THE CALIBRATION AND IMPLEMENTATION OF CR-39 NUCLEAR TRACK DETECTOR MATERIAL AS A FAST NEUTRON MICRODOSIMETER

A detailed microdosimetric characterization of the M. D. Anderson 42 MeV (p,Be) fast neutron beam was performed using the techniques of microdosimetry and a 1/2 inch diameter Rossi proportional counter. These measurements were performed at 5, 15, and 30 cm depths on the central axis, 3 cm inside, and 3 cm outside the field edge for 10 $\times$ 10 and 20 $\times$ 20 cm field sizes. Spectra were also measured at 5 and 15 cm depth on central axis for a 6 $\times$ 6 cm field size. Continuous slowing down approximation calculations were performed to model the nuclear processes that occur in the fast neutron beam. Irradiation of the CR-39 was performed using a tandem electrostatic accelerator for protons of 10, 6, and 3 MeV and alpha particles of 15, 10, and 7 MeV incident energy on target at angles of incidence from 0 to 85 degrees. The critical angle as well as track etch rate and normal incidence diameter versus linear energy transfer (LET) were obtained from these measurements. The bulk etch rate was also calculated from these measurements. Dose response of the material was studied, and the angular distribution of charged particles created by the fast neutron beam was measured with CR-39. The efficiency of CR-39 was calculated versus that of the Rossi chamber, and an algorithm was devised for derivation of LET spectra from the major and minor axis dimensions of the observed tracks. The CR-39 was irradiated in the same positions as the Rossi chamber, and the derived spectra were compared directly. ^

A biophysical model of synaptic plasticity and metaplasticity can account for the dynamics of the backward shift of hippocampal place fields.

Hippocampal place cells in the rat undergo experience-dependent changes when the rat runs stereotyped routes. One such change, the backward shift of the place field center of mass, has been linked by previous modeling efforts to spike-timing-dependent plasticity (STDP). However, these models did not account for the termination of the place field shift and they were based on an abstract implementation of STDP that ignores many of the features found in cortical plasticity. Here, instead of the abstract STDP model, we use a calcium-dependent plasticity (CaDP) learning rule that can account for many of the observed properties of cortical plasticity. We use the CaDP learning rule in combination with a model of metaplasticity to simulate place field dynamics. Without any major changes to the parameters of the original model, the present simulations account both for the initial rapid place field shift and for the subsequent slowing down of this shift. These results suggest that the CaDP model captures the essence of a general cortical mechanism of synaptic plasticity, which may underlie numerous forms of synaptic plasticity observed both in vivo and in vitro.

Alteration of CEACAM1 gene transcription in prostate cancer cells: The role of AR, Sp2, and HDAC

Cell to cell adhesion molecule (CEACAM1), a type II tumor suppressor, has been found to be down-regulated in prostate cancer cells. The mechanism that causes CEACAM1's down-regulation in tumorigenesis is unknown. Here we show that the transcriptional activity of CEACAM1 is decreased in prostate cancer cells. This decrease is not due to methylation of the CEACAM1's promoter, but rather to the alteration of transcription factors regulating CEACAM1 expression. ^ Since androgen/androgen receptors (AR) are potent regulators of prostate growth and differentiation, their role on CEACAM1 gene transcription was examined. The androgen receptor could directly increase CEACAM1 transcriptional activity in a ligand dependent manner by interacting with an AR consensus element that resides in the CEACAM1 promoter. However, AR binding to the CEACAM1 promoter is not related to the loss of CEACAM1 during prostate cancer progression. ^ Further analysis enabled us to determine the particular region in the CEACAM1 promoter that mediates a decrease in CEACAM1 transcriptional activity in prostate cancer cells. Upon further examination, we found that this CEACAM1 promoter region interacts with the Sp1, Sp2, and Sp3 transcription factors. However, only Sp2 expression was found to increase in prostate cancer cells. Inhibiting Sp2 from binding to the CEACAM1 promoter caused an increase in CEACAM1 transcriptional activity in prostate cancer cells. In addition, over-expressing Sp2 in normal prostate cells resulted in a decrease in CEACAM1 transcriptional activity and endogenous protein expression. These observations suggest that Sp2 is a transcription repressor of CEACAM1. Furthermore, prostate cancer cells treated with trichostatin A (TSA), a specific histone deacetylase (HDAC) inhibitor, activated CEACAM1 transcriptional activity. This implies that HDACs are involved in CEACAM1 transcriptional activity. Mutation of the Sp2 DNA binding region on the CEACAM1 promoter inhibited TSA activation of CEACAM1 transcriptional activity. This indicates that HDACs inhibit CEACAM1 transcriptional activity through Sp2. Base on these results, we propose that Sp2 is critical for down-regulating CEACAM1 expression, and one mechanism by which Sp2 represses CEACAM1 expression is by recruiting HDAC to the CEACAM1 promoter in prostate cancer cells. Collectively, these findings provide novel insights into mechanisms that cause the down-regulation of CEACAM1 expression in prostate cancer cells. ^

Should Texas use public funding for bariatric surgery?

Background. Obesity in America has increased exponentially since the 1970s with no sign of slowing down. It is a major public health problem, and is currently the second leading cause of preventable deaths in America (Flegal et al., 2010). Bariatric surgery is currently the only approved therapy that has shown to have a lasting impact on obese patients. While the initial cost of the surgery remains high, numerous cost-benefit analyses have demonstrated an overall cost saving within two to five years (McEwen et al., 2010). Only three states, including Texas, do not currently fund bariatric surgery through Medicare and Medicaid. ^ Objectives. To determine whether the current data on the cost-benefit analysis of bariatric surgery supports Texas' decision to not publicly fund bariatric surgery through its Medicare and Medicaid programs. ^ Methods. We conducted literature reviews to determine the current cost of obesity in Texas as well as the methods being employed to treat obesity currently. We then analyzed the history of bariatric surgery and its current implementation, looking at safety and the future benefits of bariatric surgery. We then looked at key cost-benefit analyses and meta-analyses to determine the cost effectiveness of bariatric surgery. We then analyzed both direct medical expenditures and indirect benefits of bariatric surgery. ^ Conclusions. If the obesity epidemic continues unabated, it will become one of the leading health expenditures in Texas within decades. Given that surgery is currently the only approved therapy for obesity that has been shown to be effective in the majority of patients, Texas' decision not to publicly fund bariatric surgery is short sighted.^