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DNA double-strand breaks (DSBs) are the most severe DNA damage, and defective repair can lead to apoptosis or malignant transformation. DSBs are mainly repaired by nonhomologous end joining (NHEJ) and homologous recombination (HR), while microhomology-mediated end joining (MMEJ) serves as a backup pathway. Since DNA polymerase theta (Polθ) is essential for MMEJ, this pathway is also named Polθ-mediated end joining. Polθ is barely expressed in normal tissues but overexpressed in many cancers, making it a promising therapeutic target. In recent years, Polθ inhibitors and related therapeutic strategies have emerged rapidly, with clinical trials underway. This review summarizes the structure, function and expression of Polθ in tumorigenesis, highlights synthetic lethal strategies, drug development and clinical translation, and discusses current limitations and future directions for cancer research. Polθ-mediated microhomology-mediated end joining (MMEJ) promotes genomic instability and facilitates mutation accumulation, thereby leading to cancer initiation and progression.Polθ expression is significantly upregulated in various cancer types and markedly correlates with cancer prognosis.DNA damage repair pathways and some proteins can regulate Polθ expression and mediated microhomology-mediated end joining (MMEJ) activity in cancer.Polθ inhibitor have appeared sequentially and clinical trials targeting Polθ are being gradually launched.Polθ is a highly attractive therapeutic target and synthetic lethal strategies targeting Polθ in cancer have been continuously explored.

SPO11 forms hundreds of double-strand breaks (DSBs) to initiate meiotic recombination that is normally error-free. However, SPO11 activity can be mutagenic when one chromatid incurs closely spaced DSBs (double cuts), especially when DSBs are dysregulated by loss of the ATM kinase. De novo indels and structural variants can arise via end joining at double cuts within a single hotspot (microdeletions) or at adjacent hotspots separated by at least 30 kb, as we now show, sometimes accompanied by ectopic insertions of double-cut fragments. Here, we investigate how meiotic DSB end processing influences end joining. In MRE11-deficient mouse spermatocytes, which do not resect their DSBs, deletions at double cuts occur readily, with end-joining breakpoint profiles closely matching SPO11 DSB profiles. Microdeletions suggest that two DSBs can be as close as ∼21 bp. The tyrosyl-DNA phosphodiesterase TDP2 contributes to both deletion formation and ectopic insertion of double-cut fragments, presumably by removing SPO11 from DNA ends prior to joining. Finally, observations suggest a cooperative role for MRE11 and ATM in locally regulating DSB distributions. Our findings provide insight into the mechanism of de novo mutation origin, emphasizing the role of meiotic DSBs in shaping genome evolution.

Discontinuation of infertility care without achieving a still-desired pregnancy represents a potential failure to meet patient needs and indicates healthcare system inefficiencies. While specific reasons for premature treatment cessation are documented in various populations, no study has extensively examined its prevalence or drivers within the Military Health System (MHS). This study identifies predictors and reasons for early discontinuation among active-duty servicewomen (ADSW), whose unique sociodemographic circumstances influence how and where fertility care is accessed and sustained. This cross-sectional secondary analysis used data from 3281 ADSW who received infertility services or treatments within the MHS, with a weighted response rate of 17.8%. We evaluated military and demographic characteristics, alongside care-related variables such as clinical setting, payment source, out-of-pocket expenses, care received both within and outside the MHS and unmet need for fertility services since joining the military. The outcome of the study was discontinuation of infertility treatments before achieving a desired pregnancy. A weighted binary logistic regression model calculated adjusted ORs (aORs) with 95% CIs to identify predictors of discontinuation before achieving pregnancy. The prevalence of early discontinuation among ADSW who received infertility services or treatments within the MHS was 28.2% (95% CI 26.2% to 30.2%). Factors that were related to early treatment cessation included: educational attainment of high school or less (aOR: 1.40, 95% CI 1.04 to 1.89), age 35-44 years (aOR: 1.33, 95% CI 1.07 to 1.65), receiving care both within and outside the MHS (aOR: 1.52, 95% CI 1.22 to 1.90), incurring out-of-pocket expenses (aOR: 1.31, 95% CI 1.04 to 1.65) and having an unmet need for fertility services since joining the military (aOR: 1.37, 95% CI 1.12 to 1.67). To minimise early treatment discontinuation, the MHS should expand reproductive services to more facilities, integrate standardised psychological support and conduct qualitative research to explore uncaptured reasons for ADSW to discontinue care.

Civil society organisations (CSOs) can play an important role in crisis management and facilitate effective communication and crisis response. To improve capacity for intercultural health communication in future health crises, it is crucial to learn from CSOs' experiences during the COVID-19 (SARS-CoV-2) pandemic and from their cooperation with healthcare systems. This study aims to gain insights into CSOs' experiences of intercultural health communication during the pandemic in two disadvantaged areas in Stockholm, Sweden. We also wanted to explore healthcare staff's experiences of collaboration with CSOs. We conducted a qualitative thematic analysis of interviews with informants from 15 CSOs with substantial local pandemic activity. Additionally, we conducted a secondary analysis of qualitative interview data from 21 informants involved in delivering intercultural health crisis communication during the pandemic. CSOs emphasised the importance of effective and trusted communication, which requires more than translation. They highlighted the need for a deep understanding of how language, cultural frameworks and lived experiences shape the reception of public health messages. From the perspective of healthcare staff, the collaboration with CSOs was both necessary and transformative. The partnership with CSOs was a process of "joining forces, "in which mutual learning and shared responsibility strengthened the overall intercultural communication strategy. In times of crisis, CSOs have the capacity to act as community-based knowledge brokers by strengthening trusted, understandable intercultural communication and fostering a sense of community. However, CSOs are not just an extension of the public health authorities, but independent actors with a unique ability to communicate and build trust. Collaborative structures between CSOs and healthcare need to be firmly established well ahead of future health crises. Our results emphasise the importance of culturally and linguistically adapted communication as an integral part of inclusive crisis communication. These findings position CSOs as community-engagement actors in inclusive emergency preparedness.

Bassaricyon (Carnivora, Procyonidae) is a little-known group of small Neotropical carnivores from central and northern South America. Despite their charismatic nature, they are difficult to spot in the field, and they are confused with another procyonid, the kinkajou. This poorly studied genus comprises four species: B. gabbii, B. alleni, B. medius, and B. neblina, the latter with two subspecies. In this study, the genetic diversity of Bassaricyon from eastern Amazonia was explored based on the mitochondrial gene cytochrome b. A maximum-likelihood analysis confirms the taxa recognized at the species and subspecies levels and shows that populations from the Guiana Shield (GS) are well structured relative to the lineage from western Amazonia (WA), with genetic distances among them comparable to those of other Bassaricyon subspecies. A median-joining network showed five median vectors between B. alleni lineages, more than between B. medius and B. neblina subspecies (n = 1); additionally, there are at least 10 nucleotide substitutions between them, suggesting a considerable difference between these lineages. In the last review of the genus, the estimated divergence time between B. alleni from western Amazonia and Guiana Shield was slightly less than that between B. neblina and B. medius subspecies, suggesting less time to differentiate. We collected Potos flavus in the two municipalities sampled; however, in different localities, suggesting different habitat specificities. These results, together with morphological differences among B. alleni lineages, suggest a subspecies taxonomic status for the Guiana Shield population, B. alleni beddardi.

Aberrant activation of DNA damage repair (DDR) pathways drives therapeutic resistance in cancer. Although Chromatin Assembly Factor 1 subunit A (CHAF1A) is well characterized for its role in chromatin assembly, its specific function in the DNA damage response has remained poorly defined. Here, we demonstrate that CHAF1A functions as a key regulator of DNA repair and radioresistance. Upon DNA double-strand breaks, CHAF1A is rapidly recruited to damage sites in an ATM-associated manner. Intriguingly, CHAF1A recruitment further enhances ATM phosphorylation and amplifies the DNA damage signal. Consequently, depletion of CHAF1A compromises the efficiency of both homologous recombination (HR) and non-homologous end joining (NHEJ). Mechanistically, CHAF1A governs repair pathway utilization in a cell cycle-dependent manner: during S phase, CHAF1A interacts with RAD51 in collaboration with PCNA, promoting the loading of RAD51 at DNA damage sites; whereas in non-S-phase cells, CHAF1A preferentially promotes the recruitment of KU70 to support NHEJ. Functionally, silencing CHAF1A markedly enhances tumor radiosensitivity, as robustly validated in cell-derived xenograft models and supported by proof-of-concept evidence from a patient-derived xenograft model. Collectively, our findings establish CHAF1A as a pivotal regulator of DNA damage repair in lung cancer models and position it as a promising therapeutic target for overcoming radioresistance. Cancer cells often become resistant to radiotherapy by repairing the DNA damage that radiation causes. In this study, we discovered that a protein called CHAF1A plays a key role in helping cancer cells repair this damage and survive radiation treatment. Using cell experiments, genetic approaches, and mouse tumor models—including tumors derived directly from patients (as a proof-of-concept)—we found that CHAF1A is recruited to sites of DNA damage and activates two major DNA repair pathways depending on the cell cycle stage. When we blocked CHAF1A, cancer cells became much more sensitive to radiation, and tumors shrank significantly more after treatment. These findings suggest that targeting CHAF1A could be a promising new strategy to make radiotherapy more effective for cancer patients, potentially improving treatment outcomes and reducing the chance of cancer returning after radiation therapy.

DNA double-strand breaks (DSBs) that occur during mitosis are primarily repaired by Polθ-mediated microhomology-mediated end joining (MMEJ). The CIP2A-TOPBP1 complex has been shown to tether broken chromatin at mitotic DSBs, but whether it coordinates with or functions independently of Polθ remains unknown. Here, we show that the CIP2A-TOPBP1 complex is recruited to mitotic DSB sites, where it directly interacts with Polθ and corecruits Polθ to chromatin. CIP2A sustains Polθ phosphorylation by inhibiting PP2A, thereby prolonging Polθ chromatin retention and enabling efficient repair. Upon repair completion, the CIP2A-TOPBP1 complex dissociates, PP2A dephosphorylates Polθ, and Polθ is released from chromatin. Loss of CIP2A impairs tumor growth, while disruption of CIP2A-Polθ binding leads to persistent DNA damage, micronucleus formation, and synthetic lethality in BRCA1/2-deficient cells. These findings uncover a cooperative mechanism by which CIP2A-TOPBP1 dynamically regulates Polθ in mitotic DSB repair and provide insights into the synthetic lethal interaction of CIP2A with BRCA1/2 under radiotherapy.

Radiation-resistant microorganisms that survive high doses of ionising radiation serve as valuable models for understanding stress adaptation; however, the genomic determinants underlying extreme radiation tolerance in bacteria from natural environments with high background radiation remain insufficiently characterised. Bacterial isolates from the Chavara-Neendakara HBRA (Kerala, India) were evaluated for desiccation tolerance, and the desiccation-resistant isolates were subsequently exposed to gamma irradiation (1-10 kGy) using a 60Co source. Isolates were identified through 16S rRNA sequencing, morphologically characterised by FE-SEM, and screened for antibiotic susceptibility. The highly radiation-resistant strain underwent whole-genome sequencing via Oxford Nanopore Technology, with De novo assembly, polishing, and genome annotation. Four bacterial isolates (Micrococcaceae and Paenibacillaceae) exhibited D10 values of 1-7 kGy, including one multidrug-resistant strain; no endospores were observed in the Paenibacillus isolate under the tested conditions. Paenibacillus sp. HBRA004 survived 10 kGy gamma radiation, exceeding all previously reported HBRA isolates by over fourfold. Its 5.0 Mbp genome (GC = 48.27%, ≥ 99% completeness) encodes five mechanistically independent DNA repair pathways; homologous recombination (recA, recN, radA), base excision repair (mutM, mutY, mutT), mismatch repair (mutL, mutS), nucleotide excision repair (uvrA, uvrB, uvrD), and non-homologous end joining (ku, ligD), alongside a redundant antioxidant network comprising triple-copy Fe/Mn-family superoxide dismutases and ahpC peroxiredoxin. A thioredoxin system (trxA, trxB, msrA) and manganese uptake via mntH may contribute to further layers of ROS defence. Their specific contribution to the HBRA004 phenotype remains to be experimentally and comparatively validated. These findings represent the first genomically characterised 10 kGy-resistant bacterial isolate from the Chavara-Neendakara HBRA, establishing a new benchmark for radiation tolerance within this ecologically significant environment. Pathway depth, gene copy amplification, and Mn/Fe homeostasis appear to be candidate mechanisms contributing to high-level radiation tolerance, consistent with patterns in other radiation-resistant taxa, though their contribution requires functional validation.

Physical activity engagement can improve wellbeing and social participation for individuals living with long-term neurological conditions. Student-led services enable healthcare access for those clinically underserved and increase student clinical opportunities. Furthermore, attendees become important facilitators of student learning. UMove is a free undergraduate physiotherapy student-led physical activity program aimed at improving wellbeing for people living with long-term neurological conditions. Its ongoing nature is unique for a physical activity program, with some attendees coming for over 12 years. Student experiences within physiotherapy student-led programs are well-documented, however, those of attendees, particularly those with long-term neurological conditions, remain underexplored. The primary objective was to explore the experiences of long-term UMove attendees. Secondary objectives included identifying perceived benefits and barriers to participation, and evaluating whether and how UMove affected attendees' wellbeing. Participants were 11 adults with a long-term neurological condition attending UMove for over one year. Employing Interpretive Description qualitative methodology, individualized interviews were semi-structured, audio-recorded, transcribed verbatim, and analyzed. Questions included experiences, reasons for joining, and perceived barriers and motivators to attendance. The key theme, "Valuing UMove," epitomized the value participants placed not only on this accessible program but their work with students. The flexible, tailored program met diverse and evolving needs of attendees ("Person-Centered Care"). Opportunities for social interaction with other attendees and students facilitated meaningful social connection and a sense of community, driving adherence and engagement ("Connection Conundrum" and Wise Participation). "Challenges and Improvements" highlighted improvements that could be made. Participants had positive experiences and valued the opportunities UMove provided them which went beyond physical activity to include socialization and supporting student learning.

In Canada, HIV stigma remains a persistent barrier to equitable access to health and social-services, particularly for racialized immigrants-such as African, Caribbean, and Black communities (ACB)-who remain structurally exposed to new HIV infections amidst insufficient policy attention to their distinct health needs and challenges. To bridge the knowledge-practice gap in addressing HIV-related stigma in Canada, this intervention study engaged service organizations and providers in a multi-phase implementation across Ontario and Alberta. Qualitative insights from post-intervention activity logs revealed three main areas of impact: (1) Structural reforms: Service providers are advocating for and revising organizational policies to enhance inclusivity, challenging discriminatory language and practices, organizing trainings on unconscious bias and HIV stigma, coordinating with law enforcement agencies and engaging in political mobilization to address selective criminalization of racialized immigrants for status non-disclosure; (2) Community empowerment: The service providers began engaging and educating affected communities about HIV stigma, and fostering collective empowerment against social injustices. While some are volunteering with legal aid organizations to help racialized immigrants navigate disputes, others are joining charity organizations to set up donation centres to support racialized community members; and (3) Personal and professional growth: Providers reported acknowledging the privileges they enjoy as non-racialized individuals, becoming more intentional in addressing their personal biases, and ensuring inclusive practices in service delivery. In conclusion, sustained, community-informed implementation efforts are crucial for addressing entrenched inequities and ensuring a more inclusive, just, and effective HIV response for racialized immigrant populations in Canada.

Antibody diversity is generated through stochastic rearrangement of the immunoglobulin heavy chain locus (Igh) involving the recombination of variable (VH), diversity (DH) and joining (JH) gene segments. How coding elements within the Igh locus locate one another in the complex nuclear environment is not understood. Here, we sought to identify the molecular mechanisms and physical principles that govern VH-DHJH genomic encounters. We found that transcription imposed a local confinement that stabilized interactions between spatially proximal genomic elements. The loop anchor CTCF modestly constrained population-average chromatin motion, whereas cohesin-mediated loops established large-scale confinement and reinforced self-similarity of VH-DHJH motion across spatial and temporal scales. Quantitative scaling arguments for first-passage times revealed that encounter frequencies between remote VH-DHJH genomic regions are governed by the interplay of diffusivity and spatial proximity. Together, these findings show that the hierarchy of confinements imposed by transcription and loop extrusion provides the balance between stability and mobility required to regulate genomic encounter frequencies.

Understanding Human papillomavirus (HPV) oncogenic mechanisms is essential for developing preventive and therapeutic strategies and overcoming therapy resistance in HPV-related cancers. These challenges may arise from the ability of high-risk HPV to subvert host tumor suppressors such as p53 and Rb, and to drive oncogenesis through homologous recombination deficiency (HRD) and multi-network dysregulation. Mechanistically, HPV exerts context-dependent effects on the host DNA damage response (DDR). During episomal replication, E6/E7 activate DDR and recruit BRCA1/RAD51 to replication foci to support viral replication without significantly compromising host HR repair. Upon viral integration, however, sustained E6/E7 expression drives HRD and shifts DNA repair toward error-prone end joining, generating genomic instability that fuels malignant transformation. These alterations are most clearly established in cervical cancer, whereas evidence in HPV-positive non-cervical cancer is more variable and requires further context-specific validation. In parallel, HPV E6/E7 antagonize transforming growth factor-β (TGF-β)-mediated tumor suppression and, potentially through FAT Atypical Cadherin 4 (FAT4) down-regulation, engage Wnt/β-catenin signaling. The resultant elevation of nuclear β-catenin induces programmed death-ligand 1 (PD-L1) expression promotes immune evasion, stemness, and invasiveness. Of note, while the DDR-TGF-β-β-catenin-PD-L1 axis is backed by substantial evidence in HPV-related cancers, certain connections within this pathway are extrapolated from non-HPV models or general pathway biology and are explicitly denoted as such in the main text. With residual p53 activity, HRD may confer initial sensitivity to DNA-damaging agents, but resistance frequently develops-a pattern reminiscent of the initial response followed by acquired resistance observed with immunotherapies in HPV-related cancers. Integrating these mechanistic insights, we propose ablative therapies (e.g., ablation, photodynamic therapy, surgery) for cervical intraepithelial neoplasia (CIN), and for advanced or resistant disease, a synthetic-lethality framework combining genotoxic therapies with DDR inhibitors, targeting DDR-TGF-β-β-catenin-PD-L1 axis, and antiviral approaches. The proposed therapeutic strategies, however, should be interpreted with caution, as their evidence base varies across tumor types and warrants further investigation.

This review article provides a comprehensive analysis of the synthesis, properties, and applications of Ti3SiC2 and Ti2AlC phases. It begins with an overview of the synthesis techniques for these materials, including bulk, thin film, and powder forms. Subsequently, it delves into their polymorphism, phase stability, the electrical, thermal, and elastic properties, as well as hardness, machinability, deformation, fracture, fatigue, creep, oxidation, corrosion, and friction and wear. Additionally, the review covers the advancements in composite materials, surface technologies, joining techniques, and carbide-derived carbon (CDC) based on these phases. Finally, the article suggests future research directions that aimed at guiding and inspiring further studies in the field of material sciences.

Genetic profiling of a new HPV-negative cervical cancer model identified pathogenic variants in genes implicated in oncogenic signaling, cell cycle regulation, and DNA damage repair pathways, including homologous recombination, non-homologous end-joining, and mismatch repair. Deficiencies in BRCA2, RAD51 and MLH1 were among these actionable targets. The newly described cervical cancer model revealed sensitivity towards the PARP inhibitor olaparib, which was further augmented upon combination with platinum-based chemotherapeutics. In contrast, BRCA1/2-proficient cervical cancer cells exhibited greater resistance to these strategies. This study highlights the potential of in-depth genetic analysis to identify genetic susceptibilities to guide personalized medicine approaches.

To evaluate a support structure for women victims of violence from the perspective of the survivors themselves. We conducted semi-structured interviews with 17 women attending a Maison des Femmes (MdF), a hospital-based multiprofessional structure providing medical, psychological, social, and legal support to women victims of violence, within a model currently being scaled up nationally in France. When enrolling in the MdF, participants reported seeking safety and support and expecting a therapeutic relationship tailored to their individual needs. They valued access to a wide range of professionals, coordinated by a single trusted interlocutor responsible for their care pathway. Overall, participants reported improved well-being since initiating MdF care. Experiences of group therapy were mixed: some participants described it as fostering supportive social interactions (n = 12), whereas others felt outperformed by other group members (n = 5), leading to feelings of discouragement. Frustration arose from unmet needs related to housing and income support, the slow pace of legal proceedings, and long waiting times for appointments within the structure. When considering the planned end of care, typically after 6-12 months, participants expressed uncertainty and fear of losing a vital source of support. Although women survivors of violence reported improved well-being after joining the MdF, persistent unmet social and legal needs and anxiety surrounding the end of care were identified. These findings highlight the importance of early information and anticipatory planning regarding care duration and post-discharge support.

Radiation therapy (RT) cures many patients with localized prostate cancer, but late urinary toxicity impairs quality of life and can limit dose escalation for better RT efficacy. Understanding the mechanistic bases of radiation toxicity is critical for designing effective treatment strategies to benefit prostate cancer survivors. Genome-wide association studies (GWAS) have shown that genetic susceptibility can influence toxicity risk. A GWAS of reduced urinary stream two years after RT identified rs7720298 tagging a risk locus, but the mechanism through which this SNP acts is unclear. We performed integrative bioinformatics and molecular studies that identified a nearby long non-coding RNA, LncDNAH5, whose expression is influenced by rs7720298 in human tissues, and we hypothesized it mediates RT responses. In cultured cells, LncDNAH5 suppressed the DNA repair factor TP53BP1, thus favoring homologous recombination (HR) over non-homologous end joining (NHEJ). Mechanistically, LncDNAH5 enhanced MDM2-dependent ubiquitination and degradation of TP53BP1 by promoting formation of an MDM2-TP53BP1 complex; MDM2 antagonist Nutlin-3 attenuated these effects. In vivo, a bladder-specific LncDNAH5 overexpression mouse model exhibited exacerbated RT-induced inflammatory and fibrotic responses, consistent with a heightened urothelial radiosensitivity. Together, these data support a rs7720298/LncDNAH5/MDM2/TP53BP1 axis that modulates DNA repair choice and tissue response to radiation. Clinically, LncDNAH5 expression and rs7720298 genotype may serve as complementary biomarkers to identify patients at risk for late urinary toxicity and to guide early intervention and personalized radioprotective strategies for better patient outcomes.

In 2024, there was an increase from the previous year in the number of births in South Dakota with 11,434 new babies joining the state's population. Among this birth cohort, 71% were White, 12% American Indian, 9% Hispanic, 3% Black, and 5% other races. Over recent years, a declining percent of this annual cohort is White or American Indian with other racial groups increasingly contributing to the births in the state. South Dakota's 2023 birth and fertility rates were the highest of the nation. These state rates also showed that compared to all other races, Whites also had the lowest rates of fertility in South Dakota. The state's infant mortality rate (IMR) is increased in 2024 (7.35) from the previous year (5.36) with increases in both the neonatal and post neonatal rates that occurred in only the White/Hispanic population. Five-year (2020-24) data, however, show that 71% of births are White yet they contribute to 51% of infant deaths; dissimilar to American Indians who comprise 13% of births yet contribute to 30% of all infant deaths. Almost a quarter (23%) of all infant deaths in the state are caused by sudden unexpected infant death (SUID) with a rate that is statistically significantly higher (p<.01) than what is observed nationally. Further, data show that the state's rate of SUID is not decreasing and there also has been an increasing percent of these deaths having potentially preventable risks associated with them. Overall, the state's 2020-24 total IMR (7.03) and post neonatal mortality rate (2.03) were significantly higher (p<.01) than the 2023 rates (5.6; 1.96) for the nation.

We report our experience with Holmium Laser Ablation (HOLA) of posterior urethral valves (PUV) in preterm newborns. After stabilization under anesthesia, in lithotomy position, using a 4.5/6.5 compact cystoscope (Richard Wolf) & 365-micron fibre, laser was applied at 2 J/10 Hz for HOLA. The valve leaflets were divided by short bursts of laser energy (video) joining the dots to provide complete clearance. A repeat VCUG and cystoscopy was performed in all patients after 3-6 months to confirm clearance. All patients were followed up for a median duration of 5 years (range 3-9 years). Biochemical, radiological and bladder parameters were followed up. Between 2015 and 2025, 22 neonates; median gestation 34 weeks; [32,36] underwent HOLA of PUV. Successful clearance of PUV was achieved in 20/22 neonates (90.9%), as confirmed by repeat VCUG/cystoscopy. Renal function improved significantly (p = 0.001), with the median (IQR) creatinine level decreasing from 2.6 (1,3) pre-fulguration to 0.9 (0.7,1.2) at the one-year follow-up. Upper tract dilatation persisted in seven, subsequent urodynamic evaluation identified bladder; all were successfully managed with anticholinergic medication. HOLA of PUV is feasible in preterm neonates with acceptable short-term complication profile, and without apparent excess morbidity in this small cohort.