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Background: Obesity has become a global epidemic. Bariatric surgery remains the most successful modality for producing sustained weight loss. Attrition rates after bariatric surgery are currently reported between 3 and 63% depending on the type of bariatric operation and the length of follow-up provided by the bariatric surgery team. It is currently unknown if patient attrition from bariatric surgery programs impact clinical outcomes. The availability of the Metabolic and Bariatric Surgery Accreditation and Quality Improvement Program (MBSAQIP) and the Mayo Clinic Midwest unified electronic medical record (EMR) provide a unique opportunity to explore this topic., Methods: Raw data was downloaded from MBSAQIP database for all laparoscopic Roux-en-Y gastric bypass (LRYGB) cases between May 1, 2008 and January 8, 2015 (N = 1242). Baseline weight and preexisting comorbidities (type 2 diabetes, hypertension, and hyperlipidemia) were recorded using the MBSAQIP database and the EMR. Current weight and comorbidity data (type 2 diabetes, hypertension, and hyperlipidemia) were subsequently collected at the time closest to the patient's surgical anniversary dates during the following assessment periods: years 1, 2, and 3 after surgery. Mean percentage total weight loss (TWL) was calculated at each time frame for each patient. Data was summarized using descriptive statistics, including counts and percentages for categorical variables by either year or year and location., Results: The number of patients seen by the bariatric surgery practice (BSP) compared to those seen by other providers within our practice (attrition to bariatric surgery practice (ABSP)) was highest in year 1 and reduced each subsequent year (year 1: BSP N = 740, ABSP N = 166, year 2: BSP N = 425, ABSP N = 309, and year 3: BSP N = 235, ABSP N = 325). The mean TWL in the BSP and ABSP groups at year 1 was 31.84% versus 30.19%, at year 2 was 31.34% versus 29.67%, and at year 3 was 29.01% versus 27.71% respectively. Differences were statistically significant between groups at years 1 and 2 (p < 0.05). A statistically significant difference was not found in year 3 despite a trend towards higher TWL in the BSP group. Among all patients, statistically significant differences (p < 0.0001) were observed between baseline and years 1, 2, and 3 for type 2 diabetes, hypertension, and hyperlipidemia., Conclusions: Our study confirms the problem of patient attrition to follow up at our BSP. It is also the first to suggest a difference in weight loss outcomes among patients seen in BSP compared to those seen by other providers (ABSP) at 1 and 2 years after Roux-en-Y gastric bypass (LRYGB). The potential implications of this observation on long-term weight maintenance after LRYGB and the impact on metabolic comorbidities remain unknown but warrant further investigation. It also warrants the development of strategies to improve patient retention in BSP and/or engagement of medical providers to achieve that end.

BRCA1 is a well-known tumor suppressor protein in mammals, involved in multiple cellular processes such as DNA repair, chromosome segregation and chromatin remodeling. Interestingly, homologs of BRCA1 and several of its complex partners are also found in plants. As the respective mutants are viable, in contrast to mammalian mutants, detailed analyses of their biological role is possible. Here we demonstrate that the model plant Arabidopsis thaliana harbors two homologs of the mammalian BRCA1 interaction partner BRCC36, AtBRCC36A and AtBRCC36B. Mutants of both genes as well as the double mutants are fully fertile and show no defects in development. We were able to show that mutation of one of the homologs, AtBRCC36A, leads to a severe defect in intra- and interchromosomal homologous recombination (HR). A HR defect is also apparent in Atbrca1 mutants. As the Atbrcc36a/Atbrca1 double mutant behaves like the single mutants of AtBRCA1 and AtBRCC36A both proteins seem to be involved in a common pathway in the regulation of HR. AtBRCC36 is also epistatic to AtBRCA1 in DNA crosslink repair. Upon genotoxic stress, AtBRCC36A is transferred into the nucleus.

hBRCA1 and hBARD1 are tumor suppressor proteins that are involved as heterodimer via ubiquitinylation in many cellular processes, such as DNA repair. Loss of BRCA1 or BARD1 results in early embryonic lethality and chromosomal instability. The Arabidopsis genome carries a BRCA1 homologue, and we were able to identify a BARD1 homologue. AtBRCA1 and the putative AtBARD1 protein are able to interact with each other as indicated by in vitro and in planta experiments. We have identified T-DNA insertion mutants for both genes, which show no visible phenotype under standard growth conditions and are fully fertile. Thus, in contrast to animals, both genes have no indispensable role during development and meiosis in plants. The two single as well as the double mutant are to a similar extent sensitive to mitomycin C, indicating an epistatic interaction in DNA crosslink repair. We could further demonstrate that in Arabidopsis BARD1 plays a prominent role in the regulation of homologous DNA repair in somatic cells.

Iron mobilization responses are induced by low iron supply at transcriptional level. In tomato, the basic helix-loop-helix gene FER is required for induction of iron mobilization. Using molecular-genetic techniques, we analyzed the function of BHLH029, named FRU (FER-like regulator of iron uptake), the Arabidopsis thaliana homolog of the tomato FER gene. The FRU gene was mainly expressed in roots in a cell-specific pattern and induced by iron deficiency. FRU mutant plants were chlorotic, and the FRU gene was found necessary for induction of the essential iron mobilization genes FRO2 (ferric chelate reductase gene) and IRT1 (iron-regulated transporter gene). Overexpression of FRU resulted in an increase of iron mobilization responses at low iron supply. Thus, the FRU gene is a mediator in induction of iron mobilization responses in Arabidopsis, indicating that regulation of iron uptake is conserved in dicot species.

In Arabidopsis thaliana (L.) Heynh. the seed-specific transcription factors ABI3 and FUS3 have key regulatory functions during the development of mature seeds. The highly conserved RY motif [DNA motif CATGCA(TG)], present in many seed-specific promoters, is an essential target of both regulators. Here we show that, in vitro, the full-length ABI3 protein, as well as FUS3 protein, is able to bind to RY-DNA and that the B3 domains of both transcription factors are necessary and sufficient for the specific interaction with the RY element. Flanking sequences of the RY motif modulate the binding, but the presence of an RY sequence alone allows the specific interaction of ABI3 and FUS3 with the target in vitro. Transcriptional activity of ABI3 and FUS3, measured by transient promoter activation, requires the B3 DNA-binding domain and an activation domain. In addition to the known N-terminal-located activation domain, a second transcription activation domain was found in the B1 region of ABI3.

The Arabidopsis mutants fus3 and abi3 show pleiotropic effects during embryogenesis including reduced levels of transcripts encoding embryo-specific seed proteins. To investigate the interaction between the B3-domain-containing transcription factors FUS3 and ABI3 with the RY cis-motif, conserved in many seed-specific promoters, a promoter analysis as well as band-shift experiments were performed. The analysis of promoter mutants revealed the structural requirements for the function of the RY cis-element. It is shown that both the nucleotide sequence and the alternation of purin and pyrimidin nucleotides (RY character) are essential for the activity of the motif. Further, it was shown that FUS3 and ABI3 can act independently of each other in controlling promoter activity and that the RY cis-motif is a target for both transcription factors. For FUS3, which is so far the smallest known member of the B3-domain family, a physical interaction with the RY motif was established. The functional and biochemical data demonstrate that the regulators FUS3 and ABI3 are essential components of a regulatory network acting in concert through the RY-promoter element to control gene expression during late embryogenesis and seed development.