Building the African American/Black Community's Capacity to Elucidate Factors for High Smoking Rates in Jackson, MS: Results from Implementing a Community-Led Needs Assessment.

INTRODUCTION: Although smoking has decreased dramatically over the last 50 years, reductions are uneven by race and income, specifically in the Southern United States. There is a need for intentional collaboration with communities located where large tobacco disparities exist to make lasting change. Using community-based participatory research principles, we provided intensive capacity building to a community advisory group (CAG) of 14 Jackson, MS, residents to conduct a community-led needs assessment. The aim of the community-led needs assessment was to investigate firsthand why the community smokes and the impacts of smoking-giving the CAG voice and choice to work towards reducing tobacco-related harms and inequities. METHODS: From October 2020 to September 2021, CAG members conducted thirteen interviews and nine focus groups, reaching 54 residents. We analyzed the data using a thematic and in vivo approach. RESULTS: Participants reported smoking is used to cope with systemic socio-economic issues (e.g., racism, poverty). Smoking is normalized in the community through continued use, ease of purchase, visibility of tobacco retailers, and lack of conversations or questioning surrounding smoking. Participants felt that peer and family use, addiction, and inaccessible smoking resources were the most influential factors driving smoking behaviors. CONCLUSION: This community engagement approach empowered residents to design and implement a comprehensive needs assessment resulting in rich data-a needed approach for a community experiencing enduring health inequities. Communities need to be engaged and invested in from the beginning as equal partners to learn, investigate, and develop community-relevant and innovative solutions to address tobacco social norms.

Building a baby-friendly community: Development, strategy, implementation and evaluation of a BFCI program.

AIM: The aim of the study was to investigate the impact of the use of baby-friendly community initiative (BFCI) model on various stakeholders in the community. DESIGN: Quasi-experimental research design. METHOD: The study was conducted in public premises and online workshops from April 2019 to September 2022. Participants were followed up for a period of 1 month, except for those employed at public premises. The program involved training based on an accredited BFCI framework to cultivate a breastfeeding-friendly attitude and knowledge. A paired sample t-test was used to examine breastfeeding attitude and knowledge scores before and after BFCI training among staff employed from public premises. An analysis of variance was conducted to examine the breastfeeding self-efficacy and attitude scores, measured repeatedly at different timepoints over 1-month timepoint (T0, T1 and T2) among pregnant and postpartum women. RESULTS: A total of 2340 perinatal women and 1339 staff from public premises were recruited. For staff, there was an increase in the mean score of breastfeeding knowledge and attitude by 5.8 and 6.1, respectively, at T1. Similarly, for perinatal women, there was an increase in the mean score of breastfeeding self-efficacy and attitude by 6.6 and 3.3, respectively, at T1. CONCLUSION: In summary, a BFCI model, with active community participation, accreditation and an award system, has been effective in promoting breastfeeding. Adapting the baby-friendly hospital initiative to local contexts and employing a social theory model can enhance breastfeeding promotion and improve infant health outcomes. Prioritizing culturally sensitive breastfeeding education is crucial for successful BFCI implementation. IMPLICATIONS FOR THE PROFESSION AND/OR PATIENT CARE: Healthcare professionals should consider clients' culture and socio-economic backgrounds when providing breastfeeding education to maximize effectiveness. The target audience for breastfeeding education should be expanded to include various community stakeholders beyond families. IMPACT: What problem did the study address? This study addressed the problem of knowledge gaps among stakeholders in building a breastfeeding-friendly community, particularly in implementing a baby-friendly community initiative (BFCI) as part of a baby-friendly hospital initiative (BFHI). The research filled a service gap by providing effective interventions targeting community stakeholders and assessing the impact of a BFCI program on their knowledge and attitudes towards breastfeeding. What were the main findings? The findings highlighted the effectiveness of a BFCI program in enhancing breastfeeding knowledge and attitudes among frontline staff and increasing breastfeeding confidence among mothers. These findings contribute to the understanding of the program's impact on different stakeholders in the community. Where and on whom will the research have an impact? It impacts on global policymakers by providing insights for developing comprehensive guidelines for future BFCI implementations. It also contributes to the creation of a more baby-friendly community, benefiting breastfeeding families and their infants by promoting and supporting breastfeeding families. REPORTING METHOD: This study has adhered to relevant EQUATOR guidelines using the TREND reporting guideline. PATIENT OR PUBLIC CONTRIBUTION: No patient or public contribution. WHAT DOES THIS PAPER CONTRIBUTE TO THE WIDER GLOBAL CLINICAL COMMUNITY?: This study provides an overview of the establishment of a localized BFCI program. It also opens up a new direction for the community to investigate BFCI strategies for community stakeholders. It also provides evidence to support other countries in following a similar process, as each country approaches becoming breastfeeding-friendly in its own unique way. TRIAL AND PROTOCOL REGISTRATION: No protocol.

BRCA1 heterozygosity promotes DNA damage-induced senescence in a sex-specific manner following repeated mild traumatic brain injury.

Emerging evidence suggests cellular senescence, as a consequence of excess DNA damage and deficient repair, to be a driver of brain dysfunction following repeated mild traumatic brain injury (rmTBI). This study aimed to further investigate the role of deficient DNA repair, specifically BRCA1-related repair, on DNA damage-induced senescence. BRCA1, a repair protein involved in maintaining genomic integrity with multiple roles in the central nervous system, was previously reported to be significantly downregulated in post-mortem brains with a history of rmTBI. Here we examined the effects of impaired BRCA1-related repair on DNA damage-induced senescence and outcomes 1-week post-rmTBI using mice with a heterozygous knockout for BRCA1 in a sex-segregated manner. Altered BRCA1 repair with rmTBI resulted in altered anxiety-related behaviours in males and females using elevated zero maze and contextual fear conditioning. Evaluating molecular markers associated with DNA damage signalling and senescence-related pathways revealed sex-specific differences attributed to BRCA1, where females exhibited elevated DNA damage, impaired DNA damage signalling, and dampened senescence onset compared to males. Overall, the results from this study highlight sex-specific consequences of aberrant DNA repair on outcomes post-injury, and further support a need to develop sex-specific treatments following rmTBI.

Three-Dimensional Bioprinting in Cardiovascular Disease: Current Status and Future Directions.

Three-dimensional (3D) printing plays an important role in cardiovascular disease through the use of personalised models that replicate the normal anatomy and its pathology with high accuracy and reliability. While 3D printed heart and vascular models have been shown to improve medical education, preoperative planning and simulation of cardiac procedures, as well as to enhance communication with patients, 3D bioprinting represents a potential advancement of 3D printing technology by allowing the printing of cellular or biological components, functional tissues and organs that can be used in a variety of applications in cardiovascular disease. Recent advances in bioprinting technology have shown the ability to support vascularisation of large-scale constructs with enhanced biocompatibility and structural stability, thus creating opportunities to replace damaged tissues or organs. In this review, we provide an overview of the use of 3D bioprinting in cardiovascular disease with a focus on technologies and applications in cardiac tissues, vascular constructs and grafts, heart valves and myocardium. Limitations and future research directions are highlighted.

Treatment patterns and outcomes of patients with locally advanced vulvar or vaginal cancer in British Columbia.

OBJECTIVE: As vulvar and vaginal cancers are rare malignancies, treatment is extrapolated from the cervical cancer field. Further studies are necessary to evaluate whether surgery, radiotherapy (RT), or combined chemoRT is most beneficial. METHODS: A retrospective chart review was conducted on patients diagnosed with vulvar or vaginal cancer in 2000-2017. Descriptive statistics was used to summarize demographic factors. Kaplan-Meier curves, log-rank tests, multivariate analysis with hazard ratios (HR) were conducted to compare survival outcomes, including overall survival (OS), disease-free survival, and cancer-specific survival, between surgery, RT, and chemoRT. RESULTS: This study included 688 patients with either vulvar (n = 560, 81%) or vaginal cancer (n = 128, 19%). Median age of diagnosis was 68 (27-98) years. In multivariate survival analysis, vulvar cancer was associated with more likelihood of death (HR: 1.50, p = 0.042) compared to vaginal cancer. For patients who received definitive RT, median OS was 63.8 months with concurrent chemotherapy vs. 46.3 months without for vulvar cancer (p = 0.75); for vaginal, median OS 100.4 with chemotherapy vs. 66.6 months without (p = 0.31). For vulvar cancer patients who received RT (n = 224), adding chemotherapy (n = 100) was not associated with statistically significant OS improvement (HR: 0.989, p = 0.957). Similarly, vaginal cancer patients who received chemoRT (n = 51) did not have significant OS benefit (HR: 0.720, p = 0.331) over patients who received RT (n = 49). CONCLUSIONS: In this retrospective study, chemoRT was not associated with significant improvements in survival compared to RT in vulvar or vaginal cancer. Future studies investigating novel therapies to treat these cancers are needed to improve patient outcomes.

Neurons and glial cells acquire a senescent signature after repeated mild traumatic brain injury in a sex-dependent manner.

Mild traumatic brain injury (mTBI) is an important public health issue, as it can lead to long-term neurological symptoms and risk of neurodegenerative disease. The pathophysiological mechanisms driving this remain unclear, and currently there are no effective therapies for mTBI. In this study on repeated mTBI (rmTBI), we have induced three mild closed-skull injuries or sham procedures, separated by 24 h, in C57BL/6 mice. We show that rmTBI mice have prolonged righting reflexes and astrogliosis, with neurological impairment in the Morris water maze (MWM) and the light dark test. Cortical and hippocampal tissue analysis revealed DNA damage in the form of double-strand breaks, oxidative damage, and R-loops, markers of cellular senescence including p16 and p21, and signaling mediated by the cGAS-STING pathway. This study identified novel sex differences after rmTBI in mice. Although these markers were all increased by rmTBI in both sexes, females had higher levels of DNA damage, lower levels of the senescence protein p16, and lower levels of cGAS-STING signaling proteins compared to their male counterparts. Single-cell RNA sequencing of the male rmTBI mouse brain revealed activation of the DNA damage response, evidence of cellular senescence, and pro-inflammatory markers reminiscent of the senescence-associated secretory phenotype (SASP) in neurons and glial cells. Cell-type specific changes were also present with evidence of brain immune activation, neurotransmission alterations in both excitatory and inhibitory neurons, and vascular dysfunction. Treatment of injured mice with the senolytic drug ABT263 significantly reduced markers of senescence only in males, but was not therapeutic in females. The reduction of senescence by ABT263 in male mice was accompanied by significantly improved performance in the MWM. This study provides compelling evidence that senescence contributes to brain dysfunction after rmTBI, but may do so in a sex-dependent manner.

High incidence of minor and micro breakpoints in Chronic Myeloid Leukaemia with additional cytogenetic abnormalities at diagnosis - the Western Australian series.

Introduction and objective: Chronic Myeloid Leukaemia (CML) is defined by the presence of the Philadelphia chromosome, a balanced translocation between chromosomes 9 and 22 that results in the constitutively active tyrosine kinase, BCR-ABL1. Additional chromosomal abnormalities (ACAs) at diagnosis occur in 5-10% of CML patients, and are important for prognosis. They are classified as major or minor route. The purpose of our study was to determine the frequency and type of ACAs in 193 newly diagnosed CML patients, and to evaluate patient characteristics, treatment response, and survival. Methods: Medical records, in conjunction with data from the PathWest cytogenetics and molecular laboratories, were analysed. Results: ACAs were present in 14 (7.3%) of patients at diagnosis. Seven patients had major-route abnormalities, with additional chromosome 8 (+8) the most common. All patients were treated with tyrosine kinase inhibitors (TKIs). Three patients presented in blast crisis; two patients have died. Of note, there was a high incidence of the rare minor and micro BCR-ABL1 fusion transcripts. Conclusions: Frequency of ACAs at diagnosis was similar to that of previous reports. These patients consist a higher-risk cohort, and require individualised treatment, with consideration of frontline and secondary TKIs, adjunct chemotherapy, novel agents, and allogeneic stem cell transplant.

Cellular Senescence in Traumatic Brain Injury: Evidence and Perspectives.

Mild traumatic brain injury (mTBI) can lead to long-term neurological dysfunction and increase one's risk of neurodegenerative disease. Several repercussions of mTBI have been identified and well-studied, including neuroinflammation, gliosis, microgliosis, excitotoxicity, and proteinopathy - however the pathophysiological mechanisms activating these pathways after mTBI remains controversial and unclear. Emerging research suggests DNA damage-induced cellular senescence as a possible driver of mTBI-related sequalae. Cellular senescence is a state of chronic cell-cycle arrest and inflammation associated with physiological aging, mood disorders, dementia, and various neurodegenerative pathologies. This narrative review evaluates the existing studies which identify DNA damage or cellular senescence after TBI (including mild, moderate, and severe TBI) in both experimental animal models and human studies, and outlines how cellular senescence may functionally explain both the molecular and clinical manifestations of TBI. Studies on this subject clearly show accumulation of various forms of DNA damage (including oxidative damage, single-strand breaks, and double-strand breaks) and senescent cells after TBI, and indicate that cellular senescence may be an early event after TBI. Further studies are required to understand the role of sex, cell-type specific mechanisms, and temporal patterns, as senescence may be a pathway of interest to target for therapeutic purposes including prognosis and treatment.

Breast cancer type 1 and neurodegeneration: consequences of deficient DNA repair.

Numerous cellular processes, including toxic protein aggregation and oxidative stress, have been studied extensively as potential mechanisms underlying neurodegeneration. However, limited therapeutic efficacy targeting these processes has prompted other mechanisms to be explored. Previous research has emphasized a link between cellular senescence and neurodegeneration, where senescence induced by excess DNA damage and deficient DNA repair results in structural and functional changes that ultimately contribute to brain dysfunction and increased vulnerability for neurodegeneration. Specific DNA repair proteins, such as breast cancer type 1, have been associated with both stress-induced senescence and neurodegenerative diseases, however, specific mechanisms remain unclear. Therefore, this review explores DNA damage-induced senescence in the brain as a driver of neurodegeneration, with particular focus on breast cancer type 1, and its potential contribution to sex-specific differences associated with neurodegenerative disease.

The effect of seasonal influenza vaccine on medically-attended influenza and non-influenza respiratory viruses infections at primary care level, Hong Kong SAR, 2017/18 to 2019/20.

Effectiveness of seasonal influenza vaccine (SIV) varies with the degree of matching with the vaccine and circulating viruses. We continued our SIV effectiveness against medically-attended influenza-like illness (ILI) under the Department of Health Hong Kong's sentinel private medical practitioners (PMP) network, using the test-negative case-control design, for the 2018/19 and 2019/20 season. In addition, we studied the potential interference between SIV and ILI caused by non-influenza respiratory viruses (NIRV) based on data collated from 2017/18 to 2019/20 seasons. 3404 patients were analysed. Across the 2017/18 to 2019/20 seasons, the vaccine effectiveness (VE) of SIV was 44% (95% CI 30-56%) against pan-negative controls, 57% (95%CI. 42-68%) against NIRV controls and 50% (95%CI 38-59%) against both. SIV was moderately effective against medically-attended ILI caused by influenza A/B in both 2018/19 and 2019/20 winter seasons (53.2% (95%CI 36.7-65.5%) and 41.8% (95%CI 6.3-64.1%), respectively). The VE against the main circulating subtype, influenza A(H1), was higher for the 2018/19 season (57.2% (95%CI 39.8-69.9%), compared to 34.6% (95%CI -9.6-61.4%) in the 2019/20 season). When compared to pan negative controls, those with single NIRV infections were similarly likely to have received SIV (OR 1.05 (95%CI 0.72-1.54) within the influenza season; OR 0.97 (95%CI 0.73-1.29) when including non-influenza seasons). Analyses by type of virus showed no increased risk of SIV identified among those with single infections of EV/RV, HMPV and parainfluenza but a 2-fold increased risk was shown for those with single infections of adenovirus and parainfluenza virus (adenovirus: OR 2.54 (95%CI 1.24-5.14) within influenza season and OR 1.78 (95%CI 1.01-3.09) for the whole period; parainfluenza virus: OR 2.01 (95%CI 1.22-3.29) within influenza season and OR 1.89 (95%CI 1.29-2.76) for the whole period). SIV programme and surveillance of influenza and NIRV, including SARS-CoV-2, should continue during the COVID-19 pandemic.

Puncta intended: connecting the dots between autophagy and cell stress networks.

Proteome profiling and global protein-interaction approaches have significantly improved our knowledge of the protein interactomes of autophagy and other cellular stress-response pathways. New discoveries regarding protein complexes, interaction partners, interaction domains, and biological roles of players that are part of these pathways are emerging. The fourth Vancouver Autophagy Symposium showcased research that expands our understanding of the protein interaction networks and molecular mechanisms underlying autophagy and other cellular stress responses in the context of distinct stressors. In the keynote presentation, Dr. Wade Harper described his team's recent discovery of a novel reticulophagy receptor for selective autophagic degradation of the endoplasmic reticulum, and discussed molecular mechanisms involved in ribophagy and non-autophagic ribosomal turnover. In other presentations, both omic and targeted approaches were used to reveal molecular players of other cellular stress responses including amyloid body and stress granule formation, anastasis, and extracellular vesicle biogenesis. Additional topics included the roles of autophagy in disease pathogenesis, autophagy regulatory mechanisms, and crosstalk between autophagy and cellular metabolism in anti-tumor immunity. The relationship between autophagy and other cell stress responses remains a relatively unexplored area in the field, with future investigations required to understand how the various processes are coordinated and connected in cells and tissues.Abbreviations: A-bodies: amyloid bodies; ACM: amyloid-converting motif; AMFR/gp78: autocrine motility factor receptor; ATG: autophagy-related; ATG4B: autophagy related 4B cysteine peptidase; CALCOCO2/NDP52: calcium binding and coiled-coil domain 2; CAR T: chimeric antigen receptor T; CASP3: caspase 3; CCPG1: cell cycle progression 1; CAR: chimeric antigen receptor; CML: chronic myeloid leukemia; CCOCs: clear cell ovarian cancers; CVB3: coxsackievirus B3; CRISPR-Cas9: clustered regularly interspaced short palindromic repeats-CRISPR associated protein 9; DDXs: DEAD-box helicases; EIF2S1/EIF-2alpha: eukaryotic translation initiation factor 2 subunit alpha; EIF2AK3: eukaryotic translation initiation factor 2 alpha kinase 3; ER: endoplasmic reticulum; EV: extracellular vesicle; FAO: fatty acid oxidation; GABARAP: GABA type A receptor-associated protein; ILK: integrin linked kinase; ISR: integrated stress response; MTOR: mechanistic target of rapamycin kinase; MPECs: memory precursory effector T cells; MAVS: mitochondrial antiviral signaling protein; NBR1: NBR1 autophagy cargo receptor; PI4KB/PI4KIIIß: phosphatidylinositol 4-kinase beta; PLEKHM1: pleckstrin homology and RUN domain containing M1; RB1CC1: RB1 inducible coiled-coil 1; RTN3: reticulon 3; rIGSRNAs: ribosomal intergenic noncoding RNAs; RPL29: ribosomal protein L29; RPS3: ribosomal protein S3; S. cerevisiae: Saccharomyces cerevisiae; sEV: small extracellular vesicles; S. pombe: Schizosaccharomyces pombe; SQSTM1: sequestosome 1; SF3B1: splicing factor 3b subunit 1; SILAC-MS: stable isotope labeling with amino acids in cell culture-mass spectrometry; SNAP29: synaptosome associated protein 29; TEX264: testis expressed 264, ER-phagy receptor; TNBC: triple-negative breast cancer; ULK1: unc-51 like autophagy activating kinase 1; VAS: Vancouver Autophagy Symposium.

What will it take? Using an implementation research framework to identify facilitators and barriers in implementing a school-based referral system for sexual health services.

BACKGROUND: Across the United States, sexually transmitted infections and unintended pregnancy rates are alarmingly high among youth. Schools, due to their proximity and access to youth, can increase student access to sexual health services (SHS) by creating referral systems (RS) to link students to school- and community-based SHS. From 2013 to 2018, the Centers for Disease Control and Prevention's Division of Adolescent and School Health funded 17 Local Education Agencies (LEA) to partner with priority schools and stakeholders to develop and implement RS to increase student access to SHS. Cicatelli Associates Inc. (CAI) was funded to provide capacity-building to LEA. In 2016-2017, CAI conducted case studies at two LEA, both large and urban sites, but representing different geographical and political contexts, to elucidate factors that influence RS implementation. METHODS: Nineteen LEA and community-based healthcare (CBH) staff were interviewed in the Southeastern (n = 9) and Western U.S. (n = 10). Key constructs (e.g., leadership engagement, resources, state and district policies) across the five domains of the Consolidated Framework for Implementation Research (CFIR) framework guided the methodology and analysis. Qualitative data was analyzed using the Framework Method and contextual factors and themes that led to RS implementation were identified. RESULTS: Interviewees strongly believed that school-based RS can decrease STI, HIV and unintended pregnancy and increase students' educational attainment. We identified the following contextual key factors that facilitate successful implementation and integration of an RS: enforcing state and district policies, strong LEA and CBH collaboration, positive school culture towards adolescent health, knowledgeable and supportive staff, leveraging of existing resources and staffing structures, and influential district and school building-level leadership and champions. Notably, this case study challenged our initial assumptions that RS are easily implemented in states with comprehensive SHS policies. Rather, our conversations revealed how districts and local-level policies can have significant impact and influence to impede or promote those policies. CONCLUSIONS: Through the use of the CFIR framework, the interviews identified important contextual factors and themes associated with LEAs' implementation barriers and facilitators. The study's results present key recommendations that other LEA can consider to optimize integration of RS-related evidence-based practices, systems, and policies in their districts.

Total Synthesis and Structural Establishment/Revision of Antibiotics A54145.

A54145 is a family of antibacterial cyclic lipodepsipeptides structurally resembling daptomycin. Since its discovery in 1990, only the ambiguous structures of the methoxy-aspartic acid (MeO-Asp) and the hydroxy-asparagine (HO-Asn) have been reported. We have developed efficient routes to obtain the fully protected l-MeO-Asp and l-HO-Asn building blocks compatible with Fmoc-SPPS, and a total synthesis of A54145 that enabled us to establish its structure, consisting of l-3S-HO-Asn and l-3R-MeO-Asp, revising the wrongly proposed structure of l-3S-MeO-Asp.

Nurse, Patient, and Care Partner Perceptions of a Personalized Safety Plan Screensaver.

A patient safety plan dashboard was developed that captures disparate data from the electronic health record that is then displayed as a personalized bedside screensaver. The dashboard aligns all care team members, including patients and families, in the safety plan. The screensaver content includes icons that pertain to common geriatric syndromes. In two phases, interviews were conducted with nurses, nursing assistants, patients, and informal caregivers in a large, tertiary care center. End user perceptions of the content and interface of the personalized safety plan screensavers were identified and strategies to overcome the barriers to use for future iterations were defined. Many themes were identified, ranging from appreciation of the clinical decision support provided by the screensavers to the value of the safety-centric content. Differences emerged stemming from each group of end users' role on the care team. All feedback will inform requirements for improvements to the personalized safety plan screensaver. [Journal of Gerontological Nursing, 43(4), 15-22.].

Genome-wide association study of behavioral, physiological and gene expression traits in outbred CFW mice.

Although mice are the most widely used mammalian model organism, genetic studies have suffered from limited mapping resolution due to extensive linkage disequilibrium (LD) that is characteristic of crosses among inbred strains. Carworth Farms White (CFW) mice are a commercially available outbred mouse population that exhibit rapid LD decay in comparison to other available mouse populations. We performed a genome-wide association study (GWAS) of behavioral, physiological and gene expression phenotypes using 1,200 male CFW mice. We used genotyping by sequencing (GBS) to obtain genotypes at 92,734 SNPs. We also measured gene expression using RNA sequencing in three brain regions. Our study identified numerous behavioral, physiological and expression quantitative trait loci (QTLs). We integrated the behavioral QTL and eQTL results to implicate specific genes, including Azi2 in sensitivity to methamphetamine and Zmynd11 in anxiety-like behavior. The combination of CFW mice, GBS and RNA sequencing constitutes a powerful approach to GWAS in mice.

A simplified method for quantifying cell migration/wound healing in 96-well plates.

Cell migration plays a key role in both normal physiological and pathological conditions. The study of cell migration and its underlying mechanisms is of great significance in various fields of research, including basic biology and pharmaceutical development. The cell migration or scratch wounding assay is an easy and economical in vitro method that allows researchers to assess a large number of testing compounds. Even though this simple assay has been used for decades, researchers are still trying to modify such experimental protocols and wounding devices. In this study, an 8-channel mechanical "wounder" was designed for performing a cell migration assay, particularly in a 96-well culture plate format. With special designs of a guiding bar and adjustable pins for use with disposable pipette tips, this wounder confined the scratch area within the center of each well to ensure a perfect contact between the pins and the well surface. As a result, this mechanical wounder produces a uniform denudation of a cell monolayer in a 96-well plate with a wound size of around 600 microm. Using this improved wounding device, the effects of epidermal growth factor and DL-alpha-difluoromethylornithine on the reepithelialization of rat intestinal epithelial cells (IEC-6) and serum on the wound recovery of human umbilical vein endothelial cells were demonstrated. This wounder facilitates cell migration study and can be applicable for multiple sample analysis.