Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “precision prevention”

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 145 records · Page 8Linked to original sources
PubMed1996

Burnout and related factors among HIV/AIDS health care workers.

A sample of 194 Italian health care-givers working in HIV/AIDS units was assessed to investigate whether there was a correlation between individual variables (socio-demographic and occupational characteristics, personality traits, anxiety, depression, attitudes and emotional reactions) and burnout and job satisfaction. For this proposal were used the Maslach Burnout Inventory (MBI), a socio-demographic and occupational characteristics schedule. Sixteen Personality Factor Questionnaire, Ipat Anxiety Scale, Ipat Depression Scale and AIDS Impact Questionnaire. A principal component analysis on frequency subscales scores of MBI extracted two independent dimensions labelled 'burnout' and 'personal accomplishment'. The results suggested important correlations among 'burnout', 'personal accomplishment', anxiety and depression. Age of care-givers was negatively correlated with 'burnout' and practical nurses were less personally accomplished. Anxiety, depression, emotional reactions, attitudes, ego strength, and the aptitude for interpersonal relationships and to team work were significant factors in outlining a profile of highly 'burned out' and 'personally accomplished' HIV/AIDS health care-givers. These results suggest the development of precise strategies of prevention, intervention and treatment of burnout considering not only the importance of occupational and institutional characteristics but also of individuals ones.

Adult↗
PubMed2004

The energetic conversion competence of Escherichia coli during aerobic respiration studied by 31P NMR using a circulating fermentation system.

To determine the actual potential of the energetic conversion efficiency of Escherichia coli during aerobic respiration, apparent P/O ratios (P/O(app)) under either limited or standard glucose-feeding conditions were estimated. The previously reported circulating fermentation system (CFS) was used, and (31)P NMR saturation-transfer (ST) techniques were employed. By coupling with on-line NMR observations, CFS allowed us to evaluate cellular energetics directly, with both the dissolved oxygen tension and glucose feeding precisely controlled to prevent the effect of substrate-level phosphorylation based on aerobic or anaerobic acidogenesis in E. coli cells. Phosphate consumption rates under standard and limited glucose-conditions were estimated as 4.62 +/- 0.46 and 1.99 +/- 0.11 micromol/s g of dry cell weight (DCW), respectively. Using simultaneously assessed O(2) consumption rates, the P/O(app) values under these two conditions were estimated as 1.4 +/- 0.3 and 1.5 +/- 0.1, respectively. To correlate the obtained P/O(app) values with the potential efficiency of respiratory enzymes, we determined the activities of two NADH dehydrogenases (NDH 1 and 2) and two ubiquinol oxidases (bo- and bd-type) during the periods when ST was performed. NDH-1 activities in standard or limited glucose cultures were maintained at 57% or 58% of the total NADH oxidizing activity. The percentages of bo-type oxidase activity in relation to the total ubiqinol oxidizing activity under the standard and limited glucose conditions were 32% and 36%, respectively. These percentages of enzymatic activities represent the respiratory competence of E. coli cells, suggesting that, during the NMR observatory period, the enzymatic activity was not at a maximum, which could also explain the estimated P/O(app) values. If this is the case, enhancing the expression of the bo-type oxidase or disrupting of the bd-type oxidase gene could be effective approach to increasing both the P/O ratio and cellular yields.

Biochemistry↗
PubMed2003

The molecular era of myology.

This review covers, in general terms, the salient features and impact of molecular myology under the following headings: its role in providing clues for the understanding of molecular etiology and pathogenesis of genetic myopathies, its contribution to the modernization and rationalization of the classification of muscle diseases, providing means of precise diagnosis and prevention of myopathies, development of radically new cell and gene therapies, and determination of future research directions. Myology appears to be among the medical disciplines that have benefited a great deal from molecular science. This remarkable progress will hopefully translate into effective treatment capabilities in the near future.

Animals↗
PubMed1998

What percentage of workers with work-related illnesses receive workers' compensation benefits?

This study estimates the rate at which workers suffering from occupational illnesses file for workers' compensation lost wage benefits and identifies some of the factors that affect the probability that a worker with an occupational illness will file. A database of reports of known or suspected cases of occupational illness is matched with workers' compensation claims data. Overall, between 9% and 45% of reported workers file for benefits. Data limitations prevent a more precise estimate of this rate, but a large proportion of workers with occupational illnesses clearly does not utilize the worker's compensation system. Logit analysis of a choice-based sample shows that women and employees of small firms are more likely than others to file for worker's compensation and that filing rates vary considerably across industries and diagnostic categories. Acute conditions related to the current job are no more likely to lead to claims than chronic conditions with long latency periods between exposure and development of disease.

Adult↗
PubMed2025

Longitudinal Multi-Organ Transcriptomic Atlas of Salt-Induced Hypertension.

BACKGROUND: Salt-sensitive hypertension is a prevalent and clinically significant subtype of hypertension, where increased dietary salt intake elevates blood pressure and causes injury to multiple organ systems. Despite extensive research, dynamic molecular changes and conserved versus organ-specific transcriptional programs in hypertensive multi-organ damage remain poorly understood. Defining complex molecular pathways both in a temporal sequence and in an organ-specific manner is essential for developing targeted, precision therapies to mitigate hypertensive disease burden. METHODS: We generated a longitudinal multi-organ transcriptomic atlas of salt-sensitive hypertension using RNA sequencing of kidney cortex, kidney medulla, heart, and liver from Dahl salt-sensitive rats across four disease stages. A comprehensive bioinformatic analysis mapped dynamic transcriptional programs, evaluated 50 biological pathways, and defined upstream regulators. Histological and biochemical assays complemented transcriptomic analysis, while integration with human genome-wide association studies (GWAS) and compound-transcriptome analysis provided translational insights and identified candidate therapeutics. RESULTS: Salt-induced hypertension elicited both shared and tissue-specific transcriptional programs that evolved with disease progression. The kidney medulla showed robust early immune activation with metabolic suppression, while the cortex exhibited transient metabolic activation before declining and initiating immune activation. The liver and heart showed time-dependent metabolic and inflammatory remodeling. Cross-organ comparisons revealed a shared early proliferative response that converged on proinflammatory and fibrotic signatures. Upstream regulator analysis identified 79 time- and tissue-specific transcription factors associated with gene expression dynamics. GWAS integration analysis revealed endocrine signaling, ion transport, lipid metabolism, and detoxification as conserved pathways across species, underscoring the translational relevance of the model and study. Predictive compound-transcriptome analyses identified kinase inhibitors targeting phosphoinositide 3-kinase, mechanistic target of rapamycin and cyclin-dependent kinases as top candidates to counteract maladaptive transcriptional programs. CONCLUSIONS: This study defines temporal and tissue-specific transcriptomic remodeling in salt-sensitive hypertension and highlights the need for precision interventions to prevent progressive organ damage.

Journal Article↗
PubMed2006

Wound complications following kidney and liver transplantation.

Advances in surgical techniques and immunosuppression (IS) have led to an appreciable reduction in postoperative complications following transplantation. However, wound complications as probably the most common type of post-transplantation surgical complication can still limit these improved outcomes and result in prolonged hospitalization, hospital readmission, and reoperation, consequently increasing overall transplant cost. Our aim was to review the literature to delineate the evidence-based risk factors for wound complications following kidney and liver transplantation (KTx, LTx), and to present the preventive and therapeutic modalities for this bothersome morbidity. Generally, wound complications are categorized as superficial and deep wound dehiscences, perigraft fluid collections and seroma, superficial and deep wound infections, cellulitis, lymphocele and wound drainage. The results of several studies showed that the most important risk factors for wound complications are IS and obesity. Additionally, there are surgical and/or technical factors, including type of incision, reoperation, and surgeon's expertise, as well as comorbidities such as advanced age, diabetes mellitus, malnutrition, and uremia. Preventive management of wound complications necessitates defining their etiological factors so that their detrimental effects on healing processes can be addressed and reduced. IS modalities and agents, especially sirolimus (SRL), and steroids (ST) should be adjusted according to the patient's co-existing risk factors. SRL should be administered three months after transplantation and ST should be tapered as soon as possible. A body mass index (BMI) lower than 30 kg/m2 is advisable for inclusion in a transplantation program, but higher BMIs do not exclude recipients. Surgical risk factors can be prevented by applying precise surgical techniques. Therapeutic modalities must focus on the most efficient and cost-effective medications and/or interventions to facilitate and improve wound healing.

Humans↗
PubMed1999

Transitions and inequalities in acute myocardial infarction mortality in New South Wales, 1969-94.

OBJECTIVE: To chart the transition in myocardial infarction mortality in NSW between 1969 and 1994 and to determine whether spatial, marital and occupational status differentials increased over time, despite overall mortality decline. METHOD: The study was undertaken in NSW for the 25-year period from 1969 when mortality from ischaemic heart disease declined. The demographic and spatial analysis involved descriptive epidemiology and utilised the unit list mortality files of the Australian Bureau of Statistics which are based on detailed death certificate information. RESULTS: Spatial, marital and occupational status differentials in myocardial infarction mortality increased over time, more especially variations by occupational status, inland/metropolitan differences, and married/divorced or widowed variation. Spatial variations in mortality were not simply the result of occupational status differences as mortality from white collar groups was also elevated in inland areas. Spatial variation in mortality was not diluted due to the impact of immigration. CONCLUSIONS: Particular subgroups of people remained at risk and it is likely that differential access to ambulance services and travel time contribute, more particularly in inland rural areas. IMPLICATIONS: Groups at risk need to be more precisely targeted for preventative measures and public health initiatives, with particular implications for groups in inland rural areas, the Hunter Region, and outer lower income areas of Sydney.

Adult↗
PubMed2001

The modified human DNA repair enzyme O(6)-methylguanine-DNA methyltransferase is a negative regulator of estrogen receptor-mediated transcription upon alkylation DNA damage.

Cell proliferation requires precise control to prevent mutations from replication of (unrepaired) damaged DNA in cells exposed spontaneously to mutagens. Here we show that the modified human DNA repair enzyme O(6)-methylguanine-DNA methyltransferase (R-MGMT), formed from the suicidal repair of the mutagenic O(6)-alkylguanine (6RG) lesions by MGMT in the cells exposed to alkylating carcinogens, functions in such control by preventing the estrogen receptor (ER) from transcription activation that mediates cell proliferation. This function is in contrast to the phosphotriester repair domain of bacterial ADA protein, which acts merely as a transcription activator for its own synthesis upon repair of phosphotriester lesions. First, MGMT, which is constitutively present at active transcription sites, coprecipitates with the transcription integrator CREB-binding protein CBP/p300 but not R-MGMT. Second, R-MGMT, which adopts an altered conformation, utilizes its exposed VLWKLLKVV peptide domain (codons 98 to 106) to bind ER. This binding blocks ER from association with the LXXLL motif of its coactivator, steroid receptor coactivator-1, and thus represses ER effectively from carrying out transcription that regulates cell growth. Thus, through a change in conformation upon repair of the 6RG lesion, MGMT switches from a DNA repair factor to a transcription regulator (R-MGMT), enabling the cell to sense as well as respond to mutagens. These results have implications in chemotherapy and provide insights into the mechanisms for linking transcription suppression with transcription-coupled DNA repair.

Alkylation↗
PubMed2006

TRP channels in C. elegans.

The TRP (transient receptor potential) superfamily of cation channels is present in all eukaryotes, from yeast to mammals. Many TRP channels have been studied in the nematode Caenorhabditis elegans, revealing novel biological functions, regulatory modes, and mechanisms of localization. C. elegans TRPV channels function in olfaction, mechanosensation, osmosensation, and activity-dependent gene regulation. Their activity is regulated by G protein signaling and polyunsaturated fatty acids. C. elegans TRPPs related to human polycystic kidney disease genes are expressed in male-specific neurons. The KLP-6 kinesin directs TRPP channels to cilia, where they may interact with F0/F1 ATPases. A sperm-specific TRPC channel, TRP-3, is required for fertilization. Upon sperm activation, TRP-3 translocates from an intracellular compartment to the plasma membrane to allow store-operated Ca2+ entry. The TRPM channels GON-2 and GTL-2 regulate Mg2+ homeostasis and Mg2+ uptake by intestinal cells; GON-2 is also required for gonad development. The TRPML CUP-5 promotes normal lysosome biogenesis and prevents apoptosis. Dynamic, precise expression of TRP proteins generates a remarkable range of cellular functions.

Animals↗
PubMed2006

How do heart disease and stroke become risk factors for Alzheimer's disease?

BACKGROUND: Heart disease and stroke are two of the major leading causes of death and disability in the world. Mainly affecting the elderly population, heart disease and stroke are important risk factors for Alzheimer's disease (AD). METHODS: This review examines the evidence linking chronic brain hypoperfusion (CBH) produced by several types of heart disease and stroke on the development of AD. RESULTS: The evidence indicates a strong association between such risk factors as coronary artery bypass surgery (CABG), atrial fibrillation, aortic/mitral valve damage, hypertension, hypotension, congestive heart failure, cerebrovascular-carotid atherosclerosis, and transient ischemic attacks in producing CBH. In people whose cerebral perfusion is already diminished by their advanced age, further cerebral blood flow reductions from heart-brain vascular-related risk factors, seemingly increases the probability of AD. The evidence also suggests that a neuronal energy crisis brought on by a relentless CBH is responsible for protein synthesis defects that later result in the classic AD neurodegenerative lesions such as the formation of excess beta-amyloid plaques and neurofibrillary tangles. CONCLUSIONS: Knowledge of how heart disease and stroke can progress to AD should provide a better understanding of the physiopathology characteristic of AD and also target more precise therapy in preventing, controlling or reversing this dementia.

Alzheimer Disease↗
PubMed2026

Impact of sex differences on microglial function in Alzheimer's disease.

Aging is the strongest risk factor for Alzheimer's disease (AD), a multifactorial neurodegenerative disorder characterized by amyloid-β (Aβ) accumulation, tau pathology (hyperphosphorylated tau and neurofibrillary tangles [NFTs]), and associated neuroinflammatory processes. Age-related cellular and molecular stressors, including mitochondrial dysfunction, genomic instability, and chronic low-grade inflammation, progressively increase vulnerability to neurodegeneration. In parallel, sex is increasingly recognized as a biological variable that shapes AD risk, clinical course, and neuropathological burden. Women account for roughly two-thirds of AD cases, a disparity not fully explained by longevity. Multiple factors likely contribute, including hormonal transitions across the lifespan (particularly menopausal estrogen decline), sex chromosome-linked immune regulation, sex-dependent interactions between genetic risk factors (e.g., APOE4 and TREM2) and brain aging, and differences in vascular risk, cognitive reserve, and sociocultural exposures that influence disease expression and detection. Microglia, the brain's resident immune cells, are sexually dimorphic, and respond to Aβ and tau pathology, modulating inflammatory signaling, synaptic remodeling, and neurovascular dysfunction implicated in AD. Emerging human and experimental evidence indicate that microglial activation states, immunometabolism, and functional responses differ between males and females and may contribute to sex-specific AD trajectories. Here, we synthesize current evidence supporting microglial sexual dimorphism across aging and AD, highlight possible candidates (hormonal signaling, immuno-aging, disease-associated microglial states, and immunometabolic remodeling), and discuss key knowledge gaps toward sex-informed precision approaches for prevention and treatment.

Humans↗
PubMed1989

Theoretical and practical implications for plasmapheresis in autoimmune inner ear disease.

Immune-mediated inner ear disease, by convention called autoimmune inner ear disease (AIED), has established clinical profile guidelines for diagnosis. Treatment consists of steroid and/or cytotoxic drug immunosuppression. The role of plasmapheresis (PMP) in the treatment of AIED has not been defined. Lack of a precise serological marker prevents accurate immunological understanding. Definition is, of course, difficult in a disease whose natural history is not well delineated. Successful use of PMP in one steroid and cytotoxic drug intolerant patient with AIED led to its use in a total of eight patients. The rationale for PMP was based on its known effectiveness in other autoimmune diseases and thus, its potential use in AIED. Improved auditory function occurred in 6 of the 8 patients, 3 of whom have been followed for over 3 years. Three of the six no longer require immunosuppressant medication. PMP can be used as an alternative or adjunctive therapy in AIED. These preliminary results suggest PMP can stabilize or improve auditory and vestibular symptoms in selected patients. Its use as a first line therapy followed by cytotoxic immunosuppressants bears consideration.

Adult↗
PubMed2004

G1 and S-phase checkpoints, chromosome instability, and cancer.

Mitogen-dependent progression through the first gap phase (G1) of the mammalian cell-division cycle is precisely regulated so that normal cell division is coordinated with cell growth, while the initiation of DNA synthesis (S phase) is precisely ordered to prevent inappropriate amplification of the DNA that may cause genome instability. To ensure that these fundamental requirements of cell division are met, cells have developed a surveillance mechanism based on an intricate network of protein kinase signaling pathways that lead to several different types of checkpoints. Since these checkpoints are central to the maintenance of the genomic integrity and basic viability of the cells, defects in these pathways may result in either tumorigenesis or apoptosis, depending on the severity and nature of the defects. This review summarizes the genetic and molecular mechanisms of checkpoint activation in the G1/S and S phases of the mammalian cell cycle that monitor DNA damage and replication. The relevance of these mechanisms to the origin of cancer is also discussed.

Animals↗
PubMed1999

Current patterns and future possibilities in the care of acute ischemic stroke.

Zack Hall, Director of the NINDS, succinctly described the present situation: "This is the golden age of neuroscience research" (verbal presentation at the annual meeting of the American Neurological Association, 1997). Recent trials in clinical research have demonstrated the power of thrombolytic therapy in acute ischemic stroke, and investigators across the country are now refining that therapy. The advantages of thrombolytic intervention can be provided to a much larger proportion of the population as we defined techniques to slow the rate of neuronal cell death after ischemia. However, the most exciting future opportunities for care of individuals of acute ischemic stroke arises from two somewhat unsuspected avenues. First, neuroscientists are learning in an extraordinarily rapid fashion the potentials of replacement of neural cell populations using progenitor cells. Second, the incredible explosion of genetic information has created an opportunity to identify genes responsible for atherosclerosis and other cerebrovascular disease. This, in turn, could lead to precise therapies that prevent or diminish the disease. Exploiting these opportunities requires that neural clinicians continue their cooperative efforts and, also, learn to work together with neuroscientists and geneticists. With such cooperation, we are poised to translate the golden age of neuroscience research into a genuine benefit for individuals with cerebrovascular disorders.

Cell Survival↗
PubMed1999

[Ischemic stroke: new therapeutic possibilities].

Recent randomized placebo-controlled studies have introduced new concepts in the therapy of acute ischemic stroke, such as thrombolysis either with intraarterial or intravenous administration, lowering of the level of fibrinogen or administration of aspirin. High dosis of heparin may be useful only in certain groups of patients. Stroke units proved to be effective in the acute care of stroke patients. Further advances are achieved by the introduction of new anti-platelet drugs in secondary stroke prevention and by precise definitions of the criteria for carotid surgery.

Anticoagulants↗
PubMed1999

Biomechanical evaluation of a proximal tibial opening-wedge osteotomy plate.

This biomechanical study evaluated the static response of a new opening-wedge osteotomy plate to compression and torsion loads in a human cadaver model. This plate incorporates a metal block that distracts the medial tibial cortices to ensure precise correction and prevent bone collapse. The 15-mm plate was inserted into 23 fresh cadaver specimens using a standard surgical technique. Axial loading of 13 specimens (compression) and external rotation loading of 10 specimens (torsion) was performed using a servohydraulic-testing machine. Compression loading resulted in failure at a mean of 1810 N due to bone collapse, fracture, or translation. Torsional loading resulted in failure at a mean of 10 Nm due to fracture of the lateral tibial cortex in all specimens. The ratio of the experimental failure load to the calculated estimate of the knee joint forces during gait were 1.07 in axial compression and 0.925 in torsion. This opening-wedge osteotomy plate construct appears marginally strong enough to withstand the estimated axial load on the proximal tibia during gait. Estimated torsional load on the knee during level walking slightly exceeds the failure load prior to osteotomy healing. This information can be used to guide further experimental protocols for static and dynamic testing of this device to determine the appropriate rehabilitation guidelines following opening-wedge proximal tibial osteotomy.

Aged↗
PubMed1999

Peripheral blood cells transplantation--a review article.

In the twelve years since the first PBSCT were reported, impressive advancements in BCT techniques have made it easy to perform, effective, less costly, rapid haematologically recoverable, reduced morbidity and mortality, shorten overall duration of cancer treatment and hospital stay. Development of high-dose chemotherapy and new novel effective antitumor drugs otherwise limited by haematological toxicities may now become possible. Treatment of haematological malignancies with purged autologous PBPCT, e.g. Ph Chromosome negative progenitor cells in CML or with immunologically manipulated allogeneic PC having preserved GVL but not GVHD action, with hopeful prospects, is now becoming possible. Tailoring of BC for ex-vivo selection and expansion of specially active T Iymphocytes, NK cells and other immune effector cells will enable adoptive immunotherapeutic approach and treatment of Minimal residual disease [MRD] after high-dose chemotherapy both in grafts and in patients. The discovery of a nonhaematopoietic, engraftment facilitator cell form donor BM may usher in further precision in GVHD prevention by purification and in adoptive immunotherapeutic approach. Therefore, it is likely that BCT will supersede BMT, though the follow-up is too short to draw conclusions.

Blood Transfusion, Autologous↗
PubMed1976

Correction of Type C complete atrioventricular canal. Surgical considerations.

Case histories of 8 consecutive patients who underwent surgical correction of Type C complete atrioventricular (A-V) canal at the Ochsner Medical Center over the past 2 years were analyzed. Ages ranged from 1 1/3 to 14 years. Before bypass, the level to which the common leaflets ascend and the arc that they inscribe are determined by palpation to ensure their proper reconstitution on the canal patch. The major area of closure is usually allocated to the ventricular portion. Mapping the conduction system and tying sutures with the heart beating in high-risk conduction areas prevent heart block. Precise marking and splitting of the valve leaflets and reattachment with interrupted felt-buttressed sutures avoid disruption. All patients survived the operation and have shown clinical improvement. At recatheterization, 7 of 8 patients have shown a definite decrease in mitral insufficiency. Right ventricular pressures returned toward normal and there were no significant residual shunts. Associated anomalies or previous operations have not been a contraindication, and since we have begun using the present technique, we have achieved consistently good results without prosthetic valves.

Adolescent↗