The bone marrow microenvironment (BME) in acute myeloid leukemia (AML) consists of various cell types that support the growth of AML cells and protect them from chemotherapy. Mesenchymal stromal cells (MSCs) in the BME have been shown to contribute immensely to leukemogenesis and chemotherapy resistance in AML cells. However, the mechanism of stroma-induced chemotherapy resistance is not known. Here, we hypothesized that stromal cells promote a stem-like phenotype in AML cells, thereby inducing tumorigenecity and therapy resistance. To test our hypothesis, we co-cultured AML cell lines and patient samples with BM-derived MSCs and determined aldehyde dehydrogenase (ALDH) activity and performed gene expression profiling by RNA sequencing. We found that the percentage of ALDH+ cells increased dramatically when AML cells were co-cultured with MSCs. However, among the 19 ALDH isoforms, ALDH2 and ALDH1L2 were the only two that were significantly upregulated in AML cells co-cultured with stromal cells compared to cells cultured alone. Mechanistic studies revealed that the transforming growth factor-β1 (TGF-β1)-regulated gene signature is activated in AML cells co-cultured with MSCs. Knockdown of TGF-β1 in BM-MSCs inhibited stroma-induced ALDH activity and ALDH2 expression in AML cells, whereas treatment with recombinant TGF-β1 induced the ALDH+ phenotype in AML cells. We also found that TGF-β1-induced ALDH2 expression in AML cells is mediated by the non-canonical pathway through the activation of p38. Interestingly, inhibition of ALDH2 with diadzin and CVT-10216 significantly inhibited MSC-induced ALDH activity in AML cells and sensitized them to chemotherapy, even in the presence of MSCs. Collectively, BM stroma induces ALDH2 activity in AML cells through the non-canonical TGF-β pathway. Inhibition of ALDH2 sensitizes AML cells to chemotherapy. Psychological distress following traumatic injury can influence the patient health, well-being and quality of life; however, this impact may partly vary according to the type and severity of injury. We aimed to study the predominant distress causing cluster and individual symptoms of Post-Traumatic Stress Disorders (PTSD) at the clinical and subthreshold level in patients with traumatic injuries, based on the mechanism of injury (MOI). A hospital based cross-sectional study was conducted at a Level 1 Trauma Center utilizing PTSD Checklist to diagnose PTSD after one month of the traumatic event. All patients suffering from psychological distresses were assessed by a clinical psychologist in the trauma section. PTSD diagnostic criteria from DSM-5 were used to classify the patients. Taurine clinical trial The inclusion criteria comprised of adult trauma patients who were directly involved in traumatic injuries and admitted under the Trauma Surgery services for a minimum of one day; have ability to provide written informed consent l caused higher level of distress in patients post traumatic injuries. Subthreshold symptoms of PTSD are more common and deserve more attention.Patients with different MOI showed a broad range of psychological problems with respect to symptom clusters. Negative alteration in mood and cognition followed by hyperarousal caused higher level of distress in patients post traumatic injuries. Subthreshold symptoms of PTSD are more common and deserve more attention.The development of HIV-1 vaccines is challenged by the lack of relevant models to accurately induce human B- and T-cell responses in lymphoid organs. In humanized mice reconstituted with human hematopoietic stem cells (hu-mice), human B cell-development and function are impaired and cells fail to efficiently transition from IgM B cells to IgG B cells. Here, we found that CD40-targeted vaccination combined with CpG-B adjuvant overcomes the usual defect of human B-cell switch and maturation in hu-mice. We further dissected hu-B cell responses directed against the HIV-1 Env protein elicited by targeting Env gp140 clade C to the CD40 receptor of antigen-presenting cells. The anti-CD40.Env gp140 vaccine was injected with CpG-B in a homologous prime/boost regimen or as a boost of a NYVAC-KC pox vector encoding Env gp140 clade C. Both regimens elicited Env-specific IgG-switched memory hu-B cells at a greater magnitude in hu-mice primed with NYVAC-KC. Single-cell RNA-seq analysis showed gp140-specific hu-B cells to express polyclonal IgG1 and IgG3 isotypes and a broad Ig VH/VL repertoire, with predominant VH3 family gene usage. These cells exhibited a higher rate of somatic hypermutation than the non-specific IgG+ hu-B-cell counterpart. Both vaccine regimens induced splenic GC-like structures containing hu-B and hu-Tfh-like cells expressing PD-1 and BCL-6. We confirmed in this model that circulating ICOS+ memory hu-Tfh cells correlated with the magnitude of gp140-specific B-cell responses. Finally, the NYVAC-KC heterologous prime led to a more diverse clonal expansion of specific hu-B cells. Thus, this study shows that CD40-targeted vaccination induces human IgG production in hu-mice and provides insights for the development of a CD40-targeting vaccine to prevent HIV-1 infection in humans. The prevalence of hypertension in Nigeria is high and growing. The burden and risk factor distribution also vary by geographical zone. Information about prevalence, risk factors and disease status awareness are needed to guide evidence based public health response at the national and sub- national levels. This paper describes the prevalence of hypertension and its correlates, as well as hypertension status awareness among men in North Central, Nigeria. A cross sectional survey was administered to male partners of pregnant women participating in the Healthy Beginning Initiative program from 2016-2018. Information on socio-demographic characteristics, risk factors, physical measurement and blood pressure readings were collected using a standardized protocol. Data was analyzed with simple and multiple logistic regression. The 6,538 men had a median age of 31 years [IQR 26-37]. The prevalence of hypertension was 23.3% (95% CI 22.3%-24.4%), while 46.7% had prehypertension. The odds of hypertension was associated with increasing age (OR1.