En el programa 6AM de Caracol Radio, habló Andrés Izarra de las posibles nuevas elecciones en Venezuela

En el programa 6AM de Caracol Radio, habló el gobernador del Santander y expresó su preocupación por el aprovechamiento de los grupos armados al cese al fuego. 

En 6AM Hoy por Hoy de Caracol Radio estuvo el senador Iván Cepeda, para hablar sobre la propuesta del Gobierno para salvar las negociaciones con el ELN y el paro armado que anunciaron en Chocó.

En el programa 6AM, estuvo Luz janeth Forero, directora de la Unidad de Búsqueda de Personas dadas por Desaparecidas, e hizo hincapié en las cifras de desaparecidos por el conflicto armado

En 6AM Hoy por Hoy de Caracol Radio estuvo el abogado Francisco Bernate, quien defiende a defensa de Luis Eduardo López, para hablar sobre cuáles serán los puntos con los que pedirán un “principio de oportunidad parcial”, por escándalo de la UNGRD.

En el programa de 6AM, estuvo María Isabel Ulloa, directora ejecutiva de ProPacífico, hablando sobre el trabajo que realiza ProPacífico en las poblaciones vulnerables del Valle del Cauca

En 6AM de Caracol Radio estuvo Juan Ramón Guzmán, Presidente de la Junta directiva y Co-fundador de BIVIEN, para hablar sobre en qué consiste “Compromiso territorio” y cuál será la estrategia para cerrar la brecha social en el norte del Cauca.

It's hard out here for a pimp.

How to build muscle and loose fat at the same time.

By: Tim Ernst

Is it possible to gain muscle while at the same time loose fat? Some argue that you either have to do one or the other. I'm here to tell you that it is possible, but the secret is all about nutrient timing.

There are certain times of the day when you want to be in a caloric surplus. The only way to build muscle is to be in a caloric surplus and the only way to loose fat is to be in a caloric deficit. How do you do both at the same time?

Research shows that your most optimal time for muscle growth is what you consume after your workout. If you are not consuming enough calories after your workout, then you are just wasting your time.

Here is an example on how to start your day.

8:00 am: Low-carb protein shake with a greens product.

10:30 am: 2eggs plus 4 whites scrambled with cheese, spinach, onions, peppers, and mushrooms.

1:00 pm: 2 oz of dry roasted nuts.

3:00 pm: Chicken Breast with sweet potato or brown rice.

5:00 pm (workout) Consume your a favorite pre workout shake if you want for energy but, it's not necessary.

5:30 pm 30 minutes into your workout consume a high carb drink like Karbolyn, Power Carb, or Vitargo.

5:45 pm (immediately post-workout): quickly digested protein/carb beverage.

6:15pm: 2 oz of pasta (dry weight); 4 oz of Ground Turkey mixed with egg whites.; 2 slices of 12-grain bread; package of broccoli or green beans.

7:45 pm: 1 cup brown rice, cous cous, or quinoa 4 oz of chicken breast; 2 slices of 12-grain bread, asparagus.

10:00 pm: Hand full of mixed nuts or avocado and fish oils.

That's it!

Get ready to GROW.

As you continuously approach your fitness goals, you eventually hit a plateau, which occurs when you've nearly reached your ideal fitness level. At this point, you're basically stuck at one level, but you can take it to the next level easier than you make think.

Everyone who does resistance training―from newbies to professional bodybuilders―will hit this point, but what's important is knowing how to increase your productivity and enhance your workout, and with these 21 facts, you can definitely reach your fitness goals faster.

1. Are you exactly the same as your neighbor, or for that matter, even your sibling? Since we'll assume you answered, “No,” you must understand that everyone is different and doesn't respond to the same muscle building techniques; therefore, you should alternate the speed of your repetitions for optimal results.

2. What your parents gave you doesn't have to determine your goals. You should achieve your fitness objectives despite any genetic barriers you may have―i.e. a high BMI.

3. Establish your goals on paper. Research indicates that when a person writes down detailed goals with deadlines to meet, that the individual has a specific path to follow and is more likely to be successful at achieving that goal.

4. Age is nothing but a number, so don't let your age be a factor in achieving your goals, especially since you can't change this number. Focus on what you can control, such as your sleeping patterns.

5. Find a workout buddy. When you have someone to push you, you'll work harder than you would alone.

6. Keep in mind the ratio 10:1, because you generally need to gain 10 lbs for every inch of girth you add to your arm size. For instance, a majority of people gaining 50 lbs during the course of five years will also gain five inches in their arms.

7. Prior to increasing speed or resistance, increase the range of motion first, meaning you should fully contract and stretch your muscles. If you don’t, you’ll only receive partial results.

8. You need at least eight hours of sleep per night to build muscles, so aim to get this many winks as much as possible. Remember, a few late nights won't hurt, but making it a habit will take a toll on your target fitness level.

9. Stay hydrated! Your body needs at least 1 gallon or 16 cups of water per day for proper muscle growth. The composition of your body is 70 percent water, and in order for your body to maintain an anabolic state, water is essential.

10. Consume raw vegetables whenever you can. Cooking veggies removes much of their nutritional value. In fact, boiling these healthy treats removes between 50 to 75 percent of their nutrients. You may steam them, if you can't eat them raw, but never boil them.

11. Eggs are an excellent source of protein and despite their bad reputation, they're one of the healthiest foods you can select, especially for bodybuilding.

12. If you don't have one already, go out and purchase a blender. The amount of calories that you must eat as a bodybuilder are much easier to consume in liquid form. This vital piece of equipment is definitely important if you have a busy lifestyle that doesn't allow you to eat every three to four hours.

13. When you go grocery stopping, stick to shopping in the outer aisles. These aisles are typically where the fresh dairy and meat are located. The inner portion of the grocery store consists of processed foods and canned goods that should be avoided if you want to build muscle fast.

14. Never use a supplement in place of a meal. You must put food before supplements, so that you're consuming all the nutrients you need for bodybuilding. The nutrition you receive from foods surpasses that of a supplement.

15. In regards to supplements, creatine stands out as the top bodybuilding supplement. Beginning in the 90s, creatine has been at the top of supplement charts and has not seen a decrease in popularity since. The daily dosage recommendations vary; however, the most common dosage schedule consists of taking 20-30 grams for the first 5-7 days, then reducing the amount to 3-5 grams per day.

16. Maybe you don't have enough energy to workout, or maybe you want to increase the amount of time you workout. If either of these scenarios are the case, you should choose coffee for a pick-me-up, since it contains a mild stimulant known as caffeine. Caffeine is an inexpensive and safe performance enhancer.

17. You wouldn't drive your car without warming it up on a cold day, so why would you exercise without getting your body warmed up? Get those muscles warm to avoid injury while working out. Complete at least five to 10 minutes of stretching, in addition to some light cardio before you begin heavy lifting.

18. You've heard before that cheaters never prosper, but in certain cases, this isn't true. Although cheating to finish a set quicker or to lift more weight isn't positive, cheating on the last few reps makes the weight feel easier. This stimulates more muscle fibers with greater intensity.

19. Play nice and take turns! The you-go, I-go concept leads to an intense workout, because after you do a set, your partner immediately does one after you, then before you know it, it’s your turn again. You both use the same weights, but you take turns without any rests in between, and you see who can do the most reps per set. Try this technique with your workout buddy when you do barbell curls or other simple exercises.

20. During the 1940s and 1950s, Reg Park and Vince Gironda made a super intense technique for bodybuilding popular, which consisted of doing 10 sets of 10. This old-school procedure may have a modern name of “German volume technique;” however, this has been a preferred method to build muscles for quite some time. It causes your muscles to grow rapidly. Basically, you should do 10 sets of 10 reps for one body part at a time. Then, you should superset at two different body parts each workout. Make sure you don’t rest for more than a minute in between each exercise. Use this regimen for three weeks, and then return to a more traditional approach.

21. Switch up your routine. After three weeks, you should change your program completely. Basically, it should be opposite of the original order you did the exercises in. For instance, if you worked on your chest first, you should do it last next time. If you worked on abs on Monday, you should do them on Friday next time. Change up the amount of sets you do, as well.

Vince Delmonte

Southern California’s football program has been fined $50,000 and placed on probation for one year by the NCAA because of multiple violations of coaching staff rules over two seasons

Patients' families were “horrified but not surprised” when told the blanket policy had been in place.

Carnosine (β-alanyl-l-histidine) and anserine (β-alanyl-3-methyl-l-histidine) are abundant peptides in the nervous system and skeletal muscle of many vertebrates. Many in vitro and in vivo studies demonstrated that exogenously added carnosine can improve muscle contraction, has antioxidant activity, and can quench various reactive aldehydes. Some of these functions likely contribute to the proposed anti-aging activity of carnosine. However, the physiological role of carnosine and related histidine-containing dipeptides (HCDs) is not clear. In this study, we generated a mouse line deficient in carnosine synthase (Carns1). HCDs were undetectable in the primary olfactory system and skeletal muscle of Carns1-deficient mice. Skeletal muscle contraction in these mice, however, was unaltered, and there was no evidence for reduced pH-buffering capacity in the skeletal muscle. Olfactory tests did not reveal any deterioration in 8-month-old mice lacking carnosine. In contrast, aging (18–24-month-old) Carns1-deficient mice exhibited olfactory sensitivity impairments that correlated with an age-dependent reduction in the number of olfactory receptor neurons. Whereas we found no evidence for elevated levels of lipoxidation and glycation end products in the primary olfactory system, protein carbonylation was increased in the olfactory bulb of aged Carns1-deficient mice. Taken together, these results suggest that carnosine in the olfactory system is not essential for information processing in the olfactory signaling pathway but does have a role in the long-term protection of olfactory receptor neurons, possibly through its antioxidant activity.

Cancer cachexia is characterized by reductions in peripheral lean muscle mass. Prior studies have primarily focused on increased protein breakdown as the driver of cancer-associated muscle wasting. Therapeutic interventions targeting catabolic pathways have, however, largely failed to preserve muscle mass in cachexia, suggesting that other mechanisms might be involved. In pursuit of novel pathways, we used untargeted metabolomics to search for metabolite signatures that may be linked with muscle atrophy. We injected 7-week–old C57/BL6 mice with LLC1 tumor cells or vehicle. After 21 days, tumor-bearing mice exhibited reduced body and muscle mass and impaired grip strength compared with controls, which was accompanied by lower synthesis rates of mixed muscle protein and the myofibrillar and sarcoplasmic muscle fractions. Reductions in protein synthesis were accompanied by mitochondrial enlargement and reduced coupling efficiency in tumor-bearing mice. To generate mechanistic insights into impaired protein synthesis, we performed untargeted metabolomic analyses of plasma and muscle and found increased concentrations of two methylarginines, asymmetric dimethylarginine (ADMA) and NG-monomethyl-l-arginine, in tumor-bearing mice compared with control mice. Compared with healthy controls, human cancer patients were also found to have higher levels of ADMA in the skeletal muscle. Treatment of C2C12 myotubes with ADMA impaired protein synthesis and reduced mitochondrial protein quality. These results suggest that increased levels of ADMA and mitochondrial changes may contribute to impaired muscle protein synthesis in cancer cachexia and could point to novel therapeutic targets by which to mitigate cancer cachexia.

Tirsa L. E. van Westering
Dec 1, 2020; 19:2047-2067
Research

Accompanied with nutrition transition, non-HDL-C levels of individuals in Asian countries has increased rapidly, which has caused the global epicenter of nonoptimal cholesterol to shift from Western countries to Asian countries. Thus, it is critical to underline major genetic and dietary determinants. In the current study of 2,330 Chinese individuals, genetic risk scores (GRSs) were calculated for total cholesterol (TC; GRS_TC, 57 SNPs), LDL-C (GRS_LDL-C, 45 SNPs), and HDL-C (GRS_HDL-C, 65 SNPs) based on SNPs from the Global Lipid Genetics Consortium study. Cholesterol intake was estimated by a 74-item food-frequency questionnaire. Associations of dietary cholesterol intake with plasma TC and LDL-C strengthened across quartiles of the GRS_TC (effect sizes: –0.29, 0.34, 2.45, and 6.47; P_interaction = 0.002) and GRS_LDL-C (effect sizes: –1.35, 0.17, 5.45, and 6.07; P_interaction = 0.001), respectively. Similar interactions with non-HDL-C were observed between dietary cholesterol and GRS_TC (P_interaction = 0.001) and GRS_LDL-C (P_interaction = 0.004). The adverse effects of GRS_TC on TC (effect sizes across dietary cholesterol quartiles: 0.51, 0.82, 1.21, and 1.31; P_interaction = 0.023) and GRS_LDL-C on LDL-C (effect sizes across dietary cholesterol quartiles: 0.66, 0.52, 1.12, and 1.56; P_interaction = 0.020) were more profound in those having higher cholesterol intake compared with those with lower intake. Our findings suggest significant interactions between genetic susceptibility and dietary cholesterol intake on plasma cholesterol profiles in a Chinese population.

The absence of the dystrophin protein in Duchenne muscular dystrophy (DMD) results in myofiber fragility and a plethora of downstream secondary pathologies. Although a variety of experimental therapies are in development, achieving effective treatments for DMD remains exceptionally challenging, not least because the pathological consequences of dystrophin loss are incompletely understood. Here we have performed proteome profiling in tibialis anterior muscles from two murine DMD models (mdx and mdx52) at three ages (8, 16, and 80 weeks of age), all n = 3. High-resolution isoelectric focusing liquid chromatography-tandem MS (HiRIEF-LC–MS/MS) was used to quantify the expression of 4974 proteins across all 27 samples. The two dystrophic models were found to be highly similar, whereas multiple proteins were differentially expressed relative to WT (C57BL/6) controls at each age. Furthermore, 1795 proteins were differentially expressed when samples were pooled across ages and dystrophic strains. These included numerous proteins associated with the extracellular matrix and muscle function that have not been reported previously. Pathway analysis revealed multiple perturbed pathways and predicted upstream regulators, which together are indicative of cross-talk between inflammatory, metabolic, and muscle growth pathways (e.g. TNF, INF, NF-B, SIRT1, AMPK, PGC-1α, PPARs, ILK, and AKT/PI3K). Upregulation of CAV3, MVP and PAK1 protein expression was validated in dystrophic muscle by Western blot. Furthermore, MVP was upregulated during, but not required for, the differentiation of C2C12 myoblasts suggesting that this protein may affect muscle regeneration. This study provides novel insights into mutation-independent proteomic signatures characteristic of the dystrophic phenotype and its progression with aging.

Many cell surface and secreted proteins are modified by the covalent addition of glycans that play an important role in the development of multicellular organisms. These glycan modifications enable communication between cells and the extracellular matrix via interactions with specific glycan-binding lectins and the regulation of receptor-mediated signaling. Aberrant protein glycosylation has been associated with the development of several muscular diseases suggesting essential glycan- and lectin-mediated functions in myogenesis and muscle development but our molecular understanding of the precise glycans, catalytic enzymes and lectins involved remain only partially understood. Here, we quantified dynamic remodeling of the membrane-associated proteome during a time-course of myogenesis in cell culture. We observed wide-spread changes in the abundance of several important lectins and enzymes facilitating glycan biosynthesis. Glycomics-based quantification of released N-linked glycans confirmed remodeling of the glycome consistent with the regulation of glycosyltransferases and glycosidases responsible for their formation including a previously unknown di-galactose-to-sialic acid switch supporting a functional role of these glycoepitopes in myogenesis. Furthermore, dynamic quantitative glycoproteomic analysis with multiplexed stable isotope labelling and analysis of enriched glycopeptides with multiple fragmentation approaches identified glycoproteins modified by these regulated glycans including several integrins and growth factor receptors. Myogenesis was also associated with the regulation of several lectins most notably the up-regulation of galectin-1 (LGALS1). CRISPR/Cas9-mediated deletion of Lgals1 inhibited differentiation and myotube formation suggesting an early functional role of galectin-1 in the myogenic program. Importantly, similar changes in N-glycosylation and the up-regulation of galectin-1 during postnatal skeletal muscle development were observed in mice. Treatment of new-born mice with recombinant adeno-associated viruses to overexpress galectin-1 in the musculature resulted in enhanced muscle mass. Our data form a valuable resource to further understand the glycobiology of myogenesis and will aid the development of intervention strategies to promote healthy muscle development or regeneration.

JuJu Watkins had 21 points, nine assists and six steals to help No. 3 Southern California trounce Cal State Northridge 124-39 on Tuesday night. The Trojans (3-0) had six players in double figures, including Kiki Iriafen with 15 points and Kayleigh Heckel with 14 points off the bench. All 13 Trojans who played scored.

Prithviraj Rajebhosale
Oct 23, 2024; 44:e0063242024-e0063242024
Cellular

Large-scale genome-wide association studies (GWASs) have associated intronic variants in PDE4B, encoding cAMP-specific phosphodiesterase-4B (PDE4B), with increased risk for post-traumatic stress disorder (PTSD), as well as schizophrenia and substance use disorders that are often comorbid with it. However, the pathophysiological mechanisms of genetic risk involving PDE4B are poorly understood. To examine the effects of PDE4B variation on phenotypes with translational relevance to psychiatric disorders, we focused on PDE4B missense variant M220T, which is present in the human genome as rare coding variant rs775201287. When expressed in HEK-293 cells, PDE4B1-M220T exhibited an attenuated response to a forskolin-elicited increase in the intracellular cAMP concentration. In behavioral tests, homozygous Pde4b^M220T male mice with a C57BL/6JJcl background exhibited increased reactivity to novel environments, startle hyperreactivity, prepulse inhibition deficits, altered cued fear conditioning, and enhanced spatial memory, accompanied by an increase in cAMP signaling pathway-regulated expression of BDNF in the hippocampus. In response to a traumatic event (10 tone–shock pairings), neuronal activity was decreased in the cortex but enhanced in the amygdala and hippocampus of Pde4b^M220T mice. At 24 h post-trauma, Pde4b^M220T mice exhibited increased startle hyperreactivity and decreased plasma corticosterone levels, similar to phenotypes exhibited by PTSD patients. Trauma-exposed Pde4b^M220T mice also exhibited a slower decay in freezing at 15 and 30 d post-trauma, demonstrating enhanced persistence of traumatic memories, similar to that exhibited by PTSD patients. These findings provide substantive mouse model evidence linking PDE4B variation to PTSD-relevant phenotypes and thus highlight how genetic variation of PDE4B may contribute to PTSD risk.

Neuregulin1 (Nrg1) signaling is critical for neuronal development and function from fate specification to synaptic plasticity. Type III Nrg1 is a synaptic protein which engages in bidirectional signaling with its receptor ErbB4. Forward signaling engages ErbB4 phosphorylation, whereas back signaling engages two known mechanisms: (1) local axonal PI3K-AKT signaling and (2) cleavage by -secretase resulting in cytosolic release of the intracellular domain (ICD), which can traffic to the nucleus (Bao et al., 2003; Hancock et al., 2008). To dissect the contribution of these alternate signaling strategies to neuronal development, we generated a transgenic mouse with a missense mutation (V₃₂₁L) in the Nrg1 transmembrane domain that disrupts nuclear back signaling with minimal effects on forward signaling or local back signaling and was previously found to be associated with psychosis (Walss-Bass et al., 2006). We combined RNA sequencing, retroviral fate mapping of neural stem cells, behavioral analyses, and various network analyses of transcriptomic data to investigate the effect of disrupting Nrg1 nuclear back signaling in the dentate gyrus (DG) of male and female mice. The V₃₂₁L mutation impairs nuclear translocation of the Nrg1 ICD and alters gene expression in the DG. V₃₂₁L mice show reduced stem cell proliferation, altered cell cycle dynamics, fate specification defects, and dendritic dysmorphogenesis. Orthologs of known schizophrenia (SCZ)-susceptibility genes were dysregulated in the V₃₂₁L DG. These genes coordinated a larger network with other dysregulated genes. Weighted gene correlation network analysis and protein interaction network analyses revealed striking similarity between DG transcriptomes of V₃₂₁L mouse and humans with SCZ.

Scientists have created thin polymer sheets that expand and contract when in contact with water

From the moment they arrived at the concentration camp, Jews and other Holocaust victims were treated like animals, and only a lucky group survived the experience.

The Delaware Division of the Arts’ Mezzanine Gallery presents artist Gail Husch’s exhibition, Characters, running May 6 through 30, 2022. Her exhibit will also be part of Art Loop Wilmington — the monthly self-guided tour of art in and around the city.

NEW CASTLE (Oct. 10, 2022) – Como parte de su plan estratégico para facilitar el acceso a los servicios para los residentes de Delaware a través del estado, el Departamento de Salud y Servicios Sociales (DHSS) comenzará una fase crítica de participación comunitaria en la que el público puede opinar sobre los tipos de cambios […]

Hi all,

I have been following the tutorial "Innovus Block Implementation with Stylus Common UI", version 23.1.

While I was doing the clock tree synthesis, the tutorial calls for a command

clock_opt_design

But my tool tells me this is a beta feature which needs to be enabled.

Warning: clock_opt_design requires beta feature innovusClockOptFlow enabled.

Can I ask how do I enable this beta feature?

My version of Innovus is v21.35-s114_1, is it because of the version incompatibility?

Many thanks

La enseñanza bíblica en profundidad de John MacArthur lleva la verdad transformadora de la Palabra de Dios a millones de personas cada día.

La enseñanza bíblica en profundidad de John MacArthur lleva la verdad transformadora de la Palabra de Dios a millones de personas cada día.

Title: Long-Term Exercise Can Reduce Vets' Muscle Pain
Category: Health News
Created: 8/26/2010 6:10:00 PM
Last Editorial Review: 8/27/2010 12:00:00 AM

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Category: Health News
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Title: Drug for Spinal Muscular Atrophy May Help Older Children: Study
Category: Health News
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Title: Gene 'Editing' in Dog Study Shows Promise for Kids With Muscular Dystrophy
Category: Health News
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Category: Health News
Created: 8/22/2022 12:00:00 AM
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Extract

In cystic fibrosis (CF), Pseudomonas aeruginosa acquisition represents a turning point in disease progression. The presence of chronic P. aeruginosa infection is associated with worsening lung function and increased risk of earlier death, whereas treatment substantially improves lung function and survival [1, 2]. Efforts to diagnose and eradicate early P. aeruginosa provide lasting benefits for children with CF [3, 4]. However, the timing of infection varies considerably between individuals with CF, treatment centres [5, 6], and different birth cohorts of people with the disease [7, 8].

Background

Pseudomonas aeruginosa is a common pathogen that contributes to progressive lung disease in cystic fibrosis (CF). Genetic factors other than CF-causing CFTR (CF transmembrane conductance regulator) variations contribute ~85% of the variation in chronic P. aeruginosa infection age in CF according to twin studies, but the susceptibility loci remain unknown. Our objective is to advance understanding of the genetic basis of host susceptibility to P. aeruginosa infection.

Materials and methods

We conducted a genome-wide association study of chronic P. aeruginosa infection age in 1037 Canadians with CF. We subsequently assessed the genetic correlation between chronic P. aeruginosa infection age and lung function through polygenic risk score (PRS) analysis and inferred their causal relationship through bidirectional Mendelian randomisation analysis.

Results

Two novel genome-wide significant loci with lead single nucleotide polymorphisms (SNPs) rs62369766 (chr5p12; p=1.98x10^–8) and rs927553 (chr13q12.12; p=1.91x10^–8) were associated with chronic P. aeruginosa infection age. The rs62369766 locus was validated using an independent French cohort (n=501). Furthermore, the PRS constructed from CF lung function-associated SNPs was significantly associated with chronic P. aeruginosa infection age (p=0.002). Finally, our analysis presented evidence for a causal effect of lung function on chronic P. aeruginosa infection age (β=0.782 years, p=4.24x10^–4). In the reverse direction, we observed a moderate effect (β=0.002, p=0.012).

Conclusions

We identified two novel loci that are associated with chronic P. aeruginosa infection age in individuals with CF. Additionally, we provided evidence of common genetic contributors and a potential causal relationship between P. aeruginosa infection susceptibility and lung function in CF. Therapeutics targeting these genetic factors may delay the onset of chronic infections, which account for significant remaining morbidity in CF.

Researchers describe a new nudibranch that is genetically drastically different from its closest relatives.

While each side adhered to familiar positions, the chemistry between the principals was good and the dialogue was cordial and frank.

A recent Australian study suggests that social media platforms such as TikTok and Instagram are contributing to unrealistic and unhealthy obsessions with

Your mane matters! Healthy, happy hair denotes your priorities towards self-care. Bollywood beauties including Ananya Panday, Janhvi Kapoor, Alia Bhatt, and others understand this must-do beauty ritual and ensure to keep their locks in the finest condition. Now, these celebs may

Cambridge : Cambridge University Press, 2023.

[s.l.] : Universitaire Pers Leuven, 2023.