Recent Stanford Publications in PubMedSubscribe to Recent Stanford Publications in PubMed
- Clinical Trials of Adult Stem Cell Therapy for Peripheral Artery Disease.Botham CM, Bennett WL, Cooke JPMethodist Debakey Cardiovasc J
- Deconstructing complexin function in activating and clamping Ca2+-triggered exocytosis by comparing knockout and knockdown phenotypes.Yang X, Cao P, Südhof TCProc Natl Acad Sci U S A
- Akt activation enhances ribosomal RNA synthesis through casein kinase II and TIF-IA.Nguyen LX, Mitchell BSProc Natl Acad Sci U S A
- Imputation-based assessment of next generation rare exome variant arrays.Martin AR, Tse G, Bustamante CD, Kenny EEPac Symp Biocomput
- Path-scan: a reporting tool for identifying clinically actionable variants.Daneshjou R, Zappala Z, Kukurba K, Boyle SM, Ormond KE, Klein TE, Snyder M, Bustamante CD, Altman RB, Montgomery SBPac Symp Biocomput
- Multiplex meta-analysis of medulloblastoma expression studies with external controls.Morgan AA, Achrol AS, Li MD, Khatri PJ, Cheshier SHPac Symp Biocomput
- Hierarchical Approximate Bayesian Computation.Turner BM, Van Zandt TPsychometrika
- Understanding protein folding using markov state models.Pande VSAdv Exp Med Biol
- Type I interferon signaling genes in recurrent major depression: increased expression detected by whole-blood RNA sequencing.Mostafavi S, Battle A, Zhu X, Potash JB, Weissman MM, Shi J, Beckman K, Haudenschild C, McCormick C, Mei R, Gameroff MJ, Gindes H, Adams P, Goes FS, Mondimore FM, Mackinnon DF, Notes L, Schweizer B, Furman D, Montgomery SB, Urban AE, Koller D, Levinson DFMol Psychiatry
- 18F-FDG PET/CT in the management of patients with post-transplant lymphoproliferative disorder.Takehana CS, Twist CJ, Mosci C, Quon A, Mittra E, Iagaru ANucl Med Commun
- Optimization and comprehensive characterization of a faithful tissue culture model of the benign and malignant human prostate.Maund SL, Nolley R, Peehl DMLab Invest
- Co-Stimulation Modulation with Abatacept in Patients with Recent-Onset Type 1 Diabetes: Follow-Up One Year After Cessation of Treatment.Orban T, Bundy B, Becker DJ, Dimeglio LA, Gitelman SE, Goland R, Gottlieb PA, Greenbaum CJ, Marks JB, Monzavi R, Moran A, Peakman M, Raskin P, Russell WE, Schatz D, Wherrett DK, Wilson DM, Krischer JP, Skyler JS, The Type 1 Diabetes TrialNet Abatacept Study GroupDiabetes Care
- T-cell aging in rheumatoid arthritis.Weyand CM, Yang Z, Goronzy JJCurr Opin Rheumatol
- More Than a Billion People Taking Statins?: Potential Implications of the New Cardiovascular Guidelines.Ioannidis JPJAMA
- Regulatory T Cells and the Immune Aging Process: A Mini-Review.Jagger A, Shimojima Y, Goronzy JJ, Weyand CMGerontology
- Facts about FCE (Fludarabine, Cytarabine, Etoposide) in Acute Myeloid Leukemia.Medeiros BCActa Haematol
- Helicobacter and salmonella persistent infection strategies.Monack DMCold Spring Harb Perspect Med
- The FAST and E-FAST in 2013: Trauma Ultrasonography: Overview, Practical Techniques, Controversies, and New Frontiers.Williams SR, Perera P, Gharahbaghian LCrit Care Clin
- Thoracic ultrasonography.Lobo V, Weingrow D, Perera P, Williams SR, Gharahbaghian LCrit Care Clin
- Cardiac echocardiography.Perera P, Lobo V, Williams SR, Gharahbaghian LCrit Care Clin
Clinical Trials of Adult Stem Cell Therapy for Peripheral Artery Disease.
Methodist Debakey Cardiovasc J. 2013 10;9(4):201-205
Authors: Botham CM, Bennett WL, Cooke JP
Peripheral artery disease (PAD) refers to noncoronary vascular disease affecting the peripheral arteries. Most commonly the term is applied to occlusive arterial disease affecting the limb arteries, typically due to atherosclerosis. Preclinical studies indicate that a variety of stem cell therapies provide growth factors and cytokines for therapeutic angiogenesis. Small clinical trials with bone marrow mononuclear cells, as well as other cell types, have shown promise. However, mechanisms of therapeutic effect, if any, are not understood. Definitive clinical trials are needed to determine if there are any beneficial effects on functional capacity or morbidity.
PMID: 24298310 [PubMed - as supplied by publisher]
Deconstructing complexin function in activating and clamping Ca2+-triggered exocytosis by comparing knockout and knockdown phenotypes.
Proc Natl Acad Sci U S A. 2013 Dec 2;
Authors: Yang X, Cao P, Südhof TC
Complexin, a presynaptic protein that avidly binds to assembled SNARE complexes, is widely acknowledged to activate Ca(2+)-triggered exocytosis. In addition, studies of invertebrate complexin mutants and of mouse neurons with a double knockdown (DKD) of complexin-1 and -2 suggested that complexin maintains the readily releasable pool (RRP) of vesicles and clamps spontaneous exocytosis. In contrast, studies of mouse neurons with a double knockout (DKO) of complexin-1 and -2, largely carried out in hippocampal autapses, did not detect changes in the RRP size or in spontaneous exocytosis. To clarify complexin function, we here directly compared in two different preparations, cultured cortical and olfactory bulb neurons, the phenotypes of complexin DKD and DKO neurons. We find that complexin-deficient DKD and DKO neurons invariably exhibit a ∼50% decrease in vesicle priming. Moreover, the DKD consistently increased spontaneous exocytosis, but the DKO did so in cortical but not olfactory bulb neurons. Furthermore, the complexin DKD but not the complexin DKO caused a compensatory increase in complexin-3 and -4 mRNA levels; overexpression of complexin-3 but not complexin-1 increased spontaneous exocytosis. Complexin-3 but not complexin-1 contains a C-terminal lipid anchor attaching it to the plasma membrane; addition of a similar lipid anchor to complexin-1 converted complexin-1 from a clamp into an activator of spontaneous exocytosis. Viewed together, our data suggest that complexin generally functions in priming and Ca(2+) triggering of exocytosis, and additionally contributes to the control of spontaneous exocytosis dependent on the developmental history of a neuron and on the subcellular localization of the complexin.
PMID: 24297916 [PubMed - as supplied by publisher]
Akt activation enhances ribosomal RNA synthesis through casein kinase II and TIF-IA.
Proc Natl Acad Sci U S A. 2013 Dec 2;
Authors: Nguyen LX, Mitchell BS
Transcription initiation factor I (TIF-IA) plays an essential role in regulating ribosomal RNA (rRNA) synthesis by tethering RNA polymerase I (Pol I) to the rDNA promoter. We have found that activated Akt enhances rRNA synthesis through the phosphorylation of casein kinase IIα (CK2α) on a threonine residue near its N terminus. CK2 in turn phosphorylates TIF-IA, thereby increasing rDNA transcription. Activated Akt also stabilizes TIF-IA, induces its translocation to the nucleolus, and enhances its interaction with Pol I. Treatment with AZD8055, an inhibitor of both Akt and mammalian target of rapamycin phosphorylation, but not with rapamycin, disrupts Akt-mediated TIF-IA stability, translocation, and activity. These data support a model in which activated Akt enhances rRNA synthesis both by preventing TIF-IA degradation and phosphorylating CK2α, which in turn phosphorylates TIF-IA. This model provides an explanation for the ability of activated Akt to promote cell proliferation and, potentially, transformation.
PMID: 24297901 [PubMed - as supplied by publisher]
Imputation-based assessment of next generation rare exome variant arrays.
Pac Symp Biocomput. 2014;19:241-52
Authors: Martin AR, Tse G, Bustamante CD, Kenny EE
A striking finding from recent large-scale sequencing efforts is that the vast majority of variants in the human genome are rare and found within single populations or lineages. These observations hold important implications for the design of the next round of disease variant discovery efforts-if genetic variants that influence disease risk follow the same trend, then we expect to see population-specific disease associations that require large sample sizes for detection. To address this challenge, and due to the still prohibitive cost of sequencing large cohorts, researchers have developed a new generation of low-cost genotyping arrays that assay rare variation previously identified from large exome sequencing studies. Genotyping approaches rely not only on directly observing variants, but also on phasing and imputation methods that use publicly available reference panels to infer unobserved variants in a study cohort. Rare variant exome arrays are intentionally enriched for variants likely to be disease causing, and here we assay the ability of the first commercially available rare exome variant array (the Illumina Infinium HumanExome BeadChip) to also tag other potentially damaging variants not molecularly assayed. Using full sequence data from chromosome 22 from the phase I 1000 Genomes Project, we evaluate three methods for imputation (BEAGLE, MaCH-Admix, and SHAPEIT2/IMPUTE2) with the rare exome variant array under varied study panel sizes, reference panel sizes, and LD structures via population differences. We find that imputation is more accurate across both the genome and exome for common variant arrays than the next generation array for all allele frequencies, including rare alleles. We also find that imputation is the least accurate in African populations, and accuracy is substantially improved for rare variants when the same population is included in the reference panel. Depending on the goals of GWAS researchers, our results will aid budget decisions by helping determine whether money is best spent sequencing the genomes of smaller sample sizes, genotyping larger sample sizes with rare and/or common variant arrays and imputing SNPs, or some combination of the two.
PMID: 24297551 [PubMed - in process]
Path-scan: a reporting tool for identifying clinically actionable variants.
Pac Symp Biocomput. 2014;19:229-40
Authors: Daneshjou R, Zappala Z, Kukurba K, Boyle SM, Ormond KE, Klein TE, Snyder M, Bustamante CD, Altman RB, Montgomery SB
The American College of Medical Genetics and Genomics (ACMG) recently released guidelines regarding the reporting of incidental findings in sequencing data. Given the availability of Direct to Consumer (DTC) genetic testing and the falling cost of whole exome and genome sequencing, individuals will increasingly have the opportunity to analyze their own genomic data. We have developed a web-based tool, PATH-SCAN, which annotates individual genomes and exomes for ClinVar designated pathogenic variants found within the genes from the ACMG guidelines. Because mutations in these genes predispose individuals to conditions with actionable outcomes, our tool will allow individuals or researchers to identify potential risk variants in order to consult physicians or genetic counselors for further evaluation. Moreover, our tool allows individuals to anonymously submit their pathogenic burden, so that we can crowd source the collection of quantitative information regarding the frequency of these variants. We tested our tool on 1092 publicly available genomes from the 1000 Genomes project, 163 genomes from the Personal Genome Project, and 15 genomes from a clinical genome sequencing research project. Excluding the most commonly seen variant in 1000 Genomes, about 20% of all genomes analyzed had a ClinVar designated pathogenic variant that required further evaluation.
PMID: 24297550 [PubMed - in process]
Multiplex meta-analysis of medulloblastoma expression studies with external controls.
Pac Symp Biocomput. 2014;19:99-109
Authors: Morgan AA, Achrol AS, Li MD, Khatri PJ, Cheshier SH
We propose and discuss a method for doing gene expression meta-analysis (multiple datasets) across multiplex measurement modalities measuring the expression of many genes simultaneously (e.g. microarrays and RNAseq) using external control samples and a method of heterogeneity detection to identify and filter on comparable gene expression measurements. We demonstrate this approach on publicly available gene expression datasets from samples of medulloblastoma and normal cerebellar tissue and identify some potential new targets in the treatment of medulloblastoma.
PMID: 24297537 [PubMed - in process]
Hierarchical Approximate Bayesian Computation.
Psychometrika. 2013 Dec 3;
Authors: Turner BM, Van Zandt T
Approximate Bayesian computation (ABC) is a powerful technique for estimating the posterior distribution of a model's parameters. It is especially important when the model to be fit has no explicit likelihood function, which happens for computational (or simulation-based) models such as those that are popular in cognitive neuroscience and other areas in psychology. However, ABC is usually applied only to models with few parameters. Extending ABC to hierarchical models has been difficult because high-dimensional hierarchical models add computational complexity that conventional ABC cannot accommodate. In this paper, we summarize some current approaches for performing hierarchical ABC and introduce a new algorithm called Gibbs ABC. This new algorithm incorporates well-known Bayesian techniques to improve the accuracy and efficiency of the ABC approach for estimation of hierarchical models. We then use the Gibbs ABC algorithm to estimate the parameters of two models of signal detection, one with and one without a tractable likelihood function.
PMID: 24297436 [PubMed - as supplied by publisher]
Understanding protein folding using markov state models.
Adv Exp Med Biol. 2014;797:101-6
Authors: Pande VS
PMID: 24297278 [PubMed - in process]
Type I interferon signaling genes in recurrent major depression: increased expression detected by whole-blood RNA sequencing.
Mol Psychiatry. 2013 Dec 3;
Authors: Mostafavi S, Battle A, Zhu X, Potash JB, Weissman MM, Shi J, Beckman K, Haudenschild C, McCormick C, Mei R, Gameroff MJ, Gindes H, Adams P, Goes FS, Mondimore FM, Mackinnon DF, Notes L, Schweizer B, Furman D, Montgomery SB, Urban AE, Koller D, Levinson DF
A study of genome-wide gene expression in major depressive disorder (MDD) was undertaken in a large population-based sample to determine whether altered expression levels of genes and pathways could provide insights into biological mechanisms that are relevant to this disorder. Gene expression studies have the potential to detect changes that may be because of differences in common or rare genomic sequence variation, environmental factors or their interaction. We recruited a European ancestry sample of 463 individuals with recurrent MDD and 459 controls, obtained self-report and semi-structured interview data about psychiatric and medical history and other environmental variables, sequenced RNA from whole blood and genotyped a genome-wide panel of common single-nucleotide polymorphisms. We used analytical methods to identify MDD-related genes and pathways using all of these sources of information. In analyses of association between MDD and expression levels of 13 857 single autosomal genes, accounting for multiple technical, physiological and environmental covariates, a significant excess of low P-values was observed, but there was no significant single-gene association after genome-wide correction. Pathway-based analyses of expression data detected significant association of MDD with increased expression of genes in the interferon α/β signaling pathway. This finding could not be explained by potentially confounding diseases and medications (including antidepressants) or by computationally estimated proportions of white blood cell types. Although cause-effect relationships cannot be determined from these data, the results support the hypothesis that altered immune signaling has a role in the pathogenesis, manifestation, and/or the persistence and progression of MDD.Molecular Psychiatry advance online publication, 3 December 2013; doi:10.1038/mp.2013.161.
PMID: 24296977 [PubMed - as supplied by publisher]
18F-FDG PET/CT in the management of patients with post-transplant lymphoproliferative disorder.
Nucl Med Commun. 2013 Nov 27;
Authors: Takehana CS, Twist CJ, Mosci C, Quon A, Mittra E, Iagaru A
OBJECTIVES: Post-transplant lymphoproliferative disorder (PTLD) is a rare but serious complication in transplant patients. Although fluorine-18 2-fluoro-2-deoxyglucose PET and computed tomography (F-FDG PET/CT) has been used for the evaluation and management of patients with PTLD, its utility has yet to be documented. We were therefore prompted to review our experience with F-FDG PET/CT in PTLD.
MATERIALS AND METHODS: We retrospectively reviewed the records of consecutive patients who had undergone F-FDG PET/CT for evaluation of PTLD from January 2004 to June 2012 at our institution. F-FDG PET/CT scans were compared with other imaging modalities performed concurrently. A chart review of pertinent clinical information was also conducted.
RESULTS: A total of 30 patients were identified (14 female and 16 male; 1.7-76.7 years of age, average: 23.8 years). Twenty-seven participants had biopsy-proven PTLD and another three had been treated for PTLD because of high clinical suspicion of disease and positive F-FDG PET/CT findings in the absence of histological diagnosis. Eighty-three percent of these PTLD patients had extranodal involvement. In 57% of the cases, F-FDG PET/CT detected occult lesions not identified on other imaging modalities or suggested PTLD in equivocal lesions. The more aggressive PTLD histological subtypes demonstrated higher SUVmax compared with the less aggressive subtypes.
CONCLUSION: F-FDG PET/CT is beneficial in the diagnostic evaluation of patients with PTLD. F-FDG PET/CT has the ability to detect occult lesions not identified on other imaging modalities, particularly extranodal lesions. In addition, F-FDG PET/CT may predict the PTLD subtype, as the lesions with higher pathologic grade presented with significantly higher SUVmax compared with the less aggressive forms.
PMID: 24296883 [PubMed - as supplied by publisher]
Optimization and comprehensive characterization of a faithful tissue culture model of the benign and malignant human prostate.
Lab Invest. 2013 Dec 2;
Authors: Maund SL, Nolley R, Peehl DM
Few preclinical models accurately depict normal human prostate tissue or primary prostate cancer (PCa). In vitro systems typically lack complex cellular interactions among structured prostatic epithelia and a stromal microenvironment, and genetic and molecular fidelity are concerns in both in vitro and in vivo models. 'Tissue slice cultures' (TSCs) provide realistic preclinical models of diverse tissues and organs, but have not been fully developed or widely utilized for prostate studies. Problems encountered include degeneration of differentiated secretory cells, basal cell hyperplasia, and poor survival of PCa. Here, we optimized, characterized, and applied a TSC model of primary human PCa and benign prostate tissue that overcomes many deficiencies of current in vitro models. Tissue cores from fresh prostatectomy specimens were precision-cut at 300 μm and incubated in a rotary culture apparatus. The ability of varied culture conditions to faithfully maintain benign and cancer cell and tissue structure and function over time was evaluated by immunohistological and biochemical assays. After optimization of the culture system, molecular and cellular responses to androgen ablation and to piperlongumine (PL), purported to specifically reduce androgen signaling in PCa, were investigated. Optimized culture conditions successfully maintained the structural and functional fidelity of both benign and PCa TSCs for 5 days. TSCs exhibited androgen dependence, appropriately undergoing ductal degeneration, reduced proliferation, and decreased prostate-specific antigen expression upon androgen ablation. Further, TSCs revealed cancer-specific reduction of androgen receptor and increased apoptosis upon treatment with PL, validating data from cell lines. We demonstrate a TSC model that authentically recapitulates the structural, cellular, and genetic characteristics of the benign and malignant human prostate, androgen dependence of the native tissue, and cancer-specific response to a potentially new therapeutic for PCa. The work described herein provides a basis for advancing the experimental utility of the TSC model.Laboratory Investigation advance online publication, 2 December 2013; doi:10.1038/labinvest.2013.141.
PMID: 24296879 [PubMed - as supplied by publisher]
Co-Stimulation Modulation with Abatacept in Patients with Recent-Onset Type 1 Diabetes: Follow-Up One Year After Cessation of Treatment.
Diabetes Care. 2013 Dec 2;
Authors: Orban T, Bundy B, Becker DJ, Dimeglio LA, Gitelman SE, Goland R, Gottlieb PA, Greenbaum CJ, Marks JB, Monzavi R, Moran A, Peakman M, Raskin P, Russell WE, Schatz D, Wherrett DK, Wilson DM, Krischer JP, Skyler JS, The Type 1 Diabetes TrialNet Abatacept Study Group
ObjectiveWe previously reported that two years of co-stimulation modulation with abatacept slowed decline of beta-cell function in recent-onset type 1 diabetes mellitus (T1DM). Subsequently, abatacept was discontinued, and subjects followed to determine whether there was persistence of effect.Research Design and MethodsIn 112 subjects (ages 6-36) with T1DM, 77 received abatacept and 35 received placebo infusions intravenously for 27 infusions over two years. The primary outcome - baseline-adjusted geometric mean 2-hour area under the curve (AUC) serum C-peptide during a mixed meal tolerance test (MMTT) at two years - showed higher C-peptide with abatacept versus placebo. Subjects were followed an additional year, off treatment, with MMTTs performed at 30 and 36 months.ResultsC-peptide AUC means, adjusted for age and baseline C-peptide, at 36 months were 0.217 (95% CI: 0.168, 0.268) and 0.141 (95% CI: 0.071, 0.215) nmol/L for abatacept and placebo groups, respectively (p=0.046). The C-peptide decline from baseline remained parallel with an estimated 9.5 months' delay with abatacept. Moreover, HbA1c levels remainded lower in the abatacept group than in the placebo group. The slightly lower (non-significant) mean total insulin dose among the abatacept group reported at 2 years was the same as the placebo group by 3 years.ConclusionsCo-stimulation modulation with abatacept slowed decline of beta-cell function and improved HbA1c in recent-onset T1DM. The beneficial effect was sustained for at least one year after cessation of abatacept infusions, or three years from T1DM diagnosis.
PMID: 24296850 [PubMed - as supplied by publisher]
T-cell aging in rheumatoid arthritis.
Curr Opin Rheumatol. 2014 Jan;26(1):93-100
Authors: Weyand CM, Yang Z, Goronzy JJ
PURPOSE OF REVIEW: With progressive age, the immune system and the propensity for abnormal immunity change fundamentally. Individuals greater than 50 years of age are not only more susceptible to infection and cancer, but also at higher risk for chronic inflammation and immune-mediated tissue damage. The process of immunosenescence is accelerated in rheumatoid arthritis (RA).
RECENT FINDINGS: Premature T-cell senescence occurs not only in RA, but also has been involved in morbidity and mortality of chronic HIV infection. Senescent cells acquire the 'senescence-associated secretory phenotype', which promotes and sustains tissue inflammation. Molecular mechanisms underlying T-cell aging are beginning to be understood. In addition to the contraction of T-cell diversity because of uneven clonal expansion, senescent T cells have defects in balancing cytoplasmic kinase and phosphatase activities, changing their activation thresholds. Also, leakiness in repairing DNA lesions and uncapped telomeres imposes genomic stress. Age-induced changes in the tissue microenvironment may alter the T-cell responses.
SUMMARY: Gain-of-function and loss-of-function in senescent T cells undermine protective immunity and create the conditions for chronic tissue inflammation, a combination typically encountered in RA. Genetic programs involved in T-cell signaling and DNA repair are of high interest in the search for underlying molecular defects.
PMID: 24296720 [PubMed - in process]
More Than a Billion People Taking Statins?: Potential Implications of the New Cardiovascular Guidelines.
JAMA. 2013 Dec 2;
Authors: Ioannidis JP
PMID: 24296612 [PubMed - as supplied by publisher]
Regulatory T Cells and the Immune Aging Process: A Mini-Review.
Gerontology. 2013 Nov 28;
Authors: Jagger A, Shimojima Y, Goronzy JJ, Weyand CM
Constant exposure to new and persisting antigens and the need to replace cellular attrition with newly built cells lead to profound remodeling of the immune system after the age of 50 years. The impact of the immunosenescence process varies amongst the different cellular subsets represented within the immune system. Emerging data suggest that progressive aging significantly affects frequencies, subset distribution and functional competence of regulatory T cells (Tregs). Given the central role of Tregs in immune homeostasis, age-related loss of Treg function would be predicted to cause excessive immunity, encountered in elderly humans as a syndrome of chronic, smoldering inflammation as well as the age-related increase in the risk for autoimmunity. Conversely, age-dependent gain of Treg activity would result in failing immunity, such as the rising risk of malignancies and infections amongst the elderly. Emerging data suggest that some Treg populations, specifically naturally occurring Tregs, seem to accumulate with advancing age, whereas inducible Tregs appear to be less available in the older host. More studies are necessary to elucidate functional competence of old Tregs, with an emphasis on comparing the efficacy of young and old Tregs for defined functional domains. Mechanisms of declining Treg inducibility are not understood, but may provide an opportunity for targeted immunomodulation in the elderly. On the horizon is the potential to develop novel therapeutic interventions that target Tregs to make the elderly more efficient in fighting cancers and infections and dampen the risk for senescence-associated inflammation. © 2013 S. Karger AG, Basel.
PMID: 24296590 [PubMed - as supplied by publisher]
Facts about FCE (Fludarabine, Cytarabine, Etoposide) in Acute Myeloid Leukemia.
Acta Haematol. 2013 Nov 27;131(4):200-201
Authors: Medeiros BC
PMID: 24296429 [PubMed - as supplied by publisher]
Helicobacter and salmonella persistent infection strategies.
Cold Spring Harb Perspect Med. 2013;3(12)
Authors: Monack DM
Some host-adapted bacterial pathogens are capable of causing persistent infections in humans. For example, Helicobacter pylori inhabits the human gastric mucosa and persistence can be lifelong. Salmonella enterica serovar Typhi causes systemic infections that involve colonization of the reticuloendothelial system and some individuals become lifelong carriers. In this review, I compare and contrast the different lifestyles of Helicobacter and Salmonella within the host and the strategies they have evolved to persist in mammalian hosts. Persistently infected carriers serve as the reservoirs for these pathogens, and the carrier state is an essential feature that is required for survival of the bacteria within a restricted host population. Therefore, investigating the chronic carrier state should provide insight into bacterial survival strategies, as well as new therapeutic approaches for treatments.
PMID: 24296347 [PubMed - in process]
The FAST and E-FAST in 2013: Trauma Ultrasonography: Overview, Practical Techniques, Controversies, and New Frontiers.
Crit Care Clin. 2014 Jan;30(1):119-50
Authors: Williams SR, Perera P, Gharahbaghian L
This article reviews important literature on the FAST and E-FAST examinations in adults. It also reviews key pitfalls, limitations, and controversies. A practical "how-to" guide is presented. Lastly, new frontiers are explored.
PMID: 24295843 [PubMed - in process]
Crit Care Clin. 2014 Jan;30(1):93-117
Authors: Lobo V, Weingrow D, Perera P, Williams SR, Gharahbaghian L
Thoracic ultrasonography (US) has proved to be a valuable tool in the evaluation of the patient with shortness of breath, chest pain, hypoxia, or after chest trauma. Its sensitivity and specificity for detecting disease is higher than that of a chest radiograph, and it can expedite the diagnosis for many emergent conditions. This article describes the technique of each thoracic US application, illustrating both normal and abnormal findings, as well as discussing the literature. Bedside thoracic US has defined imaging benefits in a wide range of thoracic disease, and US guidance has been shown to facilitate thoracic and airway procedures.
PMID: 24295842 [PubMed - in process]
Crit Care Clin. 2014 Jan;30(1):47-92
Authors: Perera P, Lobo V, Williams SR, Gharahbaghian L
Focused cardiac echocardiography has become a critical diagnostic tool for the emergency physician and critical care physician caring for patients in shock and following trauma to the chest, and those presenting with chest pain and shortness of breath,. Cardiac echocardiography allows for immediate diagnosis of pericardial effusions and cardiac tamponade, evaluation of cardiac contractility and volume status, and detection of right ventricular strain possibly seen with a significant pulmonary embolus. This article addresses how to perform cardiac echocardiography using the standard windows, how to interpret a focused goal-directed examination, and how to apply this information clinically at the bedside.
PMID: 24295841 [PubMed - in process]