Hoodmorales1317

From Brassica oleracea genome, 88 anthocyanin biosynthetic genes were identified. They expanded via whole-genome or tandem duplication and showed significant expression differentiation. Functional characterization revealed BoMYB113.1 as positive and BoMYBL2.1 as negative regulators responsible for anthocyanin accumulation. Brassica oleracea produces various health-promoting phytochemicals, including glucosinolates, carotenoids, and vitamins. Despite the anthocyanin biosynthetic pathways in the model plant Arabidopsis thaliana being well characterized, little is known about the genetic basis of anthocyanin biosynthesis in B. oleracea. In this study, we identified 88 B. oleracea anthocyanin biosynthetic genes (BoABGs) representing homologs of 46 Arabidopsis anthocyanin biosynthetic genes (AtABGs). Most anthocyanin biosynthetic genes, having expanded via whole-genome duplication and tandem duplication, retained more than one copy in B. oleracea. Expression analysis revealed diverse expression patterns of BoABGhould promote breeding for anthocyanin content.Otosclerosis is a bone disorder of the otic capsule and common form of late-onset hearing impairment. Considered a complex disease, little is known about its pathogenesis. Over the past 20 years, ten autosomal dominant loci (OTSC1-10) have been mapped but no genes identified. Herein, we map a new OTSC locus to a 9.96 Mb region within the FOX gene cluster on 16q24.1 and identify a 15 bp coding deletion in Forkhead Box L1 co-segregating with otosclerosis in a Caucasian family. Pre-operative phenotype ranges from moderate to severe hearing loss to profound sensorineural loss requiring a cochlear implant. Mutant FOXL1 is both transcribed and translated and correctly locates to the cell nucleus. However, the deletion of 5 residues in the C-terminus of mutant FOXL1 causes a complete loss of transcriptional activity due to loss of secondary (alpha helix) structure. FOXL1 (rs764026385) was identified in a second unrelated case on a shared background. We conclude that FOXL1 (rs764026385) is pathogenic and causes autosomal dominant otosclerosis and propose a key inhibitory role for wildtype Foxl1 in bone remodelling in the otic capsule. New insights into the molecular pathology of otosclerosis from this study provide molecular targets for non-invasive therapeutic interventions.

The determination on how antineoplastic agents interfere on the progression of periodontitis is critical for improvement and even development of novel therapeutic approaches for periodontal management. This study evaluated the influence of chemotherapy with 5-fluorouracil (5-FU) or cisplatin (CIS) on healthy periodontal tissues and on the progression of experimental periodontitis (EP).

One hundred forty-four male rats were divided into six groups (n = 24). Each group was treated with physiological saline solution (PSS) 0.9%, 5-FU, or CIS. GSK3685032 clinical trial Experimental periodontitis (EP) was induced by ligature placement. Animals were euthanized at 7, 15, and 30days after treatment. Data were statistically analyzed (p ≤ 0.05).

The groups with EP and treated with 5-FU or CIS showed lower percentage of bone volume in the furcation region and higher percentage of alveolar bone loss, higher number of TRAP-positive cells, and lower number of PCNA-positive cells when compared group with EP and treated with PSS (p ≤ 0.05). Groups with EP and treated with 5-FU or CIS showed high immunolabelling pattern of RANKL, TNF-α, and IL-1β, moderate of BAX, and low of HIF-1α. Histological analysis showed severe tissue breakdown in the groups with EP and treated with 5-FU or CIS.

Chemotherapy with antineoplastic agents 5-FU and CIS increased the intensity and duration of the inflammation and compromised tissue repair by reduction in cellular and vascular turnover. The more severe periodontal breakdown was caused by 5-FU.

Chemotherapy with antineoplastic agents 5-FU and CIS increased the intensity and duration of the inflammation and compromised tissue repair by reduction in cellular and vascular turnover. The more severe periodontal breakdown was caused by 5-FU.Using the vascularized skin allograft (VSA) model, we compared the tolerogenic effects of different allogeneic bone marrow transplantation (BMT) delivery routes into immunoprivileged compartments under a 7-day protocol immunosuppressive therapy. Twenty-eight fully MHC mismatched VSA transplants were performed between ACI (RT1a) donors and Lewis (RT11) recipients in four groups of seven animals each, under a 7-day protocol of alfa/beta TCRmAb/CsA (alpha/beta-TCR monoclonal antibodies/Cyclosporine A therapy). Donor bone marrow cells (BMC) (100 × 106 cells) were injected into three different immunoprivileged compartments Group 1 Control, without cellular supportive therapy, Group 2 Intracapsular BMT, Group 3 Intragonadal BMT, Group 4 Intrathecal BMT. In Group 2, BMC were transplanted under the kidney capsule. In Group 3, BMC were transplanted into the right testis between tunica albuginea and seminiferous tubules, and in Group 4, cells were injected intrathecally. The assessment included skin evaluation for signs and grade of rejection and immunohistochemistry for donor cells engraftment into host lymphoid compartments. Donor-specific chimerism for MHC class I (RT1a) antigens and the presence of CD4+/CD25+ T cells were assessed in the peripheral blood of recipients. The most extended allograft survival, 50-78 days, was observed in Group 4 after intrathecal BMT. The T cells CD4+/CD25+ in the peripheral blood were higher after intrathecal BMC injection than other experimental groups at each post-transplant time point. Transplantation of BMC into immunoprivileged compartments delayed rejection of fully mismatched VSA and induction of robust, donor-specific chimerism.We celebrate the 60th anniversary of Biological Cybernetics. It has also been 30 years since "Self-organized control of bipedal locomotion by neural oscillators in unpredictable environment" was published in Biological Cybernetics (Taga et al. in Biol Cybern 65(3)147-159, 1991). I would like to look back on the creation of this paper and discuss its subsequent development and future perspectives.

Mitochondria change their distribution from nuclear peripheral to uniformly distributed in cytoplasm during zygotic development of rice, and the mitochondria re-distribute around nucleus for even segregation into daughter cells. Mitochondria are highly dynamic organelles that actively move and change their localization along with actin filaments during the cell cycle. Studies of mitochondrial dynamics and distribution in plant cells have mainly been conducted on somatic cells, and our understanding about these aspects during the formation and development of zygotes remains limited. In this study, mitochondrial nucleoids of rice egg cells and zygotes were successfully stained by using N-aryl pyrido cyanine 3 (PC3), and their intracellular localization and distribution were demonstrated. Mitochondria in rice egg cells were small and coccoid in shape and were primarily distributed around the nucleus. Upon gamete fusion, the resulting zygotes showed mitochondrial dispersion and accumulation equivalent to those gg cells until 8 h after fusion (HAF). Around 12 HAF, the mitochondria started to disperse throughout the cytoplasm of the zygotes, and this dispersive distribution pattern continued until the zygotes entered the mitotic phase. At early prophase, the mitochondria redistributed from dispersive to densely accumulated around the nucleus, and during the metaphase and anaphase, the mitochondria were depleted from possible mitotic spindle region. Thereafter, during cell plate formation between daughter nuclei, the mitochondria distributed along the phragmoplast, where the new cell wall was formed. Finally, relatively equivalent amounts of mitochondria were detected in the apical and basal cells which were produced through asymmetric division of the zygotes. Further observation by treating the egg cell with latrunculin B revealed that the accumulation of mitochondria around the nuclear periphery in egg cells and early zygotes depended on the actin meshwork converging toward the egg or zygote nucleus.Non-Hodgkin lymphoma (NHL) that develops after kidney transplantation belongs to post-transplant lymphoproliferative disorders (PTLD) occurring with an incidence of 2-3%. Most pediatric cases are related to primary infection with Epstein-Barr virus (EBV), able to transform and immortalize B cells and widely proliferate due to the lack of relevant control of cytotoxic T cells in patients receiving post-transplant immunosuppression. NHL may develop as a systemic disease or as a localized lesion. The clinical pattern is variable, from non-symptomatic to fulminating disease. Young age of transplant recipient, seronegative EBV status at transplantation, and EBV mismatch between donor and recipient (D+/R-) are regarded as risk factors. Immunosuppression impacts the development of both early and late NHLs. Specific surveillance protocols, including monitoring of EBV viral load, are used in patients at risk; however, detailed histopathology diagnosis and evaluation of malignancy staging is crucial for therapeutic decisions. Minimizing of immunosuppression is a primary management, followed by the use of rituximab in B-cell NHLs. Specific chemotherapeutic protocols, adjusted to lymphoma classification and staging, are used in advanced NHLs. Radiotherapy and/or surgical removal of malignant lesions is limited to the most severe cases. Outcome is variable, depending on risk factors and timing of diagnosis, however is positive in pediatric patients in terms of graft function and patient survival. Kidney re-transplantation is possible in survivors who lost the primary graft due to chronic rejection, however may be performed after at least 2-3 years of waiting time, careful verification of malignancy-free status, and gaining immunity against EBV.

Gordonia species, aerobic, weakly acid-fast, Gram-positive bacilli, are a rare cause of peritonitis in patients undergoing peritoneal dialysis (PD). We report the first pediatric case of PD-related peritonitis caused by Gordonia bronchialis.

A 13-year-old girl with chronic kidney disease (CKD) stage 5D, on continuous cycling PD (CCPD) for 8 years, presented with cloudy PD effluent, with no abdominal discomfort or fever. Intra-peritoneal (IP) loading doses of vancomycin and ceftazidime were started at home after obtaining a PD effluent sample, which showed WBC 2,340 × 10 /L (59% neutrophils) and Gram-positive bacilli. On admission, she was clinically well and afebrile, with no history of methicillin-resistant Staphylococcus aureus (MRSA) infection, so vancomycin was discontinued, and IP ceftazidime and cefazolin were started, following a loading dose of intravenous cefazolin. Gordonia species grew after 5 days of incubation and later identified as Gordonia bronchialis. IP vancomycin was restarted as monotherapy, empirically for a total of 3 weeks therapy. A 2-week course of oral ciprofloxacin was added, based on susceptibility testing. PD catheter replacement was advised due to the risk of recurrence but was refused. A relapse occurred 16 days after discontinuing antibiotics, successfully treated with a 2-week course of IP ceftazidime and vancomycin. The PD catheter was removed and hemodialysis initiated. She received a further 2-week course of oral ciprofloxacin and amoxicillin-clavulanate post PD catheter removal.

Gordonia bronchialis is an emerging pathogen in PD peritonitis and appears to be associated with a high risk of relapse. PD catheter replacement is strongly suggested.

Gordonia bronchialis is an emerging pathogen in PD peritonitis and appears to be associated with a high risk of relapse. PD catheter replacement is strongly suggested.