Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “reprogramming”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,099 records · Page 61Linked to original sources
PubMed2006

Somatic stem cells and the origin of cancer.

Most human cancers derive from a single cell targeted by genetic and epigenetic alterations that initiate malignant transformation. Progressively, these early cancer cells give rise to different generations of daughter cells that accumulate additional mutations, acting in concert to drive the full neoplastic phenotype. As we have currently deciphered many of the gene pathways disrupted in cancer, our knowledge about the nature of the normal cells susceptible to transformation upon mutation has remained more elusive. Adult stem cells are those that show long-term replicative potential, together with the capacities of self-renewal and multi-lineage differentiation. These stem cell properties are tightly regulated in normal development, yet their alteration may be a critical issue for tumorigenesis. This concept has arisen from the striking degree of similarity noted between somatic stem cells and cancer cells, including the fundamental abilities to self-renew and differentiate. Given these shared attributes, it has been proposed that cancers are caused by transforming mutations occurring in tissue-specific stem cells. This hypothesis has been functionally supported by the observation that among all cancer cells within a particular tumor, only a minute cell fraction has the exclusive potential to regenerate the entire tumor cell population; these cells with stem-like properties have been termed cancer stem cells. Cancer stem cells can originate from mutation in normal somatic stem cells that deregulate their physiological programs. Alternatively, mutations may target more committed progenitor cells or even mature cells, which become reprogrammed to acquire stem-like functions. In any case, mutated genes should promote expansion of stem/progenitor cells, thus increasing their predisposition to cancer development by expanding self-renewal and pluripotency over their normal tendency towards relative quiescency and proper differentiation.

Animals↗
PubMed2025

Glutaryl-CoA dehydrogenase (GCDH) enhances renal malignancy risk via modulating glutarylcarnitine levels.

BACKGROUND: Crotonylation, a recently identified lysine acylation, plays a critical role in post-translational modifications [1]. It has been implicated in tumorigenesis by modulating metabolic reprogramming [2], DNA repair, immune evasion [3], and oncogenic signaling pathways, including PKA-FAK-AKT and androgen receptor signaling [4]. The specific role of crotonylation in renal malignancy (RM) remains poorly understood, especially in interaction with gene expression and metabolic pathway interactions. METHODS: This study integrates genome-wide association study (GWAS) summary statistics for RM from the FinnGen database, data on crotonylation-associated gene expression obtained from the eQTLGen consortium, and metabolite GWAS data obtained from the GWAS Catalog. A combined two-sample Mendelian randomization (MR), summary data-based Mendelian randomization (SMR), and mediation analyses were performed to investigate the causal link between Glutaryl-CoA dehydrogenase (GCDH) and RM, with a specific focus on glutarylcarnitine metabolism. RESULTS: MR analysis demonstrated a significant association; increased expression of GCDH is likely to increase the risk of RM (OR = 1.25, P = 0.0045). Mediation analysis revealed that elevated GCDH expression significantly reduced glutarylcarnitine (C5-DC) levels, which in turn was inversely associated with RM risk. A three-step MR-based mediation confirmed a significant mediating effect of glutarylcarnitine (β₁₂ = 0.0680, P = 0.002), with 30.25% of the total effect attributable to it. The robustness of these findings was further demonstrated by sensitivity analyses and SMR results. CONCLUSION: This study represents the first evidence that GCDH might exert an indirect pro-RM effect via the downregulation of glutarylcarnitine, thus providing new insights into tumor metabolic pathways and positioning glutarylcarnitine as a potentially diagnostic biomarker and therapeutic target for RM.

GCDH↗
PubMed2026

Multi-omics identification of therapeutic targets of compound sappan decoction in hepatocellular carcinoma.

BACKGROUND: Compound sappan decoction (CSD) is a multi-herbal traditional Chinese medicine formulation with clinical relevance in hepatocellular carcinoma (HCC). However, its therapeutic mechanisms remain unclear. METHODS: Bioactive compounds of CSD were identified and standardized using pharmacological and chemical databases. Potential targets were predicted via multiple target inference platforms. HCC-related genes were curated from comprehensive disease databases. Summary-data-based Mendelian randomization (SMR) was conducted to infer causal relationships between compound targets and HCC risk using large-scale quantitative trait loci (QTL) datasets and HCC genome-wide association study data. Colocalization analysis, protein-protein interaction (PPI) network construction, and GO/KEGG enrichment were performed on SMR-identified targets. Molecular docking evaluated binding affinities of representative compounds to prioritized targets. RESULTS: A total of 784 overlapping genes between predicted CSD targets and HCC-related genes were subjected to SMR analysis. Among these, 22 targets were significantly associated with HCC risk based on transcriptomic or proteomic QTLs and showed colocalization evidence. Notably, four targets (ADRB2, APOE, SYK, and PGF) were supported by both replication in an independent cohort and strong colocalization. These 22 targets were enriched in apoptosis, PI3K-Akt signaling, redox metabolism, and detoxification pathways. PPI analysis revealed central hubs including MMP9, BCL2, CASP1, and MCL1. Molecular docking demonstrated strong binding of APOE to quercetin, PGF to luteolin-7-olate, and SYK to kaempferol. CONCLUSIONS: CSD may exert therapeutic effects on HCC through modulation of genetically validated targets involved in tumor progression, inflammation, and metabolic reprogramming, supporting its potential clinical utility as an adjunctive treatment strategy. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at https://doi.org/10.1007/s12672-026-04740-8.

Caesalpinia↗
PubMed2026

A novel lactylation-related gene signature deciphers the immunosuppressive microenvironment and stratifies precision therapy in colorectal cancer.

BACKGROUND: Colorectal cancer (CRC) remains a leading cause of cancer mortality, largely due to the heterogeneity of the tumor microenvironment (TME) and the limited efficacy of immunotherapy in microsatellite stable (MSS) tumors. Histone lactylation, a post-translational modification derived from the Warburg effect, serves as a critical bridge linking metabolic reprogramming to gene regulation and immune evasion; however, its specific prognostic value and clinical implications in CRC remain to be fully elucidated. METHODS: In this study, we systematically analyzed transcriptome profiling data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) cohorts, supplemented by single-cell RNA sequencing (scRNA-seq) analysis and Human Protein Atlas (HPA) protein-level validation. By integrating univariate Cox regression, Least Absolute Shrinkage and Selection Operator (LASSO) analysis, and multivariate Cox regression, we constructed a novel lactylation-related gene (LRG) risk signature. We extensively evaluated the association between this risk signature and patient prognosis, immune infiltration patterns, somatic mutations, and therapeutic sensitivity. RESULTS: A robust 9-gene prognostic signature (DHRS7, SPR, MBD2, RBM17, CSRP2, S100A4, TMSB4X, TKT, COPS4) was identified and corroborated at the protein level. Patients with high risk scores exhibited significantly worse overall survival (OS) across the training and two independent validation cohorts. Immunogenomic and scRNA-seq analyses revealed that high-risk tumors were characterized by an immunosuppressive and stromal-dense microenvironment-with stromal cells exhibiting the highest lactylation risk scores-enriched with regulatory T cells (Tregs), and frequently harbored PIK3CA mutations. Differential expression analysis indicated that this immune exclusion is structurally maintained by enriched extracellular matrix (ECM) organization and TGF-β signaling. Conversely, low-risk tumors displayed an inflamed phenotype with active antitumor immunity. Pharmacogenomic prediction identified distinct therapeutic stratifications: low-risk patients exhibited significant sensitivity to standard chemotherapeutics (fluorouracil, oxaliplatin) and EGFR/HER2 inhibitors (e.g., lapatinib, erlotinib). In contrast, high-risk patients showed specific vulnerabilities to novel targeted agents, including PI3K pathway inhibitors (TG-100-115, XL765), microenvironment-modulating agents (sildenafil, GANT-61), and epigenetic inhibitors (UNC0638). CONCLUSION: We established a novel lactylation-related risk signature that effectively stratifies CRC patients by prognosis and TME characteristics. By elucidating the crosstalk between metabolic dysregulation, stromal barriers, and immune exclusion, this study provides potential biomarkers and stratified therapeutic strategies-ranging from standard chemotherapy to targeted metabolic and stromal interventions-to optimize precision medicine for CRC patients.

Colorectal cancer↗
PubMed2026

The mighty microproteins: from versatile cellular regulators to precision medicine therapeutics.

Microproteins, are tiny proteins encoded by small open reading frame (sORF), translation of these non-canonical open reading frames (ncORFs) has been implicated in diverse biological processes and diseases. This review summarizes recent developments in the discovery, biogenesis, and functional characterization of microproteins, and their involvement in various disease, with special focus on their roles in cancer, cardiovascular, metabolic, neurodegenerative and immune-related disorders. We emphasize the regulation of key cellular pathways by microproteins, including mitochondrial homeostasis, apoptosis, metabolic reprogramming, and immune signaling, all of which affect disease initiation and progression. Emerging evidence also supports their potential as disease biomarkers and therapeutic candidates for precision medicine. Finally, the review critically discusses the current challenges including discrepancies in microprotein annotation, the limitations of ribosome profiling and proteogenomic approaches, the gap between computationally predicted and experimentally validated microproteins, and the need for rigorous orthogonal validation by means of CRISPR-based genome editing, ribosome release assays, mutational analysis, high-resolution mass spectrometry, and functional studies. Finally, we review recent development of AI-assisted ORF prediction, single-cell translatomics, spatial proteomics, and integrated multi-omics as emerging technologies reshaping. Microprotein discovery and functional annotation. Finally, we discuss the translational potential of microproteins and highlight the remaining challenges to clinical application, including peptide stability, pharmacokinetics, tissue-specific delivery, immunogenicity, and the need for rigorous preclinical and clinical validation. Together, this review provides an updated and critical overview of the rapidly evolving microprotein field and highlights future research priorities for translating these molecules into clinically useful biomarkers and precision therapeutics.

Microproteins↗
PubMed1988

Pacemaker follow-up and adequacy of Medicare guidelines.

The time of occurrence of cardiac pacemaker problems after implantation was identified to assess the adequacy of published federal guidelines for clinic and transtelephonic follow-up. One hundred eighty-nine pacemaker patients' charts were examined retrospectively to identify pacemaker problems: inadequate sensing, non-capture, battery failure, myoinhibition, muscle stimulation, and inadequate threshold safety margin. Twenty-nine patients (15%) were identified as having pacemaker problems. A total of 41 problems were identified, of which 28 (68%) were corrected by reprogramming. Sixty-one percent of the problems were found during a clinic visit. Problems occurred more frequently during the first year in dual-chamber devices (62%) vs single-chamber devices (35%). During years 1 to 4, when few problems are expected, 30% of all problems of single-chamber devices occurred and 39% of all problems of dual-chamber devices occurred. This is a period of time that Medicare guidelines allow for one clinic visit per year for single- and two visits per year for dual-chamber devices. These data suggest: (1) Many pacemaker problems will be missed with transtelephonic follow-up alone. (2) The majority of problems involving dual-chamber devices occurred in the first year. (3) For both dual- and single-chamber devices, an unexpected significant percentage of problems occurred in 1 to 4 years. (4) Medicare guidelines may be inadequate for follow-up during this time period.

Adult↗
PubMed1991

Atrial antitachycardia pacing in children and young adults.

Atrial antitachycardia pacing was tested in 23 children and young adults. The majority of these patients had had operative repair of congenital cardiac defects and had both bradycardia and tachycardia. Pacemakers were usually implanted by the transvenous technique using bipolar leads. In each patient it was possible to find a tachycardia termination algorithm that successfully converted the tachycardia. In some patients very complex algorithms were necessary. In each patient it was also possible to find an algorithm that successfully differentiated the abnormal tachycardia from sinus tachycardia. Twelve patients required no antiarrhythmic drugs after pacemaker implantation, while 10 patients required one drug and one patient required two drugs. Eight of 23 patients had symptomatic tachycardias that required reprogramming the pacemaker to a different tachycardia termination sequence. Seven patients required reoperations, five for adapter problems and two for infection or erosion. Cardiac function improved in 15 of the 23 patients. Antitachycardia pacing is a viable option for management of tachycardias in children and young adults.

Adolescent↗
PubMed1994

Complications of pacemaker-defibrillator devices: diagnosis and management.

Treatment of resuscitated patients with implantable cardioverter defibrillators has become increasingly more common as a method for the prevention of sudden cardiac death. Major complications such as perioperative death (incidence 2% to 8%), infection (2% to 11%); and lead-related problems (3% to 27%) have been described in previous trials. In our experience with 140 patients, problems were related to leads (n = 11), the device (n = 2), pacing (n = 1), sensing (n = 13), and defibrillation function (n = 5). Additional problems that occurred during the perioperative period included infection (n = 11), hematoma, and seroma (n = 2). Thrombus formation along endocardial leads was observed in 13 of 62 (21%) patients. Different arrhythmias (n = 10), such as sinus tachycardia, atrial fibrillation, and nonsustained, slow or incessant ventricular tachycardia with shock delivery, were also detected. Surgical management (predominantly for the major problems) was used in 31 (48%) patients, drug treatment in 25 (39%), and reprogramming of the device in 24 (38%) patients. All of these problems can result in an increase in mortality rates. This article provides an overview of the complications of cardioverter defibrillator treatment and is based on both published data and our series.

Arrhythmias, Cardiac↗
PubMed1995

Implantation of transvenous nonthoracotomy cardioverter-defibrillator systems in patients with permanent endocardial pacemakers.

Among 177 patients in whom a nonthoracotomy approach was initially used to implant a cardioverter-defibrillator system, 11 (6%) patients also received a separately implanted permanent pacemaker. The main problem encountered in these patients were previously implanted unipolar pacemakers (n = 3) and ventricular pacing leads positioned at the right ventricular apex, the latter interfering with optimal placement of the tripolar implantable cardioverter-defibrillator (ICD) lead (n = 9). The approaches used to solve these problems were individualized and included placement of the ICD sensing lead at the right ventricular outflow tract (n = 3), initial placement (n = 1) or subsequent repositioning (n = 2) of the right ventricular pacing lead at the outflow tract, upgrade from unipolar to bipolar systems (n = 2), reprogramming from the DDD to AAI mode (n = 2), inactivation of the pacemaker (n = 1), and simultaneous placement of a single-chamber atrial pacemaker with the ICD lead (n = 2). These revisions fulfilled the pacing needs in each patient and prevented unfavorable sensing interaction between the two systems.

Aged↗
PubMed1983

Current physiologic pacemakers: a serious problem with a new device.

Twenty adults underwent implantation of an automatic (DDD) pacemaker (Medtronic model 7000, Versatrax I) for treatment of symptomatic bradyarrhythmias. Only 9 patients had optimal DDD mode pacing during 78 paced months. In 3 patients, the DDD mode was changed to atrioventricular (AV) sequential (DVI) early because of risk imposed by sustained tachycardia upon underlying myocardial ischemia. The remaining 8 had had tachycardia due to pacemaker reentry, and 7 had neurologic and cardiovascular symptoms. DDD pacing was abandoned in 5 when reentry could not be interrupted by digitalis administration or reprogramming. Three continue to be paced in DDD mode despite intermittent reentrant tachycardias, with digitalis diminishing episodes of reentry in only 1. Mean ventriculoatrial conduction time was 229 +/- 34 ms. Reentrant pacemaker tachycardia developed in 7 of 12 with normal or nearly normal AV conduction, but in only 1 of 5 with complete heart block. Preimplantation electrophysiologic study did not reliably detect and initial postoperative Holter monitoring did not predict reentrant tachycardia. The risk of reentry caused by a short, fixed atrial refractory period combined with the high occurrence of slow retrograde AV conduction, particularly in patients with normal or nearly normal anterograde conduction, renders the Versatrax I and other similar pacemakers unsuitable for DDD mode pacing in many patients.

Bradycardia↗
PubMed1984

Myopotential interference with DDD pacemakers: endocardial electrographic telemetry in the diagnosis of pacemaker-related arrhythmias.

Skeletal myopotentials may inhibit the output of unipolar demand ventricular pacemakers, resulting in protracted episodes of asystole in susceptible patients. The new DDD-mode pacemakers have, in addition to a unipolar ventricular lead, a unipolar atrial lead to enable atrioventricular sequential or atrial synchronous function. During clinical investigation of a new dual-unipolar cardiac pacing system programmed to operate in the DDD mode (Pacesetter AFP models 281 and 283), 6 patients were noted (5 men and 1 woman, aged 22 to 68 years) who manifested paroxysmal acceleration of ventricular pacing rate approaching the maximal tracking rate. Two patients also had abrupt slowing or cessation of ventricular output. With the use of atrial electrographic recordings (obtained with telemetry), the following mechanisms of rate change were found: myopotential tracking, myopotential inhibition, interference-mode asynchronous operation, sudden increases in sinus rate, and pacemaker-mediated reentrant tachycardia. In all patients, reprogramming of the implanted devices, based on telemetered atrial electrography, resulted in disappearance of the arrhythmias and loss of symptoms while maintaining the DDD pacing mode. Thus, several mechanisms of rhythm disturbances are peculiar to dual-chamber cardiac pacing systems that use unipolar electrodes. Endocardial telemetry combined with extensive programming capability offers the best opportunity for proper diagnosis and management of these problems.

Adult↗
PubMed1984

A temporary external DDD pacing unit.

A device for temporary external DDD pacing was developed using a modified permanent pulse generator, and temporary atrial and ventricular electrode catheters were inserted pervenously. The atrial lead was a J type and the ventricular lead had a remote anode in the superior vena cava. With a special clamp and appropriate connectors the permanent DDD pulse generator provided unipolar external DDD pacing. The device was evaluated in 13 patients to control bradyarrhythmias or for overdrive pacing in an attempt to control tachyarrhythmias. Nine patients were ambulatory; all had continuous electrocardiographic monitoring. The device was used for 1 to 12 days (mean 4.9). Eight patients benefited from temporary DDD pacing and 7 had permanent DDD pacemakers implanted. In 1 patient, atrial fibrillation developed, 2 patients had brief episodes of ventricular lead displacement and another required reprogramming because of loss of ventricular capture. Results suggest that the device is applicable for a clinical trial of DDD pacing before possible permanent implantation when attempting to improve cardiac output or control arrhythmias.

Aged↗
PubMed1988

Usefulness of transcutaneous triggering of conventional implanted pulse generators by an activity-sensing pacemaker for predicting effectiveness of rate response pacing.

A noninvasive procedure has been developed to assess effectiveness of activity-sensing rate response ventricular (VVIR) pacing systems in patients with implanted conventional fixed-rate ventricular (VVI) pacemakers capable of triggered mode operation (VVT). A VVIR pacemaker (activity threshold medium or low, rate response 6 to 10, upper rate 125 or 150 beats/min) was strapped to the chest wall (prepectoral area) of patients with previously implanted fixed-rate VVI pacemakers. In 17 of the 18 patients included in the study, the implanted pacemaker was capable of triggered mode operation (VVT). Triggering of the conventional pacemaker was achieved by reprogramming it to the VVT mode (high sensitivity, short refractory) and connecting the output of the "strapped-on" VVIR pacemaker (5 volts, 1.5-ms pulse width) to 2 standard cutaneous electrodes positioned so as to be in proximity to the implanted intracardiac electrode system. Patients underwent symptom-limited treadmill exercise tests during both VVI and VVIR pacing. Triggering conventional VVI pulse generators by a "strapped-on" VVIR pacing system proved feasible in 16 of 17 cases and improved overall heart rate response (fixed rate 86 +/- 22 vs VVIR 118 +/- 7 beats/min) and exercise duration (fixed rate 6.6 +/- 4.9 vs VVIR 10.1 +/- 4.8 minutes) (mean values for all patients studied during exercise testing). Triggering of a previously implanted permanent pacemaker by a strapped-on activity-triggered device may be useful to assess rate response pacing before implantation of a VVIR device in patients in whom elective pulse generator replacement is planned.

Adolescent↗
PubMed1988

The Activitrax rate responsive pacemaker system.

Bipolar Medtronic Activitrax rate responsive pacemakers were implanted in 31 patients for ventricular (28) or atrial (3) pacing. Mean follow-up was 16 months (range 10 to 26). Twenty pacemakers were implanted after catheter ablation of the His bundle, 7 for sick sinus syndrome. 1 for atrioventricular block and 3 for sick sinus syndrome with atrioventricular block. A rate response value was selected that gave a pacing rate of about 100 pulses/min during walking. Of the 31 patients, all had 24-hour ambulatory electrocardiographic monitoring with diary, 11 walked a 20-minute circuit, including a flight of stairs, and 20 had a treadmill exercise test. In 9 patients the pacing rate could be compared with the underlying sinus rate during exercise and was seen to match it very closely. In 12 patients the pacing rate during car driving was found to be similar to the sinus rate of 5 volunteers under similar conditions (mean minimum and maximum rate was 80 and 99 pulses/min, respectively). No pacing-induced arrhythmias were seen during ambulatory electrocardiographic monitoring. At high pacing rates slightly irregular pacing intervals were sometimes observed, which was due to polarization sensing. Sporadically, 1 pacing interval shortened to the upper rate value, because of a known and now resolved timing anomaly. Neither anomaly was of clinical consequence and the first could be resolved by reprogramming.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Cardiac pacing practices in the United States in 1985.

Physicians active in pacemaker implantation and follow-up were surveyed to obtain a profile of permanent cardiac pacing practices in the United States during 1985. Questionnaires were sent to 628 physicians, mainly in New Jersey; 145 responses were received and analyzed. A separate questionnaire was sent to 9 pacemaker manufacturers to solicit information concerning the volume of pacemaker sales and their opinions on a variety of subjects. The rate of permanent pacemaker implantation declined for the first time: it dropped from 518 devices per million population in 1981 to 374 in 1985. Sinus node dysfunction was the chief indication for permanent pacing in 52% of primary implantations; conduction disorders of the atrioventricular node and His-Purkinje system accounted for 41% and ventricular tachyarrhythmias for 2%. Dual-chamber pacing modes were used less frequently than was predicted in 1981, accounting for 30% of primary and 19% of replacement pacemakers. More than 43% of programmable pulse generators were never reprogrammed after implantation. Surveys such as this continue to provide useful information despite obstacles encountered in the use of questionnaires. Important differences in practice patterns and outcomes were identified between surgeons and nonsurgeons, and between frequent and infrequent implanters. These differences reinforce the suggestion that implanters should work at a volume sufficient to maintain their expertise, and that cooperation between surgeons and nonsurgeons would lead to improvements in patient selection, surgical results and optimal pacemaker programming and follow-up care. Better results could be achieved by adopting the continent-wide system of a pacemaker registry now used in Eastern Europe and Great Britain.

Diagnosis-Related Groups↗
PubMed1991

Experience with a third-generation implantable cardioverter-defibrillator.

A Medtronic 7216A pacemaker cardioverter-defibrillator was implanted in 16 patients (mean age 56 years) with sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) and organic heart disease with a mean left ventricular ejection fraction of 33%. Endocardial and epicardial defibrillation shock efficacy was evaluated before or at implant using 1 to 3 shock patterns, i.e., monophasic single, sequential or simultaneous shocks with dual and triple electrode configurations. Endocardial leads used a common right ventricular cathode and dual anodes, whereas epicardial leads used 2 or 3 helical coil patches. VT termination was evaluated using pacing or shock therapy, or both, whereas only shocks were used in VF. Programmable bradycardia pacing, individual zones for VT and VF detection and individualized pacing and shock therapy for VT and VF were used. Monophasic shocks had epicardial defibrillation thresholds ranging from 3 to 18 (mean 10) J and were comparable for sequential and simultaneous shocks (p greater than 0.2). VT detection rates ranged from 340 to 470 ms and VF detection rates from 270 to 330 ms. VT or VF induction, or both, was performed noninvasively in 13 patients after implant and was reproducibly terminated by rapid pacing alone (5 patients), low-energy shocks (2 patients), high-energy shocks (3 patients) and combined therapy (3 patients). Intermediate or high-energy shocks terminated all induced VF episodes. During follow-up (2 to 12 months), there have been 2 noncardiac deaths. Electrical therapy was delivered in 7 patients, for VT (3 patients), VT and VF (3 patients) and indeterminate tachyarrhythmia (1 patient). All VT/VF episodes were successfully terminated, with 78 of 96 (81%) spontaneous VT episodes terminated by pacing. Follow-up reprogramming was required in 5 patients. It is concluded that successful application of individualized electrical therapy prescriptions in patients with VT/VF is feasible. Pacing therapies, which are effective for induced VT, can be reliably used for effective long-term spontaneous VT termination in conjunction with shock therapy and can permit reduced patient exposure to shock therapy. Thus, a programmable hybrid pacemaker cardioverter-defibrillator system provides nonthoracotomy implantation, effective VT/VF termination, demand ventricular pacing and noninvasive modes for arrhythmia induction, event monitoring and clinical trouble-shooting.

Adult↗
PubMed1986

Microprocessor-based weight shift monitors for paraplegic patients.

The prevention of pressure sores for patients with spinal cord injuries includes pressure relief through the patient shifting position and, thus, weight. We have designed a microprocessor-based device to mount on the seat of a conventional wheelchair. This device has applications in hospital rehabilitation programs for improving patient care and in research to study the cause and prevention of pressure sores. It can use audible alarms, which can be disarmed, to train patients to regularly shift weight. The device stores in its memory data on the interval between and the duration of weight shifts. The contents of this memory can be transmitted to a laboratory microcomputer system and displayed in tabular, graphical, or histogram formats. This device is more versatile than previous timer-based systems, not only because its timer and alarm parameters easily can be reprogrammed, but especially because it can store and play back detailed data on the patient's performance. The device is powered by rechargeable NiCad batteries, which can last several days without recharging.

Body Weight↗
PubMed1979

Neoplastic transformation-linked alterations in arginyl-tRNA synthetase activity.

The behavior of the activity of arginyl-tRNA synthetase (L-arginine : tRNAArg Ligase(AMP-forming), EC 6.1.1.19) was determined in extracts of rat liver: normal adult, normal proliferating (from developing and from partially hepatectomized rats), and neoplastic (hepatomas of different growth rates) and in extracts of rat kidney cortex and transplantable kidney tumors. The Km values for arginine, ATP, and tRNA of the enzyme of the rapidly growing hepatoma 3924A were the same as those of the enzyme from the liver of control rats. The pH optima of the control and neoplastic livers were in the same range of 7.25-8.0. Taking the hepatic specific activity for arginyl-tRNA synthetase as 100%, deep layer of gut, thymus and testis had higher activity; renal cortex and spleen had the same activity; and skeletal muscle, brain, heart, lung, superficial layer of gut and adipose tissue had lower activity. In a wide spectrum of hepatomas of different growth rates, a significant increase of 1.4-2.4-fold in arginyl-tRNA synthetase activity was observed when compared with that of liver of control normal rats. This elevation in enzyme activity in hepatomas appears to be specific to neoplasia, since it is unaltered in regenerating and low in differentiating liver. The increase in arginyl-tRNA synthetase in the liver tumors appears to be transformation-linked, since the activity was increased in all hepatomas, even in the slowest growing ones. Furthermore, the increase in enzyme activity was not limited to hepatic neoplasms, since a rise was also observed in transplantable rat kidney tumors. Thus, the reprogramming of gene expression in neoplastic tissue entails an increase in arginine-tRNA synthetase activity.

Aging↗