Youth Voter Festival encourages maximum Youth Participation in NGE2022

308
1658
Young women from the University of Papua New Guinea and Port Moresby National High School participated in various activities at the Youth Voter Festival at Nature Park in Port Moresby.

Young people are the most diverse in a population. Together they have the power to elect the next generation of leaders who will represent their shared vision for a bright future.

The PNG Electoral Commission has taken steps through raising awareness to ensure there is maximum participation of eligible youth, women, and persons with disabilities in the 2022 National Election.

“In the NGE2022, there will be a gender split in both the voter roll and the polling booths. This is the first since Independence,” said PNG Electoral Commissioner Simon Sinai.

In recent times, the youth including disabled persons in Goroka, and Port Moresby had the opportunity to participate in a Youth Voter Festival.

The highlight of the Youth Voter Festival in Goroka and Port Moresby was the set-up of the polling simulation by the PNG Electoral Commission.

Festival participants joined the queue to ‘vote’ and asked questions to PNG Electoral Commission staff who were on hand to assist the youths in the mock polling exercise.

The polling simulation ensured that the youth become familiarized with polling places procedures and how to vote.

“Generally, we young people are reluctant to vote when we turn 18 and are eligible to vote. We have to reverse this trend of thinking and understand why it is very important for young people to get together and have a voice to elect the leaders who can best represent us in government and make decisions for a better future for us and the next generations,” said Isborn Baspen, a third year Physics major student at the University of Goroka.

The Youth Voter Festival is an initiative by the International Foundation for Electoral Systems (IFES) and supported by the American people through the United States Agency for International Development (USAID) and the Department of Foreign Affairs and Trade Australia.

The first Youth Voter Festival was held at the University of Goroka in the Eastern Highlands Province on the 2nd of June 2022. 

The Youth Voter Festival In Goroka attracted many young people from the University of Goroka, secondary schools, colleges and youth groups who participated in the event. They signed a banner to show their support that young people’s vote matter.
FM100 Talkback Show was live at the Youth Voter Festival in Port Moresby. Young people with disabilities (from left) Mark Kinito and Lovelyn Garry discuss the importance of youth voting in the 2022 National Election with FM100 Talkback Show host Douglas Dimagi.

Rolling green hills behind the university campus and an array of colourful blooms in the flower gardens meticulously kept, provided a beautiful backdrop as more than 150 youths from Eastern Highlands Province convened and joined in an array of fun activities at the Youth Voter Festival.

“Young people represent a majority of the population in Papua New Guinea, and they have the opportunity to be active participants in shaping the future of their community and country by voting,” said IFES Country Director Paul Rowland.

“IFES is happy to work with the PNG Electoral Commission and other support partners to make sure that everyone has the chance to vote in the National Election. The Youth Voter Festival is a fun-packed event that is open to young eligible voters to attend and learn more on how they can become informed voters,” Mr. Rowland added.

Participants at the festival were from youth groups in Goroka and students from the University of Goroka, Goroka Business College, Faniufa Primary School, high school students from Goroka International School, Goroka Grammar School, and Goroka Secondary School.

In Port Moresby, the Youth Voter Festival was held at Nature Park on Friday 24th June 2022.

“The youth are at the beginning of their adult lives striving for their dreams. Many will cast their votes for the first time exercising their rights as citizens. Today we celebrate them as voters,” said IFES Deputy Country Manager Robert Irish.

Over 100 youths including persons with disabilities attended the one-day event.

At the festival, an array of fun activities included quiz competitions, raffles, scavenger hunt and performances by popular PNG artists Mereani Masani and DJ Dirty Fingers was held.

Samuel Rei, a young man with a disability, sang a duet with popular artist Mereani Masani and kept the crowd entertained.

Advertise here on PNGBUZZ - Contact us today

RELATED ARTICLESMORE FROM AUTHOR

308 COMMENTS

  61. It is appropriate time to make some plans for the future and it is time to be happy. I’ve read this post and if I could I want to suggest you some interesting things or tips. Perhaps you could write next articles referring to this article. I desire to read more things about it!

  81. You actually make it seem really easy together with your presentation however I find this matter to be actually one thing which I believe I’d by no means understand. It sort of feels too complicated and very large for me. I’m taking a look ahead for your next publish, I?¦ll attempt to get the dangle of it!

  86. That is the correct blog for anyone who needs to search out out about this topic. You notice so much its almost exhausting to argue with you (not that I really would need…HaHa). You positively put a new spin on a subject thats been written about for years. Nice stuff, simply nice!

  89. This is really interesting, You’re a very skilled blogger. I have joined your feed and look forward to seeking more of your excellent post. Also, I’ve shared your website in my social networks!

  96. The next time I read a blog, I hope that it doesnt disappoint me as much as this one. I mean, I know it was my choice to read, but I actually thought youd have something interesting to say. All I hear is a bunch of whining about something that you could fix if you werent too busy looking for attention.

  98. This web site is known as a walk-by way of for all of the information you needed about this and didn’t know who to ask. Glimpse right here, and also you’ll undoubtedly uncover it.

  102. Hello there, just became alert to your blog through Google, and found that it is truly informative. I’m gonna watch out for brussels. I’ll be grateful if you continue this in future. A lot of people will be benefited from your writing. Cheers!

  104. You actually make it appear so easy with your presentation but I in finding this matter to be really something that I think I would by no means understand. It seems too complex and extremely large for me. I’m looking forward in your next submit, I’ll attempt to get the cling of it!

  108. The heart of your writing while appearing reasonable originally, did not really work properly with me after some time. Someplace within the paragraphs you were able to make me a believer unfortunately just for a very short while. I still have got a problem with your jumps in assumptions and you would do well to fill in those gaps. When you can accomplish that, I could certainly be fascinated.

  110. I believe this web site holds some rattling superb info for everyone. “The penalty of success is to be bored by the attentions of people who formerly snubbed you.” by Mary Wilson Little.

  112. What¦s Going down i am new to this, I stumbled upon this I have found It positively useful and it has aided me out loads. I hope to give a contribution & help different customers like its aided me. Good job.

  117. I’m really loving the theme/design of your web site. Do you ever run into any internet browser compatibility problems? A couple of my blog audience have complained about my blog not working correctly in Explorer but looks great in Opera. Do you have any recommendations to help fix this problem?

  147. WBCSD members demonstrated how, by leveraging more and better mobility data into MaaS applications and digital tools (e.g. digital twins), mobility providers can deploy more effective and responsive mobility services, reduce investment risks by improving 세종출장샵predictability, while increasing the effectiveness of existing mobility services.

  170. I’m really impressed along with your writing talents and also with the structure for your blog.Is this a paid topic or did you modify it your self? Anyway keepup the nice quality writing, it is uncommon to see a nice blog like this one today..

  174. I’m truly enjoying the design and layout of your website. It’s a very easy on the eyes which makes it much more enjoyable for me to come here and visit more often. Did you hire out a developer to create your theme? Fantastic work!

  176. Hi there just wanted to give you a quick heads up and let you know a few of the images aren’t loading properly. I’m not sure why but I think its a linking issue. I’ve tried it in two different browsers and both show the same outcome.

  177. Sweet blog! I found it while searching on Yahoo News. Do you have any tips on how to get listed in Yahoo News? I’ve been trying for a while but I never seem to get there! Thanks

  180. I was just searching for this info for some time. After six hours of continuous Googleing, at last I got it in your site. I wonder what’s the lack of Google strategy that do not rank this kind of informative web sites in top of the list. Generally the top web sites are full of garbage.

  181. I really like your blog.. very nice colors & theme. Did you make this website yourself or did you hire someone to do it for you? Plz answer back as I’m looking to design my own blog and would like to find out where u got this from. kudos

  182. My brother suggested I might like this blog. He was entirely right. This post truly made my day. You cann’t imagine just how much time I had spent for this information! Thanks!

  183. Its like you read my mind! You seem to know a lot about this, like you wrote the book in it or something. I think that you could do with some pics to drive the message home a bit, but other than that, this is great blog. A fantastic read. I will certainly be back.

  185. whoah this weblog is fantastic i really like reading your articles. Stay up the great paintings! You realize, a lot of individuals are looking round for this information, you can aid them greatly.

  188. Wow that was odd. I just wrote an very long comment but after I clicked submit my comment didn’t appear. Grrrr… well I’m not writing all that over again. Regardless, just wanted to say wonderful blog!

  190. Undeniably believe that which you stated. Your favorite justification appeared to be on the web the simplest thing to be aware of. I say to you, I certainly get irked while people think about worries that they plainly don’t know about. You managed to hit the nail upon the top and defined out the whole thing without having side effect , people can take a signal. Will likely be back to get more. Thanks

  204. I don’t even know how I finished up right here, but I believed this publish used to be good. I don’t realize who you are but certainly you’re going to a well-known blogger for those who are not already Cheers!

  208. Some genuinely wonderful content on this site, thanks for contribution. “Once, power was considered a masculine attribute. In fact, power has no sex.” by Katharine Graham.

  212. I’m really enjoying the design and layout of your blog. It’s a very easy on the eyes which makes it much more pleasant for me to come here and visit more often. Did you hire out a developer to create your theme? Outstanding work!

  230. Hello this is a excellent article. I’m going to mail this to my friends. I stumbled on this while searching on google I’ll be sure to come back. thanks for sharing.

  231. Hi! I just wanted to ask if you ever have any trouble with hackers? My last blog (wordpress) was hacked and I ended up losing a few months of hard work due to no backup. Do you have any solutions to prevent hackers?

  234. This is a good tip especially to those new to the blogosphere. Short but very accurate information… Thanks for sharing this one. A must read post!

  241. Epicatechin appears to augment anaerobic coaching diversifications and muscle building, both of which can be partly mediated by myostatin inhibition [10]. Myostatin is a myokine (“muscle-derived hormone”) that inhibits excess muscle development by reducing the expression of myogenic (“muscle-generating”) factors. In essence, adhering to elementary supplements like creatine is advisable for muscle development. If you’re abiding by core training principles, like a structured exercise routine, consuming extra energy than you burn, and making certain enough sleep, there’s no must stress over your myostatin ranges.
    Myostatin, also referred to as development differentiation factor 8 (GDF8), is a reworking development factor-β (TGF-β) family member that potently inhibits skeletal muscle improvement [1]. The organic perform of myostatin became evident when mice homozygous for a deletion of myostatin gene exhibited a dramatic increase in skeletal muscle mass, with particular person muscle teams enlarging to roughly twice their normal measurement [1]. In addition to its impact on skeletal muscle, myostatin has been demonstrated to play a significant position within the regulation of bone metabolism by suppressing bone formation [6] and stimulating bone resorption [7]. Indeed, myostatin null mice symbolize not only a doubling of muscle mass, but additionally enhanced bone mineral density (BMD) and bone regeneration [6,8]. Duchenne muscular dystrophy (DMD) is an incurable illness that causes the loss of muscle tissue. Myostatin inhibition has been proven to extend muscle mass in canines and mice with DMD, suggesting that the potential of myostatin inhibitors should be investigated in human patients with DMD [7, 16]. In the present examine, the impact of FOR supplementation had been compared with a macronutrient- and energy-matched placebo on indices of muscle dimension and power during two weeks of single-leg immobilization in younger, healthy men.
    EAA increased muscle quality (e.g., grip strength and maximal carrying load) without corresponding adjustments in markers of mitochondrial biogenesis and neuromuscular junction stability. In conclusion, RT amplifies muscle mass and power via changes in muscle protein turnover in conjunction with adjustments in implicated signaling, whereas EAAs improve muscle quality by way of unknown mechanisms. Beige and brown adipocytes exist in WAT, contributing to the whole body’s power expenditure. Different stimuli (i.e. complicated hormonal interplay and quite a few environmental factors) result in WAT browning. Vitamin D could be stored in adipose tissue; thus its insufficiency might contribute to aberrant adipogenesis.
    Transgenic overexpression of FST leads to a 2- to 3-fold enhance in muscle mass by way of hypertrophy and hyperplasia [21]. Nonetheless, the rise in muscle mass just isn’t solely attributed to blocking MSTN, as FST additionally inhibits the actions of multiple TGF-β members of the family, some of them play a job in limiting muscle mass [76]. FST-overexpressing MSTN-null mice show an even more excessive fourfold improve in muscle [77]. Contrarily, FST-null mice have decreased muscle mass at birth and perish inside a few hours [78]. Delivery of FST-coding mRNA gene remedy and AAV, in addition to follistatin peptide derivatives, have all been shown to supply substantial muscle increase in animal fashions [35, 79, 80]. Scholar Rock has submitted its anti-myostatin antibody apitegromab for FDA approval, simply months after reporting that it hit its primary endpoint in section III for spinal muscular atrophy (SMA). Approval would upend twenty years of failure for myostatin pathway inhibitors, a category of medicine that grows skeletal muscle.
    This means that the already low MSTN levels in DMD patients may cut back the effectiveness of MSTN inhibitors, as further lowering MSTN won’t significantly improve muscle mass, as mentioned by Mariot et al. (2017) [95]. Moreover, Mariot et al. (2017) found that in muscle wasting and atrophying ailments, not solely is myostatin downregulated, however the activin receptor is also downregulated, along with an increase in the MSTN antagonist follistatin [95]. These components additional complicate the therapeutic potential of MSTN inhibitors in muscle losing illnesses. Akt activation was not increased at 2 weeks of hindlimb suspension however was elevated via inhibition of myostatin signaling. Changes in activation of Akt signaling were measured utilizing the ratio of phosphorylated Akt (pAkt (ser 473)) to non-phosphorylated Akt (Fig. 4A; Supplemental Fig. 1A). We additional assessed the potential downstream results on activation of p70S6K (phosphorylated p70S6K/p70S6K) and located no important differences with either HS or myostatin inhibition (Fig. 4B; Supplemental Fig. 1B). Complete and phosphorylated Akt and p70s6k ranges have been variable and confirmed no variations between therapy teams.
    The effect on skeletal muscle progress is doubtless considered one of the primary causes for the huge curiosity for epicatechin in current times. One study was capable of decide that epicatechin from dark candies inhibits myostatin. Low levels of myostatin protein are desirable because it leads to increased ability to construct skeletal muscle mass. Phenolic compound resveratrol has anti-inflammatory and antioxidant properties that encourage the manufacturing of more antioxidant-related enzymes and activate transcription elements like NRF2 [189]. As a result, it might hinder the degradation of proteins, which is primarily caused by the angiotensin I and II routes, and phorbol ester via minimizing the expression of MAFbx, MuRF1, and NF-κB [190]. Furthermore, elevated NRF2 gene expression has been linked to the regulating of pro-inflammatory cytokines, primarily IL-6 and TNF.
    Discovery of this interaction between kidney and muscle tissue proposes a potential therapeutic technique to target skeletal muscle wasting in patients with CKD by modulating activin A [119]. The institution of myostatin as a robust negative regulator of muscle and bone mass has designated myostatin as a gorgeous therapeutic goal for varied musculoskeletal disorders. In truth, numerous myostatin-inhibiting pharmacological brokers have been developed, and many of them have progressed to human trials and are at present beneath evaluation (Table 1). What have to be thought-about is the fact that most myostatin inhibitors additionally block the activity of different closely-related members of the TGF-β household [9-12], raising the risk of undesired unwanted effects. In this evaluate, we’ll first describe the present understanding of the mechanism of myostatin function, and subsequently present an summary of the clinical progress, efficacy, and unwanted facet effects of different myostatin inhibitors. Lastly, we will discuss future perspectives and challenges relating to the development of effective myostatin-targeting therapeutics with minimal antagonistic results. The objective of the current examine was to find out the effect of four weeks of (–)-epicatechin supplementation on adaptations to anaerobic and aerobic cycling in a healthy adult population.
    Carlon Colker, M.D., found myostatin inhibitors in egg yolk from fertilized hen eggs. Dr. Colker developed a course of to optimize the myostatin-inhibiting exercise in yolk membranes, and the ensuing product is MYO-T12. It’s some of the talked-about myostatin inhibitors due to its potential to reduce myostatin levels, thereby allowing for increased muscle development and improved strength. Epicatechin additionally promotes nitric oxide production, which improves blood move and nutrient delivery to muscles, enhancing total muscle perform and endurance. Another potential concern is that increased muscle growth will result in an elevated threat of harm because of elevated stress on the muscle fibers.
    Change in bench press and leg press 1-repetition most levels (mean ± SD) between teams following 8 weeks of resistance coaching and supplementation. A Lot of the data about circulating MSTN ranges may be questioned due to potential methodological limitations. Binding reagent assays (e.g., immuno-assays and aptamer-based methods), the most well-liked technique for figuring out MSTN concentrations, have been shown to cross-react with GDF-11 [101, 102]. However, as GDF-11 is less abundant than GDF-8, its impression on overall MSTN measurements may be inconsequential [102].
    BYM-338 is an antibody directed to ActRIIB that’s currently in Section 2 for the remedy of cachexia in patients with stage IV nonsmall cell lung most cancers or Stage III/IV adenocarcinoma of the pancreas. Single infusions of BYM-334 in healthy volunteers were reported to be properly tolerated and resulted in a rise in TMV (D. Rook; International conference on sarcopenia analysis, Orlando, December 2012). It is crucial to acknowledge that alternative routes have been recognized that may be implicated.
    In the search for enhanced muscle development and athletic efficiency, myostatin inhibiting elements are essential. Myostatin is a protein identified for limiting muscle progress, and inhibiting its activity can considerably enhance muscle mass and strength. Sotatercept (ACE-011), developed by Acceleron Pharma to treat osteoporosis, is a fusion protein during which the extracellular area of ACVR2A is linked to a human IgG Fc area. Notably, biweekly subcutaneous injection of ACE-011 (10 mg/kg) for 3 months led to important increases in bone quantity (93%) and bone formation price (166%) in cynomolgus monkeys [55]. A substantial increase in BsALP ranges and enchancment in BMD were additionally detected in a number of myeloma patients who obtained 4 monthly doses of ACE-011 [57], indicating ACE-011 as a potentially efficient therapy in bone-loss disorders.
    Moreover, in a phase 2 trial conducted with boys affected by DMD, important enhancements were observed in muscle mass, with the group handled with 1 mg/kg each 2 weeks experiencing an approximate imply increase of 4–5%. Furthermore, improvements had been famous in 6-min walk distance (6MWD), bone mineral density, and reductions in fat mass [12, 63]. Nonetheless, non-muscle-related opposed unwanted effects including nosebleeds, gum bleeding, telangiectasia, and erythema led to the discontinuation of additional research [12]. Myostatin, a potent unfavorable regulator of skeletal muscle mass, has garnered significant consideration as a therapeutic goal for muscle dystrophies. Despite in depth research and promising preclinical outcomes, medical trials focusing on myostatin inhibition in muscle dystrophies have did not yield substantial enhancements in muscle operate or health in sufferers.
    Nevertheless, but extra analysis signifies that myostatin might simply be an anti-hypertrophy agent quite than the principle muscle atrophy trigger. The totally different strategies present there are two particular periods of muscle growth growth that myostatin regulates heavily. Obviously, anybody looking to construct muscle could be thinking about a protected approach to inhibit the myostatin protein, even just a little, to allow for greater muscle development positive aspects. Some “supplements” comprise follistatin, an experimental compound being studied for blocking the actions of myostatin. Potential side effects include muscle imbalances, elevated injury risk, and unknown long-term results on physique composition and bone metabolism. Seek The Advice Of a healthcare professional before use, especially if you have underlying health conditions. There ARE myostatin supplements on the market right now that work at reducing your body’s capability to provide this protein.
    Following birth, MSTN ranges remain high, though not as elevated as during fetal development [30]. MSTN-knockout animals, missing MSTN presence during prenatal or neonatal improvement, exhibit a dramatic 2- to 3-fold improve in muscle mass compared to wild-type animals [30]. Homozygous mutant mice show approximately 30% more physique weight, with each bigger muscular tissues fibers in cross-sectional area (hypertrophy) and a higher in fiber quantity (hyperplasia). Furthermore, MSTN-knockout animals show the next proportion of sort II fibers and a lowered variety of kind I fibers, along with decreased adipose tissue [30–32]. Postnatal suppression of MSTN, achieved via conditional gene concentrating on or the administration of MSTN inhibitors corresponding to its propeptide, antibody, or follistatin, induces important however comparatively lesser increases in skeletal muscle mass [33–35]. In contrast to MSTN-knockout fashions, muscle development from postnatal suppression of MSTN outcomes solely from muscle hypertrophy, not hyperplasia, however nonetheless predominantly induces sort II muscle fibers [36–38].
    The inhibitory role performed by MSTN in muscle improvement has made it an necessary therapeutic target for accelerating muscle mass. There are several ways of disrupting MSTN exercise ranging from the use of MSTN antibodies to pure compounds. Detailed knowledge of these methods and the use of in silico methods ought to improve information of the structural characteristics of MSTN and its bindings with inhibitory proteins, derived inhibitors, and other natural compounds.
    ACE-031 is a soluble form of ACVRIIB, and numerous research on an Amyotrophic Lateral Sclerosis mouse model have shown a single dose of ACE-031 increases muscle mass and strength. This fusion protein of ACVRIIB and IgG1-Fc acts by binding to MSTN, and thus, disrupts its inhibitory effect (Campbell et al., 2017). Experiments on ACE-031 had been subsequently suspended as a outcome of potential safety issues of epistaxis and telangiectasia. Ghrelin is essentially produced in gastric oxyntic mucosa (DeBoer, 2011), and ghrelin remedy reduces proinflammatory cytokine launch in cachexia sufferers (Kishimoto et al., 2012). Furthermore, increases in anabolic exercise by ghrelin improve GH launch and scale back the consequences of inflammation, which provides promise for the treatment of cachexia (Yanagi et al., 2018).
    It is conceivable the combination of flavonols and phytochemicals present in pure cocoa may have a special impact on skeletal muscle adaptation to train. One Other side of (–)-epicatechin supplementation worthy of further examine is the timing and length of supplementation. As An Alternative of persistent supplementation, it might show beneficial to examine the usage of (–)-epicatechin when supplemented immediately prior to train. Research have shown (–)-epicatechin increases blood flow by way of vasodilation by the use of nitric oxide production (3). Lastly, the potential inhibition of aerobic diversifications in skeletal muscle because of the antioxidant properties of (–)-epicatechin need to be instantly examined.
    All designed peptides had been docked with MSTN, and binding research have been carried out using Patchdock adopted by FireDock [46]. The top-scoring peptides had been selected based mostly on their global binding energies with MSTN. All claims expressed in this article are solely these of the authors and do not essentially represent these of their affiliated organizations, or those of the publisher, the editors and the reviewers.
    Statistical analyses were carried out by using a separate 2 × 2 (group × time point) two-way mixed model analyses of variance (ANOVA) for each criterion variable. If a bunch by time point interplay existed, a separate one-way ANOVA for every group and time level was performed to find out easy main results. All statistical procedures were carried out using the SPSS Statistics 22.zero software program (IBM, Armonk, NY). Participants warmed-up for five min at a piece fee equal to seventy five Watts on the Velotron cycle ergometer (Racer-Mate, Seattle, WA).
    Participants engaged in four cycling exercise classes per week for 4 weeks for a total of 16 sessions (Table 2). Sessions one and three of each week were accomplished independently on the University of South Alabama Recreation Middle using the prescribed depth and length and completion of each session was reported to study personnel. For the coaching classes in the recreation center, members used the True Fitness CS 800 upright bicycle (True Health, St. Louis, MO).
    Both Smad and non-Smad mediated signaling cause gene transcriptional alterations within the nucleus, in addition to activation of muscle atrophy marker genes (MuRF1 and Atrogin1), resulting in muscle loss. Extracellularly, MSTN pathway inhibitors can bind MSTN immediately or bind its receptor complicated to prevent MSTN from interacting with its receptor complex and triggering downstream indicators. SM produces and secretes IL-6 throughout prolonged exercise, and is thus reflected as myokines (Munoz-Canoves et al., 2013). Native IL-6 manufacturing improve MSCs activation and promote the regeneration of myotube (Munoz-Canoves et al., 2013). In Addition To, IL-6 remedy has been found to reinforce MSCs proliferation by controlling the cyclin D1 and c-myc genes (Serrano et al., 2008). The significance of IL-6 in myogenic differentiation has been confirmed as myoblast obtained from IL-6 null mice exhibits decreased fusion ability in vitro (Hoene et al., 2013).

    References:

    steroid Perscription (http://forum.moto-fan.pl/uzytkownik-klaudiasal)

  271. Good website! I really love how it is easy on my eyes and the data are well written. I am wondering how I might be notified whenever a new post has been made. I have subscribed to your RSS feed which must do the trick! Have a nice day!

  285. Thanks for another informative blog. Where else could I get that kind of information written in such a perfect way? I’ve a project that I’m just now working on, and I’ve been on the look out for such information.

  299. It’s really a great and useful piece of information. I am glad that you shared this useful info with us. Please keep us up to date like this. Thank you for sharing.

  302. Hello There. I found your blog using msn.This is a very well written article. I will make sure to bookmark it and return to read more of your useful info.Thanks for the post. I will definitely comeback.

  303. That is a great tip especially to those fresh to the blogosphere. Brief but very precise information… Appreciate your sharing this one. A must read post!

LEAVE A REPLY

Please enter your comment!
Please enter your name here