Race, Class and the Promise of the Public University

Commencement address by Professor Thomas Breslin at Florida International University dissects in a few words both the promise of a public university system and the threats to that system embedded in racial and class privilege

The influence of sodium salts on binary mixtures of bitter-tasting compounds

In order to study potential mixture interactions among bitter compounds, selected sodium salts were added to five compounds presented either alone or as binary bitter- ompound mixtures. Each compound was tested at a concentration that elicited &lsquo;weak&rsquo; perceived bitterness. The bitter compounds were mixed at these concentrations to form a subset of possible binary mixtures. For comparison, the concentration of each solitary compound was doubled to measure bitterness inhibition at the higher intensity level elicited by the mixtures. The following sodium salts were tested for bitterness inhibition: 100 mM sodium chloride (salty), 100 mM sodium gluconate (salty), 100 and 20 mM monosodium glutamate (umami), and 50 mM adenosine monophosphate disodium salt (umami). Sucrose (sweet) was also employed as a bitterness suppressor. The sodium salts differentially suppressed the bitterness of compounds and their binary combinations. Although most bitter compounds were suppressed, the bitterness of tetralone was not suppressed, nor was the bitterness of the binary mixtures that contained it. In general, the percent suppression of binary mixtures of compounds was predicted by the average percent suppression of its two components. Within the constraints of the present study, the bitterness of mixtures was suppressed by sodium salts and sucrose independently, with few bitter interactions. This is consistent with observations that the bitter taste system integrates the bitterness of multi-compound solutions linearly.<br /

Oral zinc sulfate solutions inhibit sweet taste perception

We investigated the ability of zinc sulfate (5, 25, 50 mM) to inhibit the sweetness of 12 chemically diverse sweeteners, which were all intensity matched to 300 mM sucrose [800 mM glucose, 475 mM fructose, 3.25 mM aspartame, 3.5 mM saccharin, 12 mM sodium cyclamate, 14 mM acesulfame-K, 1.04 M sorbitol, 0.629 mM sucralose, 0.375 mM neohesperidin dihydrochalcone (NHDC), 1.5 mM stevioside and 0.0163 mM thaumatin]. Zinc sulfate inhibited the sweetness of most compounds in a concentration dependent manner, peaking with 80% inhibition by 50 mM. Curiously, zinc sulfate never inhibited the sweetness of Na-cyclamate. This suggests that Na-cyclamate may access a sweet taste mechanism that is different from the other sweeteners, which were inhibited uniformly (except thaumatin) at every concentration of zinc sulfate. We hypothesize that this set of compounds either accesses a single receptor or multiple receptors that are inhibited equally by zinc sulfate at each concentration.<br /

Automata Learning with an Incomplete Teacher (Artifact)

We provide an implementation of the automata learning software described in the associated ECOOP article. In particular, the artifact is a Docker image with the source code for nerode and nerode-learn, along with the scripts and benchmark inputs needed to reproduce the experiments described in the paper

Voluntary Wheel Running during Weight Loss Leads to Differential Changes in Monocytes, Compared to Forced Treadmill Running

High-fat feeding and subsequent weight gain may contribute to innate immune dysfunction. Weight loss via calorie restriction and exercise represent one means to restore normal immune function. The purpose of the study was to examine how 8- weeks of aerobic exercise and low-fat diet affects weight gain, monocyte concentration, and monocyte cell-surface expression of TLR2, TLR4, CD80, and CD86. For 12- months, 24 male CD-1 mice underwent a pre-treatment phase, consuming either a low fat (10% fat) or high-fat (60% fat) diet ad libitum. Mice were randomly assigned to one of four groups (N=6/group): CN (low-fat sedentary), V-EX (voluntary wheel running), F10 EX (forced treadmill running), or SD (sedentary). V-EX, F-EX, and SD groups were switched from the high-fat to low-fat diet for an 8-week treatment period, while the CN group continued consuming the low-fat diet. Saphenous vein blood samples were analyzed using flow cytometry at baseline, week 4, and week 8. V-EX (36.4%) and F14 EX (27.1%) lost significant body weight over 8-weeks (P\u3c0.001). V-EX ran 4.4x more than F-EX (P\u3c0.001). As a group, V-EX had higher monocyte concentration than CN (48.9%) and F-EX (58.9%, P=0.004). Cell-surface expression of TLR2 (22.9%, P=0.002), TLR4 (33.3%, P\u3c0.001), and CD86 (18.6%, P\u3c0.001) increased from baseline to week 8. A time effect was seen in week 4 when CD80 expression was 42% greater for V-EX than SD (P=0.013). The present study confirms short-term exercise and low-fat diet consumption cause significant weight loss and altered immune profile as measured by increased TLR2, TLR4, CD80, and CD86 expression

Caspase-3 suppresses diethylnitrosamine-induced hepatocyte death, compensatory proliferation and hepatocarcinogenesis through inhibiting p38 activation

It is critical to understand the molecular mechanisms of hepatocarcinogenesis in order to prevent or treat hepatocellular carcinoma (HCC). The development of HCC is commonly associated with hepatocyte death and compensatory proliferation. However, the role of Caspase-3, a key apoptotic executor, in hepatocarcinogenesis is unknown. In this study, we used Caspase-3-deficient mice to examine the role of Caspase-3 in hepatocarcinogenesis in a chemical (diethylnitrosamine, DEN)-induced HCC model. We found that Caspase-3 deficiency significantly increased DEN-induced HCC. Unexpectedly, Caspase-3 deficiency increased apoptosis induced by DEN and the subsequent compensatory proliferation. Intriguingly, we discovered that Caspase-3 deficiency increased the activation of p38 with and without DEN treatment. Moreover, we demonstrated that TNFα and IL1α stimulated increased activation of p38 in Caspase-3 KO hepatocytes compared with wild-type hepatocytes. Finally, we found that inhibition of p38 by SB202190 abrogated enhanced hepatocyte death, compensatory proliferation and HCC induced by DEN in Caspase-3-deficient mice. Overall, our data suggest that Caspase-3 inhibits chemical-induced hepatocarcinogenesis by suppressing p38 activation and hepatocyte death

Exercise as a Prevention and Countermeasure to Diet-Induced Weight Gain

The purpose of this study was to evaluate the effectiveness of treadmill running at attenuating weight gain and immune dysfunction prior to or during a period of high-fat feeding in outbred CD-1 male mice. Mice were divided into four groups (N=10 mice/group): 4-weeks of treadmill running followed by 4-weeks sedentary (EX-SED), 4-weeks sedentary followed by 4 weeks of treadmill running (SEDEX), 8 weeks of treadmill running (EX), and 8 weeks sedentary (SED). After the first four weeks of the study, all groups began consumption of a high-fat diet to elicit a weight gain response. In order to track immune dysfunction, we measured peripheral blood monocytes and monocyte TLR4 expression at the conclusion of the study. We also completed a detailed analysis of body weight change over time. SED-EX was the only group that did not gain a significant amount of weight during the high-fat feeding. SED-EX had the lowest percentage of monocytes, as well as the highest total monocyte and classic subset cell surface TLR4 expression. EX and SED were not significantly different in any measurement. The present study demonstrates the importance of exercise training in counteracting the pro-inflammatory effects of diet-induced weight gain, as seen in SED-EX. Contrary to our hypothesis, exercise training prior to and throughout high-fat feeding did not prevent weight gain or attenuate the pro-inflammatory effects of weight gain. This could be due to an acclimation to the exercise intervention that blunted the anti-inflammatory effects of the exercise training during the high-fat feeding phase of the study. Similarly, exercise prior to high-fat feeding did not provide a lasting protective effect against the pro-inflammatory effects of diet-induced weight gain. Future research will endeavor to expand the current knowledge about monocyte subpopulations and to further elucidate the relationship between exercise and TLR4

Exercise Attenuates Weight Gain and Fat Accumulation in CD1- Mice Consuming a High-fat Diet

Background: Exercise training, in combination with a healthful diet, is a reliable method of weight loss or weight maintenance. It is unknown whether an exercise training program would sufficiently attenuate weight gain during chronic consumption of a high-fat diet. Purpose: Therefore, the purpose of this study was to evaluate the ability of an aerobic exercise training program to prevent excessive weight gain both before and during consumption of a high-fat diet in CD-1 male mice. Methods: Mice were divided into four groups (N=10 mice/group): 4-weeks of treadmill running followed by 6-weeks sedentary (EX-SD), 4-weeks sedentary followed by 6 weeks of treadmill running (SD-EX), 10 weeks of treadmill running (EX), and 10 weeks sedentary (SD). After the first four weeks of the study, all groups began consumption of a high-fat diet to elicit a weight gain response. The exercise program consisted of 1 hour of treadmill running 5 days/wk at ~15m/min. Body weight and body composition we measured bi-weekly. Results: EX-SD, EX, and SD gained a significant amount of both body weight and body fat after only 4 weeks of high-fat feeding (P\u3c0.05). SD-EX was the only group that did not gain a significant amount of body weight or body fat during the 6-week high-fat feeding period. Conclusions: The present study demonstrates the importance of exercise training in counteracting concurrent diet-induced weight gain, as seen in SED-EX. EX approximately matched SD in body weight gain and body fat accumulation, suggesting that exercise interventions must be progressive in order to prevent an adaptation to the training program than minimizes exercise benefits. Future research will evaluate progressive exercise training programs and their implications in various mouse models