Feedback based gas sensing setup for ppb to ppm level sensing.

Sensing and quantification of gas at low concentrations is of paramount importance, especially with highly flammable and explosive gases such as hydrogen. Standard gas sensing setups have a limit of measuring ultra-low concentrations of few parts per billion unless the external gas cylinders are changed to ones with low concentrations. In this work, we describe a home-built resistance based gas sensing setup that can sense across a wide concentration range, from parts per billion to parts per million, accurately. This was achieved using two dilution chambers: a process chamber and a feedback assembly where a part of the output gas from the dilution chamber is fed back to the inlet mass flow controller, enabling enhanced dilutions without increasing the number of mass flow controllers. In addition, the gas-sensing setup can measure across a large temperature range of 77-900 K. The developed setup was then calibrated using palladium thin films and ZnO nanoparticle thin films. The setup was tested for reproducibility, concentration response, temperature response, etc. Corresponding sensitivity values were calculated and found to be in good agreement with published values, validating our setup design.

Percutaneous CT-guided radiofrequency ablation of osteoid osteoma: Potential Pitfalls and complications and how to avoid them.

Targeted cannulation of the nidus and subsequent thermal ablation is the basis of CT-guided radiofrequency ablation (RFA) of osteoid osteoma, which is considered nowadays as the treatment of choice. The majority of complications during this procedure are due to thermal injury of adjacent structures. Specific measures as per the anatomical location of osteoid osteoma can avoid the majority of complications. This article enlists the possible complications and their necessary precautions and remedies to avoid these complications during CT-guided radiofrequency ablation of osteoid osteoma.

Transient hypothyroxinemia of prematurity and its risk factors in an extramural neonatal intensive care unit

ABSTRACT Objective: Thyroid functions in preterm newborns may be altered in the first week of life. Hypothyroxinemia has been commonly reported in these babies, which could be due to the immaturity of the hypothalamic pituitary thyroid axis or acute illness. It could have a long-term impact on the developing brain of these babies. We conducted this study to estimate the incidence of transient hypothyroxinemia of prematurity (THOP) and to determine its risk factors. Materials and methods: We analyzed thyroid stimulating hormone (TSH) and free T4 levels of 64 preterm neonates admitted in the neonatal intensive care unit. TSH and free T4 levels were measured in the first week and then at 14-21 days of life to estimate the incidence of THOP and determine its risk factors. We also estimated the incidence of congenital hypothyroidism (CH) and delayed TSH elevation in CH. Risk analysis was conducted using simple and multiple logistic regression, and numerical data was compared using the Mann Whitney U test and t test. Results: THOP was seen in 25% of the preterm babies. Caesarean delivery, presence of one or more morbidities, mechanical ventilation, birth weight ≥ 1,500 g, and gestational age ≥ 32 weeks were identified as risk factors for THOP based on simple logistic regression. In multiple regression, mechanical ventilation and gestational age ≥ 32 weeks were significantly associated with THOP. CH was seen in 2 (3.1%) babies, and 1 of these cases had delayed TSH elevation. Conclusion: Thyroid abnormalities are common in preterm admitted neonates. Mechanical ventilation is an independent risk factor for development of THOP.

Oral and Esophageal Cancer: Incidence, Prevalence and Correlation in General Indian Population: A retrospective Study.

BACKGROUND: Squamous cell carcinoma is the most frequent head-and-neck malignancy and chiefly encompasses malignancies of the upper aerodigestive tract, including the oral cavity, nasal cavity, paranasal sinuses, nasopharynx, oropharynx, hypopharynx, pharynx, and larynx. OBJECTIVES: The current study was conducted to evaluate the incidence, prevalence, and correlation of oral and esophageal cancer in the Indian population. MATERIALS AND METHODS: The present study was conducted on the basis of data collected from various government cancer hospitals in India. A total of 1000 patients of either sex admitted to the oncology ward with head-and-neck cancer from June 2018 to June 2020 were included in the study. Information regarding family history, deleterious habits, and immunity status was also collected from their medical records. The readings were recorded in a master chart, and data analysis was carried out statistically. RESULTS: A total of 1000 patients (617 males and 383 females) between the age range of 38 and 86 years were selected for the study. A total of 425 out of 1000 patients had esophageal cancer, whereas, 575 patients had oral cancer. A total of 347 males and 228 females had oral cancer, whereas 270 males and 155 females had esophageal cancer. Among the patients with oral cancer, 44 presented with a history of cigarette smoking, 49 with bidi smoking, 140 with tobacco chewing, 142 with gutkha chewing, and 159 with betel quid chewing. Majority of the patients had a habit of consuming tobacco in smokeless form. Among the patients with esophageal cancer, 175 presented with a history of cigarette smoking, 136 with bidi smoking, 12 with tobacco chewing, 13 with gutkha chewing, and nine with betel quid chewing. CONCLUSION: The incidence of both types of cancer was high in older age group, particularly in those aged above 50 years. Males had a higher predilection rate than females for both cancer types. The incidence of oral cancer was higher than that of esophageal cancer. Majority of the patients with oral cancer had a history of tobacco consumption in smokeless form, whereas the ones with esophageal cancer reported with a history of tobacco consumption in smoked form.

Comparative analysis of CT guided vertebral biopsy by a conventional bone biopsy needle versus bone biopsy needle with acquisition cradle.

BACKGROUND: We aimed to compare the rate of diagnostically successful vertebral biopsies using conventional bone biopsy needles versus those performed with bone biopsy needles with an acquisition cradle. METHODS: We retrospectively analyzed the data of patients who underwent CT-guided vertebral biopsy between December 2017 to December 2019 at our institute. From December 2017 to November 2018, the procedure was performed on 185 patients using an 11G conventional bone biopsy needle, Jamshidi needleTM "(group 1)". From December 2018 to December 2019, the procedure was performed on 242 patients using an 11G T-handle Jamshidi needle with an acquisition cradle "(group 2)". We reviewed their histopathological reports for both groups of patients to determine the rate of diagnostically successful biopsies. We also compared the crush artifact amongst the unsuccessful biopsy samples acquired by the two types of biopsy needles. RESULTS: 427 patients (270 male and 157 female patients; mean age, 46.4 years; age range, 25-67 years) who underwent CT-guided vertebral biopsy from December 2017 to December 2019 were included in our study. In group 1, diagnostic success was achieved in 136 out of 185 biopsies (73.5%); whereas in group 2, diagnostic success was achieved in 219 out of 242 biopsies (90.50%), p < 0.0001. Out of the diagnostically unsuccessful biopsies in Group 1, 36 out of 49 (73.5%) were due to crush artifact; whereas crush artifact accounted for only 3 out of 23 (13.0%) diagnostically unsuccessful biopsies in group 2, p < 0.0001. Other causes of unsuccessful biopsies (hemorrhagic contents or presence of normal osseous tissue and fibrin only) were statistically insignificant. CONCLUSION: The use of a T-handle Jamshidi needle with an acquisition cradle appears beneficial compared to the conventional Jamshidi needle in terms of the significantly higher rate of diagnostic success and a lower rate of crush artifact.

Autism-Associated Vigilin Depletion Impairs DNA Damage Repair.

Vigilin (Vgl1) is essential for heterochromatin formation, chromosome segregation, and mRNA stability and is associated with autism spectrum disorders and cancer: vigilin, for example, can suppress proto-oncogene c-fms expression in breast cancer. Conserved from yeast to humans, vigilin is an RNA-binding protein with 14 tandemly arranged nonidentical hnRNP K-type homology (KH) domains. Here, we report that vigilin depletion increased cell sensitivity to cisplatin- or ionizing radiation (IR)-induced cell death and genomic instability due to defective DNA repair. Vigilin depletion delayed dephosphorylation of IR-induced γ-H2AX and elevated levels of residual 53BP1 and RIF1 foci, while reducing Rad51 and BRCA1 focus formation, DNA end resection, and double-strand break (DSB) repair. We show that vigilin interacts with the DNA damage response (DDR) proteins RAD51 and BRCA1, and vigilin depletion impairs their recruitment to DSB sites. Transient hydroxyurea (HU)-induced replicative stress in vigilin-depleted cells increased replication fork stalling and blocked restart of DNA synthesis. Furthermore, histone acetylation promoted vigilin recruitment to DSBs preferentially in the transcriptionally active genome. These findings uncover a novel vigilin role in DNA damage repair with implications for autism and cancer-related disorders.

CT-guided radiofrequency ablation of osteoid osteoma: established concepts and new ideas.

Osteoid osteoma is a painful benign bone tumour of children and young adults with characteristic clinico-radiological features depending upon the location of the lesion. Intraoperative visualisation of the nidus is difficult and therefore curative surgery is often associated with excessive bone removal, significant perioperative morbidity and potential need of bone grafting procedures. With advancement in cross-sectional imaging and radiofrequency ablation (RFA) technology, CT-guided RFA has emerged as the treatment of choice for the osteoid osteoma. This procedure involves accurate cannulation of the nidus and subsequent thermocoagulation-induced necrosis.Multidisciplinary management approach is the standard of care for patients with osteoid osteoma. Appropriate patient selection, identification of imaging pitfalls, pre-anaesthetic evaluation and a protocol-based interventional approach are the cornerstone for a favourable outcome. Comprehensive patient preparation with proper patient position and insulation is important to prevent complications. Use of spinal needle-guided placement of introducer needle, namely, "rail-road technique" is associated with fewer needle trajectory modifications, reduced radiation dose and patient morbidity and less intervention time. Certain other procedural modifications are employed in special situations, for example, intra-articular osteoid osteoma and osteoid osteoma of the subcutaneous bone in order to reduce complications. Treatment follow-up generally includes radiographic assessment and evaluation of pain score. Dynamic contrast-enhanced MRI has been recently found useful for demonstrating post-RFA healing.

Approach-based techniques of CT-guided percutaneous vertebral biopsy.

Magnetic resonance imaging (MRI) plays an important role in the characterization of vertebral lesions. Even if latest improvements in MRI permit to understand and suspect the nature of vertebral lesions and positron emission tomography computed tomography (PET-CT) gives information about lesion metabolism, biopsy is still needed in most cases. CT-guided percutaneous vertebral biopsy is a minimally invasive, safe and accurate procedure for definitive tissue diagnosis of a vertebral lesion. CT-guided vertebral biopsy is often the best alternative to a surgical biopsy. The purpose of this technical note is to discuss the approach-based techniques for CT-guided percutaneous vertebral biopsy.

An efficient and improved method for virus-induced gene silencing in sorghum.

BACKGROUND: Although the draft genome of sorghum is available, the understanding of gene function is limited due to the lack of extensive mutant resources. Virus-induced gene silencing (VIGS) is an alternative to mutant resources to study gene function. This study reports an improved and efficient method for Brome mosaic virus (BMV)-based VIGS in sorghum. METHODS: Sorghum plants were rub-inoculated with sap prepared by grinding 2 g of infected Nicotiana benthamiana leaf in 1 ml 10 mM potassium phosphate buffer (pH 6.8) and 100 mg of carborundum abrasive. The sap was rubbed on two to three top leaves of sorghum. Inoculated plants were covered with a dome to maintain high humidity and kept in the dark for two days at 18 °C. Inoculated plants were then transferred to 18 °C growth chamber with 12 h/12 h light/dark cycle. RESULTS: This study shows that BMV infection rate can be significantly increased in sorghum by incubating plants at 18 °C. A substantial variation in BMV infection rate in sorghum genotypes/varieties was observed and BTx623 was the most susceptible. Ubiquitin (Ubiq) silencing is a better visual marker for VIGS in sorghum compared to other markers such as Magnesium Chelatase subunit H (ChlH) and Phytoene desaturase (PDS). The use of antisense strand of a gene in BMV was found to significantly increase the efficiency and extent of VIGS in sorghum. In situ hybridization experiments showed that the non-uniform silencing in sorghum is due to the uneven spread of the virus. This study further demonstrates that genes could also be silenced in the inflorescence of sorghum. CONCLUSION: In general, sorghum plants are difficult to infect with BMV and therefore recalcitrant to VIGS studies. However, by using BMV as a vector, a BMV susceptible sorghum variety, 18 °C for incubating plants, and antisense strand of the target gene fragment, efficient VIGS can still be achieved in sorghum.

ß1-Integrin Impacts Rad51 Stability and DNA Double-Strand Break Repair by Homologous Recombination.

The molecular mechanisms underlying resistance to radiotherapy in breast cancer cells remain elusive. Previously, we reported that elevated ß1-integrin is associated with enhanced breast cancer cell survival postirradiation, but how ß1-integrin conferred radioresistance was unclear. Ionizing radiation (IR) induced cell killing correlates with the efficiency of DNA double-strand break (DSB) repair, and we found that nonmalignant breast epithelial (S1) cells with low ß1-integrin expression have a higher frequency of S-phase-specific IR-induced chromosomal aberrations than the derivative malignant breast (T4-2) cells with high ß1-integrin expression. In addition, there was an increased frequency of IR-induced homologous recombination (HR) repairosome focus formation in T4-2 cells compared with that of S1 cells. Cellular levels of Rad51 in T4-2 cells, a critical factor in HR-mediated DSB repair, were significantly higher. Blocking or depleting ß1-integrin activity in T4-2 cells reduced Rad51 levels, while ectopic expression of ß1-integrin in S1 cells correspondingly increased Rad51 levels, suggesting that Rad51 is regulated by ß1-integrin. The low level of Rad51 protein in S1 cells was found to be due to rapid degradation by the ubiquitin proteasome pathway (UPP). Furthermore, the E3 ubiquitin ligase RING1 was highly upregulated in S1 cells compared to T4-2 cells. Ectopic ß1-integrin expression in S1 cells reduced RING1 levels and increased Rad51 accumulation. In contrast, ß1-integrin depletion in T4-2 cells significantly increased RING1 protein levels and potentiated Rad51 ubiquitination. These data suggest for the first time that elevated levels of the extracellular matrix receptor ß1-integrin can increase tumor cell radioresistance by decreasing Rad51 degradation through a RING1-mediated proteasomal pathway.

MOF Suppresses Replication Stress and Contributes to Resolution of Stalled Replication Forks.

The human MOF (hMOF) protein belongs to the MYST family of histone acetyltransferases and plays a critical role in transcription and the DNA damage response. MOF is essential for cell proliferation; however, its role during replication and replicative stress is unknown. Here we demonstrate that cells depleted of MOF and under replicative stress induced by cisplatin, hydroxyurea, or camptothecin have reduced survival, a higher frequency of S-phase-specific chromosome damage, and increased R-loop formation. MOF depletion decreased replication fork speed and, when combined with replicative stress, also increased stalled replication forks as well as new origin firing. MOF interacted with PCNA, a key coordinator of replication and repair machinery at replication forks, and affected its ubiquitination and recruitment to the DNA damage site. Depletion of MOF, therefore, compromised the DNA damage repair response as evidenced by decreased Mre11, RPA70, Rad51, and PCNA focus formation, reduced DNA end resection, and decreased CHK1 phosphorylation in cells after exposure to hydroxyurea or cisplatin. These results support the argument that MOF plays an important role in suppressing replication stress induced by genotoxic agents at several stages during the DNA damage response.

Differentiation of Human Induced Pluripotent or Embryonic Stem Cells Decreases the DNA Damage Repair by Homologous Recombination.

The nitric oxide (NO)-cyclic GMP pathway contributes to human stem cell differentiation, but NO free radical production can also damage DNA, necessitating a robust DNA damage response (DDR) to ensure cell survival. How the DDR is affected by differentiation is unclear. Differentiation of stem cells, either inducible pluripotent or embryonic derived, increased residual DNA damage as determined by γ-H2AX and 53BP1 foci, with increased S-phase-specific chromosomal aberration after exposure to DNA-damaging agents, suggesting reduced homologous recombination (HR) repair as supported by the observation of decreased HR-related repair factor foci formation (RAD51 and BRCA1). Differentiated cells also had relatively increased fork stalling and R-loop formation after DNA replication stress. Treatment with NO donor (NOC-18), which causes stem cell differentiation has no effect on double-strand break (DSB) repair by non-homologous end-joining but reduced DSB repair by HR. Present studies suggest that DNA repair by HR is impaired in differentiated cells.

Erratum: miR-15a/miR-16 down-regulates BMI1, impacting Ub-H2A mediated DNA repair and breast cancer cell sensitivity to doxorubicin.

A correction to this article has been published and is linked from the HTML version of this paper. The error has been fixed in the paper.

Distributions of Polycyclic Aromatic Hydrocarbons, Aromatic Ketones, Carboxylic Acids, and Trace Metals in Arctic Aerosols: Long-Range Atmospheric Transport, Photochemical Degradation/Production at Polar Sunrise.

The distributions, correlations, and source apportionment of aromatic acids, aromatic ketones, polycyclic aromatic hydrocarbons (PAHs), and trace metals were studied in Canadian high Arctic aerosols. Nineteen PAHs including minor sulfur-containing heterocyclic PAH (dibenzothiophene) and major 6 carcinogenic PAHs were detected with a high proportion of fluoranthene followed by benzo[k]fluoranthene, pyrene, and chrysene. However, in the sunlit period of spring, their concentrations significantly declined likely due to photochemical decomposition. During the polar sunrise from mid-March to mid-April, benzo[a]pyrene to benzo[e]pyrene ratios significantly dropped, and the ratios diminished further from late April to May onward. These results suggest that PAHs transported over the Arctic are subjected to strong photochemical degradation at polar sunrise. Although aromatic ketones decreased in spring, concentrations of some aromatic acids such as benzoic and phthalic acids increased during the course of polar sunrise, suggesting that aromatic hydrocarbons are oxidized to result in aromatic acids. However, PAHs do not act as the major source for low molecular weight (LMW) diacids such as oxalic acid that are largely formed at polar sunrise in the arctic atmosphere because PAHs are 1 to 2 orders of magnitude less abundant than LMW diacids. Correlations of trace metals with organics, their sources, and the possible role of trace transition metals are explained.

miR-15a/miR-16 down-regulates BMI1, impacting Ub-H2A mediated DNA repair and breast cancer cell sensitivity to doxorubicin.

The B-lymphoma Moloney murine leukemia virus insertion region-1 protein (BMI1) acts as an oncogene in various cancers, including breast cancer. Recent evidence suggests that BMI1 is rapidly recruited to sites of DNA double strand breaks where it facilitates histone H2A ubiquitination and DNA double strand break repair by homologous recombination. Here we show that miR-15a and miR-16 expression is decreased during the initial period after DNA damage where it would otherwise down-regulate BMI1, impairing DNA repair. Elevated miR-15a and miR-16 levels down-regulated BMI1 and other polycomb group proteins like RING1A, RING1B, EZH2 and also altered the expression of proteins associated with the BMI1 dependent ubiquitination pathway. Antagonizing the expression of miR-15a and miR-16, enhanced BMI1 protein levels and increased DNA repair. Further, overexpression of miR-15a and miR-16 sensitized breast cancer cells to DNA damage induced by the chemotherapeutic drug doxorubicin. Our results suggest that miR-15a and miR-16 mediate the down-regulation of BMI1, which impedes DNA repair while elevated levels can sensitize breast cancer cells to doxorubicin leading to apoptotic cell death. This data identifies a new target for manipulating DNA damage response that could impact the development of improved therapeutics for breast cancer.

Effect through inhalation on human health of PM1 bound polycyclic aromatic hydrocarbons collected from foggy days in northern part of India.

We investigated the health risk from 16 polycyclic aromatic hydrocarbons (PAHs) adsorbed on submicron particles and also reported their concentrations, spatial distribution and possible sources during foggy days at Kanpur. Twenty-four urban foggy day's samples gathered from Kanpur, an urban center in North India and most densely populated city in the Indo-Gangetic plain of India, were examined for 16 PAHs (2-6 rings).The mean concentration of PM1 was found to be 160.16±37.70µg/m(3). ∑16PAHs concentrations were 529.17ng/m(3) with a mean of 33.07ng/m(3). The compounds of higher molecular weight (4-6 rings) added to 70.67% of ∑PAHs mass concentration in the foggy day's samples. The results of source identification by using principle component analysis (PCA) and diagnostic ratios proposed that the primary sources of PAHs were vehicular emission (primarily driven by diesel fuel) and coal combustion and the secondary source. Exposure to total PAHs in the ambient air resulted in, 95% probability total Incremental Lifetime Cancer Risk (TILCR) 3.57×10(-5) for adults and 2.08×10(-5) for children or (∼35 cancer case per million in adults and ∼20 cancer case per million in children) due to inhalation in terms of ILCR were higher than the baseline value of acceptable risk (one cancer case per million people) suggesting moderate health risk to resident human population.

Source apportionment and risk assessment of PM1 bound trace metals collected during foggy and non-foggy episodes at a representative site in the Indo-Gangetic plain.

The concentration, spatial distribution and source of 13-PM1 bound trace metals (Fe, Cu, Mn, Cr, Zn, Cd, Ni, K, Mg, Na, Ca, Pb and V) and adverse health effects of 5-PM1 bound trace metals (Mn, Zn, Ni, Cr and Cd) collected during foggy and non-foggy episodes are presented. Twenty-four samples from each period (foggy and non-foggy episodes) were collected from Kanpur, a typical densely populated city and the most polluted representative site in the Indo-Gangetic plain of India, and were analyzed for carcinogenic (Ni, Cr and Cd) and non-carcinogenic metals (Mn and Zn). The average mass concentration of PM1 during foggy and non-foggy episodes was found to be 160.16±37.70 and 132.87±27.97µg/m(3). Source identification via principle component analysis suggested that vehicular emission and anthropogenic, industrial and crustal dust were the dominant sources in this region. During both episodes the decreasing order of hazard quotient (Hq) for adult and children was as Mn>Cr>Cd>Ni>Zn. In a non-foggy episode the hazardous index (Hi) values of these 5 trace metals were found to be ~3.5 times higher than a foggy episode's exposed population, respectively. In a foggy episode, due to the exposure to total carcinogenic trace metals (Ni, Cr and Cd) present in the ambient air, 95% probability total incremental lifetime cancer risks (TIlcR) were ~687 cancer cases and ~402 cancer cases per million in the adult population and children population respectively. These cancer cases were ~1.6 times higher than a non-foggy episode's exposed population.

Speciation of atmospheric polycyclic aromatic hydrocarbons (PAHs) present during fog time collected submicron particles.

Airborne submicron particles (PM1) were collected using PM1 sampler during the fog-dominated days (December 2013-January 2014). PM1 values varied between 58.12 µg/m(3) and 198.75 µg/m(3), and average mass concentration was 162.33 ± 38.25 µg/m(3) while total average concentration of particle-associated polycyclic aromatic hydrocarbon (PAHs) determined was 616.31 ± 30.31 ng/m(3). This is a signal for an alarming high pollution level at this site situated in the Indo-Gangetic Plain (IGP). PAHs were extracted from filters using toluene and acetonitrile. Quantitative measurements of polycyclic aromatic hydrocarbons (PAHs) were carried out using the high performance liquid chromatography (HPLC) technique. The extracts were analyzed for 16 target polycyclic aromatic hydrocarbons (PAHs) including carcinogenic compound benzo(a)pyrene (19.86 ± 38.98 ng/m(3)). Fluoranthene, benzo(a)anthracene, anthracene, and fluorene were the predominant compounds found in the samples collected during foggy days. Based on number of rings, four-ring PAH compounds had maximum contribution (43%) in this fog time collected submicron particles followed by three-ring (21%), five-ring (20%), six-ring (13%), and two-ring (3%), respectively. In winter and foggy days, wood and coal combustion and biomass burning also significantly contribute to the PAH levels. However, diagnostic ratio suggests diesel emissions as the prime source of PAHs at this sampling site.

RECQ helicase RECQL4 participates in non-homologous end joining and interacts with the Ku complex.

RECQL4, a member of the RecQ helicase family, is a multifunctional participant in DNA metabolism. RECQL4 protein participates in several functions both in the nucleus and in the cytoplasm of the cell, and mutations in human RECQL4 are associated with three genetic disorders: Rothmund-Thomson, RAPADILINO and Baller-Gerold syndromes. We previously reported that RECQL4 is recruited to laser-induced DNA double-strand breaks (DSB). Here, we have characterized the functional roles of RECQL4 in the non-homologous end joining (NHEJ) pathway of DSB repair. In an in vitro NHEJ assay that depends on the activity of DNA-dependent protein kinase (DNA-PK), extracts from RECQL4 knockdown cells display reduced end-joining activity on DNA substrates with cohesive and non-cohesive ends. Depletion of RECQL4 also reduced the end joining activity on a GFP reporter plasmid in vivo. Knockdown of RECQL4 increased the sensitivity of cells to γ-irradiation and resulted in accumulation of 53BP1 foci after irradiation, indicating defects in the processing of DSB. We find that RECQL4 interacts with the Ku70/Ku80 heterodimer, part of the DNA-PK complex, via its N-terminal domain. Further, RECQL4 stimulates higher order DNA binding of Ku70/Ku80 to a blunt end DNA substrate. Taken together, these results implicate that RECQL4 participates in the NHEJ pathway of DSB repair via a functional interaction with the Ku70/Ku80 complex. This is the first study to provide both in vitro and in vivo evidence for a role of a RecQ helicase in NHEJ.