Teaching Backwards: From Motion to Muscles

Have you taught those boring muscles lately? And those dreaded origins and insertions?

Bored student going through the motions of learning muscle origins and insertions...
Does this look familiar?

And when students get to the exam they are frazzled and sad? Why do we do the same things over and over and wonder why students don’t recall what we teach them? Muscles are one of the most dynamic tissues of the body so let’s teach them dynamically!

Working in healthcare for the past decade has taught me that patient “buy in” usually leads to better outcomes. Interestingly enough, students are the same way. So why not let them pick some of the muscles they have to learn? They can choose based on personal or occupational interest. For example, if your group is interested in occupational therapy, focus on muscles that are involved in activities of daily living. Are they mostly nursing students? Include muscles commonly strained by nurses in their daily practice from poor lifting mechanics or improper conditioning. This could incentivize strengthening to prevent future injuries. Student buy in may develop into personal investment, which enhances their compliance and advances their outcomes. Follow this formula, and see what happens!

Formula 1:  Buy in > Personal Investment > Compliance > Improving Outcomes

It is also important to think about the breadth of material to cover. It’s not essential that  students learn every specific muscle and attachment, and an operational method may enhance recall. Consider the following four step process starting with motion and ending with the muscle. First, focus on the motion desired. Second identify the plane of motion and axis of rotation. Third, isolate the line of action. Fourth, label the primary movers. A possible fifth addition could be offering an everyday example.

Formula 2:   Motion Desired > Plane of Motion/Axis of Rotation > Line of Action > Primary Mover

Are your students having difficulty identifying the plane of motion and axis of rotation? Try this!
Are your students having difficulty identifying the plane of motion and axis of rotation? Try this!

If students have difficulty identifying the plane of motion and axis of rotation, have them poke a pencil through the middle of a large index card. Then place the index card in the plane of motion desired. If the body part contacts the card while going through the full range of motion, they’re in the wrong plane. The axis of rotation will automatically be perpendicular to the plane of motion for easy identification.

Next, they overlay a piece of string to identify a logical line of action across the joint.

String can help students identify the logical line of action across a joint.
String can help students identify the logical line of action across a joint. 

Using this method, students can isolate the muscles in that region responsible for the action. As a bonus, they can suggest an example of how that muscle is used in everyday life.

 

If you have the students pick a few of their own muscles too, be sure they are able to complete the process despite the muscle’s obscurity. I have always included a few interesting muscles for their action, shape or function. For example, the gluteus medius not only performs hip abduction, but also executes hip internal rotation due to its line of action. The temporalis not only functions in mandibular elevation but also retraction. The piriformis, besides being a cute pennant shaped muscle, is the only gluteal muscle with a sole proximal attachment on the sacrum. If you have some high level students, dare them to discover how the gluteus maximus can perform knee extension! How else could a patient with an above knee amputation negotiate stairs in a reciprocal fashion? And if that’s not fun enough, challenge them to identify the motion that occurs if one muscle attachment is fixated and the other is not. For instance, if the distal end of the Biceps Brachii is fixated, by placing the hand under a table, then the trunk will flex forward (unfixed).  Try it with other muscles too! Muscles are dynamic and should be taught that way. Because in the end, we want our students to look like this!

This student is having her "AHA!" moment!
This student is having her “AHA!” moment!

John Zubek is a Doctor of Physical Therapy and is an Assistant Professor of  Physiology at Michigan State University. 

How does Physical Activity Exert Beneficial Effects on Atherosclerosis and Coronary Artery Disease?

This post describes an update seminar delivered by Harold Laughlin, Professor at the University of Missouri at the 2017 HAPS Annual Conference in Salt Lake City.


Update Seminar VII was given by Harold Laughlin.  In this talk, the benefits of exercise on cardiovascular health were clearly documented.  I’m sure we’ve all heard the sobering stats before.  Cardiovascular disease, largely due to atherosclerosis, is the leading cause of death in the USA, accounting for ~ 1/3rd of all deaths.  As our President-Elect Ron Gerrits announced, we were all left feeling very inspired to getting fit for the HAPS conference Fun Run next year!  

For those interested in a great review article on the regulation of coronary blood flow during exercise, Harold mentioned the Physiology Review article by Duncker and Bache (2008).   In particular, here is list of some of the things we know so far regarding coronary blood flow during exercise:

  • During exercise, heart rate and myocardial contraction increase to meet the increased oxygen demands of the body and heart itself.
  • In order to meet increased metabolic demand, coronary blood flow increases (~5 fold) and there is also a small increase in oxygen extraction.
  • An increase in heart rate, will increase the relative time spent in systole, which affects (impedes) coronary blood flow.
  • There are many factors which regulate coronary vessel dilation (neurohormones, endothelial factors, and myocardial factors)
  • During exercise, coronary vasodilation appears to be induced by many factors including: exercise-induced ischemia, shear stress, increased arterial pressure, tangential wall stress, higher levels of endogenous NO, and β-adrenergic activity.
  • Exercise training results in coronary microvascular adaptations including: the formation of new capillaries, increased arteriolar diameters, increased adrenergic receptor responsiveness, and increased endothelium-dependent vasodilation (as a result of increased expression of endothelial NO synthase (eNOS), increased NO production, and increased Kv (potassium voltage) channel activity).

In his talk, Harold brought up some current data from his experiments with swine vasculature (Simmons et al., 2012).  He noted that healthy individuals typically have good vasomotor tone, and express low levels of the inflammatory markers and adhesion molecules (e.g. E-selectin and vascular cell adhesion molecule-1, VCAM-1) that are associated with atherosclerosis.  It has been previously found that endothelial cells located at bifurcations and other points of turbulence, are more at risk for developing atherosclerotic plaques than straight conduit arteries (Davies et al. 2010).  Laughlin et al. (2012) decided to investigate the straight conduit arteries and veins in six different regions of the swine to determine whether there were any differences in susceptibility to the development of atherosclerosis.  Overall, they found conduit arteries expressed higher levels of both pro- and anti-atherogenic markers than veins.  Also as one might expect, vessels of healthy individuals that lack atherosclerosis, are the most responsive to exercise.

In this talk, the improvements in vasculature as a result of exercise training were specifically addressed (Green et al. 2017).  The exercise-induced effects on vasculature is actually remarkable.  It is estimated that physical activity increases longevity, and reduces the risk of cardiovascular mortality by 42-44%.  The positive effect of exercise is noted to have dose-dependent curve and exercise training has been found to be on par with contemporary drug interventions (Green et al. 2017).  Exercise induces structural and functional adaptations in the vascular walls that reduce the risk of atherosclerotic plaque formation.  In addition increased capillary density and formation of additional collateral circulation is observed, as exercise induces the release of VEGF (Vascular Endothelial Growth Factor) (Green et. al. 2017).  Also, exercise was found to increase endothelial progenitor cell (EPC) activity which contributes to the growth of new vessels as well as repair.

It is important to note that exercise training increases cardiac output and oxygen uptake, without increasing mean arterial pressure.  This is because as cardiac output increases, peripheral vasodilation occurs (reducing afterload).  Exercise training improves vasodilation capabilities through structural changes.  During exercise, the increased systolic pressure stimulates vascular endothelial and smooth muscle cells to grow and align in response to stress, allowing for greater vasodilation.  In addition, vessel wall stretching induces vasodilation through increased eNOS activity (which produces the vasodilator NO) and activation of Kv channels (which causes smooth muscle cells to hyperpolarize and relax).  In addition, increased blood flow, has been found to increase both acetylcholine and prostacyclin levels which have been shown to induce vasodilation.  Conversely, low levels of shear stress, has been found to increase expression of adhesion molecules (ICAM-1 and VCAM-1) and reduce levels of the endogenous vasodilator NO (Green et al. 2017).

Thankfully for those of us looking to improve vasodilatory function in our conduit arteries and increase our capillary density, improvements through exercise can be seen in as little as 1-4 weeks of exercise and of course continue with longer training sessions.  So with that in mind, I’ll be sure to grab my running shoes and sign my kids up for sports, as fewer than 30% of females and 50% of males get the recommended 60 minutes 5-7 days/ week of exercise!  Yikes-arama!  Time to unplug and play…

A big thank you to Harold Laughlin for a highly motivating talk!


Post from Dr. Zoë Soon, School of Health and Exercise Sciences, University of British Columbia Okanagan, BC, Canada


Davies, P.F., Civelek, M., Fang, Y., Guerraty, M.A. Passerini, A.G. (2010). Endothelial heterogeneity associated with regional athero-susceptiblity and adaptation to disturbed blood flow in vivo. Semin. Thromb. Hemost. 36, 265-275.

Duncker, D.J. and Bache, R.J. (2008). Regulation of coronary blood flow during exercise. Physiol. Rev. 88, 1009-1086.

Green, D.J., Hopman, M.T.E., Padilla, J., Laughlin, M.H., Thijssen, D.H.J. (2017). Vascular adaptation to exercise in humans: role of hemodynamic stimuli. Phsiol. Rev. 97, 495-528.

Simmons, G.H., Padilla, J., and Laughlin, M.H. (2012). Heterogeneity of endothelial cell phenotype within and amongst conduit vessels of the swine vasculature. Exp. Physiol. 97(9), 1074-1082.

Join HAPS– for the conversations!

The HAPS Discussion group (also known as HAPS-L and before that as “the listserv”) is the place where the most interesting conversations in A&P are happening.  This discussion group has hundreds of members, is very active, and has often features amazingly high level conversations among leaders in the field.  This group was started in 1998 as an email listserv, and some still call it that, but it is a modern discussion group with email preferences and a web archive.  The HAPS discussion group is open to all current HAPS members and is one of the most valuable perks of membership.

This week, one discussion revolved around the most accurate classification of bone types. In this discussion, Mark Nielsen (University of Utah Anatomy Professor and winner of the 2017 HAPS-Theime Excellence in Teaching Award) shared multiple illuminating contributions to the conversation. Check out the excerpt below…and then imagine having content like THIS delivered to your email box on a regular basis.

WOW, there is a lot of interesting discussion going on here, this is one of the nice things about the HAPS listserve. It is always great to share and discuss. While I agree with many of the sage comments about classification and “does it really matter because the bones do not care or know where they fit in the scheme of things”, it is still important to recognize that there is correct and incorrect within a classification scheme. Following is the bases of the classification scheme:

Long bone = what is the one characteristic shared by long bones that none of the other bone types have, one thing and one thing only, a medullary cavity, and yes all the phalanges, even the small distal phalanges have a medullary cavity, as does the clavicle. The following bones have a medullary cavity:

  • clavicle
  • humerus
  • radius
  • ulna
  • metacarpals
  • proximal phalanges of hand
  • middle phalanges of hand
  • distal phalanges of hand
  • femur
  • tibia
  • fibula
  • metatarsals
  • proximal phalanges of foot
  • middle phalanges of foot
  • distal phalanges of foot

I believe someone stated that long bones are characterized because they have a diaphysis with proximal and distal epiphyses. This is not true. Many long bones only have epiphyses at one end and not the other. This is the case for many of the phalanges. Again, the characteristic that defines a long bone is the presence of a medullary cavity. Besides, many bones have epiphyses – for example, short bones and irregular bones have epiphyses.

Short bones = are characterized by a core of spongy bone with an outer covering of compact bone. They typically have a length, width, and depth that are approximately of equal dimensions. The carpal and tarsal bones are placed in this category.

Flat bones = the true flat bones of the body all reside in the skull, but the ribs are also often considered to fall in this category because their bone structure is similar to the flat bones of the skull. These are bones that are characterized by external and internal tables (laminae) of compact bone sandwiching dense trabecular diploe, the diploic spaces of the trabecular bone being filled with hemopoetic red marrow in the living subject. This would include the parietal bones, frontal bone, squamous portion of the occipital bone and temporal bone, sutural or wormian bones that are ossification centers that never fused with the fore mentioned bones.

Most of the remaining bones did not fit into one of these three categories. Like the short bones and flat bones all the remaining bones had an outer covering of compact bone and an internal core of spongy bone and no medullary cavity, but they were not short and they were not flat. This led to the next category that became the catch all:

Irregular bones = a variety of bone shapes consisting of an outer covering of compact bone and a central core of spongy bone, with some bone surfaces that are so flat and thin that they lack spongey bone completely e.g., the scapula, ethmoid. Most of the other bones fall in this category – vertebrae, the bones of the facial skeleton and inferior cranial vault bones, hyoid, malleus, incus, stapes, and the scapula and os coxae.

The final category is the sesamoid bones = these are bones that form within tendons. In human anatomy they are similar in bony structure to short bones but have a unique classification as sesamoid bones because of their location within tendons. In some other vertebrates they are very long slender bones within tendons.

One other recognized category is a pneumatized bone. These are bones that contain air spaces within their cores and can overlap with other categories. For example, the frontal bone is both a flat bone and a pneumatized bone. The ethmoid bone, sphenoid bone, and petromastoid part of the temporal bone are both irregular bones and pneumatized bones.

So there is a logic to classification and it is not a random thing that we can bend to our whims. We now have the choice to ignore it or teach it correctly.

So if you’re a HAPS member, by all means, join this discussion group. And if you’re not a member, JOIN HAPS so you can join the discussion group. (Then adjust your email settings, because most HAPSters have experienced the infamous “blown up email box” that results from some of the more rigorous conversations! Thankfully, executive director Peter English wrote a blog post with instructions for doing just that.)

Gene Targeting into the 21st Century: Mouse Models of Human Disease from Cancer to Neuropsychiatric Disorders

This post describes an update seminar delivered by Dr. Mario R Capecchi at the 2017 HAPS Annual Conference in Salt Lake City.


Update seminar VI was a special one, given by Nobel laureate, Mario Capecchi. Having survived World War II in Italy, in part as a homeless orphan, Mario’s life story is a fascinating one.  He went on to become a graduate student at Harvard in the lab of the Nobel Prize winner and co-discoverer of the structure of DNA, James Watson.  In 2007, Mario Capecchi, now at the University of Utah, won the Nobel Prize in Physiology or Medicine jointly with Oliver Smithies and Martin Evans for their work on gene targeting. The ability to create knock-out mice is widely used to this day and has been a valuable means of mapping gene function.  Mario’s research talk at this year’s HAPS conference focussed on his current work which involves characterizing the different roles that the HOX gene family of transcription factors play during mouse development.  While most HOX (homeobox) gene members are involved in controlling embryonic body plan development in a cranio-caudal manner, Greer and Capecchi (2002) found that Hoxb8 plays a unique role in the mouse’s grooming behavior.

Most animals, including humans, perform some type of auto-grooming and in mice, a cephalocaudal pattern occurs, where the head is groomed first and the tail is groomed last.  Many regions of the brain including the brainstem appear to be involved.  Greer and Capecchi (2002) found that mice with a homozygous Hoxb8 complete loss-of-function knock-out, exhibited over-grooming to the point of hair loss and formation of deep lesions. The deep lesions suggest that the mice also may have reduced sensitivity to painful stimuli.  These mice spent twice as long grooming as wild type mice and also over-groomed their control littermates to the point of inducing hair loss.  Interestingly, in humans, obsessive-compulsive disorder (OCD) often manifests as excessive cleanliness and grooming (e.g. trichotillomania).  Greer and Capecchi mapped the murine expression of Hoxb8 and found that expression began at E7.5 in the primitive streak and yolk sac, spreading through the developing spinal ganglia, spinal cord, and then throughout grooming regions of the CNS in the adult mouse.  In many animals, the basal ganglia has been shown to be involved in modulating grooming behaviour (Aldridge et al., 1993; Berridge, 1989; Berridge and Fentress, 1987; Cromwell and Berridge, 1996; MacLean, 1985a, 1985b; Stein et al., 1992; Wise and Rapoport 1989;).  

In 2008, Capecchi’s lab (Chen et. al., 2008) found that the Hoxb8 gene was normally expressed in microglia cells, and that this expression appears to be required for regulating normal grooming time.  Chen et al. (2008) found that grooming dysfunction in Hoxb8 knockout mice, could be rescued with wild-type bone marrow transplantation. This makes sense as microglia descend from hemocytoblasts.  In addition, Chen et. al. also found that the Hoxb8 gene was normally expressed in the spinal cord where it seems to be responsible for appropriate responses to nociceptive and thermal stimuli.  In fact, Holstege et al. (2008) proposed that the nociceptive recipient interneurons in the dorsal spinal cord laminae I and II are deficient and disorganized in Hoxb8 knockout mice leading to reduced sensation.  Furthermore, Chen et. al. (2008), found that bone marrow transplantation did not rescue sensory defects, indicating that these 2 pathways of dysfunction were due to separate deficiencies (i.e. microglia cell and sensory neurons). Chen et al. (2008) found that deletion of Hoxb8 only in the hematopoietic cells resulted in mice with excessive grooming, but normal sensory responsiveness.

It is unclear how microglia cells are involved in grooming behaviour, however “immunological dysfunction is linked to many psychiatric disorders including OCD, major depression, bipolar disorder, autism, schizophrenia, and Alzheimer’s disease” Ashwood et al., 2006; da Rocha et al., 2008; Kronfol and Remick, 2000; Leonard and Myit, 2009; Strous and Shoenfeld, 2006 (Chen et al., 2008).   In this study, Hoxb8 mutant mice were found to have a deficiency of microglia (i.e. fewer microglia in the adult brain).  In terms of how microglia may control behaviour, it is speculated that microglia may be involved in modulating synaptic transmission as they surround synapses, perhaps playing a role in adjusting levels of neurotransmitters (e.g. serotonin).  In addition, microglia cells can secrete cytokines that affect both neuronal activity and longevity.  

At first glance it may seem strange that immune system cells, such as microglia, are involved in grooming.  However, upon further reflection, it does make sense that grooming behaviours may be controlled by the immune system, as the purpose of grooming in animals is to reduce the number of harmful pathogens.

Finally, it was noted that the Hoxb8 mutant mice did exhibit high levels of anxiety.   Anti-anxiety drugs were found to reduce the anxiety-induced grooming behaviour in Hoxb8 mutant mice and also improved their ability to perform the open maze test (which is a frequent measure of anxiety).   

As you can see, a lot of really interesting data was relayed to us in this update seminar and I’d really like to thank Mario Capecchi for such a thought-provoking talk!


Post from Dr. Zoë Soon, School of Health and Exercise Sciences, University of British Columbia Okanagan, BC, Canada


Aldridge, J.W., Berridge, K.C., Herman, M., and Zimmer, L. (1993). Neuronal coding of serial order: Syntax of grooming in the neostratum. Psychol. Sci. 4, 391-395.

Ashwood, P., Wills, S., and Vand Water, J. (2006). The immune response in autism: a new frontier for autism research. J. Leukoc. Biol. 80, 1-15.

Berridge, K.C. (1989). Substantia nigra 6-OHDA lesions mimic striatopallidal disruption of syntactic grooming chains: a neural systems analysis of sequence control. Psychobiol. 17, 377-385.

Berridge and Fentress (1987). Disruption of natural grooming chains after stritopallidal lesions. Psychobiol. 15, 336-342.

Chen, S.-K., Tvrdki, P., Peden, E., Cho, S., Wu, S., Spangrude, G., and Capecchi, M.R. (2010) Hematopoietic origin of pathological grooming in Hoxb8 mutant mice. Cell 141, 775-785.

Cromwell, H.C., and Berridge, K.C. (1996). Implementation of action sequences by a neostriatal site: a lesion mapping study of grooming syntax. J. Neurosci. 16, 3444-3458.

da Rocha, F.F., Correa, H., and Teixeira, S.L. (2008). Obsessive-compulsive disorder and immunology: a review. Prog. Neuropsychopharmacol. Biol. Psychiatry 32, 1139-1146.

Greer, J.M. and Capecchi, M.R. (2002). Hoxb8 is required for normal grooming behavior in mice. Neuron 33, 23-34.

Holstege, J.C., de Graaf, W., Hossani,M., Cano, S.C., Jaarsma, D., van den Akker, E., and Deschamps, J. (2008). Loss of Hoxb8 alters spinal dorsal laminae and sensory responses in mice.  Proc. Natl. Acad. Sci. USA 105, 6338-6343.

Kronfol, Z., and Remick, D.G. (200). Cytokines and the brain: implications for clinical psychiatry. Am. J. Psychiatry 157, 683-694.

Leonard, B.E., and Myint, A. (2009). The psychoneuroimmunology of depression. Hum. Psychopharmacol. 24, 165-175.

MacLean, P.D. (1985a). Brain evolution relating to family, play, and the separation call. Arch. Gen. Psychiatry 42, 405-417.

MacLean, P.D. (1985b). Evolutionary psychiatry and the triune brain. Psychol. Med. 15, 219-221.

Stein, D.J., Shoulberg, N., Helton, K., and Hollander, E. (1992). The neuroethological approach to obsessive-compulsive disorder. Compr. Psychiatry 33, 274-281.

Strous, R.D., and Shoenfeld, Y. (2006). Schizophrenia, autoimmunity and immune system dysregulation: a comprehensive model updated and revisited.  J. Auoimmun. 27, 71-80.

Wise, S., and Rapoport, J. (1989). Obsessive-compulsive disorder: is it basal ganglia dysfunction? In Osbessive-Compulsive Disorders in Children and Adolsecents, J. Rapoport, Ed. (Washington, DC: American Psychiatric Press), pp 327-344.

After the Annual – Utah Mountain Biking!

Bonneville Shore Trail
A message from HAPS Western Regional Director, Jon Jackson (left). Kerry Hull and Murray Jensen photobomb-ing.
A message from HAPS Western Regional Director, Jon Jackson (left). Photobomb by Kerry Hull and Murray Jensen.

Utah Mountain Biking is a bucket list option for interested HAPSters!

Although mountain biking is generally thought to have originated in the Marin County hills north of San Francisco, there is arguably no finer place to ride than Utah. If you have the time and inclination to hit the mountain trails and ride, there are lots of options awaiting you near the HAPS Conference this Spring.  Murray Jensen, Kerry Hull and I went out a day before the mid-year meeting to explore some biking options (and spend some time in Mark Nielsen’s lab). Here’s what we found.

Jon enforces a rest break...because rest breaks are cool.
Jon enforces a rest break…because rest breaks are cool.

Within a 10-15 minute walk up the hill from the Salt Palace (site of the HAPS Conference) you’ll find a number of shops that rent out mountain bikes.  For around $40, you will be able to rent a $2500 mountain bike for the afternoon!  Full suspensions, 29-inch wheels, and even more options can be had.  If you’re thinking or riding up in the foothills surrounding the city, you’ll have about a 20-minute uphill ride to hit the mountain trailheads that run along what was once the shore of glacial Lake Bonneville. The elevation gain from the hotel to the Bonneville Shelf is about 600-800 feet. The landscape is nothing short of spectacular, even on days with a smog layer.

Local Badger

The entire Great Basin opens up as you switch back up the foothills; it’s quiet enough that you can even surprise some locals along the way.  The uphill climbing ranges from mild to clutch-your-chest strenuous. [I suffered in particular because I was serving as the “untrained control subject,” trying to keep up with Kerry and Murray.] The altitude provided wondrous panoramic views and a kick-your-butt workout, but most importantly, it meant some SWEET downhill action.  On our segment of the Bonneville Shore Trail, the single-track path was 90-95% packed solid, and offered up a mostly smooth ride. But for those who have left their common sense behind, and seek a greater challenge, there are several advanced/expert routes down the hill that will rattle bones, loosen ligaments, and likely raise your health insurance deductibles more than Paul Ryan could.

5 Moose
Local Moose

But no fears, there are many moderate trails that can bring you back to town. Our ride lasted just under three hours, and left us euphoric, thirsty, and with a trace of sunburn (even in October).

 

6 Mid MountainIf the moderate to high euphoria levels of the HAPS meeting aren’t going to be enough — the next level up of mountain biking literally brings you up out of the Wasatch Valley to the mountains surrounding Park City, one of the nation’s premier mountain biking destinations. Lots of shops cater to people giving this level of biking a try, and so you’ll have no trouble finding a “29er” with full suspension. The uphill is even more strenuous, although some riding parks have ski-lifts 7 Elevationto take you up the mountainside. [I’m all for that, as it follows the law of conservation of energy.] This world famous Mid-Mountain Trail is definitely not for novices, but if you’re a reasonably solid mountain biker, this place is as good as it gets. Weather permitting, the miles of traversing trails running over these wooded ski hills will provide a relatively moderate-level (elevation-wise) riding experience. But the downhill can get tricky: you’re a mile and a half above sea-level, and “down” is long, long way away.

Olympic-level bikers who train in Park City power down the hills pedaling, and at high speed. Fortunately for those of us who don’t want to over-use our sympathetic nervous systems, we’re able to find more moderate slopes on which to descend.  Either way, though, it will be full-on fatigue at the finish. It was great that our intrepid riders had a “sag-wagon” to come and fetch them.

Tom Lehman joins post-ride
Tom Lehman joins post-ride

You too will probably may want to arrange for a ride, as you could be too tired and sore to drive back to SLC.  All in all, the beauty of the terrain and the challenge of the hills is a something for every mountain biker’s bucket list.  We’ll have some of the info from the bike places we used for our gear at this year’s annual conference.  We hope to see you there!

 

 


Author Jon Jackson is the HAPS Western Regional Director.

A full list of recommended post-conference activities is available on the HAPS website

Join Us at the HAPS 2017 Spring Regional

Get your taxes done early!  We are planning a full day of update speakers, workshops, and poster presentations for Saturday, April 15 in Tyler Texas.  Our morning update speaker will be Dr. Michael Beckstead, Associate Professor in the Department of Cellular and Integrative Physiology at the University of Texas Health Science Center at San Antonio. Dr. Beckstead will be speaking about dopamine neurons and Parkinson’s Disease.  In the afternoon, Dr. Lane Brunner, Dean of the College of Pharmacy at the University of Texas at Tyler, will talk about how team-based learning has been implemented in the Doctor of Pharmacy program.

As always, workshops will be given by HAPS members.  Do you have a unique approach to teaching a lab or a new angle to get complicated ideas across?  Have you found a solution to a common challenge or a new tool (or a new way to use an old tool) that helps your students?  If you need to practice your presentation for the national conference in Salt Lake City, or you won’t be able to attend the SLC conference, we’re here for you!  Submit your workshop proposal by March 24.

Posters will be set up adjacent to the workshop rooms. If you have an idea that suits a poster more than a workshop – even if it’s a poster you’ve already presented in another venue – we’ll have a place for you to share what you’ve done.  A simple idea, or an exploratory look at some new teaching tip, tool, or resource can easily be translated into a poster.  Poster submissions have the same deadline as workshop submissions, March 24.

We’ll be meeting in the newly-renovated A&P labs, so you can get some ideas from our faculty about how technology can be implemented in the lab. The use of overhead cameras to show specimens, iPads in the classroom, and structured group activities can be explored.

At the end of the day, we’ll have the opportunity to tour our new nursing and health science facility, including the simulation lab for nursing students (see image below). The first floor has an area that is set up basically as a hospital, so students get real-world training in LVN, surgical technology, and other fields. There is also a working dental clinic.

If you’re planning to come in Friday afternoon or stay over Saturday night, look for a link to the accommodations on the registration page. If you’re bringing family with you, they can explore our Center for Earth and Space Science Education (CESSE, http://sciencecenter.tjc.edu/) and the Tyler Museum of Art (http://www.tylermuseum.org/), both adjacent to the building where our conference will be held.  If there is enough interest, we can plan a social event for either Friday or Saturday evening. I look forward to seeing you all!

Betsy Ott, Conference Coordinator
aap_5257

Journal of a New HAPster: Shani Golovay

HAPS is a society focused on the teaching and learning anatomy and physiology.  We’re always looking for new members to join the community.  Check out some thoughts from new HAPSter, Shani Golovay.  

Meet Shani Golovay, a new HAPSter.
Meet Shani Golovay, a new HAPSter.

“But I have a degree in Plant Biology.  I don’t really know anything about Human Physiology, except what I teach in General Biology.”  And this started my journey to HAPS.

I found the HAPS website to be helpful as soon as I joined. I hunted down the Course Guidelines  and Learning Outcomes right away because I needed a syllabus and some ideas on how much content to cover in the course.  Then I found the Guided Inquiry Activities by Murray Jensen. I tried out the activities with my students right away- and they loved them.  I was starting to feel like I could teach this class after all, and I felt like I had a giant community of people helping me that I didn’t even know.

I learn more from the HAPS email listserv then I do from most professional journals I receive.  I was amazed how open and helpful everyone was with each other.  I look forward to the listserv conversations and I learn so much. It was so refreshing to find a whole group of people willing to share their expertise with those of us way out of our area. If I emailed someone a question, they would explain things and even send me documents or ideas.  I am much more confident about teaching this Human Physiology class because of HAPS.  I think Human Physiology may be my new favorite class to teach because of all the awesome ideas I get from other HAPSters.  I was telling my colleagues about this society where everyone was nice and actually helpful and wanted to share ideas about teaching and everyone was impressed and a bit jealous that I had found such a group.

I am just so grateful to find a community of people where those with experience and lots of talent are willing to help those of us just starting out with these classes.  We need each other because we can’t talk about this sort of stuff over dinner except with each other, right?

The best part for me was the annual meeting, but that is another blog post…..