TXN2 thioredoxin 2 [Homo sapiens (human)] - Gene - NCBI

TXN2 thioredoxin 2 [Homo sapiens (human)] - Gene - NCBI
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TXN2 thioredoxin 2 [ Homo sapiens (human) ]
Gene ID: 25828, updated on 18-Jan-2026
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Gene Sequences (FASTA)
Transcript sequences (FASTA)
Protein sequences(FASTA)
In addition, your package will include a detailed data report in both TSV and JSONL formats.
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Summary
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Official Symbol
TXN2provided by HGNC
Official Full Name
thioredoxin 2provided by HGNC
Primary source
HGNC:HGNC:17772
See related
Ensembl:ENSG00000100348 MIM:609063; AllianceGenome:HGNC:17772
Gene type
protein coding
RefSeq status
REVIEWED
Organism
Homo sapiens
Lineage
Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Primates; Haplorrhini; Catarrhini; Hominidae; Homo
Also known as
TXN; MTRX; TRX2; MT-TRX; COXPD29
Summary
This nuclear gene encodes a mitochondrial member of the thioredoxin family, a group of small multifunctional redox-active proteins. The encoded protein may play important roles in the regulation of the mitochondrial membrane potential and in protection against oxidant-induced apoptosis. [provided by RefSeq, Jul 2008]
Expression
Ubiquitous expression in adrenal (RPKM 39.7), kidney (RPKM 28.5) and 25 other tissues See more
Orthologs
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Genomic context
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See TXN2 in Genome Data Viewer
Location:
22q12.3
Exon count:
4
Annotation release
Status
Assembly
Chr
Location
RS_2025_08 current GRCh38.p14 (GCF_000001405.40) 22 NC_000022.11 (36467046..36481640, complement)
RS_2025_08 current T2T-CHM13v2.0 (GCF_009914755.1) 22 NC_060946.1 (36927219..36941813, complement)
RS_2024_09 previous assembly GRCh37.p13 (GCF_000001405.25) 22 NC_000022.10 (36863093..36877687, complement)
Chromosome 22 - NC_000022.11
Genomic regions, transcripts, and products
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Go to reference sequence details
Genomic Sequence: NC_000022.11 Chromosome 22 Reference GRCh38.p14 Primary Assembly NG_046718.1 RefSeqGene NC_060946.1 Chromosome 22 Alternate T2T-CHM13v2.0 NC_000022.10 Chromosome 22 Reference GRCh37.p13 Primary Assembly
Go to nucleotide: Graphics FASTA GenBank
Expression
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See details
Tissue-specific circular RNA induction during human fetal development RNA sequencing of total RNA from 20 human tissues HPA RNA-seq normal tissues
Project title: Tissue-specific circular RNA induction during human fetal development
Description: 35 human fetal samples from 6 tissues (3 - 7 replicates per tissue) collected between 10 and 20 weeks gestational time were sequenced using Illumina TruSeq Stranded Total RNA
BioProject: PRJNA270632
Publication: PMID 26076956
Analysis date: Mon Apr 2 22:54:59 2018
Bibliography
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Related articles in PubMed
Hypoxia inhibits expression and function of mitochondrial thioredoxin 2 to promote pulmonary hypertension. Adesina SE, et al. Am J Physiol Lung Cell Mol Physiol, 2017 May 1. PMID 28130258, Free PMC Article
Human mitochondrial thioredoxin. Involvement in mitochondrial membrane potential and cell death. Damdimopoulos AE, et al. J Biol Chem, 2002 Sep 6. PMID 12080052
Thioredoxin 2 Offers Protection against Mitochondrial Oxidative Stress in H9c2 Cells and against Myocardial Hypertrophy Induced by Hyperglycemia. Li H, et al. Int J Mol Sci, 2017 Sep 15. PMID 28914755, Free PMC Article
Genetic polymorphisms in the thioredoxin 2 (TXN2) gene and risk for spina bifida. Wen S, et al. Am J Med Genet A, 2009 Feb. PMID 19165900, Free PMC Article
Thioredoxin 2 Is a Novel E2-Interacting Protein That Inhibits the Replication of Classical Swine Fever Virus. Li S, et al. J Virol, 2015 Aug. PMID 26041303, Free PMC Article
See all (68) citations in PubMed
GeneRIFs: Gene References Into Functions
What's a GeneRIF?
scAAV2-Mediated Expression of Thioredoxin 2 and C3 Transferase Prevents Retinal Ganglion Cell Death and Lowers Intraocular Pressure in a Mouse Model of Glaucoma.
Title: scAAV2-Mediated Expression of Thioredoxin 2 and C3 Transferase Prevents Retinal Ganglion Cell Death and Lowers Intraocular Pressure in a Mouse Model of Glaucoma.
Association between genetic variants in oxidative stress-related genes and osteoporotic bone fracture. The Hortega follow-up study.
Title: Association between genetic variants in oxidative stress-related genes and osteoporotic bone fracture. The Hortega follow-up study.
Mitochondrial TXN2 attenuates amyloidogenesis via selective inhibition of BACE1 expression.
Title: Mitochondrial TXN2 attenuates amyloidogenesis via selective inhibition of BACE1 expression.
Mechanisms of Trx2/ASK1-Mediated Mitochondrial Injury in Pemphigus Vulgaris.
Title: Mechanisms of Trx2/ASK1-Mediated Mitochondrial Injury in Pemphigus Vulgaris.
Thioredoxin 2 Negatively Regulates Innate Immunity to RNA Viruses by Disrupting the Assembly of the Virus-Induced Signaling Adaptor Complex.
Title: Thioredoxin 2 Negatively Regulates Innate Immunity to RNA Viruses by Disrupting the Assembly of the Virus-Induced Signaling Adaptor Complex.
Overexpression of mitochondrial Trx2 attenuates the intracellular ROS accumulation and ATP production. Most interestingly, mitochondrial Trx2 may be involved in the cardiac hypertrophy signaling of diabetes.
Title: Thioredoxin 2 Offers Protection against Mitochondrial Oxidative Stress in H9c2 Cells and against Myocardial Hypertrophy Induced by Hyperglycemia.
Prx3 and Trx2 comprise an adaptive system to sense changes in atmospheric oxygen tension and influence cellular injury responses through both detoxification of mitochondrial oxidants and regulation of mitochondrial redox-dependent signaling
Title: Detoxification of Mitochondrial Oxidants and Apoptotic Signaling Are Facilitated by Thioredoxin-2 and Peroxiredoxin-3 during Hyperoxic Injury.
Trx2 overexpression failed to attenuate hypoxia-induced human pulmonary arterial smooth muscle cells proliferation in vitro or hypoxia-induced Pulmonary hypertension in vivo.
Title: Hypoxia inhibits expression and function o


Isolate Details | Antimicrobial Resistance Isolate Bank | Antibiotic/Antimicrobial Resistance | CDC

Isolate Details | Antimicrobial Resistance Isolate Bank | Antibiotic/Antimicrobial Resistance | CDC
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CDC & FDA Antimicrobial Resistance Isolate Bank
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View another isolate in this panel > View Another Isolate 0034 - Klebsiella pneumoniae 0040 - Klebsiella pneumoniae 0045 - Acinetobacter baumannii 0054 - Pseudomonas aeruginosa 0056 - Acinetobacter baumannii 0060 - Enterobacter cloacae 0064 - Pseudomonas aeruginosa 0075 - Klebsiella pneumoniae 0078 - Acinetobacter baumannii 0083 - Acinetobacter baumannii 0088 - Acinetobacter baumannii 0090 - Pseudomonas aeruginosa 0092 - Pseudomonas aeruginosa 0095 - Pseudomonas aeruginosa 0098 - Klebsiella pneumoniae 0100 - Pseudomonas aeruginosa 0104 - Escherichia coli 0105 - Pseudomonas aeruginosa 0118 - Escherichia coli 0132 - Enterobacter cloacae group 0143 - Klebsiella pneumoniae 0150 - Escherichia coli 0151 - Escherichia coli 0155 - Proteus mirabilis 0159 - Proteus mirabilis 0162 - Escherichia coli 0239 - Pseudomonas aeruginosa 0241 - Pseudomonas aeruginosa 0246 - Pseudomonas aeruginosa 0274 - Acinetobacter baumannii 0285 - Acinetobacter baumannii 0288 - Acinetobacter baumannii 0309 - Acinetobacter baumannii 0517 - Serratia marcescens 0555 - Klebsiella pneumoniae 0858 - Enterobacter cloacae
Panel: Cefiderocol Verification (FDC) (Custom)
AR Bank # 0033 Acinetobacter baumannii
Study ID: CarbaNP-02
Biosample Accession #: SAMN04014874
MLST: ST85(Pasteur), ST1089(Oxford)
This panels contains isolates from other AR Bank collections/panels.
MICs obtained by broth microdilution. Modal MIC is reported.
MIC results for each antimicrobial agent for an isolate may commonly be ± 1 log2 (doubling dilution) different than what is posted on the FDA & CDC AR Bank website because this is the normal technical variability of antimicrobial susceptibility testing (see J. H. Jorgensen. 1993. J Clin Microbiol. Vol 31[11]: 2841-2844).
Panel: Gram Negative Carbapenemase Detection (CarbaNP) | ARLN Verification (Custom) | Cefiderocol Verification (FDC) (Custom) | GN7F ARLN (Custom) | GAIHN (Custom)
MIC
MMR
Propagation
Temp & Biosafety
Isolate History
MIC (μg/ml) Results and Interpretation
Drug
MIC (μg/ml)
INT
Amikacin 2 S
Ampicillin/sulbactam 1 >32 R
Cefepime >32 R
Cefepime/zidebactam 5 >64 ---
Cefiderocol 16 R
Cefotaxime >64 R
Ceftazidime >128 R
Ceftriaxone >32 R
Ciprofloxacin >8 R
Colistin 4 1 I
Doripenem >8 R
Gentamicin 16 R
Imipenem 64 R
Imipenem+chelators 3 4 ---
Levofloxacin 8 R
Meropenem >8 R
Minocycline <=4 S
Piperacillin/tazobactam 1 >128 R
Tetracycline <=2 S
Tigecycline 2 <=0.5 ---
Tobramycin 16 R
Trimethoprim/sulfamethoxazole 1 >8 R
1 Reflects MIC of first component
2 Based on FDA break points
3 Screen for metallo-beta-lactamase production [Rasheed et al. Emerging Infectious Diseases. 2013. 19(6):870-878]
4 Clinical and PK/PD data demonstrate colistin has limited clinical efficacy, even if an intermediate result is obtained. Alternative agents are strongly preferred. Colistin should be used in combination with one or more active antimicrobial agents. Consultation with an infectious disease specialist is recommended.
5 Cefepime to zidebactam ratio (1:1)
Device manufacturers and users of FDA cleared devices shall consult the FDA’s Antibacterial Susceptibility Test Interpretive Criteria website for breakpoints recognized or recommended by FDA, and for information regarding FDA exceptions or additions to the applicable, recognized consensus standard.
Molecular Mechanisms of Resistance
Category Gene
Aminoglycoside ant(3")-IIa
Beta-lactam NDM-1, OXA-94
Bleomycin ble-MBL
Efflux pumps/Other ABAF
Sulfonamides sul2
Disclaimer:
The resistance mechanisms listed were identified by analysis of whole genome sequence using the ResFinder database (last updated June 2, 2016 and accessed on October 25, 2016). This analysis does not include mutations that may result in antibiotic resistance or resistance determinants added to newer versions of the ResFinder database or other antimicrobial resistance gene databases. Biosample accession numbers have been provided so that users can analyze the data on their own if so desired.
For additional gene information please visit the Reference Gene Catalog - Pathogen Detection - NCBI (https://www.ncbi.nlm.nih.gov/pathogens/refgene), a non-redundant database of bacterial genes related to antimicrobial resistance, biocide and stress resistance, general efflux, virulence, or antigenicity.
Propagation
MEDIUM
Medium: Trypticase Soy Agar with 5% Sheep Blood (BAP)
GROWTH CONDITIONS
Temperature: 35°C
Atmosphere: Aerobic
PROPAGATION PROCEDURE
Remove the sample vial to a container with dry ice or a freezer block. Keep vial on ice or block. (Do not let vial content thaw) Open vial aseptically to avoid contamination Using a sterile loop, remove a small amount of frozen isolate from the top of the vial Aseptically transfer the loop to BAP Use streak plate method to isolate single colonies Incubate inverted plate at 35°C ± 2°C for 20-24 hrs.
Storage Temperature & Biosafety
STORAGE TEMPERATURE: -70°C
BIOSAFETY LEVEL: 2
Appropriate safety procedures should always be used with this material. Laboratory safety is discussed in the current publication of 'BioSafety in Microbiological and Biomedical Laboratories' from the U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, and National Institutes of Health.
Disclaimer:
This product is sent with the condition that you are responsible for its safe storage, handling, and use. All materials are the property of the Centers for Disease Control and Prevention (CDC) and have been made available on behalf of the Food and Drug Administration (FDA). This material is not for use in human subjects and may not be redistributed. While CDC uses reasonable efforts to include accurate and up-to-date information on this product sheet, CDC makes no warranties or representations as to its accuracy. CDC is not liable for damages arising from the misidentification or misrepresentation of cultures. Please refer to the Standard Letter Agreement (SLA) for further details regarding the use of this product.
Isolate History
Date
Action Performed
10/18/23 INT was updated with a new value for Minocycline: from '---' to 'S'
10/18/23 MIC was updated with a new value for Minocycline: from '---' to '<=4'
10/18/23 Drug was added: Minocycline
03/09/23 Gene was added to 'ABAF'
03/09/23 Category was added: 'Efflux pumps/Other'
03/09/23 Gene was added to 'ble-MBL'
03/09/23 Gene was added to 'ant(3")-IIa'
03/09/23 Category was added: 'Bleomycin'
03/09/23 Category was added: 'Aminoglycoside'
12/19/22 MLST was updated: from '---' to 'ST1089(Oxford)'
12/19/22 MLST was updated: from '---' to 'ST85(Pasteur)'
12/07/22 MIC was updated with a new value for Cefepime/zidebactam: from '---' to '>64'
12/07/22 Drug was added: Cefepime/zidebactam
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4273 Willow Draw Drive #606, Park City, UT 84098 | Realty One Group

4273 Willow Draw Drive #606, Park City, UT 84098 | Realty One Group
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Taxonomy browser Taxonomy Browser (Jacqueshuberia loretensis)

Taxonomy browser Taxonomy Browser (Jacqueshuberia loretensis)
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BioProject 1 1 -
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Identical Protein Groups 2 2 -
Nucleotide 4 4 -
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Taxonomy 1 1 -
Jacqueshuberia loretensis
Taxonomy ID: 321561 (for references in articles please use ncbitaxon:321561)
current name
Jacqueshuberia loretensis R.S.Cowan, 1985
NCBI BLAST name: eudicots
Rank: species
Genetic code: Translation table 1 (Standard)
Mitochondrial genetic code: Translation table 1 (Standard)
Lineage(full)
cellular organisms; Eukaryota; Viridiplantae; Streptophyta; Streptophytina; Embryophyta; Tracheophyta; Euphyllophyta; Spermatophyta; Magnoliopsida; Mesangiospermae; eudicotyledons; Gunneridae; Pentapetalae; rosids; fabids; Fabales; Fabaceae; Caesalpinioideae; Tachigali clade; Jacqueshuberia
Comments and References:
TROPICOS (Jul 07, 2017)
Name accessed on 7 July 2017 in: Tropicos.org. Missouri Botanical Garden, 2008 - 4344 Shaw Boulevard, Saint Louis, Missouri 63110, U.S.A. on line at: http://www.tropicos.org
External Information Resources (NCBI LinkOut)
LinkOut Subject LinkOut Provider
Jacqueshuberia loretensis Cowan taxonomy/phylogenetic Encyclopedia of life
Jacqueshuberia loretensis taxonomy/phylogenetic Plants of the World Online
Jacqueshuberia loretensis taxonomy/phylogenetic The International Plant Names Index
search W3TROPICOS taxonomy/phylogenetic Vascular Tropicos
Wikipedia taxonomy/phylogenetic iPhylo
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Reference: How to cite this resource - Schoch CL, et al. NCBI Taxonomy: a comprehensive update on curation, resources and tools. Database (Oxford). 2020: baaa062. PubMed: 32761142 PMC: PMC7408187.
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Equivalent Circuit to Analyze the Transmitting Characteristics of a Cymbal Array | MDPI

Equivalent Circuit to Analyze the Transmitting Characteristics of a Cymbal Array | MDPI
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Sensors
Volume 22
Issue 22
10.3390/s22228743
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AbstractIntroductionEquivalent Circuit of a Cymbal ArrayValidation of the Equivalent Circuit AnalysisEfficiency of the Equivalent Circuit AnalysisConclusionsAuthor ContributionsFundingInstitutional Review Board StatementInformed Consent StatementData Availability StatementConflicts of InterestReferencesArticle Metrics
Article
12 November 2022
Equivalent Circuit to Analyze the Transmitting Characteristics of a Cymbal Array
Hayeong Shim1
,
Kyungseop Kim2
,
Heeseon Seo2
and
Yongrae Roh1,*
1
School of Mechanical Engineering, Kyungpook National University, Daegu 41566, Korea
2
Agency for Defense Development, Changwon 51678, Korea
*
Author to whom correspondence should be addressed.
Sensors2022, 22(22), 8743;https://doi.org/10.3390/s22228743
This article belongs to the Special Issue The Development of Piezoelectric Sensors and Actuators
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Abstract
A cymbal transducer has a simple structure consisting of a piezoceramic disk and metallic caps and has broadband characteristics when built as an array. The finite element method (FEM) is generally used to analyze the characteristics of acoustic transducers. However, the FEM requires a longer analysis time as the model becomes larger, which makes it limited and less efficient for analyzing the cymbal array. In this study, a new equivalent circuit with higher efficiency and accuracy, comparable to that of the FEM, was proposed to analyze the performance of cymbal arrays. The equivalent circuit for the array was constructed by connecting the equivalent circuits of individual cymbal transducers in parallel with a radiation impedance matrix that included both the self- and mutual radiation characteristics of the array. The validity of the new equivalent circuit was verified by measuring the transmitting voltage response of a cymbal array specimen and comparing it with that calculated using the circuit. The comparison confirmed the efficiency of the equivalent circuit in analyzing the characteristics of the cymbal array. The proposed equivalent circuit can facilitate the design of a large array of cymbal transducers.
Keywords:
cymbal transducer; equivalent circuit; broadband transducer; cymbal array
1. Introduction
A cymbal transducer is a miniaturized version of the class V flextensional transducer [1]. It consists of a piezoceramic disk and a pair of metal caps and has a low resonant frequency considering its small size. Broadband characteristics can be obtained when cymbals are arranged and used as an array [2].
Since the development of the cymbal transducer by Newnham et al. in the 1990s, various studies have been conducted by many researchers [3,4,5,6,7,8]. The performance of cymbal transducers has generally been analyzed using the finite element method (FEM). However, an equivalent circuit for cymbal transducers has recently been developed [9,10]. However, in the case of the cymbal array, an equivalent circuit for exclusive use has not yet been developed, so the FEM or experimental analysis methods are still mainly used. For instance, Tressler et al. experimentally analyzed and compared the transmitting voltage response (TVR) of a cymbal array for different constituent materials and construction methods [11]. Zhang et al. analyzed the displacement of each element constituting a cymbal array and calculated the TVR while changing the spacing between the elements using the FEM [12]. Rajapan et al. fabricated cymbal array specimens with various encapsulation materials and measured their acoustic properties [13]. Du et al. analyzed the acoustic properties of a cymbal array using an experimental method [14]. Kim et al. derived an optimized array structure to maximize the bandwidth of a cymbal array using the FEM [15].
The analysis of the acoustic characteristics of the cymbal array as conducted in all these studies using the FEM or the experimental method is very time-consuming. The cymbal transducer is small compared to the wavelength at the resonant frequency. This small and curved geometry of the cymbal requires elaborate modeling and meshing, which prolongs the analysis time so much that using the FEM to analyze a cymbal array larger than a 3 × 3 array would hardly ever be feasible.
There are positive indications that the difficulty of analyzing the cymbal array using the FEM can be resolved by developing a dedicated equivalent circuit, as inspired by the study conducted by Pyo and Roh [16]. Several related studies have been conducted. As a case in point, Zhang et al. analyzed the cymbal array using the equivalent circuit method (ECM). However, the discrepancy between the measured and analyzed TVR spectra was not ignorable. This was attributed to the inaccuracy in the mutual radiation impedance between the cymbals in the array [17]. It is necessary to supplement the equivalent circuit by deriving an accurate radiation impedance matrix dedicated to the cymbal array.
In the case of cymbal arrays, the mutual radiation impedance has a significantly large impact on the acoustic characteristics of the array because a large number of transducers, smaller than the wavelength, are arranged within a narrow area [18]. A typical equivalent circuit does not reflect such mutual radiation impedance but considers only the self-radiation impedance of each transducer [19]. The mutual radiation impedance in an array has been studied in several studies using an equivalent circuit [20,21]. Oguz et al. analyzed the effect of mutual radiation impedance on each cell in a capacitive micromachined ultrasonic transducer array using an equivalent circuit [22]. Akhbari et al. developed equivalent circuits for arrays of curved and flat piezoelectric micromachined ultrasonic transducers and analyzed the radiation characteristics of arrays using the circuits [23]. Pyo and Roh designed a structure that maximized the bandwidth of a planar Tonpilz array using an equivalent circuit that included the mutual radiation impedance [16]. Sim et al. developed an equivalent circuit model that could predict the acoustic response of a cylindrical Tonpilz array by considering the mutual radiation impedance [24]. However, all these studies were related to arrays composed of transducers with a single radiating surface. Because the upper and lower caps of a cymbal transducer act as independent radiating surfaces, as noted in Zhang’s work [17], the radiation impedance matrix used in previous studies is unsuitable for a cymbal array. The dual piston model in [17] was observed to be insufficient to express the interaction between elements in a cymbal array because the comparison between the measured and calculated results showed considerable differences.
This study proposes a new equivalent circuit that can accurately and efficiently resolve this


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TPA_inf: Coccidioides posadasii nat1 gene for arylamine N-acetyltransf - Nucleotide - NCBI

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TPA_inf: Coccidioides posadasii nat1 gene for arylamine N-acetyltransferase 1, strain RMSCC 2133, exons 1-2
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Frontiers | Analysis and Biophysics of Surface EMG for Physiotherapists and Kinesiologists: Toward a Common Language With Rehabilitation Engineers

Frontiers | Analysis and Biophysics of Surface EMG for Physiotherapists and Kinesiologists: Toward a Common Language With Rehabilitation Engineers
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METHODS article
Front. Neurol., 15 October 2020
Sec. Neurorehabilitation
Volume 11 - 2020 | https://doi.org/10.3389/fneur.2020.576729
This article is part of the Research TopicSurface Electromyography: Barriers Limiting Widespread use of sEMG in Clinical Assessment and NeurorehabilitationView all 19 articles
Analysis and Biophysics of Surface EMG for Physiotherapists and Kinesiologists: Toward a Common Language With Rehabilitation Engineers
Lara McManus1* Giuseppe De Vito2 Madeleine M. Lowery1
1Neuromuscular Systems Laboratory, School of Electrical and Electronic Engineering, University College Dublin, Dublin, Ireland
2Neuromuscular Physiology Laboratory, Department of Biomedical Sciences, University of Padova, Padova, Italy
Recent decades have seen a move toward evidence-based medicine to inform the clinical decision-making process with reproducible findings from high-quality research studies. There is a need for objective, quantitative measurement tools to increase the reliability and reproducibility of studies evaluating the efficacy of healthcare interventions, particularly in the field of physical and rehabilitative medicine. Surface electromyography (sEMG) is a non-invasive measure of muscle activity that is widely used in research but is under-utilized as a clinical tool in rehabilitative medicine. Other types of electrophysiological signals (e.g., electrocardiography, electroencephalography, intramuscular EMG) are commonly recorded by healthcare practitioners, however, sEMG has yet to successfully transition to clinical practice. Surface EMG has clear clinical potential as an indicator of muscle activation, however reliable extraction of information requires knowledge of the appropriate methods for recording and analyzing sEMG and an understanding of the underlying biophysics. These concepts are generally not covered in sufficient depth in the standard curriculum for physiotherapists and kinesiologists to encourage a confident use of sEMG in clinical practice. In addition, the common perception of sEMG as a specialized topic means that the clinical potential of sEMG and the pathways to application in practice are often not apparent. The aim of this paper is to address barriers to the translation of sEMG by emphasizing its benefits as an objective clinical tool and by overcoming its perceived complexity. The many useful clinical applications of sEMG are highlighted and examples provided to illustrate how it can be implemented in practice. The paper outlines how fundamental biophysics and EMG signal processing concepts could be presented to a non-technical audience. An accompanying tutorial with sample data and code is provided which could be used as a tool for teaching or self-guided learning. The importance of observing sEMG in routine use in clinic is identified as an essential part of the effective communication of sEMG recording and signal analysis methods. Highlighting the advantages of sEMG as a clinical tool and reducing its perceived complexity could bridge the gap between theoretical knowledge and practical application and provide the impetus for the widespread use of sEMG in clinic.
Introduction
Surface EMG is currently an under-utilized clinical tool in rehabilitative medicine, despite its clear potential as a non-invasive measure of muscle activity. It is often considered more complex to analyze than intramuscular EMG, a technique commonly applied in clinical neurology, as parameters of direct clinical relevance cannot be readily extracted (


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3FFN: Crystal structure of calcium-free human gelsolin

3FFN: Crystal structure of calcium-free human gelsolin
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3FFN: Crystal structure of calcium-free human gelsolin
PDB ID: 3FFNDownload
MMDB ID: 77149
PDB Deposition Date: 2008/12/4
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Tomar medicamentos para tratar la tuberculosis: MedlinePlus enciclopedia médica

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Tomar medicamentos para tratar la tuberculosis
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Tomar medicamentos para tratar la tuberculosis
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La tuberculosis (TB) es una infección bacterial contagiosa que compromete principalmente los pulmones, pero puede propagarse a otros órganos. El objetivo del tratamiento es curar la infección con medicamentos que combatan a la bacteria de la TB.
¿Por qué necesita medicamentos para la tuberculosis?
Usted puede tener una infección de TB pero no la enfermedad activa o los síntomas. Esto significa que la bacteria de esta enfermedad permanece inactiva (latente) en una zona pequeña de sus pulmones. Este tipo de infección puede estar presente durante años y se llama tuberculosis latente. Con la TB latente:
Usted no puede propagar la enfermedad a otras personas.
En algunas personas, la bacteria puede volverse activa. Si esto sucede, usted puede resultar enfermo o puede pasarle los gérmenes de la TB a otra persona.
Aunque usted no se sienta enfermo, necesitará tomar medicamentos para la tuberculosis durante 6 a 9 meses. Esta es la única manera de garantizar que se destruyan todas las bacterias de la TB en su cuerpo y no desarrolle una infección activa en el futuro.
Cuando usted tiene tuberculosis activa, puede sentirse enfermo o tener tos, bajar de peso, sentirse cansado o tener fiebre o sudores fríos. Con la TB activa:
Usted puede transmitir la tuberculosis a otras personas en su entorno. Esto incluye a las personas con quienes usted vive, trabaja o con quienes tiene un estrecho contacto.
Usted necesita tomar varios medicamentos para la tuberculosis durante al menos 6 meses para eliminar de su cuerpo las bacterias de esta enfermedad. Debe empezar a sentirse mejor al cabo de un mes de haber comenzado los medicamentos.
Durante las primeras 2 a 4 semanas después de empezar a tomar los medicamentos, posiblemente deba permanecer en casa para evitar la propagación de la tuberculosis a otros. Pregúntele a su proveedor de atención médica cuándo puede estar cerca de otras personas sin problema.
Su proveedor está obligado por ley a informar sobre su caso a la Secretaría de Salud Pública local.
Se le puede obligar legalmente a tomar sus medicamentos.
Pregúntele a su proveedor si otras personas con quienes usted trabaja o vive deben ser examinadas en busca de tuberculosis.
Cómo tomar los medicamentos
Los gérmenes de la tuberculosis mueren muy lentamente. Usted necesita tomar varias píldoras diferentes en distintos momentos del día, durante 6 meses o más. La única forma de eliminarlos es tomar los medicamentos para la tuberculosis de la manera como su proveedor lo haya indicado. Esto significa tomar todos los medicamentos todos los días.
Si no toma sus medicamentos para la tuberculosis de la manera correcta o deja de tomarlas antes:
Su infección de tuberculosis puede empeorar.
Su infección puede resultar más difícil de tratar. Los medicamentos que esté tomando pueden dejar de hacer efecto. Esto se denomina tuberculosis farmacorresistente y puede ser muy difícil de tratar.
Tal vez necesite tomar otros medicamentos con más efectos secundarios y menos capacidad para curar la infección.
Le puede propagar la infección a otros.
Si a su proveedor le preocupa que usted tal vez no esté tomando todos los medicamentos de acuerdo con las instrucciones, puede ordenar que alguien lo visite todos los días o unas cuantas veces a la semana para vigilar que usted tome los medicamentos para la tuberculosis. Esto se llama tratamiento de observación directa.
Efectos secundarios y otros problemas
Las mujeres que puedan estar embarazadas, que estén embarazadas o que estén amamantando deben hablar con su proveedor antes de tomar estos medicamentos. Si está utilizando pastillas anticonceptivas, pregúntele a su proveedor si los medicamentos para la tuberculosis pueden hacer que las píldoras anticonceptivas sean menos efectivas.
La mayoría de las personas no tiene efectos secundarios muy graves a raíz de los medicamentos para la tuberculosis. Los problemas con los que hay que tener cuidado y comentarle a su proveedor incluyen:
Articulaciones dolorosas
Hematomas o tendencia al sangrado
Fiebre
Poco o ningún apetito
Hormigueo o dolores en los dedos de los pies o las manos, o alrededor de la boca
Malestar estomacal, náuseas o vómitos y cólicos o dolor de estomago
Problemas de la visión
Piel u ojos amarillos (ictericia)
Orina de color del té o naranja (la orina de color naranja es normal con algunos medicamentos)
Cuándo llamar al médico
Comuníquese con su proveedor si tiene:
Cualquiera de los efectos secundarios mencionados anteriormente
Nuevos síntomas de TB activa, como tos, fiebre o sudores nocturnos, dificultad para respirar, o dolor en el pecho
Nombres alternativos
Medicamentos - tuberculosis; TVD; Terapia vigilada directamente; TB - medicamentos
Referencias
Bailey TC, Philips JA. Tuberculosis. In: Goldman L, Cooney KA, eds. Goldman-Cecil Medicine. 27th ed. Philadelphia, PA: Elsevier; 2024:chap 299.
Horne DJ, Payam N. Tuberculosis: treatment of drug-susceptible and drug-resistant. In: Broaddus VC, King TE, Ernst JD, et al, eds. Murray and Nadel's Textbook of Respiratory Medicine. 7th ed. Philadelphia, PA: Elsevier; 2022:chap 54.
Ultima revisión 11/25/2023
Versión en inglés revisada por: Denis Hadjiliadis, MD, MHS, Paul F. Harron Jr. Professor of Medicine, Pulmonary, Allergy, and Critical Care, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA. Also reviewed by David C. Dugdale, MD, Medical Director, Brenda Conaway, Editorial Director, and the A.D.A.M. Editorial team.
Traducción y localización realizada por: DrTango, Inc.
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