Employment of Family Members

The use of family labor in the farm or ranch operation can pose a number of challenges for farm managers as they try to sort through the vast quantity of regulations. While the day-to-day human-relations components of managing family members in the farm/ranch operation will differ substantially from that of non-family labor, the focus of this fact sheet will address the income tax and regulatory aspects of employing family members. Generally, the wages that you pay to family members who are also your employees are subject to social security (FICA) and Medicare taxes, federal income tax withholding, and under certain circumstances, federal and state unemployment (FUTA/SUTA). Certain exemptions may apply for your child, spouse, or parent.1In addition, employers who pay less than $150 to one individual per year, or employers who pay less than$2,500 to all employees in one year may be exempt but there are exceptions to this rule. It is important that you understand these exceptions as noted in IRS publication 51.https://digitalcommons.usu.edu/rural_tax/1007/thumbnail.jp

Unique Multiorganizational Collaborative Proves Effective in Delivering 2014 Farm Bill Education

The Agricultural Act of 2014 is critical to the economic safety net for U.S. producers. This act represented a major change in philosophy, requiring producers to make key decisions about their options on the basis of risk management. To add to the complexity of the issue, the time period for delivering applicable education to landowners before sign-up deadlines was relatively short. This article highlights a unique multiorganizational statewide approach to delivering the applicable education. It involved University of Minnesota Extension, the Center for Farm Financial Management, the U.S. Department of Agriculture, and banks and resulted in substantive evaluative outcomes

Structural changes in commercial agriculture

The basic idea of the conference on Structural Changes in Commercial Agriculture was planted in the spring of 1964 by Earl 0. Heady. He outlined for the North Central Farm Management Research Committee his concern about the kind and amount of response to both current and prospective structural changes in the commercial farm firm. Many changes represent adjustments to technological and other innovations originating in marketing, research, and educational agencies serving farmers.https://lib.dr.iastate.edu/card_reports/1025/thumbnail.jp

NEID Reveals that The Young Warm Neptune TOI-2076 b Has a Low Obliquity

TOI-2076 b is a sub-Neptune-sized planet ($R=2.39 \pm 0.10 \mathrm{R_\oplus}$) that transits a young ($204 \pm 50 \mathrm{MYr}$) bright ($V = 9.2$) K-dwarf hosting a system of three transiting planets. Using spectroscopic observations with the NEID spectrograph on the WIYN 3.5 m Telescope, we model the Rossiter-McLaughlin effect of TOI-2076 b, and derive a sky-projected obliquity of $\lambda=-3_{-15}^{+16\:\circ}$. Using the size of the star ($R=0.775 \pm0.015 \mathrm{R_\odot}$), and the stellar rotation period ($P_{\mathrm{rot}}=7.27\pm0.23$ days), we estimate a true obliquity of $\psi=18_{-9}^{+10\:\circ}$ ($\psi < 34^\circ$ at 95% confidence), demonstrating that TOI-2076 b is on a well-aligned orbit. Simultaneous diffuser-assisted photometry from the 3.5 m Telescope at Apache Point Observatory rules out flares during the transit. TOI-2076 b joins a small but growing sample of young planets in compact multi-planet systems with well-aligned orbits, and is the fourth planet with an age $\lesssim 300$ Myr in a multi-transiting system with an obliquity measurement. The low obliquity of TOI-2076 b and the presence of transit timing variations in the system suggest the TOI-2076 system likely formed via convergent disk migration in an initially well-aligned disk.Comment: Submitted to ApJL, 13 pages, 4 figures, 3 table

Estimating radiation effective doses from whole body computed tomography scans based on U.S. soldier patient height and weight

<p>Abstract</p> <p>Background</p> <p>The purpose of this study is to explore how a patient's height and weight can be used to predict the effective dose to a reference phantom with similar height and weight from a chest abdomen pelvis computed tomography scan when machine-based parameters are unknown. Since machine-based scanning parameters can be misplaced or lost, a predictive model will enable the medical professional to quantify a patient's cumulative radiation dose.</p> <p>Methods</p> <p>One hundred mathematical phantoms of varying heights and weights were defined within an x-ray Monte Carlo based software code in order to calculate organ absorbed doses and effective doses from a chest abdomen pelvis scan. Regression analysis was used to develop an effective dose predictive model. The regression model was experimentally verified using anthropomorphic phantoms and validated against a real patient population.</p> <p>Results</p> <p>Estimates of the effective doses as calculated by the predictive model were within 10% of the estimates of the effective doses using experimentally measured absorbed doses within the anthropomorphic phantoms. Comparisons of the patient population effective doses show that the predictive model is within 33% of current methods of estimating effective dose using machine-based parameters.</p> <p>Conclusions</p> <p>A patient's height and weight can be used to estimate the effective dose from a chest abdomen pelvis computed tomography scan. The presented predictive model can be used interchangeably with current effective dose estimating techniques that rely on computed tomography machine-based techniques.</p

Deletion of individual Ku subunits in mice causes an NHEJ-independent phenotype potentially by altering apurinic/apyrimidinic site repair

Ku70 and Ku80 form a heterodimer called Ku that forms a holoenzyme with DNA dependent-protein kinase catalytic subunit (DNA-PKCS) to repair DNA double strand breaks (DSBs) through the nonhomologous end joining (NHEJ) pathway. As expected mutating these genes in mice caused a similar DSB repair-defective phenotype. However, ku70-/- cells and ku80 -/- cells also appeared to have a defect in base excision repair (BER). BER corrects base lesions, apurinic/apyrimidinic (AP) sites and single stand breaks (SSBs) utilizing a variety of proteins including glycosylases, AP endonuclease 1 (APE1) and DNA Polymerase β (Pol β). In addition, deleting Ku70 was not equivalent to deleting Ku80 in cells and mice. Therefore, we hypothesized that free Ku70 (not bound to Ku80) and/or free Ku80 (not bound to Ku70) possessed activity that influenced BER. To further test this hypothesis we performed two general sets of experiments. The first set showed that deleting either Ku70 or Ku80 caused an NHEJ-independent defect. We found ku80-/- mice had a shorter life span than dna-pkcs-/- mice demonstrating a phenotype that was greater than deleting the holoenzyme. We also found Ku70-deletion induced a p53 response that reduced the level of small mutations in the brain suggesting defective BER. We further confirmed that Ku80-deletion impaired BER via a mechanism that was not epistatic to Pol β. The second set of experiments showed that free Ku70 and free Ku80 could influence BER. We observed that deletion of either Ku70 or Ku80, but not both, increased sensitivity of cells to CRT0044876 (CRT), an agent that interferes with APE1. In addition, free Ku70 and free Ku80 bound to AP sites and in the case of Ku70 inhibited APE1 activity. These observations support a novel role for free Ku70 and free Ku80 in altering BER. © 2014 Choi et al

High quality copy number and genotype data from FFPE samples using Molecular Inversion Probe (MIP) microarrays

BACKGROUND:A major challenge facing DNA copy number (CN) studies of tumors is that most banked samples with extensive clinical follow-up information are Formalin-Fixed Paraffin Embedded (FFPE). DNA from FFPE samples generally underperforms or suffers high failure rates compared to fresh frozen samples because of DNA degradation and cross-linking during FFPE fixation and processing. As FFPE protocols may vary widely between labs and samples may be stored for decades at room temperature, an ideal FFPE CN technology should work on diverse sample sets. Molecular Inversion Probe (MIP) technology has been applied successfully to obtain high quality CN and genotype data from cell line and frozen tumor DNA. Since the MIP probes require only a small (~40 bp) target binding site, we reasoned they may be well suited to assess degraded FFPE DNA. We assessed CN with a MIP panel of 50,000 markers in 93 FFPE tumor samples from 7 diverse collections. For 38 FFPE samples from three collections we were also able to asses CN in matched fresh frozen tumor tissue.RESULTS:Using an input of 37 ng genomic DNA, we generated high quality CN data with MIP technology in 88% of FFPE samples from seven diverse collections. When matched fresh frozen tissue was available, the performance of FFPE DNA was comparable to that of DNA obtained from matched frozen tumor (genotype concordance averaged 99.9%), with only a modest loss in performance in FFPE.CONCLUSION:MIP technology can be used to generate high quality CN and genotype data in FFPE as well as fresh frozen samples.This item is part of the UA Faculty Publications collection. For more information this item or other items in the UA Campus Repository, contact the University of Arizona Libraries at [email protected]

Mitochondrial Oxidative Stress Causes Hyperphosphorylation of Tau

Age-related neurodegenerative disease has been mechanistically linked with mitochondrial dysfunction via damage from reactive oxygen species produced within the cell. We determined whether increased mitochondrial oxidative stress could modulate or regulate two of the key neurochemical hallmarks of Alzheimer's disease (AD): tau phosphorylation, and ß-amyloid deposition. Mice lacking superoxide dismutase 2 (SOD2) die within the first week of life, and develop a complex heterogeneous phenotype arising from mitochondrial dysfunction and oxidative stress. Treatment of these mice with catalytic antioxidants increases their lifespan and rescues the peripheral phenotypes, while uncovering central nervous system pathology. We examined sod2 null mice differentially treated with high and low doses of a catalytic antioxidant and observed striking elevations in the levels of tau phosphorylation (at Ser-396 and other phospho-epitopes of tau) in the low-dose antioxidant treated mice at AD-associated residues. This hyperphosphorylation of tau was prevented with an increased dose of the antioxidant, previously reported to be sufficient to prevent neuropathology. We then genetically combined a well-characterized mouse model of AD (Tg2576) with heterozygous sod2 knockout mice to study the interactions between mitochondrial oxidative stress and cerebral Aß load. We found that mitochondrial SOD2 deficiency exacerbates amyloid burden and significantly reduces metal levels in the brain, while increasing levels of Ser-396 phosphorylated tau. These findings mechanistically link mitochondrial oxidative stress with the pathological features of AD