Genetic diversity analysis of mustard (Brassica spp.) germplasm using molecular marker for selection of short duration genotypes

Molecular characterization of 16 mustard (Brassica spp.) genotypes by using 12 RAPD markers revealed that three primers GLA-11, OPB-04 and OPD-02 showed good technical resolution and sufficient variations among different genotypes. A total of 40 RAPD bands were scored of which 38 (94.87%) polymorphic amplification products were obtained. Besides, the primer OPD-02 amplified maximum number of polymorphic bands (100.00%) while the primer GLA-11 and OPB-04 generated the least (92.31%) polymorphic bands, which were minimal in number. The present study produced 13.33 scorable bands per primer and 12.67 polymorphic bands per primer. Frequencies of maximum number of polymorphic loci were found to be high with the exception of GLA-11(0.750), OPB-04 (0.875) and OPD-02 (0.750). The estimate of Nei's genetic diversity for the entire genotypes of mustard was 0.3596 and Shannon's information index was 0.535. There was a high level of genetic variation among the mustard genotypes studied from the proportion of polymorphic loci point of view. The values of pair-wise comparison of Nei’s genetic distance between genotypes were computed from combined data for the three primers; ranged from 0.1054 to 0.9862. BINA Sarisha-3 and BINA Sarisha-4 showed the lowest genetic distance of 0.1054 where Tori-7 and NAP-0758-2 showed highest genetic distance of 0.9862. The 16 mustard genotypes were differentiated into three main clusters: BARI Sarisha-14, BARI Sarisha-9, BARI Sarisha-15, BINA Sarisha-4, BINA Sarisha-3, BARI Sarisha-8, Sampad and Tori-7 in cluster A, NAP-0763, NAP-0721-1, BARI Sarisha-4, BARI Sarisha-6, NAP-0762-2 and NAP-0848-2 in cluster B and NAP-0838 and NAP-0758-2 were grouped into cluster C by making dendrogram based on Nei’s genetic distance using unweighted pair group method of arithmetic means (UPGMA).Keywords: Mustard, diversity analysis, RAPD marker, genetic distance, cluster analysis.Abbreviation: UPGMA, Unweighted pair group method of arithmetic means; RFLP, restriction fragment length polymorphism; RAPDs, random amplified polymorphic DNAs; AFLP, amplified fragment length polymorphism; SSRs, simple sequence repeats; CTAB, cetyl trimethyl ammonium bromide.

Augmenting Autologous Stem Cell Transplantation to Improve Outcomes in Myeloma

Consolidation with high-dose chemotherapy and autologous stem cell transplantation (ASCT) is the standard of care for transplantation-eligible patients with multiple myeloma, based on randomized trials showing improved progression-free survival with autologous transplantation after combination chemotherapy induction. These trials were performed before novel agents were introduced; subsequently, combinations of immunomodulatory drugs and proteasome inhibitors as induction therapy have significantly improved rates and depth of response. Ongoing randomized trials are testing whether conventional autologous transplantation continues to improve responses after novel agent induction. Although these results are awaited, it is important to review strategies for improving outcomes after ASCT. Conditioning before ASCT with higher doses of melphalan and combinations of melphalan with other agents, including radiopharmaceuticals, has been explored. Tandem ASCT, consolidation, and maintenance therapy after ASCT have been investigated in phase III trials. Experimental cellular therapies using ex vivo–primed dendritic cells, ex vivo–expanded autologous lymphocytes, Killer Immunoglobulin Receptor (KIR)-mismatched allogeneic natural killer cells, and genetically modified T cells to augment ASCT are also in phase I trials. This review summarizes these strategies and highlights the importance of exploring strategies to augment ASCT, even in the era of novel agent induction

Transforming Growth Factor: β Signaling Is Essential for Limb Regeneration in Axolotls

Axolotls (urodele amphibians) have the unique ability, among vertebrates, to perfectly regenerate many parts of their body including limbs, tail, jaw and spinal cord following injury or amputation. The axolotl limb is the most widely used structure as an experimental model to study tissue regeneration. The process is well characterized, requiring multiple cellular and molecular mechanisms. The preparation phase represents the first part of the regeneration process which includes wound healing, cellular migration, dedifferentiation and proliferation. The redevelopment phase represents the second part when dedifferentiated cells stop proliferating and redifferentiate to give rise to all missing structures. In the axolotl, when a limb is amputated, the missing or wounded part is regenerated perfectly without scar formation between the stump and the regenerated structure. Multiple authors have recently highlighted the similarities between the early phases of mammalian wound healing and urodele limb regeneration. In mammals, one very important family of growth factors implicated in the control of almost all aspects of wound healing is the transforming growth factor-beta family (TGF-β). In the present study, the full length sequence of the axolotl TGF-β1 cDNA was isolated. The spatio-temporal expression pattern of TGF-β1 in regenerating limbs shows that this gene is up-regulated during the preparation phase of regeneration. Our results also demonstrate the presence of multiple components of the TGF-β signaling machinery in axolotl cells. By using a specific pharmacological inhibitor of TGF-β type I receptor, SB-431542, we show that TGF-β signaling is required for axolotl limb regeneration. Treatment of regenerating limbs with SB-431542 reveals that cellular proliferation during limb regeneration as well as the expression of genes directly dependent on TGF-β signaling are down-regulated. These data directly implicate TGF-β signaling in the initiation and control of the regeneration process in axolotls

Twelve-month observational study of children with cancer in 41 countries during the COVID-19 pandemic

Introduction Childhood cancer is a leading cause of death. It is unclear whether the COVID-19 pandemic has impacted childhood cancer mortality. In this study, we aimed to establish all-cause mortality rates for childhood cancers during the COVID-19 pandemic and determine the factors associated with mortality. Methods Prospective cohort study in 109 institutions in 41 countries. Inclusion criteria: children <18 years who were newly diagnosed with or undergoing active treatment for acute lymphoblastic leukaemia, non-Hodgkin's lymphoma, Hodgkin lymphoma, retinoblastoma, Wilms tumour, glioma, osteosarcoma, Ewing sarcoma, rhabdomyosarcoma, medulloblastoma and neuroblastoma. Of 2327 cases, 2118 patients were included in the study. The primary outcome measure was all-cause mortality at 30 days, 90 days and 12 months. Results All-cause mortality was 3.4% (n=71/2084) at 30-day follow-up, 5.7% (n=113/1969) at 90-day follow-up and 13.0% (n=206/1581) at 12-month follow-up. The median time from diagnosis to multidisciplinary team (MDT) plan was longest in low-income countries (7 days, IQR 3-11). Multivariable analysis revealed several factors associated with 12-month mortality, including low-income (OR 6.99 (95% CI 2.49 to 19.68); p<0.001), lower middle income (OR 3.32 (95% CI 1.96 to 5.61); p<0.001) and upper middle income (OR 3.49 (95% CI 2.02 to 6.03); p<0.001) country status and chemotherapy (OR 0.55 (95% CI 0.36 to 0.86); p=0.008) and immunotherapy (OR 0.27 (95% CI 0.08 to 0.91); p=0.035) within 30 days from MDT plan. Multivariable analysis revealed laboratory-confirmed SARS-CoV-2 infection (OR 5.33 (95% CI 1.19 to 23.84); p=0.029) was associated with 30-day mortality. Conclusions Children with cancer are more likely to die within 30 days if infected with SARS-CoV-2. However, timely treatment reduced odds of death. This report provides crucial information to balance the benefits of providing anticancer therapy against the risks of SARS-CoV-2 infection in children with cancer