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Chang T.P.,Childrens Hospital Los Angeles | Kriengsoontorkij W.,Mahidol University | Chan L.S.,Los Angeles CountyUniversity of Southern California Medical Center | Wang V.J.,Childrens Hospital Los Angeles
Journal of Pediatric Hematology/Oncology | Year: 2013

Objectives: The objective of this study was to determine the incidence of bacteremia in febrile sickle cell disease (SCD) children before and after the 7-valent pneumococcal vaccine (PCV7), and to determine clinical factors associated with bacteremia following PCV7. Patients and Methods: We reviewed all febrile events in SCD children from 1993 to 2009 at a tertiary care pediatric center, comparing general bacteremia and pneumococcal bacteremia incidence for 3 time periods around the PCV7. Univariate analysis and stepwise logistic regression identified clinical factors most associated with bacteremia in this population. Results: Of 466 SCD children identified, there were 2504 febrile events. We found 84 cases of bacteremia; 8 were pneumococcal. The general bacteremia incidence decreased significantly from 5.60% to 2.44% (P<0.001) over time. Pneumococcal bacteremia incidence did not decrease (P=0.13). Following PCV7, we identified 4 significant independent risk factors associated with general bacteremia: the presence of a central venous line, higher absolute band count, toxic appearance, and older age. Conclusions: In febrile SCD children, the incidence of general bacteremia decreased over time. No decrease in pneumococcal bacteremia was found. The presence of a central venous line, absolute band count, clinical appearance, and age may help predict bacteremia in this population. Copyright © 2013 by Lippincott Williams & Wilkins.


Li A.,Los Angeles CountyUniversity of Southern California Medical Center | Chan B.,Los Angeles CountyUniversity of Southern California Medical Center | Felix J.C.,Los Angeles CountyUniversity of Southern California Medical Center | Xing Y.,Los Angeles CountyUniversity of Southern California Medical Center | And 6 more authors.
PLoS ONE | Year: 2013

The molecular signals that control decisions regarding progenitor/stem cell proliferation versus differentiation are not fully understood. Differentiation of motile cilia from progenitor/stem cells may offer a simple tractable model to investigate this process. Wnt and Notch represent two key signaling pathways in progenitor/stem cell behavior in a number of tissues. Adenomatous Polyposis Coli, Apc is a negative regulator of the Wnt pathway and a well known multifunctional protein. Using the cre-LoxP system we inactivated the Apc locus via Foxj1-cre, which is expressed in cells committed to ciliated cell lineage. We then characterized the consequent phenotype in two select tissues that bear motile cilia, the lung and the testis. In the lung, Apc deletion induced β-catenin accumulation and Jag1 expression in ciliated cells and by lateral induction, triggered Notch signaling in adjacent Clara cells. In the bronchiolar epithelium, absence of Apc blocked the differentiation of a subpopulation of cells committed to the ciliogenesis program. In the human pulmonary adenocarcinoma cells, Apc over-expression inhibited Jag1 expression and promoted motile ciliogenic gene expression program including Foxj1, revealing the potential mechanism. In the testis, Apc inactivation induced β-catenin accumulation in the spermatogonia, but silenced Notch signaling and depleted spermatogonial stem cells, associated with reduced proliferation, resulting in male infertility. In sum, the present comparative analysis reveals the tissue-dependent consequences of Apc inactivation on proliferation and differentiation of ciliated cell progenitors by coordinating Wnt and Notch signaling. © 2013 Li et al.


Chan R.,Los Angeles CountyUniversity of Southern California Medical Center | Chan R.,University of Southern California | Mascarenhas L.,University of Southern California | Mascarenhas L.,Childrens Hospital Los Angeles | And 9 more authors.
American Journal of Medical Genetics, Part A | Year: 2015

Childhood malignant tumors and their treatment are not well described in the natural history of methylmalonic aciduria (MMA). Here we present a case of hepatoblastoma occurring in the native liver of a 19-month-old male with MMA. His tumor was unresectable at diagnosis and he received neoadjuvant chemotherapy with cisplatin, 5-fluorouracil and vincristine. He developed metabolic acidosis and hyperglycemia during chemotherapy. In addition, he developed anemia, thrombocytopenia and febrile neutropenia. He underwent a combined liver-kidney transplant for local control of his tumor and to treat MMA. He remains in remission more than five years after his transplant. In addition, his transplant has cured his MMA and he is able to tolerate a regular diet without developing metabolic crises. © 2015 Wiley Periodicals, Inc.


Hsu Y.-W.,Chia Nan University of Pharmacy and Science | Belcher B.R.,U.S. National Institutes of Health | Weigensberg M.J.,Los Angeles CountyUniversity of Southern California Medical Center | Spruijt-Metz D.,University of Southern California | And 3 more authors.
Pediatric Exercise Science | Year: 2014

While most studies have focused on investigating the preventive effects of physical activity on metabolic risk,the longitudinal impacts of metabolic syndrome (MetS) on activity levels is poorly understood. This study aims to examine theinfluence of MetS on initial activity levels and the trajectory of activity levels in Latina and African American female children over 12 months (n = 55, ± 1 years). Metabolic measures, including fat and lean tissue mass by BodPod, fasting glucose, lipids, blood pressure, and waist circumference, were collected at baseline.Moderate-to-vigorous physical activity and sedentary behavior by accelerometry were collected on a quarterly basis.There were no significant differences in either initial activity levels by MetS status (Moderate-to-vigorousphysical activity: 33 ± 12 mins/day for MetS, 48 ± 28 mins/day for Non-MetS, p = .12;sedentary behavior: 408 ± 57 mins/day for MetS, 421 ± 72 mins/day for Non-MetS, p = .67). Longitudinal declines in moderate-to-vigorousphysical activity (p = .038) and increases in sedentary behavior (p = .003) were found. Daily sedentary behavior increased by 82.64 more minutes in youth with MetS than in those without over one year (p = .015). This study yields the first evidence of the adverse effect of MetS on sedentary behavior. Targeted intervention strategies to reduce progressive sedentariness evident in minority youth with MetS are warranted. © 2014 Human Kinetics, Inc.


Li C.,Los Angeles CountyUniversity of Southern California Medical Center | Bellusci S.,Excellence Cluster Cardio Pulmonary System ECCPS | Bellusci S.,Universities of Giessen and Marburg Lung Center | Bellusci S.,Saban Research Institute | And 2 more authors.
Journal of Biochemistry | Year: 2015

The role of WNT signalling in metazoan organogenesis has been a topic of widespread interest. In the lung, while the role of canonical WNT signalling has been examined in some detail by multiple studies, the non-canonical WNT signalling has received limited attention. Reliable evidence shows that this important signalling mechanism constitutes a major regulatory pathway in lung development. In addition, accumulating evidence has also shown that the non-canonical WNT pathway is critical for maintaining lung homeostasis and that aberrant activation of this pathway may underlie several debilitating lung diseases. Functional analyses have further revealed that the non-canonical WNT pathway regulates multiple cellular activities in the lung that are dependent on the specific cellular context. In most cell types, non-canonical WNT signalling regulates canonical WNT activity, which is also critical for many aspects of lung biology. This review will summarize what is currently known about the role of non-canonical WNT signalling in lung development, homeostasis and pathogenesis of disease. © The Authors 2015. Published by Oxford University Press on behalf of the Japanese Biochemical Society. All rights reserved.


Lua I.,University of Southern California | Li Y.,University of Southern California | Pappoe L.S.,Los Angeles CountyUniversity of Southern California Medical Center | Asahina K.,University of Southern California
American Journal of Pathology | Year: 2015

Mesothelial cells (MCs) form a single epithelial layer and line the surface of body cavities and internal organs. Patients who undergo peritoneal dialysis often develop peritoneal fibrosis that is characterized by the accumulation of myofibroblasts in connective tissue. Although MCs are believed to be the source of myofibroblasts, their contribution has remained obscure. We determined the contribution of peritoneal MCs to myofibroblasts in chlorhexidine gluconate (CG)-induced fibrosis compared with that of phenotypic changes of liver MCs. CG injections resulted in disappearance of MCs from the body wall and the accumulation of myofibroblasts in the connective tissue. Conditional linage tracing with Wilms tumor 1 (Wt1)-CreERT2 and Rosa26 reporter mice found that 17% of myofibroblasts were derived from MCs in peritoneal fibrosis. Conditional deletion of transforming growth factor-β type II receptor in Wt1+ MCs substantially reduced peritoneal fibrosis. The CG treatment also induced myofibroblastic conversion of MCs in the liver. Lineage tracing with Mesp1-Cre mice revealed that Mesp1+ mesoderm gave rise to liver MCs but not peritoneal MCs. During recovery from peritoneal fibrosis, peritoneal MCs, but not liver MCs, contribute to the regeneration of the peritoneal mesothelium, indicating an inherent difference between parietal and visceral MCs. In conclusion, MCs partially contribute to myofibroblasts in peritoneal and liver fibrosis, and protection of the MC layer leads to reduced development of fibrous tissue. © 2015 American Society for Investigative Pathology.


PubMed | Los Angeles CountyUniversity of Southern California Medical Center and University of Southern California
Type: Journal Article | Journal: The American journal of pathology | Year: 2015

Mesothelial cells (MCs) form a single epithelial layer and line the surface of body cavities and internal organs. Patients who undergo peritoneal dialysis often develop peritoneal fibrosis that is characterized by the accumulation of myofibroblasts in connective tissue. Although MCs are believed to be the source of myofibroblasts, their contribution has remained obscure. We determined the contribution of peritoneal MCs to myofibroblasts in chlorhexidine gluconate (CG)-induced fibrosis compared with that of phenotypic changes of liver MCs. CG injections resulted in disappearance of MCs from the body wall and the accumulation of myofibroblasts in the connective tissue. Conditional linage tracing with Wilms tumor 1 (Wt1)-CreERT2 and Rosa26 reporter mice found that 17% of myofibroblasts were derived from MCs in peritoneal fibrosis. Conditional deletion of transforming growth factor- type II receptor in Wt1(+) MCs substantially reduced peritoneal fibrosis. The CG treatment also induced myofibroblastic conversion of MCs in the liver. Lineage tracing with Mesp1-Cre mice revealed that Mesp1(+) mesoderm gave rise to liver MCs but not peritoneal MCs. During recovery from peritoneal fibrosis, peritoneal MCs, but not liver MCs, contribute to the regeneration of the peritoneal mesothelium, indicating an inherent difference between parietal and visceral MCs. In conclusion, MCs partially contribute to myofibroblasts in peritoneal and liver fibrosis, and protection of the MC layer leads to reduced development of fibrous tissue.


Talving P.,Divisions of Trauma and Surgical Critical Care | Branco B.C.,Divisions of Trauma and Surgical Critical Care | Plurad D.,Divisions of Trauma and Surgical Critical Care | Inaba K.,Divisions of Trauma and Surgical Critical Care | And 4 more authors.
Journal of Emergencies, Trauma and Shock | Year: 2012

Post-traumatic cardiac pseudoaneurysm (PSA) is a rare, potentially life-threatening complication after penetrating cardiac injury. Early surgical intervention has been the treatment of choice for this sequela due to the risk of rupture. Nevertheless, selective non-operative management (SNOM) has been practiced in patients with postinfarct PSA that are small and stable. We report a case of a post-traumatic cardiac PSA subjected to SNOM.

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