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Article ; Online: New Drugs and Regimens for Tuberculosis Disease Treatment in Children and Adolescents.

Garcia-Prats, Anthony J / Starke, Jeffrey R / Waning, Brenda / Kaiser, Brian / Seddon, James A

Journal of the Pediatric Infectious Diseases Society

2022 Volume 11, Issue Supplement_3, Page(s) S101–S109

Abstract: After almost 30 years of relative stagnation, research over the past decade has led to remarkable advances in the treatment of both drug-susceptible (DS) and drug-resistant (DR) tuberculosis (TB) disease in children and adolescents. Compared with the ... ...

Abstract	After almost 30 years of relative stagnation, research over the past decade has led to remarkable advances in the treatment of both drug-susceptible (DS) and drug-resistant (DR) tuberculosis (TB) disease in children and adolescents. Compared with the previous standard therapy of at least 6 months, 2 new regimens lasting for only 4 months for the treatment of DS-TB have been studied and are recommended by the World Health Organization (WHO), along with a shortened 6-month regimen for treatment of DS-TB meningitis. In addition, the 18- to 24-month regimens previously used for DR-TB that included painful injectable drugs with high rates of adverse effects have been replaced with shorter, safer all-oral regimens. Advances that have improved treatment include development of new TB drugs (bedaquiline, delamanid, pretomanid), reapplication of older TB drugs (rifampicin and rifapentine), and repurposing of other drugs (clofazimine and linezolid). The development of child-friendly formulations for many of these drugs has further enhanced the ability to safely and effectively treat DS- and DR-TB in children and adolescents. The characteristics and use of these drugs, regimens, and formulations are reviewed.
MeSH term(s)	Adolescent ; Humans ; Antitubercular Agents/therapeutic use ; Tuberculosis/drug therapy ; Tuberculosis, Multidrug-Resistant/drug therapy ; Clofazimine/therapeutic use ; Linezolid
Chemical Substances	Antitubercular Agents ; Clofazimine (D959AE5USF) ; Linezolid (ISQ9I6J12J)
Language	English
Publishing date	2022-10-31
Publishing country	England
Document type	Journal Article
ZDB-ID	2668791-4
ISSN	2048-7207 ; 2048-7193
ISSN (online)	2048-7207
ISSN	2048-7193
DOI	10.1093/jpids/piac047
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Clinical signs of the transition of syncope into hypoxic coma: a case report.

van Dijk, J Gert / van Rossum, Ineke A / van Waning, Jaap I / Westra, Sjoerd W / Thijs, Roland D

Clinical autonomic research : official journal of the Clinical Autonomic Research Society

2023 Volume 33, Issue 6, Page(s) 915–918

MeSH term(s)	Humans ; Coma/etiology ; Syncope/etiology ; Syncope/diagnosis ; Syncope, Vasovagal ; Hypoxia/etiology
Language	English
Publishing date	2023-09-05
Publishing country	Germany
Document type	Case Reports ; Letter
ZDB-ID	1080007-4
ISSN	1619-1560 ; 0959-9851
ISSN (online)	1619-1560
ISSN	0959-9851
DOI	10.1007/s10286-023-00978-2
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Zs.A 3270: Show issues

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Article ; Online: Asia emerges as a hotbed of diagnostic innovations for tuberculosis.

Bigio, Jacob / van Gemert, Wayne / Kaiser, Brian / Waning, Brenda / Pai, Madhukar

Journal of clinical tuberculosis and other mycobacterial diseases

2021 Volume 25, Page(s) 100267

Language	English
Publishing date	2021-08-25
Publishing country	England
Document type	Editorial
ISSN	2405-5794
ISSN (online)	2405-5794
DOI	10.1016/j.jctube.2021.100267
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Article ; Online: Bone metastases induce metabolic changes and mitophagy in mice.

Wilcox-Hagerty, Jenna / Xu, Haifang / Hain, Brian A / Arnold, Amy C / Waning, David L

Experimental physiology

2021 Volume 106, Issue 2, Page(s) 506–518

Abstract: New findings: What is the central question of this study? Cachexia causes severe changes in skeletal muscle metabolism and function and is a key predictor of negative outcomes in cancer patients: what are the changes in whole animal energy metabolism ... ...

Abstract	New findings: What is the central question of this study? Cachexia causes severe changes in skeletal muscle metabolism and function and is a key predictor of negative outcomes in cancer patients: what are the changes in whole animal energy metabolism and mitochondria in skeletal muscle? What is the main finding and its importance? There is decreased whole animal energy expenditure in mice with cachexia. They displayed highly dysmorphic mitochondria and mitophagy in skeletal muscle. Abstract: Cachexia causes changes in skeletal muscle metabolism. Mice with MDA-MB-231 breast cancer bone metastases and cachexia have decreased whole animal energy metabolism and increased skeletal muscle mitophagy. We examined whole animal energy metabolism by indirect calorimetry in mice with MDA-MB-231 breast cancer bone metastases, and showed decreased energy expenditure. We also examined skeletal muscle mitochondria and found that mitochondria in mice with MDA-MB-231 bone metastases are highly dysmorphic and have altered protein markers of mitochondrial biogenesis and dynamics. In addition, LC3B protein was increased in mitochondria of skeletal muscle from cachectic mice, and colocalized with the mitochondrial protein Tom20. Our data demonstrate the importance of mitophagy in cachexia. Understanding these changes will help contribute to defining treatments for cancer cachexia.
MeSH term(s)	Animals ; Bone Neoplasms/metabolism ; Bone Neoplasms/secondary ; Cachexia/metabolism ; Cachexia/pathology ; Energy Metabolism/physiology ; Female ; Mammary Neoplasms, Experimental/metabolism ; Mammary Neoplasms, Experimental/pathology ; Mice ; Mitochondria, Muscle/metabolism ; Mitophagy/physiology ; Muscle, Skeletal/metabolism ; Organelle Biogenesis
Language	English
Publishing date	2021-01-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1016295-1
ISSN	1469-445X ; 0958-0670
ISSN (online)	1469-445X
ISSN	0958-0670
DOI	10.1113/EP089130
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Article ; Online: LP07 and LLC preclinical models of lung cancer induce divergent anabolic deficits and expression of pro-inflammatory effectors of muscle wasting.

Belcher, Daniel J / Guitart, Maria / Hain, Brian / Kim, Hyo-Gun / Waning, David / Barreiro, Esther / Nader, Gustavo A

Journal of applied physiology (Bethesda, Md. : 1985)

2022 Volume 133, Issue 6, Page(s) 1260–1272

Abstract: Preclinical models have been instrumental to elucidate the mechanisms underlying muscle wasting in lung cancer (LC). We investigated anabolic deficits and the expression of proinflammatory effectors of muscle wasting in the LP07 and Lewis lung carcinoma ( ...

Abstract	Preclinical models have been instrumental to elucidate the mechanisms underlying muscle wasting in lung cancer (LC). We investigated anabolic deficits and the expression of proinflammatory effectors of muscle wasting in the LP07 and Lewis lung carcinoma (LLC) tumor models. Tumor growth resulted in significant weakness in LP07 but not in LLC mice despite similar reductions in gastrocnemius muscle mass in both models. The LP07 tumors caused a reduction in ribosomal (r)RNA and a decrease in rRNA gene (rDNA) transcription elongation, whereas no changes in ribosomal capacity were evident in LLC tumor-bearing mice. Expression of RNA Polymerase I (Pol I) elongation-associated subunits Polr2f, PAF53, and Znrd1 mRNAs was significantly elevated in the LP07 model, whereas Pol I elongation-related factors FACT and Spt4/5 mRNAs were elevated in the LLC mice. Reductions in RPS6 and 4E-BP1 phosphorylation were similar in both models but were independent of mTOR phosphorylation in LP07 mice. Muscle inflammation was also tumor-specific, IL-6 and TNF-α mRNA increased with LLC tumors, and upregulation of NLRP3 mRNA was independent of tumor type. In summary, although both models caused muscle wasting, only the LP07 model displayed muscle weakness with reductions in ribosomal capacity. Intracellular signaling diverged at the mTOR level with similar reductions in RPS6 and 4E-BP1 phosphorylation regardless of tumor type. The increase in proinflammatory factors was more pronounced in the LLC model. Our results demonstrate novel divergent anabolic deficits and expression of proinflammatory effectors of muscle wasting in the LP07 and LLC preclinical models of lung cancer.
MeSH term(s)	Mice ; Animals ; Carcinoma, Lewis Lung/genetics ; Carcinoma, Lewis Lung/metabolism ; Carcinoma, Lewis Lung/pathology ; Cachexia/etiology ; Muscular Atrophy/metabolism ; Muscle, Skeletal/metabolism ; Lung Neoplasms/complications ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; TOR Serine-Threonine Kinases/metabolism ; RNA, Messenger/metabolism ; Mice, Inbred C57BL
Chemical Substances	TOR Serine-Threonine Kinases (EC 2.7.11.1) ; RNA, Messenger
Language	English
Publishing date	2022-10-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	219139-8
ISSN	1522-1601 ; 0021-8987 ; 0161-7567 ; 8750-7587
ISSN (online)	1522-1601
ISSN	0021-8987 ; 0161-7567 ; 8750-7587
DOI	10.1152/japplphysiol.00246.2022
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Article ; Online: The great medicines scandal: access is not just about cost.

Waning, Brenda J

BMJ (Clinical research ed.)

2006 Volume 333, Issue 7557, Page(s) 44

MeSH term(s)	Developing Countries ; Drug Costs ; Humans ; Pharmaceutical Preparations/supply & distribution
Chemical Substances	Pharmaceutical Preparations
Language	English
Publishing date	2006-07-01
Publishing country	England
Document type	Comment ; Letter
ZDB-ID	1362901-3
ISSN	1756-1833 ; 0959-8154 ; 0959-8146 ; 0959-8138 ; 0959-535X ; 1759-2151
ISSN (online)	1756-1833
ISSN	0959-8154 ; 0959-8146 ; 0959-8138 ; 0959-535X ; 1759-2151
DOI	10.1136/bmj.333.7557.44-a
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Article ; Online: State-of-the art review: Noncompaction cardiomyopathy in pediatric patients.

Rohde, Sofie / Muslem, Rahatullah / Kaya, Emrah / Dalinghaus, Michel / van Waning, Jaap I / Majoor-Krakauer, Danielle / Towbin, Jeffery / Caliskan, Kadir

Heart failure reviews

2021 Volume 27, Issue 1, Page(s) 15–28

Abstract: Noncompaction cardiomyopathy (NCCM) is a disease characterized by hypertrabeculation, commonly hypothesized due to an arrest in compaction during fetal development. In 2006, NCCM was classified as a distinct form of cardiomyopathy (CMP) by the American ... ...

Abstract	Noncompaction cardiomyopathy (NCCM) is a disease characterized by hypertrabeculation, commonly hypothesized due to an arrest in compaction during fetal development. In 2006, NCCM was classified as a distinct form of cardiomyopathy (CMP) by the American Heart Association. NCCM in childhood is more frequently familial than when diagnosed in adulthood and is associated with other congenital heart diseases (CHDs), other genetic CMPs, and neuromuscular diseases (NMDs). It is yet a rare cardiac diseased with an estimated incidence of 0.12 per 100.000 in children up to 10 years of age. Diagnosing NCCM can be challenging due to non-uniform diagnostic criteria, unawareness, presumed other CMPs, and presence of CHD. Therefore, the incidence of NCCM in children might be an underestimation. Nonetheless, NCCM is the third most common cardiomyopathy in childhood and is associated with heart failure, arrhythmias, and/or thromboembolic events. This state-of-the-art review provides an overview on pediatric NCCM. In addition, we discuss the natural history, epidemiology, genetics, clinical presentation, outcome, and therapeutic options of NCCM in pediatric patients, including fetuses, neonates, infants, and children. Furthermore, we provide a simple classification of different forms of the disease. Finally, the differences between the pediatric population and the adult population are described.
MeSH term(s)	Adult ; Arrhythmias, Cardiac ; Cardiomyopathies/diagnosis ; Cardiomyopathies/epidemiology ; Child ; Heart ; Heart Defects, Congenital/complications ; Heart Defects, Congenital/diagnosis ; Heart Defects, Congenital/epidemiology ; Humans ; Infant ; Infant, Newborn ; Thromboembolism
Language	English
Publishing date	2021-03-14
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1336499-6
ISSN	1573-7322 ; 1382-4147
ISSN (online)	1573-7322
ISSN	1382-4147
DOI	10.1007/s10741-021-10089-7
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Zs.A 5212: Show issues

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Article ; Online: Cancer- and Chemotherapy-Induced Musculoskeletal Degradation.

Sturgeon, Kathleen M / Mathis, Katlynn M / Rogers, Connie J / Schmitz, Kathryn H / Waning, David L

JBMR plus

2019 Volume 3, Issue 3, Page(s) e10187

Abstract: Mobility in advanced cancer patients is a major health care concern and is often lost in advanced metastatic cancers. Erosion of mobility is a major component in determining quality of life but also starts a process of loss of muscle and bone mass that ... ...

Abstract	Mobility in advanced cancer patients is a major health care concern and is often lost in advanced metastatic cancers. Erosion of mobility is a major component in determining quality of life but also starts a process of loss of muscle and bone mass that further devastates patients. In addition, treatment options become limited in these advanced cancer patients. Loss of bone and muscle occurs concomitantly. Advanced cancers that are metastatic to bone often lead to bone loss (osteolytic lesions) but may also lead to abnormal deposition of new bone (osteoblastic lesions). However, in both cases there is a disruption to normal bone remodeling and radiologic evidence of bone loss. Many antitumor therapies can also lead to loss of bone in cancer survivors. Bone loss releases cytokines (TGFβ) stored in the mineralized matrix that can act on skeletal muscle and lead to weakness. Likewise, loss of skeletal muscle mass leads to reduced bone mass and quality via mechanical and endocrine signals. Collectively these interactions are termed bone-muscle cross-talk, which has garnered much attention recently as a prime target for musculoskeletal health. Pharmacological approaches as well as nutrition and exercise can improve muscle and bone but have fallen short in the context of advanced cancers and cachexia. This review highlights our current knowledge of these interventions and discusses the difficulties in treating severe musculoskeletal deficits with the emphasis on improving not only bone mass and muscle size but also functional outcomes. © 2019 The Authors.
Language	English
Publishing date	2019-02-25
Publishing country	England
Document type	Journal Article ; Review
ISSN	2473-4039
ISSN (online)	2473-4039
DOI	10.1002/jbm4.10187
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Article ; Online: Systematic Review of Genotype-Phenotype Correlations in Noncompaction Cardiomyopathy.

van Waning, Jaap I / Moesker, Joost / Heijsman, Daphne / Boersma, Eric / Majoor-Krakauer, Danielle

Journal of the American Heart Association

2019 Volume 8, Issue 23, Page(s) e012993

Abstract: Background A genetic cause can be identified in 30% of noncompaction cardiomyopathy patients (NCCM) with clinical features ranging from asymptomatic cardiomyopathy to heart failure with major adverse cardiac events (MACE). Methods and Results To ... ...

Abstract	Background A genetic cause can be identified in 30% of noncompaction cardiomyopathy patients (NCCM) with clinical features ranging from asymptomatic cardiomyopathy to heart failure with major adverse cardiac events (MACE). Methods and Results To investigate genotype-phenotype correlations, the genotypes and clinical features of genetic NCCM patients were collected from the literature. We compared age at diagnosis, cardiac features and risk for MACE according to mode of inheritance and molecular effects for defects in the most common sarcomere genes and NCCM subtypes. Geno- and phenotypes of 561 NCCM patients from 172 studies showed increased risk in children for congenital heart defects (
MeSH term(s)	Adolescent ; Adult ; Age Factors ; Cardiomyopathies/complications ; Cardiomyopathies/diagnosis ; Cardiomyopathies/genetics ; Child ; Child, Preschool ; Female ; Genetic Association Studies ; Heart Diseases/etiology ; Humans ; Infant ; Male ; Risk Assessment ; Sarcomeres/genetics ; Young Adult
Language	English
Publishing date	2019-11-27
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't ; Systematic Review
ZDB-ID	2653953-6
ISSN	2047-9980 ; 2047-9980
ISSN (online)	2047-9980
ISSN	2047-9980
DOI	10.1161/JAHA.119.012993
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Article ; Online: Zoledronic Acid Improves Muscle Function in Healthy Mice Treated with Chemotherapy.

Hain, Brian A / Jude, Baptiste / Xu, Haifang / Smuin, Dallas M / Fox, Edward J / Elfar, John C / Waning, David L

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

2019 Volume 35, Issue 2, Page(s) 368–381

Abstract: Carboplatin is a chemotherapy drug used to treat solid tumors but also causes bone loss and muscle atrophy and weakness. Bone loss contributes to muscle weakness through bone-muscle crosstalk, which is prevented with the bisphosphonate zoledronic acid ( ... ...

Abstract	Carboplatin is a chemotherapy drug used to treat solid tumors but also causes bone loss and muscle atrophy and weakness. Bone loss contributes to muscle weakness through bone-muscle crosstalk, which is prevented with the bisphosphonate zoledronic acid (ZA). We treated mice with carboplatin in the presence or absence of ZA to assess the impact of bone resorption on muscle. Carboplatin caused loss of body weight, muscle mass, and bone mass, and also led to muscle weakness as early as 7 days after treatment. Mice treated with carboplatin and ZA lost body weight and muscle mass but did not lose bone mass. In addition, muscle function in mice treated with ZA was similar to control animals. We also used the anti-TGFβ antibody (1D11) to prevent carboplatin-induced bone loss and showed similar results to ZA-treated mice. We found that atrogin-1 mRNA expression was increased in muscle from mice treated with carboplatin, which explained muscle atrophy. In mice treated with carboplatin for 1 or 3 days, we did not observe any bone or muscle loss, or muscle weakness. In addition, reduced caloric intake in the carboplatin treated mice did not cause loss of bone or muscle mass, or muscle weakness. Our results show that blocking carboplatin-induced bone resorption is sufficient to prevent skeletal muscle weakness and suggests another benefit to bone therapy beyond bone in patients receiving chemotherapy. © 2019 American Society for Bone and Mineral Research.
MeSH term(s)	Animals ; Bone Density Conservation Agents ; Diphosphonates/pharmacology ; Imidazoles/pharmacology ; Mice ; Muscle, Skeletal ; Zoledronic Acid/pharmacology
Chemical Substances	Bone Density Conservation Agents ; Diphosphonates ; Imidazoles ; Zoledronic Acid (6XC1PAD3KF)
Language	English
Publishing date	2019-10-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	632783-7
ISSN	1523-4681 ; 0884-0431
ISSN (online)	1523-4681
ISSN	0884-0431
DOI	10.1002/jbmr.3890
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