001). Messaging was much less common for VEHs ages 55 to 64 or older, non-Latino Blacks, those receiving homeless-tailored primary care, and those with SUDs (all P < 0.001). VEHs with opioid use disorder were even less likely than those with other SUDs to use secure messaging (P = 0.047).
 
  Persons with homeless experiences might require assistance to engage with secure messaging technology. As health systems limit in-person care during a national pandemic, alternative solutions may be needed to facilitate health communications and prevent care disruptions for patients experiencing homelessness and SUDs.
 Persons with homeless experiences might require assistance to engage with secure messaging technology. As health systems limit in-person care during a national pandemic, alternative solutions may be needed to facilitate health communications and prevent care disruptions for patients experiencing homelessness and SUDs.
  Hyperbilirubinemia is a predictor of severe drug-induced liver injury (DILI). Hepatobiliary ATP-binding cassette (ABC) transporters play an important role in the transportation of many drugs and bilirubin; however, little is known about these transporters and the risk of DILI. The aim of this study was to explore associations between genetic variations in important ABC transporters and susceptibility to DILI, with a particular focus on hyperbilirubinemia.
 
  A total of 200 patients with DILI and 200 healthy controls were enrolled as the training dataset. Another 106 patients with DILI were recruited as the validation dataset. They were genotyped for ABCB11 (BSEP) rs2287622, ABCB1 (MDR1) rs1128503, rs1045642, ABCB4 (MDR3) rs2230028, ABCC2 (MRP2) rs1885301, rs717620, rs2273697, rs3740066 and rs8187710 using polymerase chain reaction-based TaqMan genotyping assays.
 
  There were no statistical differences in any of the nine ABC transporter single nucleotide polymorphisms between the DILI and control groups. Howein patients with DILI. Screening for this variant may help to prevent and mitigate drug-induced hyperbilirubinemia.
  The aim of the present study was to investigate the risk factors for amputation in patients with diabetic foot ulcer (DFU).
 
  Between 2012 and 2017, 646 patients with DFU were admitted to our diabetic foot care center. A retrospective chart review was performed, and the end point was limb salvage and minor or major amputation. Chi-square test, dependent t test, and a multivariate logistic regression analysis were performed to identify risk factors in patients with DFUs.
 
  A total of 399 male and 247 female patients (mean age 64.6 years) were included in this study, of whom 159 (24.6%) underwent lower limb amputation (minor, 17.5; major, 7.1%). Independent risk factors of amputation were peripheral arterial disease (PAD) (odds ratio [OR], 3.196; p < 0.001), C-reactive protein (CRP) level (OR, 1.046; p = 0.001), and hospital stay (OR, 1.019; p = 0.001). Subgroup analysis based on all patients with PAD who underwent amputation showed that endovascular intervention (OR, 0.271; p = 0.049) was a protective factor for major amputation in addition to CRP level (OR, 1.116; p = 0.008).
 
  DFU remains a major medical and public health issue. PAD, CRP level, and hospital stay are independent risk factors for amputation. Endovascular intervention is an independent protective factor against major amputation among patients with PAD who underwent amputation.
 DFU remains a major medical and public health issue. PAD, CRP level, and hospital stay are independent risk factors for amputation. Endovascular intervention is an independent protective factor against major amputation among patients with PAD who underwent amputation.DNA-damaging chemotherapy is a major component of therapy for high-risk neuroblastoma, and patients often relapse with treatment-refractory disease. We hypothesized that DNA repair genes with increased expression in alkylating agent resistant models would provide therapeutic targets for enhancing chemotherapy. In-vitro cytotoxicity of alkylating agents for 12 patient-derived neuroblastoma cell lines was assayed using DIMSCAN, and mRNA expression of 57 DNA repair, three transporter, and two glutathione synthesis genes was assessed by TaqMan low-density array (TLDA) with further validation by qRT-PCR in 26 cell lines. O6-methylguanine-DNA methyltransferase (MGMT) mRNA was upregulated in cell lines with greater melphalan and temozolomide (TMZ) resistance.  https://www.selleckchem.com/products/elexacaftor.html  MGMT expression also correlated significantly with resistance to TMZ+irinotecan (IRN) (in-vitro as the SN38 active metabolite). Forced overexpression of MGMT (lentiviral transduction) in MGMT non-expressing cell lines significantly increased TMZ+SN38 resistance. The MGMT inhibitor O6-benzylguanine (O6BG) enhanced TMZ+SN38 in-vitro cytotoxicity, H2AX phosphorylation, caspase-3 cleavage, and apoptosis by terminal deoxynucleotidyl transferase dUTP nick end labeling. TMZ+IRN+O6BG delayed tumor growth and increased survival relative to TMZ+IRN in two of seven patient-derived xenografts established at time of death from progressive neuroblastoma. We demonstrated that high MGMT expression was associated with resistance to alkylating agents and TMZ+IRN in preclinical neuroblastoma models. The MGMT inhibitor O6BG enhanced the anticancer effect of TMZ+IRN in vitro and in vivo. These results support further preclinical studies exploring MGMT as a therapeutic target and biomarker of TMZ+IRN resistance in high-risk neuroblastoma.Activation and proliferation of cancer stem cells exert an important role in the invasion, metastasis, and recurrence of malignant tumors, including lung cancer. Therefore, exploring molecular targets related to self-renewal and mobility of lung cancer stem cells has important clinical significance. In our present study, we aimed to explore the effects of miR-138-5p on lung cancer stem-like cells and associated regulatory mechanism. In our present study, enhanced self-renewal capacity and elevated expression of cancer stem cells markers CD133, CD44, aldehyde dehydrogenase 1 of lung cancer stem-like cells derived from A549 cells were firstly verified. Then, obviously enhanced autophagy was found in lung cancer stem-like cells compared with parental cells A549. Besides, we found that enhanced autophagy induced by rapamycin promoted self-renewal and cell mobility of lung cancer stem-like cells and suppression of autophagy by 3-methyladenine exerted just opposite effects. In addition, miR-138-5p was found to be downregulated in lung cancer stem-like cells compared with that in parental cell A549.