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PubMed1996

Nanocontrollers for biomedical applications.

Several semiconductor companies now manufacture low cost single-chip microcontrollers in dual inline packages having twenty or fewer pins. The controllers are field programmable by means of inexpensive development boards linked to personal computers. These processors were designed with a minimalist philosophy which provide them with only a few dozen bytes of on-chip RAM, hundreds of bytes of PROM, a parallel port, a counter/timer, and reduced instruction sets. The better-equipped members of this class may have special on-chip hardware, such as analog-to-digital input, pulse-width modulation output and a serial port. Most must be programmed in assembler, although some support BASIC, "C" or other languages. Their tiny size, design simplicity and operational single-mindedness earn them the nickname "nanocontrollers". Despite meager resources, these controllers can be successfully employed in a variety of biomedical applications. Such uses include: consolidation of multi-chip "glue logic" circuitry; functioning as subsystem elements in complex designs; serving as device drivers or protocol converters; and forming the building blocks of hypercube processor arrays or artificial neural networks. This paper describes the general capabilities, special features, and some application examples of "nanocontroller" technology.

Biomedical Engineering↗

PubMed1995

Strenuous physical activity in young adulthood and risk of breast cancer (United States).

The epidemiologic data on the relation between strenuous physical activity and breast cancer are limited and inconsistent. Because risk of breast cancer may be influenced by ovarian function which, in turn is modulated by physical activity, the hypothesis that exercise may be associated with a reduced risk of breast cancer merits further investigation. We, therefore, conducted a large case-control study in 1988-1991, and interviewed 6,888 women (17 to 74 years of age) with breast cancer in Maine, Massachusetts, New Hampshire, and Wisconsin (United States). Interviewed controls (9,539 women, 18 to 74 years of age) were selected randomly from lists of licensed drivers (for younger women) or from a roster of Medicare enrollees (for older women). We used multivariate adjusted odds ratios (OR) and 95 percent confidence intervals (CI) from logistic regression models to estimate relative risks between self-reported physical activity when 14 to 22 years of age and breast cancer. When compared with sedentary controls, women who reported any strenuous physical during ages 14 to 22 years had a modest reduction in the risk of breast cancer (OR = 0.95, CI = 0.93-0.97). However, those who exercised vigorously at least once a day had a 50 percent reduction in risk of breast cancer (OR = 0.5, CI = 0.4-0.7). These data support the hypothesis that women who are physically active have a reduced risk of breast cancer.

Adolescent↗

PubMed2024

eQTLs identify regulatory networks and drivers of variation in the individual response to sepsis.

Sepsis is a clinical syndrome of life-threatening organ dysfunction caused by a dysregulated response to infection, for which disease heterogeneity is a major obstacle to developing targeted treatments. We have previously identified gene-expression-based patient subgroups (sepsis response signatures [SRS]) informative for outcome and underlying pathophysiology. Here, we aimed to investigate the role of genetic variation in determining the host transcriptomic response and to delineate regulatory networks underlying SRS. Using genotyping and RNA-sequencing data on 638 adult sepsis patients, we report 16,049 independent expression (eQTLs) and 32 co-expression module (modQTLs) quantitative trait loci in this disease context. We identified significant interactions between SRS and genotype for 1,578 SNP-gene pairs and combined transcription factor (TF) binding site information (SNP2TFBS) and predicted regulon activity (DoRothEA) to identify candidate upstream regulators. Overall, these approaches identified putative mechanistic links between host genetic variation, cell subtypes, and the individual transcriptomic response to infection.

Humans↗

PubMed2006

Transcriptome analysis in Catharanthus roseus leaves and roots for comparative terpenoid indole alkaloid profiles.

In Catharanthus roseus (L.) G. Don each tissue is known to produce a distinct spectrum of terpenoid indole alkaloids. Since the invaluable antineoplastic bisindole alkaloids are restricted to the aerial parts of the plant and do not occur in its underground tissues, identification of the structural and regulatory factors operating distinctly in the shoot/leaf of the plant will be a necessity for modulation of bisindole alkaloid biosynthesis. This study aimed at elucidating the differential gene expression in the two main tissues (leaf and root) of the plant, well known for their distinct terpenoid indole alkaloid profiles. The leaf and root transcriptomes of C. roseus were comparatively analysed using two different approaches: (i) indirectly through construction and characterization of separate cDNA libraries; and (ii) directly through a strategically designed suppression subtractive hybridization, using the leaf and root cDNA populations as tester and driver, respectively. A total of 155 ESTs (55 and 45 from the separate leaf and root cDNA libraries, respectively, and 55 from the subtracted leaf-specific cDNA library) were subjected to homology-based classification and submitted to dbEST. The direct approach yielded an EST for sgd (strictosidine beta-D-glucosidase) and 16 novel ESTs. Dat (acetyl-CoA: 4-O-deacetylvindoline 4-O-acetyl-transferase) and sgd transcripts could not be detected in the root system of the plant (cv. 'Dhawal') at any developmental stage (6 d, 6 weeks, or 6 months). The growth-related decrease in shoot/leaf dat and sgd transcript levels was paralleled by a concomitant decrease in shoot/leaf vindoline content.

Acetyltransferases↗

PubMed2026

IL1B-centered immune dysregulation involving IL7R, CCR7, ITGB2 and IRF1 across insomnia and inflammatory bowel disease.

BACKGROUND: Insomnia is a prevalent sleep disorder that strongly affects one's quality of life and physical well-being. Inflammatory bowel disease (IBD) is a chronic inflammatory condition of the intestines, and a majority of IBD patients suffer from comorbid insomnia. However, the shared molecular features linking insomnia and IBD remain poorly characterized. METHODS: Common differentially expressed genes (DEGs) were identified in datasets of insomnia (GSE208668) and IBD (GSE179285) using the Limma package. Functional enrichment was performed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. Protein-protein interaction (PPI) network construction and hub gene identification was subsequently performed. Furthermore, we validated the reliability of the hub genes using qRT-PCR and Enzyme-linked immunosorbent assay (ELISA). In addition, we constructed a TF-miRNA regulatory network of hub genes and assessed the abundance of immune cell infiltration in insomnia and IBD using CIBERSORT, EPIC, and xCell algorithms. Finally, we utilized the DsigDB to predict potential therapeutic candidates. RESULTS: The analysis revealed 75 upregulated and 32 downregulated common DEGs. Functional enrichment analysis revealed the inflammatory response and immune activation as pivotal drivers underlying the pathogenesis of both insomnia and IBD. Five hub DEGs, namely, IL1B, IL7R, CCR7, ITGB2, and IRF1, were subsequently screened and validated. The TF-miRNA-mRNA regulatory network consisted of 5 TFs, 14 miRNA nodes and 5 core mRNA nodes. Immune cell infiltration analysis revealed several patterns shared between insomnia and IBD. Additionally, 10 potential therapeutic drugs for insomnia and IBD were proposed. CONCLUSION: Integrative coexpression network analysis reveals convergent dysregulation of an IL1B-centered immune module (comprising IL7R, CCR7, ITGB2, and IRF1) across insomnia and IBD, a shared immune disturbance and candidate targets for simultaneous intervention upon further mechanistic validation.

Humans↗

PubMed2001

Neurobiological measures of human selective attention.

Selective attention allows people to process some stimuli more thoroughly than others. This is partly under voluntary control, and partly determined by stimulus salience. Selective attention has been studied with psychological methods for many years, but recent cognitive neuroscience studies using brain-imaging methods (and other neurobiological measures) have transformed the topic. Such studies have demonstrated that sensory processing can be strongly modulated by attention throughout perceptual networks, including even processing in primary sensory cortex. They have shown that some of these modulations can be anticipatory, arising prior to stimulus presentation, while other components reflect a changed neural response to an incoming stimulus. Recent imaging studies have also examined the mechanisms involved in controlling such attentional modulation of sensory processing. In addition to answering many long-standing questions about selective attention, such research also raises new questions. The various contributions in this volume provide an overview of the spectacular recent advances in attention research using neurobiological measures, and they outline critical issues to be resolved in the future.

Attention↗

PubMed2006

Attentional preparation for a lateralized visual distractor: behavioral and fMRI evidence.

Attending to the location of an expected visual target can lead to anticipatory activations in spatiotopic occipital cortex, emerging before target onset. But less is known about how the brain may prepare for a distractor at a known location remote from the target. In a psychophysical experiment, we found that trial-to-trial advance knowledge about the presence of a distractor in the target-opposite hemifield significantly reduced its behavioral cost. In a subsequent functional magnetic resonance imaging experiment with similar task and stimuli, we found anticipatory activations in the occipital cortex contralateral to the expected distractor, but no additional target modulation, when participants were given advance information about a distractor's subsequent presence and location. Several attention-related control structures (frontal eye fields and superior parietal cortex) were active during attentional preparation for all trials, whereas the left superior prefrontal and right angular gyri were additionally activated when a distractor was anticipated. The right temporoparietal junction showed stronger functional coupling with occipital regions during preparation for trials with an isolated target than for trials with a distractor expected. These results show that anticipation of a visual distractor at a known location, remote from the target, can lead to (1) a reduction in the behavioral cost of that distractor, (2) preparatory modulation of the occipital cortex contralateral to the location of the expected distractor, and (3) anticipatory activation of distinct parietal and frontal brain structures. These findings indicate that specific components of preparatory visual attention may be devoted to minimizing the impact of distractors, not just to enhancements of target processing.

Adult↗

PubMed1988

Studies on the crustacean cardiac ganglion.

1. An overview of studies on the decapod crustacean cardiac ganglion is given emphasizing contributions to questions of general interest in cellular neurophysiology. 2. John Welsh, in 1951, introduced this 9-celled, semi-autonomous ganglion as a preparation offering physiologists unique experimental possibilities. 3. It exhibits remarkable reliability and stability in rhythmic pattern generation. The neurons show endogenous burst-forming capability mediated by "driver potentials". 4. These regenerative, Ca-mediated potentials are restricted to the soma, while impulse-generating membrane is segregated to the distal axon. 5. Thus, voltage-clamp analysis of the ionic currents underlying the burst-forming potentials is possible by isolating the soma with a ligature. 6. The isolated ganglion is spontaneously active, but the normal mechanism of pacemaking remains to be clarified, including the possible contribution of stretch-sensitive dendrites. 7. The activity of the ganglion is subject to modulation by neurohumors. These include the transmitter at intraganglionic synapses, transmitters of the pair of inhibitory and the two pairs of acceleratory fibers, and neurohormones released from the pericardial organs. The transmitters are not established. 8. Effects on the ganglion of substances isolated from the pericardial organs have been described. 9. These include 5-hydroxytryptamine, dopamine, octopamine, and two peptides. 10. One of these, proctolin, produces a long-lasting sequence of effects. 11. The work continues to raise new questions for which the ganglion offers excellent research material.

Animals↗

PubMed2001

A self-oscillating detuning-insensitive class-E transmitter for implantable microsystems.

This paper describes a low-cost, self-oscillating, detuning-in-sensitive, class-E driver for transcutaneous power and data transmission to implantable microsystems. A voltage feedback scheme using a fast comparator for zero-crossing detection and a CMOS start-up circuit were used to stabilize the class-E operation for various transmitter coil inductance values. This technique solves the common problem of mismatch between the switching frequency of the driving device and the resonant frequency of the load network, which can cause excessive power loss and damage to the active device. Data is transmitted by AM modulation of the carrier through switching the power supply between two levels. The transmitter uses a 9-V supply, consumes 212 mA, operates at 3.9 MHz, and has an efficiency of 71%. The efficiency is stable (< 2% change) against 13% variations in the inductance value of a pancake shaped transmitter coil. Index Terms-Biomedical microsystems, class-E transmitter, implantable electronics, inductive powering, transcutaneous links.

Electric Power Supplies↗

PubMed2026

Hypoxia-Induced ADAM23 Drives Neuron-Tumor Crosstalk and Therapeutic Resistance in Hepatocellular Carcinoma.

Hypoxia and nutrient deprivation are fundamental drivers of tumor aggressiveness and therapeutic resistance in hepatocellular carcinoma (HCC). While the involvement of neural components in the tumor microenvironment (TME) is increasingly recognized, the molecular transducers linking metabolic stress to neuron-tumor crosstalk remain elusive. Here, we identify ADAM23 (A disintegrin and metalloproteinase 23) as a hypoxia-responsive mediator that mediates communication between HCC cells and neuronal cells. ADAM23 expression was markedly upregulated in HCC cells under both chemical (CoCl2) and physical hypoxia (1% O2), a process further amplified by glucose deprivation and directly modulated by HIF-1α. Functional assays revealed that ADAM23 overexpression promotes epithelial-mesenchymal transition (EMT) and enhances cell viability under metabolic stress. Notably, sorafenib-resistant HCC cells (Huh7SR) exhibited high levels of ADAM23 secretion, which triggered proliferative and metabolic activation in neuronal SH-SY5Y cells. In 3D co-culture spheroid models, Huh7SR cells mixed with SH-SY5Y cells displayed significantly larger spheroid volumes and enhanced neuronal fluorescence compared with parental controls, suggesting that ADAM23-mediated interactions facilitate a supportive neural niche. Analysis of The Cancer Genome Atlas (TCGA) datasets and patient microarrays confirmed that ADAM23 is significantly overexpressed in HCC and positively correlates with HIF-1α expression. Moreover, elevated expression of ADAM23 was significantly correlated with poor overall survival. Collectively, our findings underscore ADAM23 as a critical metabolic-neural linker that promotes HCC progression and drug resistance. These findings suggest that the ADAM23-mediated neuron-tumor axis may represent a potential therapeutic target in aggressive HCC.

ADAM23↗

PubMedDate not supplied

A short history of the second messenger concept in neurons and lessons from long lasting changes in two neuronal systems producing afterdischarge and circadian oscillations.

This paper gives a short historical summary of how the second messenger concept, introduced by Earl Sutherland some three decades ago, has been refined and applied by neurobiologists to account for long-lasting changes in the membrane properties of certain neurons. Such refinements in the second messenger hypothesis have application to two specific long-lasting changes in neurons in Aplysia. In the bag cell neuroendocrine system, a brief synaptic input induces an afterdischarge lasting about 30 minutes. Both cAMP-dependent and Ca2+ and phospholipid-dependent protein kinases are activated by the synaptic input and a variety of potassium and calcium channels are modulated. In the eye of Aplysia a spontaneous circadian modulation of ion channels takes place over a twenty-four hour period. In addition phase shifts of this circadian oscillator are mediated, for light by cGMP and for serotonin by cAMP. The circadian oscillator, unlike the bag cell afterdischarge mechanism, is sensitive to ionizing radiation as well as to transcriptional inhibitors. Evidence is presented that specific proteins are synthesized at different times in the circadian cycle. One of these proteins (m.w. 41.9, pI 5.5) accumulates linearly with time of day, resembling a sawtooth oscillator. This protein may be the driver for the circadian oscillation itself. The role of second messengers in various forms of plasticity in neuronal systems (sensitization, long-term potentiation, long-term depression, "learning") may just be part of a very widespread mechanism by which neurons and other cells can generate long-lasting changes in membrane and other cellular properties with brief inputs (synaptic, hormonal) that are of some special adaptive value to the organism.

Animals↗

PubMed2003

Multimodal visual-somatosensory integration in saccade generation.

Neurophysiological studies have demonstrated multisensory interaction effects in the neural structures involved in saccade generation when visual, auditory or somatosensory stimuli are presented bimodally. Visual-auditory interaction effects have been demonstrated in numerous behavioural studies of saccades but little is known about interaction effects involving somatosensory stimuli. The present study examined visual-somatosensory interaction effects on saccade generation using a multisensory paradigm, whereby task-irrelevant distractors appeared spatially-coincident with, or remote from the designated saccade target. Somatosensory distractors reduced the latency of saccades when presented before the visual target and the greatest facilitation effect was observed with spatially-coincident stimuli. Visual distractors spatially-coincident with a somatosensory target reduced latency (and increased peak velocity) when presented before and after the target. Visual distractors contralateral to somatosensory targets increased saccade latency and produced high error rates of saccades made to the distractor. The high error rates and latency modulation with visual distractors is consistent with a bias for visual stimuli in the saccadic system. In the visual target condition, saccade latency was modulated by a somatosensory distractor that was entirely task-irrelevant and this effect was always greatest with spatially-coincident distractors. The multisensory distractor effects are discussed in terms of saccades being programmed to the non-target modality, the early triggering of a non-spatial saccade 'when' signal, and multisensory neuronal enhancement effects.

Acoustic Stimulation↗

PubMed1992

The neurobiology of selective attention.

Research in the field of selective visual attention has recently seen substantial progress in several areas. Neuroimaging and electrical recording results have indicated that selective attention amplifies neural activity in prestriate areas concerned with basic visual processing. Imaging and cellular studies are delineating the networks of anatomical areas that serve as the source of attentional modulation and have suggested that these networks are anatomically distinct from the sites of the resulting amplifications. Cognitive studies of visual search have explored the role of these amplified computations in the integration of visual features into objects. Attentional effects in normal subjects, and their disruption following brain injury, have revealed the mental representations upon which attention operates.

Animals↗

PubMed2002

Driver and front seat passenger fatalities associated with air bag deployment. Part 2: A review of injury patterns and investigative issues.

Assessment of the role of air bag deployment in injury causation in a crash of any severity requires analysis of occupant, vehicle, and impact data. The potential injurious role of an air bag is independent of crash severity and is more obvious in minor collisions, particularly those involving "out-of-position" occupants. Factors such as occupant height and other constitutional and medical factors, intoxication, age, type, and proper use of other restraint systems, pre-impact braking and multiple impacts can contribute to an occupant being "out-of-position." Two injury mechanisms are described in out-of-position occupants: "punch-out" when the individual covers the air bag module before deployment and "membrane-force" when the occupant contacts a partly deployed air bag. Each mechanism is associated with injury patterns. In adults, "punch-out" can cause thoraco-abdominal trauma and "membrane-force" loading can lead to craniocervical injury. This can also occur in short-statured occupants including children subjected to both types of loading. In more severe collisions, other factors, e.g., intrusion, steering column and seatbelt loading and other occupant compartment contacts, can contribute to trauma.

Abdominal Injuries↗

PubMed2004

Microvascular patterning is controlled by fine-tuning the Akt signal.

We investigated the functions of Akt during vascular development and remodeling by using an inducible endothelial cell-specific driver of the dominant-active myrAkt. We found that sustained signaling in response to overexpression of myrAkt led to embryonic lethality, edema, and vascular malformations. In addition to the morphological malformations, the vascular phenotype was consistent with a failure in remodeling, such that the normal patterning and vessel hierarchy was disturbed. Examination of the well studied retinal vasculature during the remodeling phases revealed that transient expression of myrAkt was capable of altering the normal response to oxygen-induced remodeling without causing vascular malformations. These findings suggest that physiological levels of Akt signaling modulated microvascular remodeling and support the hypothesis that, although Akt may be required for vascular growth and homeostasis, appropriate down-regulation is also an essential aspect of normal vascular patterning.

Animals↗

PubMed2000

[Clinical practice guidelines of the Spanish Society of Cardiology on pacemakers].

Following a brief introduction on the history and generic codification of the different cardiac stimulation methods available, the implantation techniques are described and the requisites, such as human resources, their qualifications and the materials required, which are essential in the organization of a Pacemaker Unit are discussed. The current indications for permanent cardiac stimulation are reported and are classified by sections in tales following the 1998 norms of the ACC/AHA. In another section, the indications in special situations such as hypertrophic or dilated cardiomyopathy are described. Stimulation frequency modulation with the incorporation of biodetectors in modern pacemakers or in the probes are commented upon as is atriosynchronic ventricular stimulation with a single electrode (VDD). The recent automatisms which have been implemented in the current pacemakers are discussed and the most adequate selection of the stimulation mode for each patient is analyzed and demonstrated in a table which may be easily interpreted. On establishing the recommendable protocol for undertaking the follow up of the patient with a pacemaker, the criteria accepted as replacement indicators are discussed. In a brief section some legal aspects (drivers license, informed consent) are commented upon and the possible sources of interference with the function of the system implanted, whether medical or environmental or laboral, have been analyzed more in depth. The chapter ends with a brief discussion on the survival of patients with pacemakers.

Adolescent↗

PubMed1995

Physical and chemical characterization of airbag effluents.

OBJECTIVE: This paper describes a study aimed at characterizing the exposure to physical and chemical by-products from the deployment of airbag restraint systems. DESIGN, MATERIALS AND METHODS: Specifically, the levels of particulates and the composition of gases and bag fabric speed were measured in the passenger compartment following deployment of either a driver's side or driver's side/passenger's side airbag system. MEASUREMENTS: A Fourier transform infrared analyzer (FTIR) and chemiluminescence analyzers were used for gas analysis, a cascade impactor and gravimetric filter measurements for aerosol determination and high-speed films to determine fabric speed. MAIN RESULTS AND CONCLUSIONS: The measured gases were found to be within the recommended guidelines for human exposures, but no guidelines exist for particle exposures of this magnitude (150-220 mg/m3) but short duration. High-speed films were also taken of the deployments to obtain an estimate of the fabric speed as it leaves the module. The maximum average speed for both types of airbag was approximately 100 mph and in both cases average speeds ranged from lows near 50 mph to highs of over 200 mph.

Air↗

PubMed2006

Cyclin D1 in non-small cell lung cancer: a key driver of malignant transformation.

PURPOSE: To review the evidence implicating the deregulation of cyclin D1 in the pathogenesis of non-small cell lung cancer (NSCLC), and to discuss the opportunities for targeted clinical intervention. METHODS: Data published until June 2006 are summarized, and previously unpublished results from our own research are included. RESULTS: In normal cells, cyclin D1 complexes with and activates cyclin-dependent kinases (CDK) and acts as a transcriptional regulator. The protein is frequently overexpressed in a wide range of cancers, sometimes coincident with CCND1 (cyclin D1) gene amplification (5-20% of tumours). A low level of somatic mutations have been seen in certain tumours. CCND1 is amplified in NSCLC and cyclin D1 is frequently overexpressed in tumours and pre-invasive bronchial lesions, generally from one parental allele. Mutation analyses revealed a frequent CCND1 gene polymorphism (A870G) that modulates alternative splicing and allows expression of an alternative cyclin D1 transcript (transcript cyclin D1b). The encoded cyclin D1b protein lacks a specific phosphorylation site required for nuclear export. Genotype has been correlated with the risk and/or severity of disease or drug response across a range of malignancies, including lung cancer. Together, these findings suggest a strong pathological role for cyclin D1 deregulation in bronchial neoplasia. CONCLUSION: Current data indicate that cyclin D1 overexpression is not a consequence of, but rather a pivotal element in the process of malignant transformation in the lung and other tissues. This understanding may open new avenues for lung cancer diagnosis, treatment and prevention.

Adenoma↗