Carbon footprint and net carbon gain of major long-term cropping systems under no-tillage.

Due to increased contribution from agriculture sector to total greenhouse gas emissions, there is need to study the ability of no-tilled diverse cropping systems including crop sequences and bio-covers to mitigate C equivalent emissions. Thus, C-footprint was calculated for a long-term experiment at the University of Tennessee's Research and Education Center in Milan with six-crop sequences: continuous cotton (Gossypium hirsutum L.), cotton-corn (Zea mays L.), continuous corn, corn-soybean (Glycine max L.), continuous soybean, and soybean-cotton interacted with four bio-covers: poultry litter, hairy vetch (Vicia villosa), winter wheat (Triticum aestivum), and fallow control with three replicates in a strip-plot design. During the experiment duration (2002-2017), field inputs (fertilizers, pesticides, and machinery used for planting, chemical applications, and harvesting) and outputs (crop yield, aboveground, and belowground residue) were assessed for each crop sequence/bio-cover combination to calculate total C equivalence of inputs and outputs, net C gain, C footprint per kg yield, sustainability index, and nitrous oxide emissions. For continuous corn, C-based input emissions were significantly higher by 0.28-0.62 Mg CO2 eq. ha-1 yr-1 than all other sequences, however, a greater net C gain (5.4 Mg C eq. ha-1 yr-1) was also observed due to increased crop yield, aboveground and belowground residues. Poultry litter application resulted in lower C-footprint (1.59-2.09 kg CO2 eq. kg-1 yield) than hairy vetch, wheat, and fallow under all crop sequences. Hairy vetch also lowered C-footprint per kg yield (∼2-14%) when compared with wheat under continuous systems of corn, soybean, and cotton, and cotton-corn rotation. Poultry litter application increased sustainability index (23-45) of all cropping sequences compared with other bio-covers. Hairy vetch improved sustainability index of corn including cropping sequences as compared with wheat and fallow. Inclusion of soybean and cotton with corn significantly decreased nitrous oxide emissions by 20-25%. The major factor contributing towards C-based input emissions was N fertilizer with 68% contribution to total emissions on average. It is concluded that application of poultry litter can reduce per yield C-footprint and enhance production system sustainability compared with hairy vetch, wheat, and fallow for monocultures or rotations of corn, soybean, cotton. Additionally, hairy vetch can outperform wheat in reducing the per yield C-footprint for continuous corn/soybean/cotton, and cotton-corn rotation. Especially for corn production systems, hairy vetch can enhance sustainability index compared with wheat and fallow. In order to increase per hectare net C gain, reduce per yield C-footprint and enhance sustainability index simultaneously, integration of continuous corn or corn-soybean/cotton rotation with bio-cover poultry litter or hairy vetch may perform better than the monocultures of soybean or cotton integrated with bio-cover wheat or fallow control in the Mid-south USA.

The glioma-associated protein SETA interacts with AIP1/Alix and ALG-2 and modulates apoptosis in astrocytes.

Expression of the src homology 3 (SH3) domain-containing expressed in tumorigenic astrocytes (SETA) gene is associated with the tumorigenic state in astrocytes. SETA encodes a variety of adapter proteins containing either one or two SH3 domains, as suggested by the sequence heterogeneity of isolated cDNAs. Using both SH3 domains in a yeast two-hybrid screen of a glial progenitor cell cDNA library, we isolated the rat homolog of the ALG-2-interacting protein 1 or ALG-2-interacting protein X (AIP1/Alix). In vitro confrontation experiments showed that the SH3-N domain of SETA interacted with the proline-rich C terminus of AIP1. In co-immunoprecipitation experiments, SETA and AIP1 interacted and could form a complex with apoptosis-linked gene 2 protein. Endogenous SETA and AIP1 proteins showed similar patterns of staining in primary rat astrocytes. Misexpression of a variety of SETA protein isoforms in these astrocytes revealed that they localized to the actin cytoskeleton. Furthermore, SETA proteins containing the SH3-N domain were able to sensitize astrocytes to apoptosis induced by UV irradiation. Expression of the isolated SH3-N domain had the greatest effect in these experiments, indicating that interference in the interaction between endogenous SETA and AIP1 sensitizes astrocytes to apoptosis in response to DNA damage.

SETA is a multifunctional adapter protein with three SH3 domains that binds Grb2, Cbl, and the novel SB1 proteins.

Expression of the src homology 3 (SH3)-encoding, expressed in tumorigenic astrocytes (SETA) gene is associated with astrocyte transformation in culture and tumors in the adult brain. SETA binds to the apoptosis regulator apoptosis-linked gene 2 (ALG-2) interacting protein 1 (AIP1), and modulates apoptosis in astrocytes. The predicted protein structure of SETA revealed two SH3 domains, while related proteins were reported to have three. Here we report the identification of an additional SH3 domain N-terminal to the previously identified SETA sequence. Yeast two-hybrid screening of a p53(-/-) astrocyte cDNA library with this SH3 domain identified a novel gene, SETA binding protein 1 (SB1), with 55% amino acid identity to the renal tumor antigen, NY-REN-45. In vitro confrontation and co-immunoprecipitation experiments confirmed the binding of SB1 to SETA. Evidence that SETA binds to the CD2 protein, the proto-oncogene c-Cbl, and the signal transduction molecule Grb2, and can dimerize via its C-terminal coiled coil (CC) domain is also presented.

SETA: a novel SH3 domain-containing adapter molecule associated with malignancy in astrocytes.

Differential display polymerase chain reaction analysis was used to compare five differentiation states of the O-2A progenitor-like cell line CG4: progenitor cells and cells at 12 h or 4 days after the induction of differentiation into oligodendrocytes or astrocytes. This led to the identification of 52 sequence tags that were expressed differentially with cellular phenotype. One sequence was upregulated during differentiation of CG4 cells and represented a novel gene that we named SETA (SH3 domain-containing gene expressed in tumorigenic astrocytes). This gene encodes an SH3 domain-containing adapter protein with sequence similarity to the CD2AP (CD2 adapter protein) and CMS (Cas ligand with multiple Src homology) genes. SETA mRNA was expressed at high levels in the developing rat brain but was barely detectable in the normal adult rat or human brain. However, SETA mRNA was found in approximately one half of the human gliomas tested, including astrocytomas grades II, III, and IV, as well as oligodendrogliomas, mixed oligoastrocytomas, and human glioma-derived cell lines. A rat glioma generated by treatment with the alkylating carcinogen ethylnitrosourea on postnatal day 1 and a derived cell line also expressed SETA mRNA. Furthermore, in an in vitro model of astrocytoma progression based on p53-/- astrocytes, expression of SETA was restricted to cells that are tumorigenic.

Detection of both mutant and wild-type p53 protein in normal skin fibroblasts and demonstration of a shared 'second hit' on p53 in diverse tumors from a cancer-prone family with Li-Fraumeni syndrome.

Germline transmission of mutant p53 gene in cancer-prone families with Li-Fraumeni syndrome has revealed a new role for p53 in the genetic predisposition to cancer. The studies reported here focus on the analysis of the expression of normal and mutant p53 RNA and protein in germline configuration and demonstrate that normal skin fibroblasts derived from members of a family with Li-Fraumeni syndrome express mutant p53Gly----Asp(245) protein and RNA at levels similar to the wild-type p53. Thus, these fibroblasts represent a unique biological system in which endogenous promoters are utilized for the expression of both mutant and normal p53. We have further extended the earlier observations on the analysis of mutant p53 with a limited number of tumors derived from individuals with Li-Fraumeni syndrome. Tumors arising from two different germ layers in four individuals in a single family clearly exhibited the loss of the wild-type allele and the retention of the mutant allele observed in the normal skin fibroblasts derived from the same individuals. These observations further support the notion that germline p53 mutation plays a key role in the tumorigenesis of individuals with Li-Fraumeni syndrome.

Phase II study of combination 4'-epidoxorubicin and mitomycin C in recurrent epithelial ovarian cancer.

Thirty-three evaluable patients who had epithelial ovarian cancer that had not responded to treatment were entered into a phase II study of combination epirubicin and mitomycin C. Epirubicin (65 mg/m2) and mitomycin C (4 mg/m2) were administered separately, each as an i.v. bolus every 4 weeks. Ten patients (30%) had a complete or partial responses. The median duration of response was 20 weeks (range, 9-53). The regimen was well tolerated. Myelotoxicity occurred in four patients requiring hospitalization for septicaemia. Eleven patients had a blood transfusion. Alopecia was common, and nausea and vomiting, though frequent, usually mild. Cardiological toxicity was observed in one patient only. She developed congestive cardiac failure after an acute myocardial infarction. This regimen is active in advanced ovarian cancer that has not responded to prior treatment and warrants further study combination with other active drugs as a first-line regimen for ovarian cancer.