule-GSTKar3 complex in comparison to the microtubule-Kar3 motor domain complex to determine the distinctive mechanistic features required for GSTKar3 motility. Our results indicate that ATP binding was significantly faster for GSTKar3 than that observed previously for the Kar3 motor domain. In addition, microtubule-activated ADP release resulted in an intermediate that bound ADP weakly in contrast to the Kar3 motor domain, suggesting that after ADP release, the microtubule-GSTKar3 motor binds ATP in preference to ADP. The kinetics also showed that GST-Kar3 readily detached from the microtubule rather than remaining bound for multiple ATP turnovers. These results indicate that the extended alpha-helical domain NH2-terminal to the catalytic core provides the structural transitions in response to the ATPase cycle that are critical for motility and that dimerization is not specifically required. This study provides the foundation to define the mechanistic contributions of Cik1 and Vik1 for Kar3 force generation and function in vivo.

Adenosine Diphosphate↗

PubMed2002

Adaptive skills and executive function in autism spectrum disorders.

There is active debate regarding the nature of executive dysfunction in autism. Additionally, investigations have yet to show a relationship between deficits in executive function and the everyday behavioral difficulties that may originate from them. The present study examined the relationship between executive abilities and adaptive behavior in 35 children with Autism Spectrum Disorders, using two parent reports of everyday functioning, the Vineland Adaptive Behavior Scales (VABS) and the Behavior Rating Inventory of Executive Function (BRIEF). Results found several relationships: The Initiate and Working Memory domains were negatively correlated with most domains of adaptive behavior. Also, the Communication and Socialization domains of the VABS were negatively correlated with several areas of executive functioning, suggesting that impairments in executive abilities are strongly associated with the deficits in communication, play and social relationships found in children with autism.

Adaptation, Psychological↗

PubMed2004

Electrophysiological alterations during hypnosis for ego-enhancement: a preliminary investigation.

EEG activity at the midfrontal (Fz) region was recorded during pre- and postbaselines, live hypnotic induction, arm levitation and progressive relaxation (PNR) deepening, and therapeutic ego-enhancing suggestions among 60 college student volunteers, previously screened with the Stanford Hypnotic Susceptibility Scale, Form C. Comparisons across conditions for delta, theta, alpha, and beta activity were made between low, moderate, high, and very high hypnotizable groups. Results indicated (a) significant increases in theta EEGs across the hypnosis process with a peak at PNR and a drop in theta thereafter to termination, with highs showing significantly more dramatic effects than moderates; (b) a similar inverted U-shaped pattern for beta EEGs across hypnosis conditions, with very highs significantly higher in beta power than moderates and lows, and with highs significantly higher than moderates; (c) general profile differences between the highs for theta and the highs and very highs for beta in comparison to the moderates and lows, with peak theta and beta power occurring during ego-enhancing suggestions for more highly hypnotizable participants; (d) a drop in alpha EEGs across the trance process with a return to baseline after hypnosis, with moderates showing significantly lower alpha power; and (e) an increase in delta power across conditions to PNR and then a decrease to post-hypnosis baseline, with moderates significantly lower than highs.

Adult↗

PubMedDate not supplied

Factors affecting parenting stress among biologically vulnerable toddlers.

Parenting a child with, or at risk for, a developmental delay or disability can be stressful. Abidin's parenting stress model was used as a framework to examine how several maternal, child, and family factors predict parent stress outcomes. Stepwise regression models revealed that maternal and child factors were significant contributors to parenting stress. However, family factors (income and family functioning) were not retained. Parenting stress was lower when child (cognitive and adaptive ability) and maternal (depression and child care competence) characteristics were more positive. Child cognitive ability was a strong contributor to total parenting stress and two parenting stress subscales. Findings suggest that these parents need stress lowering interventions such as supportive child care, respite relief, and a child behaviour-focused program.

Adaptation, Psychological↗

PubMed2002

Genomic rearrangements resulting in PLP1 deletion occur by nonhomologous end joining and cause different dysmyelinating phenotypes in males and females.

In the majority of patients with Pelizaeus-Merzbacher disease, duplication of the proteolipid protein gene PLP1 is responsible, whereas deletion of PLP1 is infrequent. Genomic mechanisms for these submicroscopic chromosomal rearrangements remain unknown. We identified three families with PLP1 deletions (including one family described elsewhere) that arose by three distinct processes. In one family, PLP1 deletion resulted from a maternal balanced submicroscopic insertional translocation of the entire PLP1 gene to the telomere of chromosome 19. PLP1 on the 19qtel is probably inactive by virtue of a position effect, because a healthy male sibling carries the same der(19) chromosome along with a normal X chromosome. Genomic mapping of the deleted segments revealed that the deletions are smaller than most of the PLP1 duplications and involve only two other genes. We hypothesize that the deletion is infrequent, because only the smaller deletions can avoid causing either infertility or lethality. Analyses of the DNA sequence flanking the deletion breakpoints revealed Alu-Alu recombination in the family with translocation. In the other two families, no homologous sequence flanking the breakpoints was found, but the distal breakpoints were embedded in novel low-copy repeats, suggesting the potential involvement of genome architecture in stimulating these rearrangements. In one family, junction sequences revealed a complex recombination event. Our data suggest that PLP1 deletions are likely caused by nonhomologous end joining.

Base Sequence↗

PubMed2004

Clinical, epidemiologic, and molecular evaluation of a clonal outbreak of methicillin-resistant Staphylococcus aureus infection.

San Francisco General Hospital (San Francisco, CA) experienced an overall increase in the recovery of methicillin-resistant Staphylococcus aureus (MRSA) isolates that were shown by pulsed-field gel electrophoresis to have a genotype (genotype A1) that was new to this institution. We performed a case-control study to identify risk factors for acquiring genotype A1 MRSA infection from 1 October 2001 to 19 July 2002. Patients with genotype A1 MRSA infection were compared with 2 control groups: MRSA-infected control patients (i.e., patients with infection due to non-genotype A1 MRSA) and non-MRSA infected control patients (i.e., hospitalized patients without MRSA infection). There were 41 case patients infected with genotype A1 MRSA, 99 control patients infected with MRSA, and 41 control patients without MRSA infection. Pneumonia, surgical wound infections, and line infections occurred more frequently among case patients. Intensive care unit exposure and invasive procedures conferred the greatest risk for genotype A1 MRSA infection in multivariate models. Case patients were not associated with increased mortality, after adjusting for age, comorbidities, and intensive care unit exposure. Genotype A1 MRSA caused a large nosocomial outbreak of infection that was associated with distinct risk factors and clinical manifestations.

Bacterial Typing Techniques↗

PubMed2004

Body-composition changes in the simian immunodeficiency virus-infected juvenile rhesus macaque.

BACKGROUND: Body-composition changes are common in individuals infected with human immunodeficiency virus. The purpose of the present study was to measure, as a model of wasting in acquired immunodeficiency syndrome (AIDS), longitudinal body-composition changes in macaques infected with simian immunodeficiency virus (SIV). METHODS: Twelve juvenile macaques were inoculated with SIVmac239. Immunologic, virologic, somatometric, and dual-energy x-ray-absorptiometry measurements were performed prospectively every 4 weeks for 72 weeks and were compared to measurements taken from 8 uninfected control macaques. RESULTS: During the first 4 weeks, body-fat percentage decreased in the SIV-infected macaques while lean-tissue percentage increased; during weeks 4-72, these macaques lost a greater percentage of total fat tissue but had more subcutaneous-fat deposition than did the uninfected control macaques. Just prior to death, the SIV-infected macaques that died (n=7) had a greater loss in body-mass index, abdominal fat, fat tissue, and lean tissue, compared with that in SIV-infected macaques that survived (n=5). CONCLUSIONS: Body-composition changes in SIV-infected juvenile macaques exhibit 3 phases: during acute infection, loss of body weight from fat tissue; a compensation period during which macaques grow, but at a reduced rate; and a terminal phase, during which tissue is lost from all body compartments. The SIV-infected juvenile macaque provides a useful model for the investigation of wasting in AIDS, particularly for pediatric AIDS wasting.

Abdomen↗

PubMed2005

The effect of micronutrient supplementation on disease progression and death in simian immunodeficiency virus-infected juvenile male rhesus macaques.

BACKGROUND: We investigated the impact that micronutrient supplementation has on the progression of simian acquired immunodeficiency syndrome (SAIDS). METHODS: Twenty-four simian immunodeficiency virus-infected juvenile male rhesus macaques were randomized into 2 groups. One group was given certified chow, and the other group was given chow and a supplement that contained 2-3 times the estimated nutritional requirement of micronutrients. Virological, immunological, and body composition measurements were taken every 4 weeks for 120 weeks. RESULTS: There was no difference between groups in weight gain, body mass index (BMI), crown-heel length, waist circumference, total tissue mass, lean mass, bone mineral content, or bone mineral density. The rhesus macaques on the supplemented diet had a higher death rate (hazard ratio, 2.39; P<.001) than those on the nonsupplemented diet; death in both groups was associated with a higher viral load set point during the early phase of infection. Additionally, higher body weight, BMI, crown-rump length, and lower viral load set point were protective from death in both groups. CONCLUSIONS: Micronutrient supplementation did not significantly alter the progression of SAIDS with respect to changes in body composition and immunological characteristics. A significantly higher rate of death was observed in rhesus macaques on the supplemented diet.

Animals↗

PubMed2006

Preoperative use of mupirocin for the prevention of healthcare-associated Staphylococcus aureus infections: a cost-effectiveness analysis.

OBJECTIVE: Staphylococcus aureus is the most common cause of healthcare-associated infections. Intranasal mupirocin treatment probably decreases S. aureus infections among colonized surgical patients. Using cost-effectiveness analysis, we evaluated the cost-effectiveness of preoperative use of mupirocin for the prevention of healthcare-associated S. aureus infections. METHODS: Three strategies were compared: (1) screen with nasal culture and give treatment to carriers, (2) give treatment to all patients without screening, and (3) neither screen nor treat. A societal perspective was taken. Adverse outcomes included bloodstream infection, pneumonia, surgical site infection, death due to underlying illness or infection, readmission, and the need for home health care. Data inputs were obtained from an extensive MEDLINE review and from publicly available government data sources. The following base-case data inputs (and ranges) for sensitivity analysis were used: rate of S. aureus carriage, 23.1% (19%-55%); efficacy of mupirocin treatment, 51% (8%-75%); mupirocin treatment cost, 48.36 US Dollars (24.18-57.74 US Dollars); and hospital costs of bloodstream infection, 25,128 US Dollars (6,194-40,211 US Dollars), pneumonia, 18,366 US Dollars (5,574-28,952 US Dollars), and surgical site infection 16,256 US Dollars (5,119-22,553 US Dollars). Widespread use of mupirocin has been associated with high levels of mupirocin resistance; therefore, a broad range of estimates for efficacy was tested in the sensitivity analysis. PATIENTS: The target population included patients undergoing nonemergent surgery requiring postoperative hospitalization. RESULTS: Both the screen-and-treat and treat-all strategies were cost saving, saving 102 US Dollars per patient screened and 88 US Dollars per patient treated, respectively. In 1-way sensitivity analyses, the model was robust with respect to all data inputs except for the efficacy of mupirocin treatment. If the efficacy is less than 16.1%, then the screen-and-treat strategy is cost incurring. A treat-all strategy was more cost saving if the rate of S. aureus carriage was greater than 42.7%, the mupirocin cost was less than 29.87 US Dollars, or nursing compensation was greater than 64.21 US Dollars per hour. CONCLUSION: Administration of mupirocin before surgery is cost saving, primarily because healthcare-associated infections are very expensive. The level of mupirocin efficacy is critical to the cost-effectiveness of this intervention.

Anti-Bacterial Agents↗

PubMed2006

Caspase-2-induced apoptosis requires bid cleavage: a physiological role for bid in heat shock-induced death.

The mechanisms through which Caspase-2 leads to cell death are controversial. Here we show, using a combination of cell-free and cell culture-based approaches, that cleavage of the Bcl-2-family protein Bid is required for the induction of apoptosis by Caspase-2. Caspase-2 promoted cytochrome c release from mitochondria in the presence of cytosol from wild-type, but not Bid-deficient, mouse embryonic fibroblasts (MEFs). Recombinant wild-type Bid, but not a noncleavable mutant (D59E), restored cytochrome c release. Similarly, Bid-null MEFs were relatively resistant to apoptosis triggered by active Caspase-2, and apoptosis was restored in Bid-null cells by the expression of wild-type, but not D59E, Bid. Finally, Bid-null MEFs were substantially more resistant to apoptosis induced by heat shock, which has been shown to be dependent on apical activation of Caspase-2. The data are consistent with a model in which Caspase-2 induces apoptosis via cleavage of Bid at D59 and the subsequent engagement of the mitochondrial (intrinsic) pathway.

Animals↗