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Making Masa for Tamales
Making tamales is for people who do not have a life and that is why we only make them once a year. This is the most labor intensive hobby in the world. This makes baking bread seem like a simple project. Let’s start with the simple task of finding organic dried corn. That was my first career in this undertaking. I didn’t need a resume to find this job. This brings me to the midlife crisis of converting this organic whole yellow corn into masa. I now consider masa a four-letter word.
1 ½ lbs. of Dried Whole Organic Yellow Corn
2 Quarts Filtered Water
1 Tbs of Pickling Lime
2-3 Tbs of Organic Chicken Broth
For a start, place 1 1/2 pounds of dried yellow corn in a large pan and fill with 2 quarts of filtered water. Add one tablespoon of pickling lime, bring to a boil then let simmer for ten minutes. After it cools down place in a glass bowl (not metal) cover with a cheese cloth and let it soak for one to two weeks. This is a long wait, so I suggest you find other things to do, such as changing the baby’s diaper, building a house or baking bread.
Now we are ready for the exciting part, take the freshly soaked corn and rinse it thoroughly. Put this in a heavy-duty food processor one cup at a time and let run a couple of minutes (I suggest pulsing part of the time). Also stop every minute or so and push the corn down into the blades with a spatula. The corn will be coarse and dry at this point so let the processor run for two minutes. Add broth one spoon at a time. (The last time I did these two tablespoons of broth worked perfectly.) As the processor continues to run the masa should be clinging together and start forming into a ball. This is the moment of truth, yielding a major league size glob of masa is the objective. The food processor will start bouncing from side to side as the ball forms. If not, then phone the local Mexican Market and order five pounds of masa. This is like brain surgery: if you know how to do it, it’s easy.
Now we move swiftly into phase two of this project. We add the final ingredients that transforms this ball into masa. I use the Bosch mixer to blend the secret recipe of the tamale masa.
Add the following:
1.5 lbs. processed corn (the baseball)
¾ Cup coconut oil or 6 ounces (organic preferred)
1 Teaspoon sea salt
1.5 Teaspoons Baking Powder
You will also need about one pack of husks. Please don’t put these in the mixer, trust me it makes a big mess. You will need something to fill the tamale with. The technical Mexican term for this is called Spreading the Masa, then place the filler of your choice on top of the spread and close the tamale. This makes a great healthy tamale. Now the cloud of gloom lifts; it is almost time to eat the tamales. All the hard work pays off... the greatest, healthiest tamales this side of Heaven. With this corn Masa you can make masa for tamales and corn tortillas (we will show you how to make corn tortillas in a future blog post).
My mother in law Mercy Montes, my favorite mother-in-law of all times, started this tamale tradition. I miss her dearly. She always prayed for me, spent time with me and defended me even when I was wrong. She brought this wonderful tradition and recipe from Mexico many years ago. The Christmas and tamale season are always sprinkled with a bit of sadness without her. She will never be forgotten.
If you have any problems with this recipe or questions, please email my wife at firstname.lastname@example.org. You can purchase your organic yellow whole corn here. Survival hand grinders coming soon!
Happiest of Holidays!
-Jerry, from Survival General


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- Label free proteomics. Here no labels are used and the quantitation is relying on for example extracted ion chromatograms.
Many proteins are post-translationally modified and it is those modifications that often determine the function, interaction and physio-chemical properties of these proteins. A posttranslational modification (PTM) is the covalent attachment of a chemical group to a protein after protein synthesis or the proteolytical removal of a signal peptide after localization. PTMs are essential for the function and localization of proteins. Therefore, the analysis of PTMs in clinical proteomics might provide new discoveries both in the disease understanding and in the biomarker discovery areas.
CCP has a world recognized experience in identification, characterization and quantitation of various PTMs, including phosphorylation, glycosylation, acetylation, etc. We have robust protocols for quantitative analysis of the above mentioned PTMs and are routinely identifying thousands of phosphorylation sites and sialylated glycosylation sites from low amount of primary cell material.


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|San Diego Visual Art Collaborations is an multi-facet exhibition featuring collaborations between local artists, patrons and The Studio Door running from May 1 - 28, 2021 produced by The Studio Door.
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The gallery's 2021 Celebration of Sculpture also continues with sculptor Manuelita Brown artworks in the gallery for May and June.


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Audi Sport customer racing has announced the successful delivery of its first customer racing R8 LMS GT4 competition cars. Customers from America, Australia, China and Europe took delivery of the first twelve examples of the car, at a special event at Audi’s Neuburg an der Donau facility.
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text: Penarth was an agricultural community but the Industrial Revolution brought a great change. The town owes its early development to the success of the South Wales coalfields and the necessity for additional port facilities to accommodate the industry that followed. A tidal harbour was planned, which became a dock. The beach and Esplanade provided relaxation for locals and tourists alike and Penarth could boast a pier constructed by James & Arthru Mayoh in 1894. It was from Penarth beach that Kathleen Thomas became the first person to swim the Bristol Channel in 1927. She swam into Weston-super-Mare in seven hours and eighteen minutes. The book contains over 200 fascinating photographs, some loaned from family albums and others from prized postcard collections. It explores the dock, the town and includes its churches, as well as Penarth's gardens and the Esplanade, before travelling on to Sully via Lavernock and Swanbridge. Penarth holds many happy childhood memories for the author and the book will be enjoyed by all who have lived in Penarth or know it as a place they have visited since their childhood.

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Potential conflict of interest: Nothing to report.
We have been using polarized hepatic WIF-B cells to examine ethanol-induced liver injury. Previously, we determined microtubules were more highly acetylated and more stable in ethanol-treated WIF-B cells. We proposed that the ethanol-induced alterations in microtubule dynamics may explain the ethanol-induced defects in membrane trafficking that have been previously documented. To test this, we compared the trafficking of selected proteins in control cells and cells treated with ethanol or with the histone deacetylase 6 inhibitor trichostatin A (TSA). We determined that exposure to 50 nM TSA for 30 minutes induced microtubule acetylation (∼3-fold increase) and stability to the same extent as did ethanol. As shown previously in situ, the endocytic trafficking of the asialoglycoprotein receptor (ASGP-R) was impaired in ethanol-treated WIF-B cells. This impairment required ethanol metabolism and was likely mediated by acetaldehyde. TSA also impaired ASGP-R endocytic trafficking, but to a lesser extent. Similarly, both ethanol and TSA impaired transcytosis of the single-spanning apical resident aminopeptidase N (APN). For both ASGP-R and APN and for both treatments, the block in trafficking was internalization from the basolateral membrane. Interestingly, no changes in transcytosis of the glycophosphatidylinositol-anchored protein, 5′-nucleotidase, were observed, suggesting that increased microtubule acetylation and stability differentially regulate internalization. We further determined that albumin secretion was impaired in both ethanol-treated and TSA-treated cells, indicating that increased microtubule acetylation and stability also disrupted this transport step. Conclusion: These results indicate that altered microtubule dynamics explain in part alcohol-induced defects in membrane trafficking. (HEPATOLOGY 2008.)
Alcoholic liver disease is a major biomedical health concern in the United States. Although the progression of this disease has been well described clinically, little is known about the molecular basis for liver injury. Research aimed at identifying the molecules and pathways that promote alcohol-induced hepatotoxicity has been hampered by the lack of good in vitro models. Our recent studies have been performed in WIF-B cells, an emerging model system for the study of alcohol-induced liver injury. These hepatic cells are highly differentiated and form discrete apical and basolateral membrane domains in culture. Domain-specific membrane proteins are localized in WIF-B cells as they are in hepatocytes in situ, and many liver-specific functions are maintained.1 Importantly, WIF-B cells metabolize ethanol using alcohol dehydrogenase (ADH) and cytochrome P4502E1.2 Like hepatocytes, ethanol-treated WIF-B cells display a reduced redox state and increased triglycerides.2
More recently, we discovered that microtubule repolymerization was impaired in ethanol-treated WIF-B cells,3 consistent with reports performed in vitro and in isolated hepatocytes.4–6 We also found that steady-state microtubules in alcohol-treated WIF-B cells were more stable and were acetylated 2-3-fold more than were those in control cells.3 This posttranslational modification is characteristic of stable microtubule populations (see Westermann and Weber7 and the Discussion section). We confirmed these results in livers from ethanol-fed rats, indicating the findings have physiologic importance.3 We further determined that increased microtubule acetylation and stability in WIF-B cells was dependent on ethanol metabolism and was likely mediated by acetaldehyde. Thus, alcohol consumption and metabolism alter hepatic microtubule dynamics.
Because microtubules are central to multiple cellular processes, changes in their dynamics will likely alter hepatic function. This study was aimed at understanding the relationship between protein trafficking and alterations in microtubule dynamics. Not only is protein trafficking microtubule dependent, it is also selectively impaired by ethanol.8–10 Two transport pathways appear to be affected: transport of newly synthesized secretory or membrane proteins from the Golgi to the basolateral membrane and receptor-mediated endocytosis from the sinusoidal surface. Can the defects in secretion and endocytosis be explained by increased microtubule acetylation and stability?
To answer this question, we examined the trafficking of selected proteins in WIF-B cells treated with ethanol or trichostatin A (TSA), an inhibitor of histone deacetylase 6 (HDAC6). HDAC6 is the major tubulin deacetylase in liver and WIF-B cells (Grozinger et al.12 and manuscript in preparation), and when inhibited with TSA, increased microtubule acetylation and stability is observed.13–15 We determined that 50 nM TSA for 30 minutes induced microtubule acetylation and stability to the same extent in WIF-B cells as did ethanol, allowing us to test our hypothesis. This result also suggested that acetylation induced microtubule stability, a topic that is currently controversial (for example, see Tran et al.15 and Palazzo et al.16 and the Discussion section). As shown in situ,8–10 ethanol impaired albumin secretion and internalization of asialoglycoprotein receptor (ASGP-R), further confirming that WIF-B cells are a good model for studying alcoholic liver injury. Similarly, TSA treatment impaired albumin secretion and ASGP-R internalization, but to a lesser extent. Both agents impaired internalization of the single-spanning apical resident aminopeptidase N (APN), but distribution of the glycophosphatidylinositol (GPI)–anchored protein 5′-nucleotidase (5′-NT) was not altered, suggesting that microtubule acetylation and stability selectively regulate internalization. We concluded that increased microtubule acetylation and stability in part explain the alcohol-induced defects in membrane trafficking.
F12 (Coon's) medium, 4-methylpyrazole (4-MP), nocodazole, and TSA were purchased from Sigma-Aldrich (St. Louis, MO). Fetal bovine serum came from Gemini Bio-Products (Woodland, CA) and Hepes from HyClone (Logan, UT). Alexa-466-conjugated and Alexa-568-conjugated secondary antibodies were purchased from Invitrogen (Carlsbad, CA). HRP-conjugated secondary antibodies and the monoclonal antibodies against α-tubulin and acetylated α-tubulin came from Sigma-Aldrich. Polyclonal antibodies against rat serum albumin were from ICN Kappel (Costa Mesa, CA). Antibodies against ASGP-R, APN, HA321, and 5′-NT were all kindly provided by Dr. Ann Hubbard (Johns Hopkins School of Medicine, Baltimore, MD).
WIF-B cells were grown in a humidified 7% CO2 incubator at 37°C as described.1 Briefly, cells were grown in F12 medium (pH 7.0) supplemented with 5% FBS, 10 μM hypoxanthine, 40 nM aminopterin, and 1.6 μM thymidine. Cells were seeded on glass coverslips at 1.3 × 104 cells/cm2 and grown for 8–12 days until they reached maximum density and polarity. In general, cells were treated on day 7 with 50 mM ethanol in medium buffered with 10 mM Hepes (pH 7.0) for 72 hours as described.2 Cells were additionally treated with 4-MP or TSA as described in the figure captions.
WIF-B cells were fixed on ice with chilled phosphate-buffered saline (PBS) containing 4% paraformaldehyde for 1 minute and permeabilized with ice-cold methanol for 10 minutes as described.17 When staining for acetylated or total α-tubulin, cells were fixed and permeabilized with methanol at −20°C for 5 minutes. Cells were processed for indirect immunofluorescence as described.17 Alexa-conjugated secondary antibodies were used at 5 μg/mL.
Labeled cells were visualized by epifluorescence using an Olympus BX60 Fluorescence Microscope (OPELCO, Dulles, VA). Images were taken with a Coolsnap HQ2 digital camera (Photometrics, Tucson, AZ) and IPLabs image analysis software (Biovision, Exton, PA) or with a SPOT digital camera (Diagnostic Instruments, Sterling Heights, MI) and SPOT Advanced software. Adobe Photoshop (Adobe Systems Inc., Mountain View, CA) was used to compile images.
To quantitate the relative distributions of APN, 5′-NT, and ASGP-R, random fields from each slide were visualized by epifluorescence and digitized. From micrographs, the average pixel intensity of selected regions of interest (ROIs) placed at the apical or basolateral surface of the same WIF-B cell (APN and 5′-NT) were measured using the Measure ROI tool of ImageJ imaging software (National Institutes of Health). For ASGP-R, the average pixel intensity at the intracellular compartment or plasma membrane of the same cell was measured. The averaged background pixel intensity was subtracted from each value, and the ratio of apical to basolateral membrane (APN and 5′-NT) or intracellular to plasma membrane fluorescence intensity (ASGP-R) was determined.
ASGP-R was surface-labeled in control or treated cells for 15–30 minutes at 37°C with antibodies (diluted 1:25) specific to an extracellular epitope as described.17 Cells were washed 3 times with PBS, fixed as described above, and labeled with Alexa-488-conjugated secondary antibodies.
To analyze whole-cell lysates, cells grown on coverslips were washed 3 times in prewarmed PBS and lysed directly in 200 μL of SDS-PAGE sample buffer and boiled. To assess the relative amounts of soluble and insoluble tubulin, microtubules were depolymerized with 33 μM nocodazole for increasing times as described in the figure captions. Cells were washed 3 times with prewarmed PEM (80 mM PIPES, 2 mM EGTA, 1 mM MgCl2 [pH 6.8]) and extracted in 300 μL of PEM containing 0.15% Triton X-100 at 37°C for l minute. The supernatant (containing soluble tubulin) was collected, and SDS-PAGE sample buffer was added. The cells (containing polymeric tubulin) were washed 3 times in prewarmed PEM without detergent and lysed in SDS-PAGE sample buffer. Samples were immunoblotted with anti-α-tubulin (1:7,500) or anti-acetylated α-tubulin (1:4,000). Immunoreactivity was detected using enhanced chemiluminescence (PerkinElmer, Waltham, MA). The relative levels of tubulin were determined by densitometric analysis of immunoreactive bands.
Cells were pretreated in the absence or presence of 50 mM ethanol for 72 hours or in the absence or presence of 50 nM TSA for 15 minutes. Cells were rinsed 5 times with prewarmed serum-free medium and then reincubated in serum-free medium in the continued absence or presence of either agent. Either 0, 15, 30, or 60 minutes after reincubation, aliquots of the media were collected and analyzed for albumin secretion by immunoblotting. The cell lysates were also collected by solubilization directly into SDS-PAGE sample buffer. Samples were processed for immunoblotting and densitometry as described above. At each time, the percentage of secreted albumin was determined and plotted. A rate of albumin secretion (percentage of albumin secreted/minute) was calculated for each experiment.
The results are expressed as means ± SEMs. Comparisons between control, TSA- or ethanol-treated cells were made using the Student t test for paired data. P values ≤ 0.05 were considered significant.
TSA Induced Increased Microtubule Acetylation and Stability to an Extent Similar to Ethanol.
To test our hypothesis that microtubule acetylation is responsible for alcohol-induced defects in membrane trafficking, we established TSA conditions that promoted equivalent levels of microtubule acetylation in the absence of alcohol. As shown in Fig. 1A, TSA promoted the concentration-dependent acetylation of microtubules, saturating at 500 nM. From this analysis and from time-dependence studies (data not shown), we chose 50 nM TSA for 30 minutes for subsequent analysis. These conditions generally led to a 2-5-fold increase in microtubule acetylation, approximating the approximately 3-fold increase observed with ethanol.3
Previously, we observed that ethanol promoted the formation of microtubules that appeared thicker and more gnarled, features of stable microtubules.3 However, when TSA-treated cells were stained for total α-tubulin, the change in morphology was much less pronounced. The tubules appeared somewhat thicker but not shorter or more gnarled (Fig. 1B[a,b]). This may likely be explained by the short TSA treatment (30 minutes versus 72 hours of ethanol treatment). In contrast, the acetylated α-tubulin staining pattern in TSA-treated cells was similar to that in ethanol-treated cells (Fig. 1B[c,d]), where increased labeling was detected in the microtubule organizing centers just adjacent to the apical membrane (the bile canalicular-like structures are indicated by asterisks).
Because microtubule acetylation is a marker for stable microtubules7 and because increased acetylation in ethanol-treated cells correlated with increased microtubule stability, we examined the effect of TSA on microtubule stability. We assayed intact cells for soluble versus polymeric acetylated tubulin after treatment with the microtubule poison nocodazole. Cells were treated with 33 μM nocodazole for the indicated times (Fig. 2) and lysed in a microtubule stabilizing buffer containing 0.15% Triton X-100. The soluble (S) tubulin (that is deacetylated) was released into the supernatant, whereas the stable polymeric (P) tubulin (that is acetylated) remained cell associated. In control cells, acetylated microtubule polymers were significantly depolymerized after 15 minutes of nocodazole; less than 50% remained polymeric (Fig. 2). In contrast, the polymers in TSA-treated cells were nocodazole resistant. Even after 60 minutes, 72% ± 11% of the acetylated polymeric tubulin remained compared with the 16% ± 8% observed in the controls. The levels of polymeric tubulin in TSA-treated cells were remarkably similar to values from ethanol-treated cells (72% versus ∼75% polymeric tubulin, respectively, after 60 minutes; see Kannarkat et al.3), These data indicate that the TSA-induced increase in microtubule acetylation and stability was similar to that induced by ethanol, thus providing us with the appropriate agent to test our hypothesis. Also, these results suggest that increased acetylation induced microtubule stability, a topic currently being debated (see Discussion section).
Ethanol and TSA Impair Internalization of Selected Proteins.
We first examined the steady-state distributions of ASGP-R, a receptor whose itinerary is impaired by ethanol consumption.8–10 In control cells, the majority of ASGP-R was on intracellular, perinuclear structures (Fig. 3A). Although this intracellular staining was present in ethanol-treated cells, a striking increase in staining at or near the basolateral membrane was observed (Fig. 3B). Such a shift in distribution is consistent with impaired internalization of this recycling receptor from the basolateral surface. These results are also consistent with reports of impaired internalization in situ,8–10 further confirming that WIF-B cells are a good model for studying alcohol-induced hepatic injury.
To confirm our morphological observations, we quantitated ASGP-R distribution from micrographs using our previously published method.18 The ratio of intracellular to basolateral fluorescence for ASGP-R in control cells was 1.53, indicating that most receptors were intracellular (Table 1). In the presence of ethanol, this ratio was decreased to 0.88 (56% of control, P < 0.006), indicating more receptors were present at the basolateral surface, consistent with decreased internalization. The addition of the ADH inhibitor 4-MP prevented redistribution, and the ratio was similar to that of the control (1.28, P < 0.02), indicating that ethanol metabolism was required for the trafficking defect and that the impairment was likely mediated by acetaldehyde, results also consistent with previous studies.11 An increased basolateral population of ASGP-R was also observed in TSA-treated cells (Fig. 5A,B) but to a lesser extent than in ethanol treated cells (Table 1). Nonetheless, the 20% decrease in the ratio of intracellular to basolateral staining was found to be statistically significant (P < 0.02). As described above, the less dramatic TSA effect was likely a result of the short treatment time.
Table 1. Ethanol- and TSA-Impaired Trafficking of ASGP-R and APN, But Not 5′-NT
EtOH + 4-MP
For experiments summarized on the left side of the table, cells were treated for 72 hours in the absence or the presence of 50 mM ethanol and/or 3 mM 4-MP as indicated. For the experiments on the right side, cells were treated for 30 minutes with 50 nM TSA. Cells were fixed and stained for the indicated proteins. Random fields were visualized by epifluorescence and digitized. From micrographs, the average pixel intensity from selected regions of interest placed at the apical or basolateral membrane of the same WIF-B cell was measured to analyze the distribution of APN and 5′-NT. For ASGP-R, the average pixel intensity in the intracellular structures or plasma membrane of the same cell was measured. The averaged background pixel intensity was subtracted from each value, and the ratio of apical to basolateral membrane (for APN and 5′-NT) or intracellular to membrane fluorescence intensity (for ASGP-R) was determined. Values are expressed as the mean ±SEM; the percentage of the control for each treatment condition is shown in parentheses.
To determine if the internalization defect was specific to recycling receptors, we examined the distribution of another class of proteins, apical residents. In hepatocytes, newly synthesized apical residents take an indirect route to the apical surface. They are transported from the TGN to the basolateral surface, where they are selectively retrieved by endocytosis and transcytosed to the apical surface.19 We tested whether ethanol impaired the basolateral internalization of transcytosing proteins by examining the distributions of APN (single-spanning protein) and 5′-NT (GPI-anchored protein). Importantly, these proteins are likely internalized via different mechanisms.19
In control cells, APN was found exclusively at the apical surface (Fig. 4A), whereas 5′-NT was found mainly at the apical surface, with a small population of the transcytosing population at the basolateral surface (Fig. 4C). Interestingly, increased basolateral staining was only observed for APN in the presence of ethanol (Fig. 4B). To ensure that the increased basolateral staining was not a result of the loss of tight junction integrity, which would allow lateral diffusion, we examined the distribution of HA321, a basolateral resident. In both control and treated cells, HA321 distribution was restricted to the basolateral surface (Fig. 4E,F; note the absence of staining at the canaliculi, indicated by asterisks), showing that lateral diffusion to the apical surface was blocked and confirming the integrity of the tight junctions.
Our morphological observations were confirmed when the ratio of apical to basolateral membrane staining was measured in control and treated cells (Table 1). The ratio for APN staining was drastically reduced, from 10.89 to 4.49 (41% of control values) in ethanol-treated cells, indicating increased basolateral levels, and as for ASGP-R, implying decreased basolateral internalization. In contrast, no significant change in the fluorescence intensity ratio was detected for 5′-NT (Table 1), suggesting no impairment of its internalization.
Remarkably, this selectivity was observed in TSA-treated cells. Morphologically, a slightly increased basolateral population of APN was observed in treated cells (Fig. 5C,D), but no change in the distributions of 5′-NT or HA321 was observed (Fig. 5E,F and G,H, respectively). These observations were confirmed quantitatively (Table 1). Despite the smaller difference for APN, the values were statistically significant when normalized to the percent inhibition for each experiment (P < 0.05). As described earlier, this was likely a result of the short TSA incubation. However, it is interesting to note that the ratios for both ASGP-R and APN decreased to nearly the same levels in TSA-treated cells (19.5% and 21%, respectively), supporting the significance of these findings.
Ethanol- and TSA-Impaired Basolateral Internalization of ASGP-R.
These results suggest that both agents impaired basolateral internalization. To confirm this directly, we monitored the trafficking of antibody-labeled ASGP-R. Live cells were labeled with ASGP-R antibodies specific to external epitopes and internalized for 15–30 minutes. Because tight junctions restrict antibody access to the apical surface, only antigens at the basolateral membrane were labeled. Cells were fixed and labeled with secondary antibodies to detect the trafficked antigen–antibody complexes. In control cells, a significant intracellular ASGP-R population was detected (Fig. 6A,C, arrows) with very little basolateral labeling, indicating that ASGP-R was rapidly internalized. In contrast, in both ethanol-treated cells (Fig. 6B) and TSA-treated cells (Fig. 6D), ASGP-R was mainly detected at the basolateral surface; very little intracellular labeling was observed. These results indicate that the increased ASGP-R steady-state basolateral staining was a result of impaired internalization.
TSA and Ethanol Impair Albumin Secretion.
Because ethanol is known to impair secretion in situ and in isolated hepatocytes, we examined whether ethanol and TSA impaired albumin secretion in WIF-B cells. For these experiments, cells were pretreated in the absence or the presence of 50 mM ethanol for 72 hours or of 50 nM TSA for 15 minutes. Cells were washed and reincubated in serum-free medium in the continued absence or presence of either agent. Either 0, 15, 30, or 60 minutes after reincubation, aliquots of the media were collected and analyzed for albumin secretion by immunoblotting. Values were plotted, and rates of albumin secretion were calculated. As in situ, ethanol impaired albumin secretion in WIF-B cells (Table 2). Although the rate decreased by only about 20%, this was significant (P < 0.03). TSA treatment also led to decreased secretion (Table 2), but in this case the impairment was more dramatic (>26% impaired) and was highly significant (P < 0.0001). We believe that this disparity might be explained by the ability of WIF-B cells to compensate for decreased secretion during the longer ethanol incubation. Nonetheless, microtubule acetylation and increased stability appear to correlate with impaired secretion.
Table 2. Ethanol- and TSA-Impaired Albumin Secretion
Secretion rate (% secreted/min)
Cells were pretreated in the absence or the presence of 50 mM ethanol for 72 hours or in the absence or the presence of 50 nM TSA for 15 minutes. Cells were washed and reincubated in serum-free medium in the continued absence or presence of ethanol or TSA. Either 0, 15, 30, or 60 minutes after reincubation, aliquots of media were collected and analyzed for albumin secretion by immunoblotting. The percent secreted was graphed for each time, and the rate of albumin secretion was determined for each experiment. Values are the average ± SEM of at least 3 independent experiments; *P < 0.03; †P < 0.0001.
1.03 ± 0.05
0.84 ± 0.03*
1.04 ± 0.02
0.76 ± 0.02†
We previously determined that ethanol induced increased acetylation and stability of microtubules in WIF-B cells and in livers from ethanol-fed rats.3 In the present study, we asked whether these microtubule alterations could explain ethanol-induced defects in protein trafficking. We compared the distribution and dynamics of selected proteins in ethanol- and TSA-treated cells. Importantly, TSA led to increased microtubule acetylation and stability to the same extent as that in ethanol. Both treatments led to the impaired internalization of ASGP-R and APN. Interestingly, the internalization of 5′-NT, a GPI-anchored protein, was not impaired, implying the effect was selective (that is, only certain internalization mechanisms were impaired) and specific (that is, the changes were due to altered microtubule dynamics). Furthermore, we determined that albumin secretion was impaired in ethanol- and TSA-treated cells. We concluded that increased microtubule acetylation and stability in part explain ethanol-induced defects in protein trafficking. These studies also further confirmed that WIF-B cells are a good model for studying alcohol-induced hepatotoxicity.
TSA-Induced Microtubule Acetylation and Stability.
Microtubules exist as both dynamic and stable polymers. The latter population is characterized by a longer half-life, resistance to microtubule poisons (for example, cold and nocodazole), and specific posttranslational modifications.7 These modifications include the removal of a carboxy-terminal tyrosine, polyglutamylation, polyglycylation, and acetylation of lysine 40 on α-tubulin.7 The functions of these modifications and how they contribute to microtubule stability are not yet understood. In particular, the role of acetylation-induced microtubule stability has been the subject of debate. In some studies, acetylation appeared independent of microtubule stability,16, 20, 21 whereas in other studies including this one, increased acetylation induced increased microtubule stability.13–15 The reasons for these conflicting results are not known but may reflect cell type differences in microtubule dynamics. Also, different assays were used to determine stability that likely vary in sensitivity and approach (for example, measuring nocodazole resistance versus real-time tubulin dynamics) such that conflicting results were obtained.
How Might Increased Microtubule Acetylation and Stability Impair Protein Trafficking?
There is evidence that different microtubule populations (and/or modification of these populations) support specific protein transport steps.22 Of particular interest are studies performed in WIF-B cells that used a novel microtubule depolymerizing drug, 201-F.23 This drug specifically depolymerized dynamic microtubules, leaving only stable acetylated polymers behind. In 201-F–treated cells, both secretion and transcytosis were impaired. Although the specific impaired transcytotic step was not identified, increased basolateral labeling of the apical proteins was observed. These results are remarkably consistent with our findings that in ethanol-treated or TSA-treated cells in which increased populations of stable microtubules were observed (presumably at the expense of dynamic microtubules), both albumin secretion and basolateral internalization were impaired.
How Does Increased Microtubule Acetylation and Stability Alter Protein Trafficking?
Although lysine 40 is thought to reside in the lumen of the microtubule,24 it is possible that its acetylation may lead to altered tubulin conformation such that there are altered interactions with microtubule-associated proteins and motors. This hypothesis is supported by the findings that kinesin, dynein, and dynactin preferentially bound acetylated microtubules in neuronal cells.21, 25, 26 Enhanced kinesin binding to acetylated microtubules correlated with increased anterograde vesicle motility in these neuronal cells,21, 26 a result inconsistent with the decreased secretion observed in our studies. However, secretion of interkleukin 1β was impaired in blood cells treated with specific HDAC6 inhibitors,27 consistent with our results suggesting that microtubule dynamics may differentially regulate vesicle trafficking in neuronal cells. This is further supported by the finding that vesicles recovered from livers of ethanol-fed rats had decreased motility in vitro.28 Clearly, further studies are needed to fully understand these results.
Another open question is why the distribution of 5′-NT was not altered in treated cells. One possibility is that internalization mechanisms were differentially impaired. There are at least 3 major internalization routes in mammalian cells—clathrin-mediated, caveolae-mediated/raft-mediated, and non–clathrin-mediated/non–raft-mediated29—which are characterized by specific molecular players, cargoes, and regulators. In general, the receptors that displayed impaired endocytosis in ethanol-treated hepatic cells are internalized via clathrin-mediated pathways (ASGP-R, epidermal growth factor receptor, and insulin via its receptor).8–10, 30, 31 Although the basolateral internalization mechanism for 5′-NT has not been identified, its GPI anchor suggests it is internalized via a caveolae-mediated/raft-mediated pathway. Furthermore, from work performed in hepatocytes,32 5′-NT is known to have a longer apical arrival time than other residents (3.5 versus 1.5–2 hours), which may reflect differences in their internalization routes. Thus, we propose that the molecular machinery that drives clathrin-mediated endocytosis is more prone to adduction by acetaldehyde or other reactive metabolites such that it is selectively impaired by alcohol treatment. This is a hypothesis we are actively testing.
WIF-B Cells Are a Good Model System for Studying Alcohol-Induced Liver Injury.
This study further confirms that WIF-B cells are a good model for studying alcohol-induced hepatotoxicity. Not only does this cell line exhibit a polarized phenotype in culture, it also maintains numerous liver-specific activities normally lost in isolated hepatocytes or missing from other hepatic cell lines. Importantly, these cells metabolize ethanol2 and display alcohol-induced defects in cellular processes as described in situ or in isolated hepatocytes. These impairments include decreased microtubule polymerization,3 defects in ASGP-R trafficking, and albumin secretion. Furthermore, we determined that microtubules in both WIF-B cells and in livers from alcohol-fed rats were hyperacetylated.3 Thus, we believe that WIF-B cells will enable meaningful mechanistic studies, allowing us to examine the molecular basis of alcohol-induced hepatic-injury.


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This little Jack Russell dog has gone missing between Richhill and Armagh.
His owners are desperate for his safe return following his disappearance yesterday morning (Wednesday).
If anyone sees him or hears of anyone finding a dog can you please let Alice Todd know on Facebook or by calling her on 07463240597.
She’s hoping he’s around the Mullanasilla Road area between Richhill and Armagh.
She posted: “Please keep an eye out, he’s very friendly and wouldn’t hurt a fly Thankyou,”
Please help by sharing her appeal.
Read more news:
Exciting plans to redevelop one of borough’s forgotten forest park gems
Suspected Class A drugs worth £20,000 seized in Co Armagh raid
Appeal for witnesses as thieves damage van and steal tools
Baby Ruby suffered THREE heart attacks at just eight weeks old

domain: pet


In the realm of concealed carry, the Sig Sauer P365-XMacro Tacops emerges as a game-changer, offering a compact design without compromising on power or precision. This exceptional firearm is not just a concealed carry option; it’s an experience that goes beyond expectations, providing users with unparalleled versatility and reliability.
Compact Brilliance: Sig Sauer P365-XMacro Tacops Unveiled
The Sig Sauer P365-XMacro Tacops stands as a testament to Sig Sauer’s commitment to innovation. Combining a micro-compact frame with tactical features, this firearm redefines what is possible for concealed carry enthusiasts. The P365-XMacro Tacops is not just a gun; it’s a statement that compact firearms can deliver uncompromising performance.
Tactical Precision at Its Core
One of the standout features of the P365-XMacro Tacops is its emphasis on tactical precision. The incorporation of advanced sighting options, coupled with a crisp trigger, ensures that every shot fired is a calculated and controlled action. This level of precision is a game-changer for those who demand accuracy in a compact package.
Beyond Concealed Carry: Versatility Redefined
While the P365-XMacro Tacops is an excellent concealed carry option, its versatility extends beyond that role. This firearm is equally adept at home defense or as a backup for professionals requiring a discreet yet powerful sidearm. The adaptability of the P365-XMacro Tacops makes it an ideal companion for a variety of scenarios.
For those in pursuit of the Sig Sauer P365-XMacro Tacops, the opportunity to acquire this compact powerhouse is now at hand. The firearm is not just for sale; it’s an invitation to experience a new level of concealed carry excellence. The P365-XMacro Tacops is more than a firearm; it’s a lifestyle choice for those who refuse to compromise on quality.
Micro Meets Macro: The Sig Sauer P365-XMacro Tacops Advantage
The marriage of micro and macro elements in the P365-XMacro Tacops sets it apart from traditional concealed carry options. The compact design conceals effortlessly, while the tactical features provide users with capabilities usually associated with larger firearms. Sig Sauer has ingeniously combined the best of both worlds to create an advantage that defies expectations.
Elevate Your EDC: Sig Sauer P365-XMacro Tacops
Elevating your Everyday Carry (EDC) goes beyond just carrying a firearm; it’s about carrying confidence. The Sig Sauer P365-XMacro Tacops empowers users with a compact solution that doesn’t compromise performance. Whether you’re navigating crowded urban spaces or venturing into the great outdoors, the P365-XMacro Tacops is a reliable companion that enhances your EDC experience.
Unveiling Tactical Mastery with Sig Sauer
The tactical brilliance of the P365-XMacro Tacops is not just a feature; it’s a philosophy that Sig Sauer has embedded into this firearm. From its compact dimensions to its advanced sighting system, every element is designed with the user’s tactical advantage in mind. The P365-XMacro Tacops is a masterclass in blending form and function for optimal performance.
The Sig Sauer P365-XMacroTacops is not just a concealed carry firearm; it’s an experience that transcends the limitations of size. For those who seek compact brilliance without compromising on tactical features, the P365-XMacro Tacops is the answer. Visit Standard Gun Shop to explore and acquire the Sig Sauer P365-XMacro Tacops for sale and elevate your concealed carry experience. Where precision meets compact perfection, the P365-XMacro Tacopsstands ready to redefine your expectations.


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For the 1950 Le Mans 24 Hours the American sportsman Briggs Cunningham entered two Cadillacs, one being standard and the other extensive modified. One was a standard Cadillac Series 61 sedan whereas the other, nicknamed by the French “Le Monstre,” used a Cadillac 61 chassis but with a special body constructed as an experiment by an aerodynamicist from Grumman Aircraft to lower wind resistance and reduce weight. The team at Frick-Tappett Motors on Long Island, working closely with the designer and Cunningham, prepared both cars. Le Monstre’s engine was still fairly standard, but with five carburetors. It was successful in that it was substantially faster in top speed than its unmodified sister. French journalists also had a name for that standard Cadillac, Petit Pataud (little clumsy puppy).
Le Monstre was driven by Cunningham and Phil Walters who was a very accomplished driver in his own right as the prewar Midget racer “Ted Tappet.” Walters was an owner of Frick-Tappett, makers of the Fordillac, a kind of hot-rodded Ford with a more powerful Cadillac motor. The Cunningham Cadillac sedan was piloted by brothers Miles and Sam Collier who were good friends of Cunningham. Here the two cars pass in line through the dangerous White House Corner (part of that house being visible to the right) which led onto the Le Mans start/finish straight.
The obvious damage to the right front of Le Monster arose from a Phil Walters practice crash and the resulting informal repairs. In spite of this and other first time troubles both entries finished the race with the sedan in 10th position and Le Monstre following in 11th due to an early sandbank excursion by Cunningham that cost four laps. Today these two icons of Le Mans history remain in their original Le Mans condition in the Collier Collection in Naples, Florida.
Photo by Louis Klemantaski ©The Klemantaski Collection – http://www.klemcoll.comn

domain: design


Create a color palette using Adobe Color, then import that palette into Adobe InDesign.
Written by Paulina Rios Colordot: Available both online and in the App Store, Colordot is a simple way of picking colors for any occasion. Adobe Color CC: Adobe Color CC is perfect for creating color palettes that are analogous, complementary, monochromatic and more. Also available online and in the App Store. Colourlovers: Colorlovers is an … Continue reading Color Inspiration


text:
As the sun sets across the Palo Alto Hills in Silicon Valley, you would think that life is as peaceful as the quaint orchards and rolling farmlands nearby. Looks can be deceiving. The rumbling throughout the valley isn’t the San Andreas fault murmuring, it’s the tremors of acceleration taking place. Start-up acceleration has been part of the technology landscape in Silicon Valley for as long as entrepreneurs have been in residence and ideas have been incubated inside funds and research teams. However, this era of acceleration has taken a different tune. It is faster paced, broader reaching and more successful than its incubator predecessors. Part of that success is founded on the technology available to get a product to market faster and the absolute growth in angels and mentors involved.
Y Combinator, the original start-up accelerator, was conceived in 2005 and became the blueprint seed fund for more than 500 start-up launches. Accelerators offer a blend of valuable advice and seed funding (typically around $20,000 for 6-7 per cent equity) and a critical path to a community of experienced entrepreneurs, angel investors and venture capital funds. Other accelerator programs include Alchemist, Founder Institute, Seedcamp, 500Startups and TechStars.
Closer to home, the movement in Australia has built to an impressive wave. Startmate, PushStart, Pollenizer, AngelCube, BlueChilli and Ignition Labs/ATP and thriving workspaces such as Fishburners and iLab have cultivated a new generation of aspiring start-up founders. Specialised accelerator Right Pedal, founded by Steve Baxter, focuses on gaming, leveraging the community of game developer successes in Queensland.To whet your appetite before taking the plunge, you might opt for Pollenizer’s Brown Bag Design in Sydney on June 26. If you want to take the leap to the US, TechStars Austin is open for application, final deadline June 30.
After graduating from these programs with a working product and initial customer traction, options going forward include garnering angel funding or simply selling more. The pool of venture capital is slim in Australia. Self-funded and angel-funded paths to profitability and the rumbling of cash flow and a dividend or an acquisition offer may well serve accelerated graduates best. A couple of examples of accelerator-direct-to-exit include Wufoo acquired by SurveyMonkey straight from Y Combinator, and Grabble acquired by WalMark straight from StartMate. These are few and far between, however, and while the preponderance of accelerated companies may fail, failing fast serves as the ultimate platform from which to learn, rapidly hone skills, and get the entrepreneurial bug.
It’s the best way to bring ideas to fruition with nimble resources and the ticking of time.
Tristen Langley is a venture partner with Southern Cross Venture Partners and a director with Amalfi Capital. You will find her in Sydney, Shanghai and Silicon Valley.

domain: geography


text:
Afternoon everyone. It's a sultry, soporific afternoon in Ischia, sunny at times and kind of cloudy at others with an unpredictable wind that comes in fits and starts. Right now at 3:45pm it's 31° Celcius (88° Fahrenheit) and we're expecting another warm evening with a minimum of 21°C (70°F). Actually today is a special day in Ischia and Italy in general. In the country where every name of a saint is celebrated each day, today happens to be the name day of San Giovanni. There's myth that says you shouldn't swim in the sea today because it's full of knives, a legend that derives from a terrible battle that was fought off the coast of Forio between pirates and islanders! Thankfully the town is a much calmer place these days as you can see in today's photo. A domani, ciao :-)
ISCHIA DAILY WEATHER, PHOTO & UPDATE:
Today's weather in Ischia plus a nice photo and a little news...


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Joan Aiken The Wolves of Willoughby Chase
Illustrated from drawings by Pat Marriott
Puffin Books 1968 (1962)
The action of this book takes place in a period of English history that never happened — shortly after the accession to the throne of Good King James III in 1832 …
Joan Aiken’s The Wolves of Willoughby Chase fits into no one category. From the introductory note one might assume it belongs to the genre called Uchronia (“no time”) in which it becomes clear that at some stage in the past history diverged from its familiar course; in this case the Jacobite rebellion succeeded and the Stuarts continued to reign in Britain from the middle of the 18th century. It is also on the frontiers of Utopia (“no place”) in that the England described includes places and distances which only by a large stretch of the imagination co-exist in our own world: Willoughby Chase House and the town of Blastburn seem to be located somewhere around Humberside, and yet we’re told the walking distance from Blastburn to London is about four hundred miles (in reality from the Humber to the capital is only around 200 miles by modern roads).
On another level the novel is a Dickensian parody: orphans (real or assumed) have to cope with bitter winters, reversals of fortunes and conniving villains with quirky names only to — one hopes — overcome their plight with a mixture of natural cunning, kind helpers and a measure of good luck. But this is also a children’s book and, as such books usually confirm, events are seen almost entirely through the eyes of youngsters. It lingers somewhere on the continuum between fairytale and fantasy, albeit that there is no magic involved, but with a large pinch of Gothick thrown in for good measure, complete with secret passages and rambling suites of rooms.
And where do the wolves come in?

domain: literature


text:
This article is more than 1 year old
UK distie fights Cisco injunction
Spot the difference
A Shropshire distie is threatening to report Cisco to the DTI for uncompetitive behaviour after the networking giant's lawyers began moves to stop it selling kit from Chinese equipment manufacturer Huawei.
Spot Distribution's robust response comes after receiving a "cease and desist" letter from Cisco for distributing Huawei products that allegedly copy Cisco's intellectual property.
In a parallel move, Cisco yesterday announced it had filed a law suit in Texas alleging that Huawei "unlawfully copied and misappropriated Cisco's IOS software, including source code, copied Cisco documentation and other copyrighted materials, and infringed numerous Cisco patents."
Cisco accusations against Huawei are unusually detailed. Amongst other things, it alleges the operating system used by Huawei's Quidway routers and switches "contains a number of text strings, file names, and bugs that are identical to those found in Cisco's IOS source code".
Spot Distribution claims Cisco's actions against it and Huawei are unfounded. Huawei has not stolen Cisco's technology, it says, arguing that the networking giant is running scared of its competition.
In a statement issued today, George (Georgina) Wellings, a director at Spot Distribution, stated: "On inspecting the Huawei manuals we have in stock, it appears that Spot Distribution Ltd has no case to answer."
"We hope this attempt to prevent the distribution of Huawei products is not just the result of a major manufacturer running scared of the competition."
Casting herself in the role of David (Davina?) against Cisco's Goliath, Wellings is reaching for her slingshot.
"It is our intention to refer this matter to the Office of Fair Trading and DTI to ensure there has been no attempt to act in an anti-competitive manner," she added.
We wanted to discuss the legal basis of this unorthodox move with Spot Distribution (along with other matters), but no directors were available for comment at the time of going to press. ®
Cisco sues Huawei over IP 'theft'
Conspiracy to create 'Cisco of China'

domain: law


text:
Ten years ago, Forrester published some research with the slightly awkward title of ‘New Payment Systems’ Survival Guide’. One of our findings was that many successful new payment systems have some kind of ‘must-have’ transaction that encourages customers to go through the hassle of learning how to use a new system in the first place. Good examples of ‘must-have’ transactions include eBay’s auctions for PayPal, travel to work for Transport for London’s Oyster, and online shopping for iDeal.
Ever since, I’ve been seeking the ‘must-have’ transaction that will spark consumer adoption of mobile payments in developed economies. But what if there isn’t one? (And, after 10 years, it’s probably time to admit that there isn’t). The answer is to focus relentlessly on both lowering the barriers to mobile payment by making it as easy as possible for customers to use a new system and to increase the benefits by maximizing the number of ways and places customers can use a system.
- Transfers between a customer’s own accounts;
- Transfers to other accounts;
- Bill payments through Australia’s BPay service;
- MasterCard PayPass contactless payments at the point of sale (using an iCarte case, not an integrated Near Field Communications chip);
- Payments to friends through email addresses and mobile numbers;
- Payments to friends on Facebook; and
- 'Bump’ payments to friends (based on two iPhones being bumped together in close proximity using the handsets’ accelerometers and GPS to confirm the transfer).
By enabling so many types of payment through a mobile phone, Commonwealth Bank is teaching its customers that if they want to make a payment – in any situation – they should use the Kaching app. In doing so, the bank is successfully encouraging customers to adopt mobile payment without the magic of a single ‘must-have’ transaction.
In the 18 months since launch in October 2011, some 800,000 people have downloaded the Kaching app (compared with the bank's 4.3 million active online banking users). Those customers used Kaching to transfer or pay more than A$1 billion ($1.02 billion) in 11 months from October 2011 to September 2012.

domain: economics


text:
Today.Az » Business » BP-Azerbaijan plans to deliver 2.1 bln cu m of gaz to the state
14 August 2006 [00:50] - Today.Az
According to press service of BP Azerbaijan, the company plans to deliver a total amount of 2.1 billion cubic meters of gas produced from the Central Azeri and West Azeri platforms to Azerbaijan until the end of this year.
Associated gas is being transported via the underwater gas pipeline into the Sangachal Terminal and onward via a new gas export pipeline connecting the terminal's gas processing facilities and Azerigas's national grid system.
Since the beginning of the year, the company has delivered 488.5 million cubic meters of Chirag and 930 million cubic meters of Sangachal gas to the State.


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A Dutch police officer ended an hours-long standoff by running over the hostage-taker with a car Tuesday evening, according to Reuters.
A man armed with a pistol, an automatic rifle and explosives held a man hostage for at least four hours in the Amsterdam Apple Store while demanding $226 million in cryptocurrency from the police as ransom and threatening to blow himself up, Reuters reported.
Clearly Amsterdam isn’t only a city of bicycles. 😉 This is how Dutch police last night stopped an armed hostage taker in Amsterdam after the man tried to recapture his hostage who moments earlier managed to escape.pic.twitter.com/BntCfQBsU3
— Harald Doornbos (@HaraldDoornbos) February 23, 2022
The police sent a robot to deliver water to the door at the hostage-taker’s request, at which point the suspect chased the hostage out of the building and was hit by a police car, according to Reuters. He reportedly sustained serious injuries.
The suspected hostage-taker, a 27-year-old man from Amsterdam, had a criminal record, police told Reuters.
The police described the hostage as “heroic” for “forcing a breakthrough” in a situation that could have gone on much longer, Reuters reported. (RELATED: Fireball In BYU Dorm: Student Causes Explosion With Homemade Rocket Fuel)
About 70 people escaped the store during the hostage situation and there were no reported injuries besides the hostage-taker’, according to Reuters.
“We are so incredibly grateful and relieved that our employees and customers in Amsterdam are safe after this terrifying experience,” Apple commented in a statement obtained by Reuters.
All content created by the Daily Caller News Foundation, an independent and nonpartisan newswire service, is available without charge to any legitimate news publisher that can provide a large audience. All republished articles must include our logo, our reporter’s byline and their DCNF affiliation. For any questions about our guidelines or partnering with us, please contact firstname.lastname@example.org.

domain: news


text:
An anonymous businesswoman donated one million dollars to the charity.
Please donate generously.
The appeal for people to donate blood was very successful.
WordNet 3.0 Sense Numbers: 1
In a normal covalent bond each atom donates one electron to make a shared pair.
An ionic bond is when one atom donates an electron to another atom.

domain: chemistry


text:
The International Business Times and others covered Kino Lorber's acquisition of Daniel Leconte's 2008 documetnary, "It's Hard To Be Loved By Jerks." Read more below:
An American film distributor (Kino Lorber) has purchased the rights to a documentary about Charlie Hebdo, the French satirical magazine that was attacked on Jan. 7 by extremists who killed 12 people, including some of the magazine's most prominent cartoonists. Kino Lorber, the company, bought the rights from French company Pyramide International, which holds the rights to the documentary, "It's Hard Being Loved by Jerks" ("C'est dur d'être aimé par des cons").
The documentary, released in France in 2008 and directed by Daniel Leconte, is named after the caption of a popular Charlie Hebdo cartoon. In 2006, the magazine sparked an uproar in France when it reprinted a set of highly controversial cartoons of the Prophet Muhammad originally published in a Danish paper. The documentary examined the legal battle that ensued in France after Charlie Hebdo was charged with defamation, is considered sympathetic to the cause of freedom of expression for which the magazine championed. Some of those interviewed in the documentary were killed in the January attacks. When the documentary was first released, it sold about 40,000 tickets, according to Eric Lagesse, president of Pyramide.
The day after the January attack, the film was re-released in France, eventually playing in 110 theaters and selling about 10,000 tickets, according to Variety magazine. Pyramide is offering the film again to distributors at the Berlin Film Festival, which ends Feb. 15.
Lagesse told AFP he thinks the film will succeed in American universities and arthouse cinemas. Kino Lorber is expected to release the film in universities and major U.S. cities this spring. Elizabeth Sheldon, a senior vice president at Kino Lorber, said the film would be "a catalyst for conversation."
"As a distributor, freedom of speech concerns me at first range and today it is more important to keep defending those ideas," Pyramide's Lagesse said. "More than ever."
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text:
Proton Therapy Makes Way to Oklahoma
OKLAHOMA CITY -- Cancer patients in Oklahoma now have an opportunity to receive a more advanced form of radiation treatment. It's called proton therapy. And the new proton treatment center in Oklahoma City is only the sixth in the nation.
It's an exclusive treatment that was only available on either end of the country. But now, Oklahomans and people from neighboring states will benefit from another weapon in the fight against cancer.
Since his diagnosis of cancer last year, Steve White has been in and out of exam rooms.
"My family doctor sent me to an urologist and he did a biopsy and determined that I had prostate cancer," White said. "So, then the question becomes, ‘What do you do about it?'"
Initially, White opted for surgery. But then the Oklahoman settled on treatment at Pro-Cure in Florida, where he underwent proton therapy. As it turns out, the usually tough side effects that come along with traditional radiation didn't affect White.
"I felt great," White said. "We were playing gold, going fishing, going to the beach and just, you know, had a vacation for a couple months.
To administer proton therapy, a series of magnets sit inside the "cyclotron." When fired up, protons are generated, ejected from the machine, and travel to the body. Inside the body -- the protons only attack the tumor. Chances of damaging the surrounding tissues, like in traditional radiation treatments, are dramatically decreased.
"With protons, doesn't mean side affects there, but have a much better chance of avoiding them," Radiation Oncologist Dr. Sameer Keole said. "For instance, for a pediatric child, we can decrease the dose to the normal brain by anywhere from 70 to 80 percent."
Doctors estimate that 3,500 Oklahomans would benefit from proton therapy this year.
Steve White went through two months of the treatment. Now it's one year later, and he's living cancer free.
"You know, I'm convinced it's gone and I'm cured," White said.
Doctors at Pro-Cure plan to treat patients with brain tumors, head and neck tumors, prostate cancer as well as patients with pediatric cancers at the Oklahoma City center. There are plans to move into breast and lung cancer treatments, among other illnesses, in the future.

domain: health


2020 Dodge Durango Specs, Engine, Review, & Changes – The Dodge vehicle family muscle mission does not end with the 2020 Dodge Durango crossover. The brawny ride with its steel unibody isn’t by definition an SUV, as it lacks body-on-frame construction. CUV classification does not end Durangos from transporting three rows of passenger seats, towing as a lot as to 8,700 pounds, or lighting up the pavement in the SRT version.
Fiat Chrysler Automobiles’ Jeep Grand Cherokee shares two engines and a few other mechanized elements with the Durango, but the Grand Cherokee is a five-passenger vehicle. The Durango is longer, broader, taller, and heavier than the Grand Cherokee, plus, depending on trim, the Durango can seat six or seven travelers, including the driver.
Dodge’s 2020 mission for the Durango: Distribute SRT styling qualities to other trim amounts to bring up the Durango’s overall badass quotient. The 2020 Durango R-T has the exact same front styling as the SRT, which include a front fascia, performance hood, decrease valence, and fog lighting fixtures. Other trims and powertrains and appearance deals for all powertrains. All 2020 Durangos have rearview file backup video cameras, new sport steering wheels, and a driver-driven electronic T-shifters.
Three engines power 2020 Durango models. The most compact of the three mills, with the greatest fuel economy, is a 3.6L Pentastar V6. The V6 tends to make 293 horsepower at 6,400 rpm with a single exhaust and 295 horsepower with dual exhaust. Torque with possibly exhaust system is 260 pound-feet at 4,000 rpm. Durangos with the V6 can pull up to 6,200 pounds of motorboat, camper, or trailer.
Fueling the V6 with 87 octane gas is fine. Rear wheel drives Durango with the V6 offer an EPA average score of 19 mpg in city driving, 26 mpg on the highway, and 21 mpg combined. With AWD the put together V6 mileage score stays the same at 21 mpg but the city and highway driving each drop one mile per gallon to 18 mpg and 25 mpg, respectively. The V6 is standard on the SXT, SXT Plus, GT, and Citadel Durango trim. The Durango R/T goes a 5.7L Hemi V8 rated at 360 hp at 5,150 rpm and 390 lb-ft of torque at 4,250 rpm. You can use 87 octane gas, but Dodge advocates midrange 89 octane. Rear wheel and all-wheel drive Durango with the 5.7L Hemi is EPA rated at 14 mpg in the city, 22 mpg on the highway, and 17 mpg in mixed driving. The 5.7L Hemi is a choice on the Durango Citadel.
The high-performance Durango SRT gets its power from a 6.4L V8 that wails with 475 hp at 6,000 rpm and 470 lb-ft of torque at 4,300 rpm. Supply the SRT 91 octane premium gas. The SRT’s EPA fuel economy status probable issues very little to those who will buy it, but for the record, it’s 13 mpg in city driving, 19 mpg on the highway and 15 mpg combined. Handling, suspension, brakes, and drivetrain methods change amid Durango trims. The SXT and GT trims have anti-lock four-wheel disc brakes, with heavy-duty enhancements for the Citadel and R/T trims and high-performance Brembo brakes on the SRT. The R/T has a reduced-height sports suspension when the SRT has a Bilstein high-performance active damping suspension. AWD SXT, GT, and Citadels use a single-speed full-time AWD set up. The R/T has two-speed, active on-need AWD. The SRT uses FCA’s Quadra-Trac active on-desire 4WD system.
All Durango models have electronic stability control, including vehicle stability administration, electronic roll mitigation, all-speed traction control, brake assist, and 4-channel anti-lock brakes. Also, all trims include hill-start assist to stop rolling back when starting upon an incline, rainfall brake assists, ready alert braking, and trailers sway control. Unaggressive safety and driver assistance features are available in choice deals for most models (not the base SXT), but the only feature across all trims is a rearview backup camera. The dining tables listed below suggest indirect safety and assist features that are standard (in striking), optional, or otherwise available for each trim.


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Pink Willpower Bracelet (Item #713)
This unique bracelet makes a statement with stunning shades of pink and beautiful sparkles. The combination of Sara Yo and top-grade freshwater pearls is luxurious, elegant and chic. The adjustable bracelet is easy to slip on and off and is even more stunning in person with gorgeous sparkles.
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Former presidential candidate speaks out on health care reform and stirs up the GOP
McCain ad calls Obama 'biggest celebrity in the world'
Former McChrystal adviser on next step in Afghanistan
'Live Desk' panel weighs in on GOP's attempt to portray Obama as extremely liberal
Florida Senator Mel Martinez holds news conference on his retirement
Dow soars despite tanking dollar and spiking gold prices. Home Depot co-founder weighs in
Mini van crashes into restaurant wall
'Special Report' panel on czars in Obama administration, Afghanistan and GAO report on federal office security
Sen. Barrasso reacts to new health care reform bill audit
Part 1: The president sits down with FNC's Bret Baier to discuss the health care reform bill
Go behind the scenes as Greta prepares for Wednesday's 'On the Record'
Sen. John Kerry stirs controversy with below the belt Sen. John McCain joke
Listeners have their say in one sentence or less.
Former Senator Bob Dole (R-KS) tells Alan why he wants the Republican Party to support health care reform.
We will take a look at the turmoil in the Middle East from a National Security standpoint, and what the government should and can do to protect the Nation. Mike Baker and Bill Daly are here with the weekly hit list.
Reform bill put back to the test
Panel weighs in on content of Obama's address
Former HHS sec'y on health care reform
Once again, McCain reveals his lighter side on 'Saturday Night Live'
'Hannity & Colmes' pays tribute to over a decade on FOX News Channel


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Welcome to FindLaw's Cases & Codes, a free source of state and federal court opinions, state laws, and the United States Code. For more information about the legal concepts addressed by these cases and statutes, visit FindLaw's Learn About the Law.
(1) Life insurance may be made payable to a trustee to be named as beneficiary in the policy and the proceeds of such insurance shall be paid to such trustee and shall be held and disposed of by the trustee as provided in a trust agreement made by the insured during his lifetime. It shall not be necessary to the validity of any such trust agreement or declaration of trust that it have a trust corpus other than the right of the trustee to receive such insurance proceeds as beneficiary.
(2) A policy of life insurance may designate as beneficiary a trustee or trustees named by will. The proceeds of such insurance shall be payable to the trustee or trustees to be held and disposed of under the terms of the will as they exist as of the time of the death of the testator. If no such trustee makes claim to the proceeds from the insurance company within eighteen (18) months after the death of the insured, or if satisfactory evidence is furnished to the insurance company within such eighteen-month period showing that there is or will be no trustee to receive the proceeds, payment shall be made by the insurance company to the executors, administrators, or assigns of the insured, unless otherwise provided by agreement with the insurance company during the lifetime of the insured.
(3) The proceeds of the insurance as received by the trustee or trustees shall not be subject to debts of the insured nor to transfer or estate tax to any greater extent than if such proceeds were payable to the beneficiary or beneficiaries named in the trust and not to the estate of the insured.
(4) Such insurance proceeds so held in trust may be commingled with any other assets which may properly come into such trust.
(5) Nothing in this section shall affect the validity of any life insurance policy beneficiary designation heretofore made naming trustees of trusts established by living trust or by will.
Cite this article: FindLaw.com - Mississippi Code Title 83. Insurance § 83-7-7. Beneficiary designations of trustees - last updated January 01, 2018 | https://codes.findlaw.com/ms/title-83-insurance/ms-code-sect-83-7-7.html
FindLaw Codes may not reflect the most recent version of the law in your jurisdiction. Please verify the status of the code you are researching with the state legislature or via Westlaw before relying on it for your legal needs.
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Celiac disease is the permanent intolerance to gluten present in food. This is because the body does not produce or produce little enzyme capable of degrading gluten, which causes a reaction of the immune system that results in lesions in the intestine.
Celiac disease can manifest itself in infants as they begin to vary their diet at 6 months or during adulthood and is characterized by diarrhea, irritability, fatigue, unwarranted weight loss or anemia without apparent cause.
There is no specific treatment for celiac disease, however, symptoms related to the disease can be controlled by eliminating any food or product that contains gluten or traces. Gluten may also be present in small amounts in toothpaste, moisturizers or lipstick, and people who have skin manifestations while consuming gluten, such as itching or dermatitis, should also avoid these products. Therefore, it is always recommended to carefully read the labels and packaging to make sure the presence of gluten in the products. Learn where gluten can be found.
Symptoms of Celiac disease in Adults
The symptoms of celiac disease vary according to the degree of intolerance of the person, usually:
- Swollen belly;
- Weight loss;
- Lack of appetite;
- Frequent diarrhea;
- Irritability or apathy;
- Large and bulky evacuation of pale and very smelly feces.
When the person has the mildest form of the disease, the symptoms of gluten intolerance manifest themselves through the following symptoms:
- Dyspepsia, which is the difficulty of digestion;
- Fragile bones;
- Irregular or absent menstruation;
- Feeling tingling in the arms and legs;
- Injuries to the tongue or fissures in the corners of the mouth;
- Elevation of liver enzymes with no apparent cause;
- Swelling that arises abruptly after infection or surgery;
- Iron deficiency anemia or folate deficiency and vitamin B 12;
- Bleeding gums when brushing teeth or flossing.
In addition, low levels of protein, potassium, and sodium in the blood can be noted, as well as impairment of the nervous system, leading to epilepsy, depression, autism, and schizophrenia. Learn more about gluten intolerance.
The symptoms of celiac disease disappear completely with the elimination of gluten from the diet. And to determine the diagnosis, the best doctors are the immunoallergologist, and the gastroenterologist. Here are the top 7 symptoms of gluten intolerance.
Diagnosis of celiac disease
The diagnosis of celiac disease is made by the gastroenterologist through the evaluation of the symptoms presented by the person and the family history, since the celiac disease is mainly caused by genetics.
In addition to the clinical evaluation, the doctor may request some tests, such as blood from blood, urine, stool and biopsy of the small intestine through a high digestive endoscopy. To confirm the disease, the doctor may also request a second biopsy of the small intestine after exclusion of gluten from the diet for 2 to 6 weeks. It is through the biopsy that the doctor can assess the integrity of the intestine and check for any signs that indicate gluten intolerance.
Treatment for celiac disease
Celiac disease has no cure, and treatment should be done throughout life. Treatment for celiac disease is made exclusively with the suspension of use of products containing gluten and a gluten-free diet, which should be indicated by a specialist nutritionist. See which foods contain gluten.
The diagnosis of celiac disease in adults is made when there is already a nutritional deficiency, so the doctor may indicate that supplementation of nutrients that may be lacking in the body due to the common malabsorption in celiac disease is done, in order to prevent other diseases such as osteoporosis or anemia.


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