Cause Of Death Research Articles

Mortality and Years of Life Lost from Diabetes Mellitus in Poland: A Register-Based Study (2000–2022)

Background: The aim of the study was to assess mortality and years of life lost from diabetes mellitus in Poland between 2000 and 2022. Methods: The database was created from death cards made available for the purposes of this study by Statistics Poland. The study used data on deaths caused by type 1 diabetes mellitus, T1DM (N = 33,328), and type 2 diabetes mellitus, T2DM (N = 113,706). Standardized death rates (SDRs) and standard expected years of life lost per person (SEYLLp) and per death (SEYLLd) were calculated. A time trend analysis was performed using joinpoint models. The annual percentage change (APC) and the average annual percentage change (AAPC) were estimated. Results: Between 2000 and 2022, 33,328 people died from T1DM in Poland. The SDR rate increased from 6.0 to 8.8 per 100,000 population in the analyzed period. The APC was 1.3% (p < 0.05). SEYLLp rates per 100,000 population were 79.3 in 2000 and 109.2 in 2022. SEYLLd rates were 22.9 and 17.9 years, respectively (APC = −1.0%, p < 0.05). The mean age of those who died from T1DM increased from 66.1 in 2000 to 72.5 in 2022. Between 2000 and 2022, 113,706 people died from T2DM. The SDR increased from 12.5 to 37.7 per 100,00 (APC = 5.5%, p < 0.05). SEYLLp rates were 88.8 and 296.0 per 100,000 population (APC = 6.4%, p < 0.05). SEYLLd rates decreased from 16.9 in 2000 to 13.4 in 2022 (AAPC = −1.0%, p < 0.05). The mean age of those who died from T2DM increased from 73.1 to 78.1 years. Conclusions: The study showed a growing problem of diabetes as a cause of death and years of life lost.

The Role of Screening for Venous Thromboembolism in Pelvic Trauma Patients: A Single-Centre Retrospective Study

Background: Venous thromboembolism (VTE) is a severe complication following pelvic trauma. Thromboprophylaxis has reduced the risk of VTE in the pelvic trauma population; nevertheless, the risk remains high. A substantial pulmonary embolism has emerged as the unexpected cause of death among patients presenting with ‘minor pelvic fractures’. The purpose of this study was to analyse the single-centre experience with a surveillance protocol. We hypothesised that DVT surveillance with VUS and CTPA may reduce the perioperative mortality–morbidity rate in the subpopulation of patients with pelvic or acetabular fractures. Methods: This is a retrospective analysis of patients admitted with pelvic or acetabular fractures between January 2001 and December 2021. In April 2013, a screening protocol for VTE was introduced. This protocol included venous ultrasound and CTPA for patients with chest injuries. Patients from two groups—one screened for VTE and one without screening—were compared. Results: Of the 3186 patients with pelvic and/or acetabular fractures who were admitted, 1975 were not screened for VTE and 1211 underwent screening. There were more VTE cases in the screening group (5.62% vs. 0.86%, p < 0.001). Nine (0.46%) cases of sudden death occurred in the non-screening group, and all of them died with symptoms of acute PE. Since the screening was introduced, we have not encountered any deaths in the perioperative period (0.46 vs. 0, p = 0.02). Conclusions: The combined use of VUS and CTPA in chest-injured patients is a trustworthy means of screening for VTE, resulting in decreased mortality rates for those with pelvic and acetabular fractures by accurately diagnosing VTE during the perioperative phase.

Characterising fire or burn-related fatalities in the USA using the National Violent Death Reporting System, 2003–2020

ObjectivesIntentional fire or burn-related deaths are rare in the USA compared with some countries, but do occur, and our knowledge of their epidemiology is limited. The objective of this study...

Causes of admission and mortality in European Hedgehog (Erinaceus europaeus, Linnaeus, 1758)

Erinaceus europaeus, a key indicator species for health ecosystems, faces various threats that impact the survival of the species. Most factors of threat are associated with human activity. The authors present a review of E. europaeus admission causes in wildlife rehabilitation centres and the mortality pattern of free-ranging animals. The review includes 20 papers spanning a considerable timespan from 1981 to 2024. The main causes of admission to wildlife rehabilitation centres are hoglets and starvation. The main causes of death in hedgehogs are vehicle collision and predation. It can be concluded that humans and human activity play a significant role in the mortality of these animals. In the future, a more standardised analysis of hedgehog carcasses is necessary to understand their threats and diseases and to design significant measures to protect the species.

Inclusive intervention design for vulnerable road users: Applying co-design and behaviour change model in Bangladesh

In developing countries, it is debatable whether poor design of facilities or violation of traffic rules by road users is the leading cause of pedestrian injuries and deaths. Professionals, pedestrians and drivers tend to blame each other. Shared responsibility for road safety is crucial for protecting vulnerable road users such as commuting students and workers who face higher injury risks while crossing highways. While the Safe System approach emphasises authorities’ responsibility for safe facilities, understanding user needs and promoting behaviour change remain underexplored. This study investigates the current design practices in Bangladesh. It compares the impact of conventional design with co-design on intervention quality and examines the further benefits of integrating a behaviour change model ‘COM-B’.Local road agency professionals applied the design process and suggested interventions at four highway sites. Subsequently, four focus group sessions were conducted with students and workers, followed by four design workshops. In each workshop, participants were randomly assigned to two design groups (without and with the application of the behaviour change model), where they designed interventions facilitated by professionals. Lastly, perception ratings of stakeholders and safety assessments by four experts were conducted to evaluate the efficacy of all interventions.The findings highlight major usability problems in conventional designs, while co-designed interventions demonstrate clear improvements. Notably, integrating a behaviour change model further enhances effectiveness. Stakeholder interviews reveal that co-design fosters shared responsibility and addresses the blame culture. The co-design approach and application of the behaviour change model can address design flaws and promote the proper use of facilities.

Detection of circulating tumor cells in non-metastatic prostate cancer through integration of a microfluidic CTC enrichment system and multiparametric flow cytometry.

Prostate cancer (PCa) is the second most common cancer among men and the fifth leading cause of cancer death. Circulating tumor cell (CTC) enumeration and characterisation in PCa has been shown to provide valuable information on prognosis of disease, therapy management and detection of resistance. Here, Cellsway's microfluidic platform for high-throughput enrichment of intact CTC populations was used to isolate CTCs from the blood of 20 localised PCa patients and 10 healthy donor samples to evaluate the clinical performance of the technology. To enumerate and characterise CTCs, a multi-parameter flow cytometry analysis was performed on the enriched CTC suspension using CTC-specific biomarkers. CTCs were detected in 17 of 20 patient samples, which corresponds to 85% CTC positivity. The median CTC count per 7.5 ml blood was 2 (1-9). In 80% of patients (n = 16), the number of CTCs ranged from 1 to 5, and in 5% of patients (n = 1) the number of CTCs was above 5. No CTCs were observed in the blood samples of 10 healthy volunteers, demonstrating the high specificity and low risk of false positives of the technology.

Central nervous system tumors in adolescents and young adults: A Society for Neuro-Oncology consensus review on diagnosis, management, and future directions.

Adolescents and young adults (AYAs; ages 15-39 years) are a vulnerable population facing challenges in oncological care, including access to specialized care, transition of care, unique tumor biology, and poor representation in clinical trials. Brain tumors are the second most common tumor type in AYA, with malignant brain tumors being the most common cause of cancer-related death. The 2021 WHO Classification for central nervous system (CNS) Tumors highlights the importance of integrated molecular characterization with histologic diagnosis in several tumors relevant to the AYA population. In this position paper from the Society for Neuro-Oncology (SNO), the diagnosis and management of CNS tumors in AYA is reviewed, focusing on the most common tumor types in this population, namely glioma, medulloblastoma, ependymoma, and CNS germ cell tumor. Current challenges and future directions specific to AYA are also highlighted. Finally, possible solutions to address barriers in the care of AYA patients are discussed, emphasizing the need for multidisciplinary and collaborative approaches that span the pediatric and adult paradigms of care, and incorporating advanced molecular testing, targeted therapy, and AYA-centered care.

Robotic manipulation of cardiomyocytes to identify gap junction modifiers for arrhythmogenic cardiomyopathy.

Arrhythmogenic cardiomyopathy (ACM) is a leading cause of sudden cardiac death among young adults. Aberrant gap junction remodeling has been linked to disease-causative mutations in plakophilin-2 (PKP2). Although gap junctions are a key therapeutic target, measurement of gap junction function in preclinical disease models is technically challenging. To quantify gap junction function with high precision and high consistency, we developed a robotic cell manipulation system with visual feedback from digital holographic microscopy for three-dimensional and label-free imaging of human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs). The robotic system can accurately determine the dynamic height changes in the cells' contraction and resting phases, microinject drug-treated healthy and diseased iPSC-CMs in their resting phase with constant injection depth across all cells, and deposit a membrane-impermeable dye that solely diffuses between cells through gap junctions for measuring the gap junction diffusion function. The robotic system was applied toward a targeted drug screen to identify gap junction modulators and potential therapeutics for ACM. Five compounds were found to dose-dependently enhance gap junction permeability in cardiomyocytes with PKP2 knockdown. In addition, PCO 400 (pinacidil) reduced beating irregularity in a mouse model of ACM expressing mutant PKP2 (R735X). These results highlight the utility of the robotic cell manipulation system to efficiently assess gap junction function in a relevant preclinical disease model, thus providing a technique to advance drug discovery for ACM and other gap junction-mediated diseases.

The effect of drugs and guns on life expectancy in the United States, 2000–2020

ObjectivesThis study estimated the effect of changing trends in drug- and firearm-related mortality on life expectancy in the U.S. over the last two decades. Study designRetrospective cross-sectional study. MethodsWe used national vital registration data from CDC WONDER, stratified by sex, to estimate the mortality rate due to accidental and intentional poisoning (ICD Codes X40-X49, X60-X69, Y10-Y19 and X85), and firearm deaths (ICD codes W32-W34, X72-X74, X93-X95, Y22-Y24) for the period 2000–2020. We applied standard life table methods to all cause mortality rates with and without these mortality causes to estimate the life expectancy at each age over this period. ResultsIn 2020, mortality due to drugs and firearms combined reduced male life expectancy by1.67 years compared to 0.67 years in 2000, and without the effect of these two causes of death, male life expectancy in 2019 would have been 78.02 years. For women, drugs and firearm-related mortality reduced life expectancy by 0.20 years in 2000 and 0.63 years in 2020, and female life expectancy would have been 82.25 years in 2019 without the retarding effect of these two preventable causes. ConclusionsDrug- and firearm-related deaths have increased so rapidly, especially among younger populations, that life expectancy at birth is significantly reduced by these causes of death. Without urgent action to tackle these preventable causes of death, US life expectancy will continue to stagnate and may even decline, even without the effect of COVID-19.

Prevalence, Reasons, and Prevention for Drug Related Death After Release from Prisons: A Systematic Review and Meta-analysis

Context: Drug-related mortality is a major concern in public and global health discussions. Objectives: Therefore, the aim of this study was to investigate the prevalence, causes, and prevention of death after individuals are released from prison. Methods: This study was conducted systematically using MeSH keywords with no language or time restrictions. PubMed, Scopus, and Web of Science databases were extensively searched for observational studies from 1980/1/1 to 2023/12/30, following the PRISMA checklist. Fourteen research studies were ultimately included in the systematic review process. The CRD code is CRD42024571756. Results: The two-week period following release, with an 18% prevalence, was identified as the time when most overdose deaths occurred. The leading causes of death included prior heroin use, previous experiences with drug withdrawal, drug injection, and sedative use within six months before death. Compared to other unnatural causes of death, there was an increased risk of fatal drug overdose for individuals who died within the first two months of release. Men had higher death rates from all causes compared to women. Most studies reported that substance abuse treatment during imprisonment and providing take-home naloxone for emergencies protected against mortality from all causes. Conclusions: In conclusion, evidence from these systematic investigations highlights the urgent need for targeted interventions to address substance use disorders and overdose prevention among individuals recently released from prison. Efforts to bridge the gap between incarceration and community reintegration should prioritize comprehensive substance abuse treatment programs to reduce the heightened risk of mortality in this vulnerable population.

Blestriarene C exerts an inhibitory effect on triple-negative breast cancer through multiple signaling pathways

IntroductionBreast cancer is the most common cancer worldwide, the leading cause of cancer death in women, and the fifth leading cause of cancer death. Triple negative breast cancer (TNBC), with high metastasis and mortality rates, is the most challenging subtype in breast cancer treatment. There is an urgent need to develop anti-TNBC drugs with significant efficacy, low side effects and good availability. In early drug screening, blestriarene C was found to have inhibitory effects on TNBC cells. In this article, we further explore the mechanisms associated with blestriarene C for breast cancer.MethodsIn this article, we take the approach of network pharmacology combined with in vivo and in vitro experiments. Network pharmacology analysis was used to predict the active components in Baiji, and to investigate the hub targets and related mechanisms of BC in TNBC treatment. The mechanism of anti-TNBC in vitro was evaluated by CCK-8 assay, cell apoptosis and cell cycle assays, wound healing assay, WB assay, and molecular docking analysis. The inhibition effect in vivo was test in subcutaneous tumor models established in mice.ResultsThrough network pharmacology analysis and experiments, we screened out BC as the main active ingredient, and found that BC could inhibit the Ras/ERK/c-Fos signaling pathway while downregulating the expression of HSP90AA1 and upregulating the expression of PTGS2, thereby promoting apoptosis, causing S-phase cycle arrest, and inhibiting the proliferation and migration of BT549 cells. The in vivo results illustrated that BC inhibited the growth of TNBC tumors and has a high safety profile. By integrating network pharmacology with in vitro and in vivo experiments, this study demonstrated that BC inhibited the proliferation and migration of TNBC cells by inhibiting the Ras/ERK/c-Fos signaling pathway, promoting apoptosis, and causing S-phase cycle arrest.DiscussionThis study provides new evidence for the use of BC as a novel drug for TNBC treatment.

Determinants of unsuccessful tuberculosis treatment outcome in Southwest Ethiopia regional state public hospitals, 2022: a multi-center case control study

BackgroundTuberculosis is the major cause of morbidity, and it is one of the top ten causes of death globally. In Africa, the overall pooled estimate of unsuccessful tuberculosis treatment outcome was reported to be 21.1%, which is above the World Health Organization defined threshold of 15%. Unsuccessful treatment outcomes result in drug resistance, prolonged periods of infection, and increased morbidity and mortality. Therefore, this study aimed to assess determinants of unsuccessful treatment outcomes among tuberculosis patients in Southwest Ethiopia regional state public hospitals, in 2022.MethodA retrospective unmatched case–control study was employed by recruiting 570 study units (190 cases and 380 controls) in three randomly selected public hospitals from 1 August 2022 to 21 August 2022. Data were collected by using a data extraction checklist adapted from tuberculosis registration logbook. Bivariate and multivariate logistic regression models were employed. A predictor variable with a p-value of less than 0.05 in the multivariate logistic regression model was taken as statistically significant. The odds ratio and 95% confidence level were used to measure the strength of the association.ResultA total of 561 records (187 cases and 374 controls) were included from tuberculosis registers. In this study, the factors independently associated with unsuccessful tuberculosis treatment outcome were older age (AOR = 1.68, 95% CI: 1.142, 2.472), rural residence (AOR = 1.548, 95% CI: 1.055, 2.272), retreatment category (AOR = 2.12, 95% CI: 1.339, 3.357), underweight (BMI < 18.5 kg/m2) (AOR = 1.952, 95% CI: 1.240, 3.071), being HIV positive (AOR = 2.144, 95% CI: 1.372, 3.349) and having no treatment adherence support (AOR = 2.016, 95% CI: 1.270, 3.201).Conclusion and recommendationIn this study, socio-demographic, clinical, and treatment-related factors contributed to the risk of unsuccessful treatment outcomes. Targeted interventions should be taken into consideration to diminish poor tuberculosis treatment outcomes among high-risk groups throughout the whole tuberculosis treatment course.

Adunctin E from Conamomum rubidum Induces Apoptosis in Lung Cancer via HSP90AA1 Modulation: A Network Pharmacology and In Vitro Study

Lung cancer stands out as a leading cause of death among various cancer types, highlighting the urgent need for effective anticancer drugs and the discovery of new compounds with potent therapeutic properties. Natural sources, such as the Conamomum genus, offer various bioactive compounds. Adunctin E (AE), a dihydrochalcone derived from Conamomum rubidum, exhibited several pharmacological activities, and its potential as an anticancer agent remains largely unexplored. Thus, this study aimed to elucidate its apoptotic-inducing effect and identify its molecular targets. The network pharmacology analysis led to the identification of 71 potential targets of AE against lung cancer. Subsequent gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Reactome pathway enrichment analyses revealed the involvement of these targets in cancer-associated signaling pathways. Notably, HSP90AA1, MAPK1, and PIK3CA emerged as key players in apoptosis. In silico molecular docking and dynamic simulations suggested a strong and stable interaction between AE and HSP90AA1. In vitro experiments further confirmed a significant apoptotic-inducing effect of AE on lung cancer cell lines A549 and H460. Furthermore, immunoblot analysis exhibited a substantial decrease in HSP90AA1 levels in response to AE treatment. These findings support the potential anticancer activity of AE through the HSP90AA1 mechanism, underscoring its promise as a novel compound worthy of further research and development for anti-lung cancer therapy.

Criteria air pollutants and HIV-related mortality: Insights from a nationwide case-crossover investigation

The heightened vulnerability of individuals with HIV to environmental stressors is well-recognized, yet the role of air pollution in exacerbating HIV-related mortality remains underexplored. In this nationwide, individual-level case-crossover study conducted from 2013 to 2019, we investigated the association between short-term exposure to criteria air pollutants and HIV-related mortality. Our analysis of 38,510 HIV-related deaths revealed significant associations between exposure to PM2.5, PM10, NO2, and CO and increased mortality risk. The effects of PM2.5 and PM10 persisted for two days, whereas NO2 and CO had immediate, same-day impacts. Vulnerability was heightened in individuals under 65 years, males, those with lower educational attainment, and unmarried individuals. Among causes of death, HIV-related malignant neoplasms exhibited the highest sensitivity to particulate matter. Our findings provide novel insights into the relationship between short-term air pollution exposure and HIV-related mortality, emphasizing the increased susceptibility of this immunocompromised population. The results underscore the need for targeted public health interventions to reduce pollution exposure, particularly for the most at-risk demographic groups. This study contributes to a deeper understanding of environmental health risks faced by individuals living with HIV and informs evidence-based policy recommendations.

Current Insights into Therapeutic Potential of Terpenoids as Anticancer Agents.

Cancer is regarded as one of the main causes of death globally. Future predictions indicate that the death rate from cancer will keep rising, which may reach 11.4 million in 2030. Carcinogenesis refers to the phenomenon of transforming a normal cell into a cancer cell. Cancer is characterized by unregulated and uncontrolled cell division due to alterations at the molecular and genetic levels. Gene mutations can speed up the rate of cell division, which leads to cancer. Metastasis entails the dissemination of cancer cells from the primary site to distant regions of the body via the circulatory or lymphatic systems. This review is mainly focusing on the anticancer properties of terpenoids. In the case of human beings, several types of cancers can be treated clinically based on the form and phase of the cancer. So, there are different types of treatment regimens available for the management of cancer, such as immunotherapy, hormonal therapy, radiation therapy, and chemotherapy. Several problems are associated with cancer therapy, including chemoresistance, severe toxicity, relapse, and metastasis. To minimize these complications, natural products like terpenoids seem to be beneficial for the effective management of cancer. Experimental results revealed that the anticancer potential of terpenoids is due to activation of apoptosis and stimulation of cell cycle arrest. Some of the terpenoids exhibit anticancer effects by inhibiting angiogenesis and metastasis via the regulation of several signaling pathways intracellularly. Certain terpenoids have been shown to work in concert with anticancer medications (doxorubicin, cisplatin, paclitaxel, and 5-fluorouracil) to provide synergistic effects. These terpenoids have also been shown to be effective against cancer cells that are resistant to several drug therapies. The current study will focus on signaling pathways and mode of action of several types of terpenoids as anticancer agents. Further, it will provide insights into the ongoing clinical trials and prospective pathways for the advancement of terpenoids as possible anti-cancer agents.

Circulating Blood-Brain Barrier Proteins for Differentiating Ischaemic Stroke Patients from Stroke Mimics

Background: Stroke is one of the leading causes of death and disability worldwide. The diagnosis of stroke remains largely clinical, yet widely used stroke scoring systems and brain imaging do not satisfactorily allow the distinction of ischaemic stroke (IS) patients from stroke mimics (SMs). Blood biomarkers are promising tools that could facilitate clinical triage. Methods: This study recruited 66 patients with IS and 24 SMs. The levels of Glial fibrillary acidic protein (GFAP), Neuron-specific enolase (NSE), Neurofilament light chain (NfL) and blood-brain barrier (BBB) proteins [Occludin (OCLN), Zonula occludens 1 (ZO-1), Claudin-5] in blood serum were measured by enzyme-linked immunosorbent assay technique. Biomarker levels in IS patients and SMs were compared using the Mann–Whitney U test. Multivariable logistic regression analysis was used to evaluate the diagnostic performance of biomarkers in combination with the National Institutes of Health Stroke Scale (NIHSS) score. Results: More significant differences in circulating GFAP, NfL, OCLN, ZO-1, and Claudin-5 but not NSE were found in IS patients compared to SMs. A combination of circulating ZO-1, Claudin-5, and OCLN with NIHSS score gives the highest diagnostic accuracy, sensitivity, and specificity. Conclusions: A prediction model with circulating BBB proteins in combination with NIHSS score differentiates between IS patients and SMs.

The role of IL-17 family cytokines in cardiac fibrosis

Myocardial fibrosis is a common pathological feature in various cardiovascular diseases including myocardial infarction, heart failure, and myocarditis. Generally, persistent myocardial fibrosis correlates with poor prognosis and ranks among the leading causes of death globally. Currently, there is no effective treatment for myocardial fibrosis, partly due to its unclear pathogenic mechanism. Increasing studies have shown IL-17 family cytokines are strongly associated with the initiation and propagation of myocardial fibrosis. This review summarizes the expression, action, and signal transduction mechanisms of IL-17, focusing on its role in fibrosis associated with cardiovascular diseases such as myocardial infarction, heart failure, hypertension, diabetes, and myocarditis. It also discusses its potential as a therapeutic target, offering new insights for the clinical treatment of myocardial fibrosis.

Epicardial transplantation of antioxidant polyurethane scaffold based human amniotic epithelial stem cell patch for myocardial infarction treatment

Myocardial infarction (MI) is a leading cause of death globally. Stem cell therapy is considered a potential strategy for MI treatment. Transplantation of classic stem cells including embryonic, induced pluripotent and cardiac stem cells exhibited certain repairing effect on MI via supplementing cardiomyocytes, however, their clinical applications were blocked by problems of cell survival, differentiation, functional activity and also biosafety and ethical concerns. Here, we introduced human amniotic epithelial stem cells (hAESCs) featured with immunomodulatory activities, immune-privilege and biosafety, for constructing a stem cell cardiac patch based on porous antioxidant polyurethane (PUR), which demonstrated decent hAESCs compatibility. In rats, the administration of PUR-hAESC patch significantly reduced fibrosis and facilitated vascularization in myocardium after MI and consequently improved cardiac remodeling and function. Mechanistically, the patch provides a beneficial microenvironment for cardiac repair by facilitating a desirable immune response, paracrine modulation and limited oxidative milieu. Our findings may provide a potential therapeutic strategy for MI.

Improving Biomedical Science Literacy and Patient-Directed Knowledge of Tuberculosis (TB): A Cross-Sectional Infodemiology Study Examining Readability of Patient-Facing TB Information

BackgroundTuberculosis (TB) continues be the leading cause of death globally due to an infectious agent. There is a paucity of data describing the readability of patient-facing TB information for service users. The aim of this study was to calculate the readability of multiple global TB information sources.MethodsInformation on tuberculosis (n = 150 sources) included nine categories, Patient-facing information: WHO publications (n = 17), International governments (n = 19), Hospitals (n = 10), Non-government organisations (NGOs)/charities (n = 20), Cochrane Plain Language Summaries (n = 20); LabTestsOnlineUK (n = 4) and Scientific-facing information: Clinical trials (n = 20), Cochrane abstracts (n = 20), Scientific abstracts (n = 20). Readability was calculated using Readable software, defined by (i) Flesch Reading Ease (FRE), (ii) Flesch-Kincaid Grade Level (FKGL), (iii) Gunning Fog Index and (iv) SMOG Index and two text metrics [words/sentence, syllables/word].ResultsMean readability values for TB information for the FRE and FKGL were 35.6 ± 1.6 (standard error of mean (SEM)) (US Target ≥60; UK Target ≥90) and 12.3 ± 0.3 (US Target ≤8; UK Target ≤6), respectively, with mean words per sentence and syllables per word of 17.2 and 1.8, respectively. Cochrane Plain Language Summaries had similar readability scores to their matching scientific abstract (p = 0.15). LabTestsOnlineUK yielded a mean FRE score of 51.5 ± 1.2, a mean FKGL score of 10.2 ± 0.5 and text metric scores of 16.7 ± 2.3 and 1.6, for words per sentence and syllables per word, respectively. In descending order, TB information from international governments, hospitals and LabTestsOnlineUK were the most readable (FRE = 57.9, 54.1 and 51.5, respectively), whereas scientific abstracts and Cochrane abstracts were the most difficult to read (13.0 and 30.2, respectively).ConclusionPatient-facing TB information analysed had poor readability. Effective communication of biomedical science concepts and information relating to TB is vital for service users to enhance their health literacy of tuberculosis, thereby promoting better clinical outcomes. Biomedical scientists are important custodians of scientific information for their service user populations, including other healthcare professionals within the TB multidisciplinary (MDT) team and patient service users. When preparing TB information, this should be checked and modified in real time employing readability calculators, to align with health readability targets.

Tubulin-Targeted Therapy in Melanoma Increases the Cell Migration Potential by Activation of the Actomyosin Cytoskeleton─An In Vitro Study.

One of the most dangerous aspects of cancers is their ability to metastasize, which is the leading cause of death. Hence, it holds significance to develop therapies targeting the eradication of cancer cells in parallel, inhibiting metastases in cells surviving the applied therapy. Here, we focused on two melanoma cell lines─WM35 and WM266-4─representing the less and more invasive melanomas. We investigated the mechanisms of cellular processes regulating the activation of actomyosin as an effect of colchicine treatment. Additionally, we investigated the biophysical aspects of supplement therapy using Rho-associated protein kinase (ROCK) inhibitor (Y-27632) and myosin II inhibitor ((-)-blebbistatin), focusing on the microtubules and actin filaments. We analyzed their effect on the proliferation, migration, and invasiveness of melanoma cells, supported by studies on cytoskeletal architecture using confocal fluorescence microscopy and nanomechanics using atomic force microscopy (AFM) and microconstriction channels. Our results showed that colchicine inhibits the migration of most melanoma cells, while for a small cell population, it paradoxically increases their migration and invasiveness. These changes are also accompanied by the formation of stress fibers, compensating for the loss of microtubules. Simultaneous administration of selected agents led to the inhibition of this compensatory effect. Collectively, our results highlighted that colchicine led to actomyosin activation and increased the level of cancer cell invasiveness. We emphasized that a cellular pathway of Rho-ROCK-dependent actomyosin contraction is responsible for the increased invasive potential of melanoma cells in tubulin-targeted therapy.