Pub Date : 2022-06-06DOI: 10.1186/s40348-022-00143-1
H. Mentzel, K. Glutig, Stephanie Gräger, Paul C. Krüger, M. Waginger
{"title":"Ultrasound elastography in children — nice to have for scientific studies or arrived in clinical routine?","authors":"H. Mentzel, K. Glutig, Stephanie Gräger, Paul C. Krüger, M. Waginger","doi":"10.1186/s40348-022-00143-1","DOIUrl":"https://doi.org/10.1186/s40348-022-00143-1","url":null,"abstract":"","PeriodicalId":74215,"journal":{"name":"Molecular and cellular pediatrics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47122683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-05-20DOI: 10.1186/s40348-022-00142-2
Sina Neyazi, Michelle Ng, Dirk Heckl, Jan-Henning Klusmann
Long noncoding RNAs (lncRNAs) are increasingly emerging as regulators across human development and disease, and many have been described in the context of hematopoiesis and leukemogenesis. These studies have yielded new molecular insights into the contribution of lncRNAs to AML development and revealed connections between lncRNA expression and clinical parameters in AML patients. In this mini review, we illustrate the versatile functions of lncRNAs in AML, with a focus on pediatric AML, and present examples that may serve as future therapeutic targets or predictive factors.
{"title":"Long noncoding RNAs as regulators of pediatric acute myeloid leukemia.","authors":"Sina Neyazi, Michelle Ng, Dirk Heckl, Jan-Henning Klusmann","doi":"10.1186/s40348-022-00142-2","DOIUrl":"10.1186/s40348-022-00142-2","url":null,"abstract":"<p><p>Long noncoding RNAs (lncRNAs) are increasingly emerging as regulators across human development and disease, and many have been described in the context of hematopoiesis and leukemogenesis. These studies have yielded new molecular insights into the contribution of lncRNAs to AML development and revealed connections between lncRNA expression and clinical parameters in AML patients. In this mini review, we illustrate the versatile functions of lncRNAs in AML, with a focus on pediatric AML, and present examples that may serve as future therapeutic targets or predictive factors.</p>","PeriodicalId":74215,"journal":{"name":"Molecular and cellular pediatrics","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2022-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9123150/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47297273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-05-05DOI: 10.1186/s40348-022-00141-3
M. Bartosova, S. Zarogiannis, C. Schmitt, Klaus Gema Aysun K. Rainer Salim Rimante Dorota Sahar Gü Arbeiter Ariceta Bayazit Büscher Caliskan Cerkausk, K. Arbeiter, G. Ariceta, A. Bayazıt, R. Büscher, S. Çalışkan, R. Čerkauskienė, D. Drożdż, S. Fathallah-Shaykh, G. Klaus, R. Krmar, J. Oh, V. Peters, U. Querfeld, B. Ranchin, P. Sallay, B. Schaefer, C. Taylan, S. Testa, J. Vandewalle, E. Verrina, K. Vondrák, B. Warady, Y. Yap, A. Zaloszyc
{"title":"How peritoneal dialysis transforms the peritoneum and vasculature in children with chronic kidney disease—what can we learn for future treatment?","authors":"M. Bartosova, S. Zarogiannis, C. Schmitt, Klaus Gema Aysun K. Rainer Salim Rimante Dorota Sahar Gü Arbeiter Ariceta Bayazit Büscher Caliskan Cerkausk, K. Arbeiter, G. Ariceta, A. Bayazıt, R. Büscher, S. Çalışkan, R. Čerkauskienė, D. Drożdż, S. Fathallah-Shaykh, G. Klaus, R. Krmar, J. Oh, V. Peters, U. Querfeld, B. Ranchin, P. Sallay, B. Schaefer, C. Taylan, S. Testa, J. Vandewalle, E. Verrina, K. Vondrák, B. Warady, Y. Yap, A. Zaloszyc","doi":"10.1186/s40348-022-00141-3","DOIUrl":"https://doi.org/10.1186/s40348-022-00141-3","url":null,"abstract":"","PeriodicalId":74215,"journal":{"name":"Molecular and cellular pediatrics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41895546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-04-20DOI: 10.1186/s40348-022-00137-z
Lena Holzfurtner, T. Shahzad, Ying Dong, Lisa Rekers, Ariane Selting, B. Staude, Tina Lauer, A. Schmidt, S. Rivetti, K. Zimmer, Judith Behnke, S. Bellusci, H. Ehrhardt
{"title":"When inflammation meets lung development—an update on the pathogenesis of bronchopulmonary dysplasia","authors":"Lena Holzfurtner, T. Shahzad, Ying Dong, Lisa Rekers, Ariane Selting, B. Staude, Tina Lauer, A. Schmidt, S. Rivetti, K. Zimmer, Judith Behnke, S. Bellusci, H. Ehrhardt","doi":"10.1186/s40348-022-00137-z","DOIUrl":"https://doi.org/10.1186/s40348-022-00137-z","url":null,"abstract":"","PeriodicalId":74215,"journal":{"name":"Molecular and cellular pediatrics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43276843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-04-05DOI: 10.1186/s40348-022-00139-x
Sarah Peters, Serdar Cantez, Jan De Laffolie
Background: Exclusive enteral nutrition (EEN) is the first-line therapy for pediatric-onset Crohn's disease (CD) patients. CEDATA-GPGE® is the largest patient registry for children and adolescents with inflammatory bowel disease (IBD) in Europe, collecting data from over 5000 patients since 2004 in Germany and Austria. Since the application of EEN over 8 weeks is difficult and a high dropout rate is often described, the mode of application including a supporting structure is crucial for success. The aim of this study was to ascertain the variation in the application of EEN across the participating centers and to associate these with the outcome.
Results: Thirty-one centers responded to the survey (81.6%). 88.5% of CD patients were recommended EEN for induction therapy, 71.8% actually started with EEN, and 22.1% terminated the EEN prematurely. The duration of EEN typically lasted 6 to 8 weeks, and the polymeric formula was mainly used. 80.6% of the clinics added flavorings to the formulas. After EEN, the most preferred diet for maintenance therapy was a healthy, well-balanced diet considering individual intolerances.
Conclusions: EEN is widely recommended as an induction therapy by the German and Austrian pediatric gastroenterologists for children and adolescents with CD. However, this questionnaire-based study has shown a wide variation in EEN protocols used by the different pediatric clinics of CEDATA-GPGE®.
背景:纯肠内营养(EEN)是儿科克罗恩病(CD)患者的一线疗法。CEDATA-GPGE® 是欧洲最大的儿童和青少年炎症性肠病 (IBD) 患者登记处,自 2004 年以来收集了德国和奥地利 5000 多名患者的数据。由于在 8 周内应用 EEN 比较困难,而且经常有辍学率较高的描述,因此包括支持结构在内的应用模式是成功的关键。本研究的目的是确定各参与中心在应用 EEN 方面的差异,并将这些差异与结果联系起来:31个中心(81.6%)对调查做出了回应。88.5%的 CD 患者被推荐接受 EEN 诱导治疗,71.8%的患者实际开始接受 EEN,22.1%的患者提前终止了 EEN。肠易激综合征的治疗时间一般为 6 至 8 周,主要使用聚合配方。80.6%的诊所在配方奶粉中添加了香料。EEN 结束后,考虑到个体的不耐受性,最受欢迎的维持治疗饮食是健康、均衡的饮食:结论:德国和奥地利的儿科胃肠病专家广泛推荐将 EEN 作为 CD 儿童和青少年的诱导疗法。然而,这项基于调查问卷的研究表明,CEDATA-GPGE® 的不同儿科诊所所采用的 EEN 方案存在很大差异。
{"title":"Implementation of exclusive enteral nutrition in pediatric patients with Crohn's disease-results of a survey of CEDATA-GPGE reporting centers.","authors":"Sarah Peters, Serdar Cantez, Jan De Laffolie","doi":"10.1186/s40348-022-00139-x","DOIUrl":"10.1186/s40348-022-00139-x","url":null,"abstract":"<p><strong>Background: </strong>Exclusive enteral nutrition (EEN) is the first-line therapy for pediatric-onset Crohn's disease (CD) patients. CEDATA-GPGE® is the largest patient registry for children and adolescents with inflammatory bowel disease (IBD) in Europe, collecting data from over 5000 patients since 2004 in Germany and Austria. Since the application of EEN over 8 weeks is difficult and a high dropout rate is often described, the mode of application including a supporting structure is crucial for success. The aim of this study was to ascertain the variation in the application of EEN across the participating centers and to associate these with the outcome.</p><p><strong>Results: </strong>Thirty-one centers responded to the survey (81.6%). 88.5% of CD patients were recommended EEN for induction therapy, 71.8% actually started with EEN, and 22.1% terminated the EEN prematurely. The duration of EEN typically lasted 6 to 8 weeks, and the polymeric formula was mainly used. 80.6% of the clinics added flavorings to the formulas. After EEN, the most preferred diet for maintenance therapy was a healthy, well-balanced diet considering individual intolerances.</p><p><strong>Conclusions: </strong>EEN is widely recommended as an induction therapy by the German and Austrian pediatric gastroenterologists for children and adolescents with CD. However, this questionnaire-based study has shown a wide variation in EEN protocols used by the different pediatric clinics of CEDATA-GPGE®.</p>","PeriodicalId":74215,"journal":{"name":"Molecular and cellular pediatrics","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2022-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8982684/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47855012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-03-20DOI: 10.1186/s40348-022-00138-y
M. Sigler, H. Rouatbi, J. Vázquez-Jiménez, M. Seghaye
{"title":"Uni-ventricular palliation vs. bi-ventricular repair: differential inflammatory response","authors":"M. Sigler, H. Rouatbi, J. Vázquez-Jiménez, M. Seghaye","doi":"10.1186/s40348-022-00138-y","DOIUrl":"https://doi.org/10.1186/s40348-022-00138-y","url":null,"abstract":"","PeriodicalId":74215,"journal":{"name":"Molecular and cellular pediatrics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44725631","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-03-10DOI: 10.1186/s40348-022-00140-4
S. Burdach, M. Westhoff, M. Steinhauser, K. Debatin
{"title":"Correction to: Precision medicine in pediatric oncology","authors":"S. Burdach, M. Westhoff, M. Steinhauser, K. Debatin","doi":"10.1186/s40348-022-00140-4","DOIUrl":"https://doi.org/10.1186/s40348-022-00140-4","url":null,"abstract":"","PeriodicalId":74215,"journal":{"name":"Molecular and cellular pediatrics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48599681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-03-05DOI: 10.1186/s40348-022-00136-0
Alexander Kiefer, Erika Plattner, R. Ruppel, C. Weiss, Z. Zhou-Suckow, M. Mall, M. Renner, H. Müller
{"title":"DMBT1 is upregulated in cystic fibrosis, affects ciliary motility, and is reduced by acetylcysteine","authors":"Alexander Kiefer, Erika Plattner, R. Ruppel, C. Weiss, Z. Zhou-Suckow, M. Mall, M. Renner, H. Müller","doi":"10.1186/s40348-022-00136-0","DOIUrl":"https://doi.org/10.1186/s40348-022-00136-0","url":null,"abstract":"","PeriodicalId":74215,"journal":{"name":"Molecular and cellular pediatrics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49654119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-02-21DOI: 10.1186/s40348-022-00135-1
Michaela Plamper, Bettina Gohlke, Joachim Woelfle
Background: The PTEN hamartoma tumor syndrome (PHTS) encompasses several different syndromes, which are linked to an autosomal-dominant mutation of the tumor suppressor PTEN gene on chromosome 10. Loss of PTEN activity leads to an increased phosphorylation of different cell proteins, which may have an influence on growth, migration, and apoptosis. Excessive activity of the PI3K/AKT/mTOR pathway due to PTEN deficiency may lead to the development of benign and malignant tumors and overgrowth. Diagnosis of PHTS in childhood can be even more challenging than in adulthood because of a lack of well-defined diagnostic criteria. So far, there are no official recommendations for cancer surveillance in affected children and adolescents.
Main body: All individuals with PHTS are at high risk for tumor development and thus might benefit from cancer surveillance strategies. In childhood, macrocephaly may be the only evident symptom, but developmental delay, behavioral problems, dermatological features (e.g., penile freckling), vascular anomalies, lipoma, or enlarged perivascular spaces in cerebral magnetic resonance imaging (cMRI) may help to establish the diagnosis. Regular psychomotor assessment and assistance in subjects with neurological impairment play an important role in the management of affected children. Already in early childhood, affected patients bear a high risk to develop thyroid pathologies. For that reason, monitoring of thyroid morphology and function should be established right after diagnosis. We present a detailed description of affected organ systems, tools for initiation of molecular diagnostic and screening recommendations for patients < 18 years of age.
Conclusion: Affected families frequently experience a long way until the correct diagnosis for their child's peculiarity is made. Even after diagnosis, it is not easy to find a physician who is familiar with this rare group of diseases. Because of a still-limited database, it is not easy to establish evidence-based (cancer) surveillance recommendations. The presented screening recommendation should thus be revised regularly according to the current state of knowledge.
{"title":"PTEN hamartoma tumor syndrome in childhood and adolescence-a comprehensive review and presentation of the German pediatric guideline.","authors":"Michaela Plamper, Bettina Gohlke, Joachim Woelfle","doi":"10.1186/s40348-022-00135-1","DOIUrl":"https://doi.org/10.1186/s40348-022-00135-1","url":null,"abstract":"<p><strong>Background: </strong>The PTEN hamartoma tumor syndrome (PHTS) encompasses several different syndromes, which are linked to an autosomal-dominant mutation of the tumor suppressor PTEN gene on chromosome 10. Loss of PTEN activity leads to an increased phosphorylation of different cell proteins, which may have an influence on growth, migration, and apoptosis. Excessive activity of the PI3K/AKT/mTOR pathway due to PTEN deficiency may lead to the development of benign and malignant tumors and overgrowth. Diagnosis of PHTS in childhood can be even more challenging than in adulthood because of a lack of well-defined diagnostic criteria. So far, there are no official recommendations for cancer surveillance in affected children and adolescents.</p><p><strong>Main body: </strong>All individuals with PHTS are at high risk for tumor development and thus might benefit from cancer surveillance strategies. In childhood, macrocephaly may be the only evident symptom, but developmental delay, behavioral problems, dermatological features (e.g., penile freckling), vascular anomalies, lipoma, or enlarged perivascular spaces in cerebral magnetic resonance imaging (cMRI) may help to establish the diagnosis. Regular psychomotor assessment and assistance in subjects with neurological impairment play an important role in the management of affected children. Already in early childhood, affected patients bear a high risk to develop thyroid pathologies. For that reason, monitoring of thyroid morphology and function should be established right after diagnosis. We present a detailed description of affected organ systems, tools for initiation of molecular diagnostic and screening recommendations for patients < 18 years of age.</p><p><strong>Conclusion: </strong>Affected families frequently experience a long way until the correct diagnosis for their child's peculiarity is made. Even after diagnosis, it is not easy to find a physician who is familiar with this rare group of diseases. Because of a still-limited database, it is not easy to establish evidence-based (cancer) surveillance recommendations. The presented screening recommendation should thus be revised regularly according to the current state of knowledge.</p>","PeriodicalId":74215,"journal":{"name":"Molecular and cellular pediatrics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8859017/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39940726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The purpose of the current study was to evaluate the phenotypic and genotypic patterns of aminoglycoside resistance among the Gram-negative bacteria (GNB) isolates collected from pediatric and general hospitals in Iran. A total of 836 clinical isolates of GNB were collected from pediatric and general hospitals from January 2018 to the end of December 2019. The identification of bacterial isolates was performed by conventional biochemical tests. Susceptibility to aminoglycosides was evaluated by the disk diffusion method (DDM). The frequency of genes encoding aminoglycoside-modifying enzymes (AMEs) was screened by the PCR method via specific primers. Among all pediatric and general hospitals, the predominant GNB isolates were Acinetobacter spp. (n = 327) and Escherichia coli (n = 144). However, E. coli (n = 20/144; 13.9%) had the highest frequency in clinical samples collected from pediatrics. The DDM results showed that 64.3% of all GNB were resistant to all of the tested aminoglycoside agents. Acinetobacter spp. and Klebsiella pneumoniae with 93.6%, Pseudomonas aeruginosa with 93.4%, and Enterobacter spp. with 86.5% exhibited very high levels of resistance to gentamicin. Amikacin was the most effective antibiotic against E. coli isolates. In total, the results showed that the aac (6')-Ib gene with 59% had the highest frequency among genes encoding AMEs in GNB. The frequency of the surveyed aminoglycoside-modifying enzyme genes among all GNB was found as follows: aph (3')-VIe (48.7%), aadA15 (38.6%), aph (3')-Ia (31.3%), aph (3')-II (14.4%), and aph (6) (2.6%). The obtained data demonstrated that the phenotypic and genotypic aminoglycoside resistance among GNB was quite high and it is possible that the resistance genes may frequently spread among clinical isolates of GNB.
{"title":"Evaluation of phenotypic and genotypic patterns of aminoglycoside resistance in the Gram-negative bacteria isolates collected from pediatric and general hospitals.","authors":"Leila Azimi, Shahnaz Armin, Hossein Samadi Kafil, Nafiseh Abdollahi, Kiarash Ghazvini, Sepide Hasanzadeh, Shahram Shahraki Zahedani, Sedigheh Rafiei Tabatabaei, Fatemeh Fallah","doi":"10.1186/s40348-022-00134-2","DOIUrl":"https://doi.org/10.1186/s40348-022-00134-2","url":null,"abstract":"<p><p>The purpose of the current study was to evaluate the phenotypic and genotypic patterns of aminoglycoside resistance among the Gram-negative bacteria (GNB) isolates collected from pediatric and general hospitals in Iran. A total of 836 clinical isolates of GNB were collected from pediatric and general hospitals from January 2018 to the end of December 2019. The identification of bacterial isolates was performed by conventional biochemical tests. Susceptibility to aminoglycosides was evaluated by the disk diffusion method (DDM). The frequency of genes encoding aminoglycoside-modifying enzymes (AMEs) was screened by the PCR method via specific primers. Among all pediatric and general hospitals, the predominant GNB isolates were Acinetobacter spp. (n = 327) and Escherichia coli (n = 144). However, E. coli (n = 20/144; 13.9%) had the highest frequency in clinical samples collected from pediatrics. The DDM results showed that 64.3% of all GNB were resistant to all of the tested aminoglycoside agents. Acinetobacter spp. and Klebsiella pneumoniae with 93.6%, Pseudomonas aeruginosa with 93.4%, and Enterobacter spp. with 86.5% exhibited very high levels of resistance to gentamicin. Amikacin was the most effective antibiotic against E. coli isolates. In total, the results showed that the aac (6')-Ib gene with 59% had the highest frequency among genes encoding AMEs in GNB. The frequency of the surveyed aminoglycoside-modifying enzyme genes among all GNB was found as follows: aph (3')-VIe (48.7%), aadA15 (38.6%), aph (3')-Ia (31.3%), aph (3')-II (14.4%), and aph (6) (2.6%). The obtained data demonstrated that the phenotypic and genotypic aminoglycoside resistance among GNB was quite high and it is possible that the resistance genes may frequently spread among clinical isolates of GNB.</p>","PeriodicalId":74215,"journal":{"name":"Molecular and cellular pediatrics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8816979/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39889775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}