google-site-verification=Gv0qWfGxN8mQFdnttVkBdb0UtF7P8_087tr3-YUQ9Ko

5 Reasons Why Your Website Is Not Converting

https://www.interco.mjfgroup.biz/herearethereasons

How do you measure the success of a site? Conversion is an issue if you are not converting so read this Blog 5 Reasons Why Your Website Is Not Converting an see if this will help.

You could have a lot of traffic going to your site, but those visits don’t really matter if you aren’t converting them into customers. The only visitors that matter are those that are adding to your bottom-line. All other traffic is essentially wasted.

https:/www.mjfgroup.biz/5reasonswhyyoursiteisnotconverting

5 Reasons Why Your Website Is Not Converting

Are you finding yourself with a lot of traffic, selling the right products at competitive prices, yet not with many paying customers? Then read on to find out why your site isn’t converting and what you can do about it.

Check Your Current Conversion Rate

First things first, you should know your current conversion rate. Whether you measure your conversions by product purchases, brochure downloads or email newsletter signups: you need to be measuring and tracking those conversions regularly. You can track your conversion rate using Goals in Google Analytics, or through any other analytics platform of your choosing.

So what’s considered a good conversion rate? The ideal rate is between 2 to 3 percent. This rate could be higher or lower based on the value of the conversion (e.g. you’d have more difficulty converting customers if you’re selling products or services worth $10,000+). But if you’re having less than 2 percent conversion and your conversion value isn’t very high, then you might have a problem on your hands.

5 Reasons Why Your Website Is Not Converting

Here are five reasons why your site may be underperforming.

#1. You’re Providing a Bad Mobile Experience

If your website isn’t mobile-friendly, there is no way it will survive in these times. It isn’t enough for your site to be responsive, it has to be designed specifically for mobile in terms of content and structure. Failure to do so would mean marginalizing a substantial portion of your customer base and in turn, decreasing your conversion rate.

But what does designing for mobile entail?

  • Using large and easily legible text
  • Using short paragraphs
  • Making sure that every key feature is just a tap away
  • Having just a single call-to-action

The key is to keep testing your mobile site. Perhaps you should even ask customers and family members for feedback on your site’s mobile experience. Afterwards, you should review what is working and what is not – and address those issues.

5 Reasons Why Your Website Is Not Converting

As long as you do not ignore the importance of having a good mobile experience for your site, you can easily hone in on the reason(s) your site is not converting.

#2. No Call to Action

Your website could be user-friendly with engaging and quality content, but without a clear and concise call-to-action, you simply won’t convert. Users may want to convert but just don’t have the opportunity or means to do so. Because you haven’t provided it.

Make your call-to-action clear, concise, prominent, specific and compelling. Provide all the information users need so they know exactly what you want them to do next. Create calls-to-action that are relevant and specific; and place them in a prominent place on every page of your site.

Whatever you do, make sure it is very easy for the user to convert when they are ready to.

#3. Your Users Are Annoyed with Your Website

You may be missing out on conversion opportunities if there is something off-putting about your site. Look at your bounce rate: if it is high, then you know there is something that is not appealing to users.

In such a case, you need to find out what the problem is – directly from the user. You may use heat maps and look at your user journeys via Google Analytics, but perhaps it will make your job easier to ask users directly (e.g. via a quick survey).

A few common annoyances on websites:

  • You do not offer any useful information
  • Navigation is too difficult
  • You have too many ads or popups
  • Your site doesn’t look good

These are all problems with a rather easy fix. Take your time investigating them and fix the errors as soon as you can.

5 Reasons Why Your Website Is Not Converting

#4. You’re Off-Target

Your website should be anything but general. A lot of website owners aim to please everyone – but they can’t – and end up isolating their entire audience.

Perhaps you’re writing for the wrong audience, perhaps you’re writing for a larger demographic than you should be; whatever the case, inaccurate targeting could negatively impact your conversion rate. Your copy, branding, marketing and site design should speak directly to a niche demographic.

Conduct market research to properly define and know your audience.

#5. You Have a Slow Site

We previously covered the importance of website load speed and provided tips on to speed up your site. When your website doesn’t load fast, your visitors leave and are unlikely to visit again in the near future.

5 Reasons Why Your Website Is Not Converting

There are many factors that can slow down your site, such as:

  • A site that isn’t optimized for mobile
  • Broken links
  • Not using caching
  • Messy code
  • Images that aren’t optimized
  • Flash and Java
  • Average web hosting

You can check your current site speed via Page Speed Insights. If your site is taking longer than 3 seconds to load, you need to work on it. Studies show that most users quickly exit sites that take longer than 3 seconds to load.

Measure, Measure and Measure

This is actually a sixth reason why your site may not be converting. The measure, measure and keep measuring. If you’re not measuring, you’re guessing, and in turn, not really making any strides.

The problem most website owners encounter is that they are either not tracking their website traffic or that they are tracking but not reviewing their metrics. Some do know they should be tracking, but just aren’t sure what to look for or what to make of the results.

Well, you should always start with your goals in mind. Then you can identify which key metrics will help you to measure your progress towards those goals.

Once you start measuring, you can improve on those metrics; figure out what is working, what isn’t, and then fine-tune and optimize.

5 Reasons Why Your Website Is Not Converting

Wrapping Up

These five reasons are just a starting point to help boost your conversion rates. There are many other reasons why your site may not be converting. However, these are fairly common in under-converting sites.

If you find that any of these reasons apply to your business, simply make the changes and you’ll see a big difference or improvement in your conversion rates and bottom line.

If you need any Digital Marketing help please contact me.

Contact Me

De-Risk Future Growth

https://www.interco.mjfgroup.biz/derisk

De-Risk Future Growth as Financial targets are at risk more than at any other time in recent history due to the prevailing business climate and associated uncertainty.

What then, can business leaders do to configure their companies to navigate the difficult path ahead?

https://www.interco.mjfgroup.biz/driskfuturegrowth

New insight

The Index measures your company’s Entrepreneurial Dynamic™. This assesses the underlying strengths and weaknesses of your operational capability, which fundamentally underpins future commercial success. It accurately identifies where and why your financial targets are at risk, provides actionable insight to help mitigate that risk and increases the probability that future growth will be achieved.

De-Risk Future Growth


…for more information, please contact me.

10 Tools for Your Students’ Creativity Toolbox

https://www.interco.mjfgroup.biz/creativity

10 Tools for Your Students’ Creativity Toolbox as “Creativity involves breaking out of established patterns in order to look at things in a different way.” —Edward de Bono.

Read all our blogs by signing up.

[wpmem_form register]

When I write an article, I usually draft two or three versions before I find the one I call the first draft. Creating an article requires exploring what I want to say and how I want to say it for my audience. I tell my children and students that the best writing begins during the revisions.

Creativity does not just occur in the arts—it happens within engineering design, policy making, problem solving, game strategizing, and especially lesson planning. And it’s a process that takes many forms, from conceiving an idea to shaping thoughts into something tangible to polishing a draft. During the process, there are likely many redos, as each draft and conversation inspires a new take on the idea, which may sharpen the picture of one’s creation.

It’s a mistake to believe that creativity is an inherent ability that some people have in plenty while others have little. Those are the thoughts of either self-doubters or people who struggle with explaining how to be creative. There are people who are gifted with a natural attunement to creative thinking, just as there are gifted athletes, scientists, and teachers, but dedicated study and practice can hone one’s creativity.

10 Tools for Your Students’ Creativity Toolbox

“Creativity is the process of having original ideas that have value. It is a process; it’s not random.” —Ken Robinson

Creativity is a fluid and flexible process. Sometimes the best way to make something new is to muck around. Accept that the first, second, or nth round or draft may not be what is wanted. It’s a messy process. In the act of doing, we find pieces that become the foundation of the product that is eventually shaped.

The Creativity Toolbox

Here are a few tools for your students’ creativity toolbox. Practice these techniques with students and they’ll begin to understand how to use them for themselves.

    1. Don’t settle for the first great idea. Keep generating until you have at least three workable ideas. Chalk Talk (pdf) is a silent idea-mapping activity where participants dialog through writing. Affinity Mapping (pdf) is a mixture of shared reflective responses to prompts followed by collaborative organizing of the ideas. Much can be recorded in the students’ journals.
    2. Draft and redraft an idea, concept, solution, or product. Redraft from different perspectives, such as audience, cultural viewpoint, or supporter vs. antagonist.
    3. Participate in structured conversations. Dialog with reflection can lead to new and revised ideas. Use structured protocols that support reflection, such as Spider Web (Harkness) Discussions, and feedback, like the Charrette Protocol.
    4. Make mistakes through trial and error. Finding flaws is a treasured opportunity to design something better or see a new approach.
    5. Set the product or idea aside to marinate for some time. Work on something else for a day, or a week. Return to the creative work with a fresh perspective. When I do this, my revision work is more effective.

10 Tools for Your Students’ Creativity Toolbox

  1. Grow a work portfolio. Produce a collection of first drafts to draw inspiration for creative projects.
  2. Keep a journal. Start small with a journal for a scientist, writer, mathematician, engineer, or other. Inspiration strikes in the moment. As students capture their thinking through writing, they can find connections between two or three notes, which can result in an epiphany.
  3. Research to learn new ideas. We don’t know what we don’t know. Research deepens students’ knowledge base and opens up ways of thinking that they were previously unaware of.
  4. Critique peer work. Feedback protocols for writing, designs, or solutions to problems are good ways for students to express their thinking, get feedback, and then process how they might incorporate some into their work. Try gallery walks and Charrette.
  5. Solve problems and puzzles for exercise on how to think differently. Use team builders like ones from Teampedia for students to practice creative problem-solving. Conduct a post-reflection experience where students unpack the tools used from their creativity toolbox.

Expand your students’ creativity toolbox by exploring and teaching three or four of these tools. As with curriculum skills, students build understanding and competency with the tools themselves, so that they can select the one that fits their current need. Conducting science experiments is unnecessarily difficult if one does not know the purpose and use of the scientific method or engineering design steps. Composing a quality research paper is hopeless if one does not have the skills for information fluency and finding authoritative references. The same is true with creativity.

“Creativity is a wild mind & a disciplined eye.” —Dorothy Parker
Eat That Frog - Watch the inspirational movie now

Being creative requires development of tools. Being creative means that a person can look in their toolbox and try one of the strategies they’ve practiced—and if the results are a failure, they can use that opportunity to rummage around for another tool. Students can practice independence when their creativity toolbox is well equipped. What matters most with creativity is getting started.

ABOUT THE AUTHOR

An excellent post.

Now if you need any Training, Development using our management Consulting division or Funding using our Fundinglines division Contact us.

Contact Us.

Urban farms on rooftops and underground

https://www.inerco.mjfgroup.biz/innercityfarms

Urban farms on rooftops and underground as City agriculturalists are harnessing technologies such as……

Register online to get to see all our blogs.

[wpmem_form register]

LED bulbs, 3D printers and data analysis to speed up growth and create farms virtually anywhere

 

Are Vertical Farms The Future Of Agriculture?

Let us help you put your innercity garden grow plans together.

Contact Us.

To Stay Young, Kill Zombie Cells

https://www.interco.mjfgroup.biz/stayyoung

To Stay Young, Kill Zombie Cells as an An anti-aging strategy that works in mice is about to be tested in humans.

Jan van Deursen was baffled by the decrepit-looking transgenic mice he created in 2000. Instead of developing tumours as expected, the mice experienced a stranger malady. By the time they were three months old, their fur had grown thin and their eyes were glazed with cataracts. It took him years to work out why: the mice were ageing rapidly, their bodies clogged with a strange type of cell that did not divide, but that wouldn’t die.

That gave van Deursen and his colleagues at Mayo Clinic in Rochester, Minnesota, an idea: could killing off these ‘zombie’ cells in the mice delay their premature descent into old age? The answer was yes. In a 2011 study, the team found that eliminating these ‘senescent’ cells forestalled many of the ravages of age. The discovery set off a spate of similar findings. In the seven years since, dozens of experiments have confirmed that senescent cells accumulate in ageing organs, and that eliminating them can alleviate, or even prevent, certain illnesses (see ‘Becoming undead’). This year alone, clearing the cells in mice has been shown to restore fitness, fur density and kidney function. It has also improved lung disease and even mended damaged cartilage. And in a 2016 study, it seemed to extend the lifespan of normally ageing mice.

“Just by removing senescent cells, you could stimulate new tissue production,” says Jennifer Elisseeff, senior author of the cartilage paper and a biomedical engineer at Johns Hopkins University in Baltimore, Maryland. It jump-starts some of the tissue’s natural repair mechanisms, she says.

To Stay Young, Kill Zombie Cells

250x250 ; 12/5

This anti-ageing phenomenon has been an unexpected twist in the study of senescent cells, a common, non-dividing cell type first described more than five decades ago. When a cell enters senescence—and almost all cells have the potential to do so—it stops producing copies of itself, begins to belch out hundreds of proteins, and cranks up anti-death pathways full blast. A senescent cell is in its twilight: not quite dead, but not dividing as it did at its peak.

Now biotechnology and pharmaceutical companies are keen to test drugs—known as senolytics—that kill senescent cells in the hope of rolling back, or at least forestalling, the ravages of age. Unity Biotechnology in San Francisco, California, co-founded by van Deursen, plans to conduct multiple clinical trials over the next two-and-a-half years, treating people with osteoarthritis, eye diseases and pulmonary diseases. At Mayo, gerontologist James Kirkland, who took part in the 2011 study, is cautiously beginning a handful of small, proof-of-concept trials that pit senolytic drugs against a range of age-related ailments. “I lose sleep at night because these things always look good in mice or rats, but when you get to people you hit a brick wall,” says Kirkland.

No other anti-ageing elixir has yet cleared that wall, and for a few good reasons. It’s next to impossible to get funding for clinical trials that measure an increase in healthy lifespan. And even as a concept, ageing is slippery. The US Food and Drug Administration has not labelled it a condition in need of treatment.

 

Still, if any of the trials offer “a whiff of human efficacy”, says Unity’s president, Ned David, there will be a massive push to develop treatments and to better understand the fundamental process of ageing. Other researchers who study the process are watching closely. Senolytics are “absolutely ready” for clinical trials, says Nir Barzilai, director of the Institute for Aging Research at the Albert Einstein College of Medicine in New York City. “I think senolytics are drugs that could come soon and be effective in the elderly now, even in the next few years.”

Credit: Nature, October 24, 2017, doi:10.1038/550448a

To Stay Young, Kill Zombie Cells

THE DARK SIDE

When microbiologists Leonard Hayflick and Paul Moorhead coined the term senescence in 1961, they suggested that it represented ageing on a cellular level. But very little research was done on ageing at the time, and Hayflick recalls people calling him an idiot for making the observation. The idea was ignored for decades.

Although many cells do die on their own, all somatic cells (those other than reproductive ones) that divide have the ability to undergo senescence. But, for a long time, these twilight cells were simply a curiosity, says Manuel Serrano of the Institute for Research in Biomedicine in Barcelona, Spain, who has studied senescence for more than 25 years. “We were not sure if they were doing something important.” Despite self-disabling the ability to replicate, senescent cells stay metabolically active, often continuing to perform basic cellular functions.

By the mid-2000s, senescence was chiefly understood as a way of arresting the growth of damaged cells to suppress tumours. Today, researchers continue to study how senescence arises in development and disease. They know that when a cell becomes mutated or injured, it often stops dividing—to avoid passing that damage to daughter cells. Senescent cells have also been identified in the placenta and embryo, where they seem to guide the formation of temporary structures before being cleared out by other cells.

But it wasn’t long before researchers discovered what molecular biologist Judith Campisi calls the “dark side” of senescence. In 2008, three research groups, including Campisi’s at the Buck Institute for Research on Aging in Novato, California, revealed that senescent cells excrete a glut of molecules—including cytokines, growth factors and proteases—that affect the function of nearby cells and incite local inflammation. Campisi’s group described this activity as the cell’s senescence-associated secretory phenotype, or SASP. In recent unpublished work, her team identified hundreds of proteins involved in SASPs.

In young, healthy tissue, says Serrano, these secretions are probably part of a restorative process, by which damaged cells stimulate repair in nearby tissues and emit a distress signal prompting the immune system to eliminate them. Yet at some point, senescent cells begin to accumulate—a process linked to problems such as osteoarthritis, a chronic inflammation of the joints, and atherosclerosis, a hardening of the arteries. No one is quite sure when or why that happens. It has been suggested that, over time, the immune system stops responding to the cells.

Surprisingly, senescent cells turn out to be slightly different in each tissue. They secrete different cytokines, express different extracellular proteins and use different tactics to avoid death. That incredible variety has made it a challenge for labs to detect and visualize senescent cells. “There is nothing definitive about a senescent cell. Nothing. Period,” says Campisi.

In fact, even the defining feature of a senescent cell—that it does not divide—is not written in stone. After chemotherapy, for example, cells take up to two weeks to become senescent, before reverting at some later point to a proliferating, cancerous state, says Hayley McDaid, a pharmacologist at Albert Einstein College of Medicine. In support of that idea, a large collaboration of researchers found this year that removing senescent cells right after chemotherapy, in mouse models for skin and breast cancer, makes the cancer less likely to spread.

The lack of universal features makes it hard to take inventory of senescent cells. Researchers have to use a large panel of markers to search for them in tissue, making the work laborious and expensive, says van Deursen. A universal marker for senescence would make the job much easier—but researchers know of no specific protein to label, or process to identify. “My money would be on us never finding a senescent-specific marker,” Campisi adds. “I would bet a good bottle of wine on that.”

Earlier this year, however, one group did develop a way to count these cells in tissue. Valery Krizhanovsky and his colleagues at the Weizmann Institute of Science in Rehovot, Israel, stained tissues for molecular markers of senescence and imaged them to analyse the number of senescent cells in tumours and aged tissues from mice. “There were quite a few more cells than I actually thought that we would find,” says Krizhanovsky. In young mice, no more than 1% of cells in any given organ were senescent. In two-year-old mice, however, up to 20% of cells were senescent in some organs.

But there’s a silver lining to these elusive twilight cells: they might be hard to find, but they’re easy to kill.

OUT WITH THE OLD

In November 2011, while on a three-hour flight, David read van Deursen and Kirkland’s just-published paper about eliminating zombie cells. Then he read it again, and then a third time. The idea “was so simple and beautiful”, recalls David. “It was almost poetic.” When the flight landed, David, a serial biotech entrepreneur, immediately rang van Deursen, and within 72 hours had convinced him to meet to discuss forming an anti-ageing company.

Kirkland, together with collaborators at the Sanford Burnham Medical Research Institute in La Jolla, California, initially attempted a high-throughput screen to quickly identify a compound that would kill senescent cells. But they found it to be “a monumental task” to tell whether a drug was affecting dividing or non-dividing cells, Kirkland recalls. After several failed attempts, he took another tack.


Senescent cells depend on protective mechanisms to survive in their ‘undead’ state, so Kirkland, in collaboration with Laura Niedernhofer and others from the Scripps Research Institute in Jupiter, Florida, began seeking out those mechanisms. They identified six signalling pathways that prevent cell death, which senescent cells activate to survive.

Then it was just a matter of finding compounds that would disrupt those pathways. In early 2015, the team identified the first senolytics: an FDA-approved chemotherapy drug, dasatinib, which eliminates human fat-cell progenitors that have turned senescent; and a plant-derived health-food supplement, quercetin, which targets senescent human endothelial cells, among other cell types. The combination of the two—which work better together than apart—alleviates a range of age-related disorders in mice.

Ten months later, Daohong Zhou at the University of Arkansas for Medical Sciences in Little Rock and his colleagues identified a senolytic compound now known as navitoclax, which inhibits two proteins in the BCL-2 family that usually help the cells to survive. Similar findings were reported within weeks by Kirkland’s lab and Krizhanovsky’s lab.

By now, 14 senolytics have been described in the literature, including small molecules, antibodies and, in March this year, a peptide that activates a cell-death pathway and can restore lustrous hair and physical fitness to ageing mice.

So far, each senolytic kills a particular flavour of senescent cell. Targeting the different diseases of ageing, therefore, will require multiple types of senolytics. “That’s what’s going to make this difficult: each senescent cell might have a different way to protect itself, so we’ll have to find combinations of drugs to wipe them all out,” says Niedernhofer. Unity maintains a large atlas documenting which senescent cells are associated with which disease; any weaknesses unique to given kinds of cell, and how to exploit those flaws; and the chemistry required to build the right drug for a particular tissue. There is no doubt that for different indications, different types of drug will need to be developed, says David. “In a perfect world, you wouldn’t have to. But sadly, biology did not get that memo.”

For all the challenges, senolytic drugs have several attractive qualities. Senescent cells will probably need to be cleared only periodically—say, once a year—to prevent or delay disease. So the drug is around for only a short time. This type of ‘hit and run’ delivery could reduce the chance of side effects, and people could take the drugs during periods of good health. Unity plans to inject the compounds directly into diseased tissue, such as a knee joint in the case of osteoarthritis, or the back of the eye for someone with age-related macular degeneration.

And unlike cancer, in which a single remaining cell can spark a new tumour, there’s no need to kill every senescent cell in a tissue: mouse studies suggest that dispatching most of them is enough to make a difference. Finally, senolytic drugs will clear only senescent cells that are already present—they won’t prevent the formation of such cells in the future, which means that senescence can continue to perform its original tumour-suppressing role in the body.

Those perks haven’t convinced everybody of the power of senolytics. Almost 60 years after his initial discovery, Hayflick now believes that ageing is an inexorable biophysical process that cannot be altered by eliminating senescent cells. “Efforts to interfere with the ageing process have been going on since recorded human history,” says Hayflick. “And we know of nothing—nothing—that has demonstrated to interfere with the ageing process.”

Fans of senolytics are much more optimistic, emboldened by recent results. Last year, van Deursen’s lab went beyond its tests on super-aged mice and showed that killing off senescent cells in normally ageing mice delayed the deterioration of organs associated with ageing, including the kidney and heart. And—to the joy of anti-ageing enthusiasts everywhere—it extended the animals’ median lifespan by about 25%.

Successful results from mouse studies have already lured seven or eight companies into the field, Kirkland estimates. At Mayo, one clinical trial has opened, pitting dasatinib and quercetin in combination against chronic kidney disease. Kirkland plans to try other senolytics against different age-related diseases. “We want to use more than one set of agents across the trials and look at more than one condition,” he says.

If eliminating senescent cells in humans does improve age-related illnesses, researchers will aim to create broader anti-ageing therapies, says David. In the meantime, researchers in the field insist that no one should take these drugs until proper safety tests in humans are complete. In rodents, senolytic compounds have been shown to delay wound healing, and there could be additional side effects. “It’s just too dangerous,” says Kirkland.

Van Deursen says that continuing to answer basic biological questions is the field’s best shot at success. “Only then will we be able to understand what ageing really is, and how we can, in an intelligent way, interfere with it.”

This article is reproduced with permission and wasfirst publishedon October 24, 2017.

 

%d bloggers like this: