Author: Mokhtar

  • What does my KOOS score mean and is my KOOS score normal?

    What does my KOOS score mean and is my KOOS score normal?



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    If you weigh yourself on a scale and receive a number, how do you understand the value? How do you know if you are overweight, underweight or normal? Who do you compare yourself to?

    To determine what’s normal and understand your own score, you’ll likely compare your weight to other people who have similar characteristics to you, such as gender, age, and height. There would be no point in comparing yourself to someone with different characteristics, since what is normal for him or her is likely different for you. This same concept applies to normative values.

    Normative data identify what is common or typical and describe observed characteristics of a specific population at a specific time.[1] Using normative values ​​allows you to give meaning to your test scores by comparing your score to scores of people with similar characteristics to you.[2]

    As explained in part 1 of the KOOS blog series, the Knee Injury and Osteoarthritis Score (KOOS) is a questionnaire specifically designed for people with various knee conditions.[3] By completing the KOOS you will gain insight into the course of your knee injury and you and your healthcare provider can monitor the effects of the treatment over time.[3] While comparing your own preoperative and postoperative KOOS scores provides insight into your recovery process, you can also compare your scores to normative KOOS values ​​to determine your degree of disability or your level of progress compared to people who have had a similar injury, surgery, or have undergone treatment. .

    View the normal KOOS scoring blog for populations that have suffered an ACL injury,[4][5][6] total knee replacement (TKR) surgery, [7][8][9] as well as those who have knee osteoarthritis,[10] and populations without known knee disorders [11] in part 2 of the KOOS blog series.

    If you have had a knee injury or surgery, try our Curovate app for your daily recovery. Curovate offers video-guided daily exercises, progress tracking, the ability to measure the range of motion of your knee and hip, and the ability to complete the KOOS outcome measurement, all within the app.

    If you need more tailored help during your surgery or recovery from your injury, check out our Virtual Physiotherapy page to book your 1-on-1 video session with a physiotherapist.

    Learn more about the KOOS and what normative values ​​are. Also learn how to interpret your KOOS score in this YouTube video presented by Joey Wong, kinesiologist.

    acl knee physical therapy 1080x1080 2
    Download it on Google Play



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  • Research Fellow – Rubin Institute for Advanced Orthopedics (RIAO) at Sinai Hospital in Baltimore

    This new position is intended for medical students who wish to strengthen their competitive position to obtain a residency position in the field of orthopedic surgery. Research assistants will work with national and international leaders in the field of total joint replacement to assist in preparing manuscripts for publication in peer-reviewed journals, to collect and analyze data, to attend and present your work at regional and national conferences, and to assist with FDA investigations of new drugs and devices. This is a large-scale research center where numerous projects have not only been published in PubMed-indexed journals, but have also been selected to present at national orthopedic meetings, namely the AAOS and AAHKS.

    Research assistants have the opportunity to attend daily morning conferences at the orthopedic surgery residency, led by program director Dr. Jack Ingari, MD. This is an excellent opportunity to strengthen your resume and increase your chances of matching with an orthopedic surgery residency.

    Student researchers will work under the guidance of:

    -Ronald E. Delanois, MD

    -Michael A. Mont, MD

    -James Nace, DO, MPT

    GOALS:

    – Research into basic scientific and clinical aspects of total joint arthroplasty and preservation.

    – Learn to create and extract clinical data from institutional and national databases

    – Develop a better appreciation for biostatistics in the orthopedics setting

    – Prepare manuscripts and textbook chapters.

    – Present at research meetings, seminars, journal clubs, symposia and professional association meetings.

    EDUCATIONAL LEVEL REQUIREMENT OR REASONS: All candidates who have completed their third year and passed their USMLE Step 1 and/or COMLEX Level 1 board exams. It is preferable that USMLE Step 2 be completed before beginning the research program. Experience in writing and biostatistics is a plus.

    APPLICATION: Attach the following materials This email address is being protected from spambots. You need JavaScript enabled to view it.:

    – Application letter OR letter of interest

    – PDF of Curriculum Vitae

    – All available USMLE AND/OR COMLEX score reports

    – ≥ 1 letters of recommendation

    RIAO website: www.lifebridgehealth.org/RIAO/RIAO.aspx

    Twitter handle: @RIAOResearch Instagram handle: @RIAOorthopedics

    US/Canadian MD/DO preferred. US IMGs will be considered on a case-by-case basis. J-1 visa is possible.

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  • The histone acetyltransferases CBP and p300 regulate stress response pathways in synovial fibroblasts at transcriptional and functional levels

    Hypoxia, the formation of reactive oxygen species (ROS) and subsequent oxidative stress in synovial tissues are key events in the pathogenesis of RA1. We provide evidence here that CBP and p300 are critical regulators of the adaptive response of SF that integrate the transcriptional and functional regulation of stress response pathways throughout the cell.

    CBP and p300 are HATs and H3K27ac mark writers, which activate post-translational histone modifications present in enhancers and promoters20. Among the CBP/p300 target proteins are several non-histone proteins in addition to histones, including many transcription factors and signaling effectors16.21. Despite their high protein sequence homology, CBP and p300 have distinct individual functions identified by our own and other studies12,13,14.

    In SF, persistent H3K27ac in inflammatory gene promoters was associated with long-lasting and persistent expression of the corresponding genes22. We recently demonstrated that p300 is the major HAT in SF that exerts a pro- and anti-inflammatory role. This is in contrast to CBP, which exerted anti-inflammatory effects upon silencing, and specifically regulated TNF-induced interferon signature gene expression14. Although we have ruled out that silencing p300 additionally reduced CBP and vice versa, we cannot completely rule out other potential off-target effects after our silencing approach. Krosel etc already. have shown that inhibitors targeting the HAT or bromodomain of CBP/p300 closely resemble the effects of p300 silencing, including increased expression of TNF-induced proinflammatory gene expression14.

    Our RNAseq data provide evidence that the number of p300-regulated target genes is greater than that of CBP-regulated target genes, also in terms of stress response. While the cellular response to oxidative stress and autophagy was co-regulated by CBP and p300, genes associated with response to oxygen levels, hypoxia, and pathways associated with proteasome regulation and function were specifically enriched upon knockdown of p300. In pathways co-regulated by CBP and p300, we identified several genes that were regulated in opposite directions. These results point to individual functions of the two enzymes at the level of target genes, similar to what we have already observed for many inflammatory genes14. Furthermore, a small number of measured CBP and p300 target genes, namely BCL2, SOD3 and HDAC6, could be regulated in a joint-specific manner, as indicated by our Real-time PCR results in a limited number of samples for each joint site. Frank-Bertoncelj et al. have previously shown that H3K27ac is one of the mechanisms controlling the joint-specific expression of homeobox (HOX) transcription factors in SF from different locations7. To draw a definitive conclusion whether stress-associated target genes are regulated in a joint-specific manner, larger numbers of SF from different joints would be needed, together with H3K27ac ChIPseq data in unstimulated and TNF-stimulated SF from different joints.

    In addition to the differential roles of CBP and p300 in regulating target gene expression, we showed here a differential regulation of CBP and p300 by stimulating SF with 4-HNE and TNF (Fig. 6). These factors are present in the synovial microenvironment in RA and mimic the oxidative stress and inflammation, respectively. While 4-HNE and TNF, similar to H2O2suppressed the expression of p300, CBP was not affected. 4-HNE is a lipid peroxidation product generated at elevated levels of ROS. Levels of 4-HNE are elevated in serum, synovial fluids, and synovial tissues of RA patients, and serum levels of 4-HNE correlate with structural damage such as erosions in the early stage of RA23,24. As mimicked by our silencing approach, the TNF- and 4-HNE-mediated suppression of p300 expression in the synovial RA microenvironment has fundamental consequences for SF behavior. Our datasets from the previous one14 and the present study indicates that reduced expression of p300 was associated with increased expression of many inflammatory cytokines, chemokines matrix metalloproteinases and stress response genes in SF. Among these genes were HK2, a marker indicating the metabolic switch from SF to glycolysis, and VEGF, a pro-angiogenic factor secreted to overcome hypoxia.1.

    Figure 6
    figure 6

    Summary of CBP- and p300-regulated pathways in SF. The expression of p300 but not CBP is down-regulated in synovial fibroblasts after exposure to TNF and oxidative stress. The effects of p300 and CBP silencing are demonstrated based on findings from this and a previous study14. Downward arrows indicate suppressed expression or function, upward arrows indicate increased expression or function. The figure was created by BioRender.com.

    TNF stimulation of SF markers of endoplasmic reticulum (ER) was shown to induce stress and autophagy25. Our data suggest that CBP and p300 regulate autophagy at the transcriptional level and influence autophagic flux. The assessment of autophagy in the presence of the lysosomal inhibitor bafilomycin A1 indicated that CBP and p300 regulate autophagy function at different stages within the autophagic process. CBP silencing affected autophagosome synthesis. In contrast, knockdown of p300 induced autophagy in unstimulated SF, and induced a late-stage block of autophagy in TNF-stimulated SF, a condition in which polyubiquitinated proteins in SF accumulated. Accordingly, knocking down p300 only increased cell death in the presence of TNF, as previously indicated14. Kato etc already. have previously shown that autophagy induction partially compensated for reduced clearance of polyubiquitinated proteins in SF after blocking proteasome function, indicating a protective effect of autophagy induction in SF under such conditions5. Here we observed a similar compensatory mechanism after p300 knockdown, which was associated with a suppression of proteasome enzymatic activities and an induction of autophagy. This finding is consistent with a previous study in HeLa cells in which p300 knockdown was associated with reduced acetylation of autophagy-related proteins and increased levels of autophagy.26.

    Acetylation and deacetylation of components of the autophagy machinery control all steps of this catabolic process, from autophagosome initiation to LC3 conjugation, cargo assembly, and autophagosome-lysosome fusion27,28. Several classes of acetyltransferases, including CBP and p300, and deacetylases, including sirtuin1, HDAC4 and HDAC6 are involved in the regulation of autophagy27.29. Furthermore, the function of autophagy-related transcription factors, such as transcription factor EB (TFEB), Foxo1 and Foxo3, is regulated by deacetylation28.30. Recently, the increased translation of FOXO3 mRNA has been described to facilitate the initiation of autophagy31. We showed here that in unstimulated SF, FOXO3 mRNA increased after p300 knockdown, a condition in which autophagic flux increased. HDAC6 binds to polyubiquitinated proteins in SF29and promotes autophagy by facilitating autophagosome-lysosome fusion27. On the other hand, HDAC6 was also shown to suppress autophagy by deacetylating TFEB and Foxo130. This could explain the inverse regulation of HDAC6 and ATG5 and ATG16L1 in SF.

    A global analysis of the CBP/p300-dependent acetylome in mouse embryonic fibroblasts (MEF) suggested that proteasome functions might also be regulated by these enzymes.21. The majority of proteasome machinery components showed numerous CBP/p300-dependent acetylation sites in regulatory and enzymatic subunits in MEF (http://p300db.choudharylab.org). Furthermore, ATG5 and ATG16L1, two proteins essential for autophagosome assembly, showed CBP/p300-dependent acetylation sites21. Whether proteasome and autophagy components are acetylated in a CBP- and p300-dependent manner in SF remains to be functionally evaluated21. Because CBP/p300-dependent acetylation sites in MEF were analyzed after a combinatorial knockout of both enzymes, it is not clear which of them is the key enzyme in regulating the post-translational acetylation of proteins involved in the regulation of autophagy and proteasome activities.

    In summary, we have identified CBP and p300 in particular as critical regulators of stress response pathways in SF, with overlapping and distinct functions within specific pathways. The downregulation of p300 by TNF and oxidative stress provides a mechanism underlying SF activation in the synovial microenvironment.

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  • My Personal Journey to Osteoporosis Care and Awareness in Underserved Communities – Bone Talk

    My Personal Journey to Osteoporosis Care and Awareness in Underserved Communities – Bone Talk

    IMG 20230830 WA0029

    My personal journey to osteoporosis care and awareness in underserved communities
    By Dr. Tasneem Hassan

    My name is Dr. Tasneem Hassan and I work as a general practitioner in Nairobi, Kenya. After graduating in 2019, I started working in a public hospital in Nairobi.

    Later I started working at Rayhaan Healthcare, where I met Dr. Mustafa Bhaiji, a consultant radiologist with a special interest in osteoporosis. I also learned about the DXA technology, which further sparked my interest in osteoporosis. As I learned more about my family’s history and observed many people with poor bone mass, I started to pay more attention to it.

    This is the story of my grandmother, who fell a few years ago and broke her hip, needing hip replacement surgery and leaving her bedridden for a while. All these difficulties contributed to her death. For starters, we know she had low bone mass, but the lack of a bone DXA scan in Mombasa, Kenya delayed early diagnosis and treatment. She also had dementia and her recovery was difficult. In addition, there is a lack of awareness in our system about osteopenia and osteoporosis, which hinders early diagnosis and prevention. If our thinking about osteoporosis had advanced significantly earlier at the time, she might not have died from the comorbidities associated with the fracture.

    Another interaction I had was with my mother, who had already suffered a fracture. She is currently going through menopause and a few months ago she broke her foot as a result of a fall. This could be a stress fracture. But given her age and menopause, higher risk of falls, and history of two fractures, I wouldn’t be shocked if she has poor bone mass, and thus osteopenia. Individualizing care is simple; we do it all the time. We shouldn’t allow people to walk around with untreated osteoporosis because they will eventually stop walking. It’s no longer the 1900s.

    Osteoporosis is a disease that roughly causes 8.9 million fractures per yearculminating in one osteoporosis fracture every 3 seconds. One in three women and one in five men those aged 50 and over will experience an osteoporotic fracture. Osteoporosis causes bones to become weak and brittle, causing them to break easily even after a minor fall, bump, sneeze, or quick movement. I have seen people who have fractures that damage them not only physically, but emotionally as well. It reduces their overall quality of life, sometimes resulting in despair and isolation as people reduce social connection or are no longer able to do the activities they used to do. The prolonged loss of freedom and freedom of movement has caused physical, emotional and financial hardship to patients as well as their relatives and friends.

    80% of it who have had at least one osteoporotic fracture are not diagnosed or treated for osteoporosis.

    As a GP, I tried to read as much as I could after recovering from my pity party, which I felt was tragically avoidable. Over the past few weeks I have been focusing on a study of the prevalence of osteoporosis in our organization, particularly as it relates to ethnicity, age, menopause and risk factors.

    Many women experience decreased bone mass after menopause and aging. I am very interested in following up on this group of patients and referring them to the best available care. We also conduct research based on the few DXA scans we have completed to help future generations.

    It is also overlooked as a health problem in Africa for several reasons, including:

    Overburdened by communicable diseases such as tuberculosis (TB) and human immunodeficiency virus (HIV).

    Not long ago there was a widespread belief that osteoporosis and resulting fragility fractures were uncommon among black Africans, but this is no longer the case.

    We have come across many people of all races affected by osteopenia. However, the problem remains that there is no African research. This brings the FRAX scoring guideline into conflict because it does not take African race into account.

    In our region, healthcare professionals also lack insights about osteoporosis.

    Despite advances in scientific research and available therapies and diagnostic techniques, osteoporosis remains a global health problem with potentially disastrous consequences for patients and enormous costs to healthcare systems.

    In this context, we can probably all agree that we need to improve osteoporosis treatment and raise awareness in underserved communities.

    My goal is for more physicians to be informed about this topic and for this disease to be prioritized alongside other chronic conditions.

    This story is part of a support initiative called Voices of Osteoporosis: Stories of Hope and Inspiration. If you have experienced osteoporosis as a patient or caregiver, we invite you to share your story. Your story can inspire others to learn how to protect their ability to live their best life and stay strong. click here learn more.

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  • A lockdown can lead to an increase in the number of injuries

    A lockdown can lead to an increase in the number of injuries

    Injury rates at an NCAA Division I institution following the COVID-19 lockdown.

    Angileri HS, Rosenberg SI, Tanenbaum JE, Terry MA, Tjong VK. Orthop J Sport Med. 2023;11(8). doi:10.1177/23259671231187917.
    Full text freely available

    Take home message

    Injury rates at one NCAA Division I institution have increased by more than 10% following the return of athletes from the COVID-19 pandemic. While the number of injuries increased, the total time lost due to injury decreased.

    Background

    The COVID-19 pandemic created an unprecedented event that dramatically impacted sports at all levels, causing athletic competitions and training to be suspended. Professional athletic organizations experienced an increase in injuries during the first season after the pandemic. Unfortunately, we know little about how the COVID-19 pandemic has affected injury rates among college athletes.

    Study aim

    The researchers completed an epidemiological study to evaluate injury rates in collegiate athletics at a single NCAA Division I institution following the COVID-19 pandemic using data collected from the institution’s injury surveillance database.

    Methods

    The authors extracted injury data from 18 sports during the three seasons before the pandemic (2017-2020) and one season after (2020-2021). The researchers defined an injury as an event that causes an athlete to miss practice or competition time or a problem that persists for more than 3 days. The total number of days the patient was unavailable and the anatomic area of ​​the injury were also recorded. The authors ruled out non-sports-related medical problems.

    Results

    Post-pandemic athletes experienced an 11% increase in overall injury incidence compared to pre-pandemic. While the overall injury rate increased, the reported number of days off work dropped from pre-pandemic to 21% post-pandemic.

    Viewpoints

    Overall, these findings among college athletes are consistent with previous evidence among professional athletes that more injuries occurred in the post-pandemic season. Other SMR posts have suggested that testing positive for COVID-19 increases an athlete’s risk of injury. Moreover, another explanation is that healthcare professionals were more vigilant in monitoring athletes after the pandemic, as they suspected that problems might arise when resuming sports after a long break. More studies with data from multiple institutions should investigate why athletes may experience more injuries post-pandemic (e.g., deconditioning, COVID-19 infections, better monitoring). Interestingly, athletes missed fewer days due to injuries after the pandemic, indicating that less severe injuries were driving the increase in injuries.

    Clinical implications

    Unfortunately, the COVID-19 pandemic may not be the last time we have to suspend sporting activities. The growing evidence suggests that we need to be cautious when returning to exercise after long-term exercise restrictions. During this time, it may be valuable to adapt current warm-up programs to include key components of injury prevention warm-up programs.

    Questions for discussion

    What changes have you made as a result of the pandemic? What was your reason for continuing these services years later?

    Written by Kyle Harris
    Reviewed by Jeffrey Driban

    related posts

    Tested positive for COVID? Be careful out there
    We need a better understanding of how COVID-19 has affected our athletes
    Use of cardiovascular magnetic resonance (CMR) imaging for return to athletic activities after COVID-19 infection: an expert consensus document on behalf of the American Heart Association Council on Cardiovascular Radiology and Intervention (CVRI) Leadership and endorsed by the Society for Cardiovascular Magnetic Resonance (SCMR)
    Adapted physical activity in subjects and athletes recovering from Covid-19: a position statement of the Società Italiana Scienze Motorie e Sportive

    9 EBP CEU courses

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  • 3 Ways to Categorize Bones – Biogennix

    3 Ways to Categorize Bones – Biogennix

    Cross section of long bone showing both cancellous bone and compact bone.

    Cross section of a long bone showing the result of endochondral formation. Cortical bone (COR) and cancellous bone (CAN) form inferiorly and superiorly to the articular (joint) surface (AS) from the growth plate (GP).

    To understand what role bone graft products In the process of bone fracture repair, it is important to understand the architecture of the bone and the different bone categories involved in the healing process. As with most complex subjects, there are many ways to characterize bone. This blog describes the three main methods of bot categorization.

    1. Macroscopic appearance: cancellous bone versus cortical bone
    2. Degree of maturity: woven versus lamellar bone
    3. Embryological development: membrane versus endochondral bone

    Macroscopic appearance: cancellous bone versus cortical bone

    At the macroscopic level, bone can be classified as either cancellous bone or cortical bone. Synonyms for cancellous bone are trabecular or spongy bone. Cortical bone can be referred to as stretched or compact bone. When you look at bones with the naked eye, you can easily see distinct differences in porosity or density. Cancellous bone tissue is typically found on the inside of the bone, while cortical bone is found on the outside (Figure 1). In a serious bone fracture, both cortical and cancellous bone are often broken.

    Cancellous bone porosity typically ranges from 75-95% with an average pore size of 200-600 μm in diameter. This gives it a honeycomb-shaped, spongy appearance and light weight. It is found in the inner chamber of most bones, usually at the ends, near joints. This type of bone is made of beamsThese are curved beams or arches specially arranged to evenly distribute biomechanical loads across the articular surfaces of joints.

    The low density of cancellous bone makes it more fragile than cortical bone, but it is also more flexible. In technical terms it has a lower one elastic modulus. This cushioning effect prevents or delays arthritis of the more vulnerable and non-regenerative tissues, especially cartilage or intervertebral discs. The high porosity of cancellous bone also serves as a reservoir for bone marrow, which is essential for the regeneration of a variety of tissues. Finally, cancellous bone serves as a source of storing calcium and phosphorus for use throughout the body.

    Unlike cancellous bone, cortical bone is very dense and only 5-10% porous. Therefore, it is heavier in weight. The pores are very small, usually 10-100 μm in diameter. In fact, the pore size of the channels that feed the osteocytes is called channels, are less than 500 nm (0.5 μm). For the most part, the pores of cortical bone are not visible without magnification. These pores are just large enough in diameter to allow blood and lymphatic vessels, as well as nerves, to snake through the cortical bone and support all the osteocytes and other cells in the bone. Due to its high density, cortical bone serves as a hard protective layer around the internal bone marrow cavity and bears most of the biomechanical loads placed on our bones.

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  • Quick Guide to MCL Sprains – ACL Strong

    Quick Guide to MCL Sprains – ACL Strong

    Do you have pain on the inside of the knee after receiving a direct hit on the side of your leg? Does your knee feel unstable or loose when you step or turn sideways?

    If you have pain in the “medial” or inner side of your knee, an injury to the Medial Collateral Ligament, also known as the MCL, may be the reason for this.

    The MCL is a stabilizing ligament in the knee that can be acutely injured by an awkward fall or sudden contact with another person or object. It can also become injured gradually through repetitive stress.

    If you have medial knee pain and have not fallen or hit the knee, you may be making a crucial mistake in your daily activities that is putting stress on the MCL.

    Read this quick guide to the MCL sprain to find out what it is, what you can do about it, and how to prevent it.

    What is the medial collateral ligament (MCL)?

    MCL Sprains2

    The MCL consists of connective tissue that connects the femur to the tibia at the medial portion of the knee joint. The femur is the bone in the thigh and the tibia is the weight-bearing bone of your lower leg, also called the tibia.

    The MCL stabilizes the knee during everyday movements, such as walking, running, and going up and down stairs. The MCL also provides important structural support for your knee during athletic movements such as cutting, twisting, jumping and landing. Like the anterior cruciate ligament, or ACL, the MCL provides support and stability to the overall structure of the knee. Unlike ACL, MCL often heals on its own without the need for surgery.

    What can cause an MCL sprain?

    What can cause an MCL sprain?
    Injury 2

    Sprains occur to ligaments when they are stretched beyond what they are capable of. The result can range from micro-tears of the fibers to a full-thickness tear of the ligament.

    • A grade 1 sprain involves an overloaded ligament with micro-tearing of some fibers.
    • A grade 2 sprain involves a partial tear of the ligament, while the ligament is still largely intact.
    • A grade 3 sprain involves a more extensive or complete tear (rupture) of the ligament.

    Think of a sprain as a spectrum of severity, and therefore some recovery time will be required and treatment may vary. No two sprains are exactly the same.

    Acute or sudden MCL sprains usually happen during a slip and fall, a twist of the knee, or from a direct blow to the knee (usually from the outside of the knee), such as a tackle in football or soccer. Pain, swelling, loss of range of motion, and/or difficulty walking may follow the injury.

    Another way to aggravate MCL is through poor mechanics during daily activities. A mistake that many people make without realizing it is allowing their knee to drop into valgus, a medial direction, during normal movements such as getting in or out of the car, walking up or down stairs, and running. This extra stress on the inside of the knee can cause the MCL to break down over time, be more vulnerable to injury and likely become more painful. This type of injury can start as pain or tenderness along the medial knee, and over time can progress to degenerative joint disease or osteoarthritis if left unchecked. Watch this video to see how daily activities can contribute to knee problems.

    What is the best treatment for MCL sprains?

    MCL sprains are normally treated non-operatively, meaning they usually do not require surgery. In some cases, surgery is only recommended if there is other knee damage as a result of the injury.

    An avulsion fracture occurs when trauma to the knee causes the ligament to disrupt a piece of bone at the bony attachment, causing a piece of bone to pull away with the ligament. Still, some MCL sprains with associated avulsion fractures are treated nonoperatively because the area receives good blood flow and the body can heal these structures on its own.

    With rehabilitation exercises that focus on range of motion, balance, stability and strengthening of the leg, the MCL will normally heal after a short period of immobilization to the knee.

    Immobilization is an important first step in the non-operative treatment of an MCL sprain. Medical professionals often recommend treating the injury by keeping the knee straight (in a brace) and walking with crutches. This strategy allows the area to heal without stretching or straining the sprained fibers.

    Once the knee immobilizer is removed, physical therapy is recommended to begin moving the knee and promote circulation so that the tissue continues to heal. Deep knee bending is usually avoided, but walking and other gentle activities are recommended to increase blood flow to the area, which can help speed the healing process. Physiotherapy and progressive increases in activity are crucial to returning to normal life and preventing a similar injury.

    By strengthening the muscles around the entire leg, hip and torso and improving the body’s ability to withstand forces in multiple directions, you can bulletproof the knee for a safe return to lifelong sports and activities.

    What Exercises Should You Do to Recover from (or Prevent) an MCL Sprain?

    Exercises after an MCL sprain should include strengthening the leg muscles and working on balance and stability of the knee. A lot of stability at the knee actually comes from the hips and core, so targeting the hips and core is essential.

    Strengthening the hip musculature allows force to be absorbed into the legs more efficiently, which can help protect the knee from injury during athletic maneuvers. Strengthening the muscles of the lower and upper legs also allows the body to better withstand the forces of athletic movements. By incorporating an ACL Strong course into your routine, you can reduce your risk of not only an MCL sprain, but also other knee, hip, or ankle injuries.

    Whether you’re recovering from an MCL injury, trying to prevent another one, or want to be the best athlete you can be without knee problems, the ACL Strong courses can help you focus on your knee health from the comfort of your own home. , without you having to figure anything out yourself. The process was designed by physiotherapists and is educational and useful, so you can do that too transform from not knowing where your weaknesses are, to becoming stronger and more balanced in the right places, so you’ll be more resilient in the long run.

    The goal of ACL Strong is to help you reduce pain, prevent knee injuries, perform better and get you on your way to doing what you love for as long as possible. The courses are intended for anyone who wants to protect their lifestyle and have the freedom to do what they want without being limited by pain, injury or aging.

    Not convinced yet? Read our testimonials or frequently asked questions to see how ACL Strong can help you. Once you’ve made the decision to get exactly the exercises you need and expert support, don’t wait any longer because in just 6 weeks you can experience a transformation like never before and protect your lifestyle in the long term.

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  • Medicare enrollees can now switch coverage.  Here’s what’s new and what you should keep in mind.

    Medicare enrollees can now switch coverage. Here’s what’s new and what you should keep in mind.

    Consumers know it’s fall when stores start offering Halloween candy and flu shots — and the airwaves and mailboxes fill with ads for Medicare options.

    It’s annual open enrollment time again for the 65 million Americans covered by Medicare, the federal health program for the elderly and some people with disabilities.

    From October 15 to December 7, participants in the traditional program or Medicare Advantage plans, which are offered by private insurers, can change their coverage. (First-time enrollees typically sign up within a few months of their 65th birthday, whether during open enrollment season or not.)

    There are a few new features for 2024, including a lower out-of-pocket limit for some patients on expensive medications.

    Whatever happens, experts say, it’s a good idea for beneficiaries to examine their current coverage, because health and drug plans may have made changes, including to the pharmacies or medical providers in their networks and how much prescriptions cost.

    “The advice is to check, check and check again,” says Bonnie Burns, a consultant with California Health Advocates, a nonprofit Medicare advocacy program.

    But as anyone in the program or who helps friends or family members with coverage decisions knows, it’s complicated.

    Here are a few things to keep in mind.

    Know the Basics: Medicare vs. Medicare Advantage

    People in traditional Medicare can see any participating doctor or hospital (and most do participate), while those in Medicare Advantage must choose from an itemized list of providers – a network – that is unique to that plan. Some Advantage plans offer a broader network than others. Always check whether your preferred doctors, hospitals and pharmacies are covered.

    Because traditional Medicare does not cover prescriptions, members should also consider signing up for Part D, the optional drug benefit, which includes a separate premium.

    Conversely, most Medicare Advantage plans include drug coverage, but be sure to check before you enroll because some do not. These private plans are heavily advertised, often touting that they offer “extras” not available in traditional Medicare, such as dental or vision coverage. Read the fine print to see what restrictions, if any, are placed on such benefits.

    Those age 65 and older who are new to traditional Medicare can purchase a supplemental or “Medigap” policy, which covers many out-of-pocket costs, such as deductibles and copays, which can be significant. Generally, beneficiaries have six months after enrolling in Medicare Part B to purchase a Medigap policy.

    So switching from Medicare Advantage to traditional Medicare during open enrollment could pose problems for those who want to purchase a supplemental Medigap policy. That’s because private insurers offering Medigap plans, with some exceptions, can turn away applicants with health problems, or increase premiums or limit coverage of pre-existing conditions.

    Some states offer beneficiaries more guarantees that they can switch Medigap plans without answering health questions, although the rules vary.

    To make all this even more confusing, there is a second open enrollment period each year, but it is only for those with a Medicare Advantage plan. They can change their plans or return to traditional Medicare from January 1 to March 31.

    Drug coverage has changed – for the better

    Beneficiaries who have enrolled in a Part D drug plan or receive drug coverage through their Medicare Advantage plan know that there are many copays and deductibles. But by 2024, some of these expenses will disappear for those who need a lot of expensive medicines.

    President Joe Biden’s Inflation Reduction Act places a new annual cap on Medicare beneficiaries’ out-of-pocket costs for medications.

    “That policy is going to help people who are taking very expensive medications for conditions like cancer, rheumatoid arthritis and hepatitis,” said Tricia Neuman, senior vice president and head of KFF’s Medicare policy program.

    The cap will greatly help beneficiaries who fall into Medicare’s “catastrophic” coverage — an estimated 1.5 million Americans in 2019, according to KFF.

    Here’s how it works: The cap is triggered after patients and their drug plans together spend about $8,000 on medications. KFF estimates that this means about $3,300 in out-of-pocket expenses for many patients.

    Some people could reach the limit within one month, given the high prices of many drugs for serious conditions. After the limit is reached, beneficiaries will not have to pay anything out of pocket for their medications that year, saving them thousands of dollars annually.

    It is important to note that this new limit will not apply to medications administered to patients, usually in doctor’s offices, such as many cancer chemotherapeutics. These drugs are covered by Medicare Part B, which pays for doctor visits and other outpatient services.

    According to the Medicare Rights Center, next year Medicare will also expand opportunities for some low-income beneficiaries to qualify for low- or zero-premium drug coverage with no deductibles and lower copayments.

    Insurers offering Part D and Advantage plans may also have made other changes to drug coverage, Burns said.

    Beneficiaries should consult their plan’s “formulary,” a list of covered medications, and how much they will have to pay for the medications. Be sure to note whether prescriptions require a co-pay, which is a fixed dollar amount, or coinsurance, which is a percentage of the drug cost. In general, copayments mean lower out-of-pocket costs than coinsurance, Burns said.

    Help is available

    In many parts of the country, consumers can choose from more than 40 Medicare Advantage plans. That can be overwhelming.

    Medicare’s online plan finder provides details on the Advantage and Part D drug plans available by zip code. Allows users to view details about each plan’s benefits, costs, and healthcare provider network.

    Insurers are expected to keep their supplier directories up to date. But experts say enrollees should contact directly the doctors and hospitals they would most like to confirm that they are participating in a particular Advantage plan. People concerned about drug costs should “check to see if their pharmacy is a ‘preferred pharmacy’ and if it is in network” under their Advantage or Part D plan, Neuman said.

    “There can be a significant difference in out-of-pocket expenses between one pharmacy and another, even in the same plan,” she said.

    To get the most complete picture of estimated drug costs, Medicare beneficiaries should look up their prescriptions, dosages and their pharmacies, says Emily Whicheloe, education director at the Medicare Rights Center.

    “For people with specific drug needs, it’s also a good idea to contact the plan and say, ‘Hey, will you still cover this drug next year?’ If not, change to a plan,” she said.

    Additional enrollment assistance can be obtained for free through the State Health Insurance Assistance Program, which operates in all states.

    Beneficiaries can also ask questions through a toll-free Medicare hotline: 1-800-633-4227 or 1-800-MEDICARE.

    Insurance brokers can also help, but with a caveat. “Working with a broker can be fun for that personal touch, but know that they may not represent all plans in their state,” says Whicheloe.

    Whatever you do, avoid telemarketers, Burns said. In addition to TV and mail ads, many Medicare beneficiaries are inundated with phone calls promoting private plans.

    “Hang up,” Burns said.




    Kaiser health newsThis article was adapted from khn.org, a national newsroom that produces in-depth journalism on health issues and is one of the core operating programs at KFF – the independent source for health policy research, polling and journalism.

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  • Chronic pain and movement and why I went to my physiotherapist for help

    Chronic pain and movement and why I went to my physiotherapist for help

    woman lifting dumbbell
    Photo by Leon Ardho on Pexels.com

    Okay, so I wanted to get back into doing more resistance training. Currently my resistance training involves my dogs pulling on the leash when we go for walks. While that certainly gives me a solid upper body workout, it is neither consistent nor conducive to gradually building strength and capacity.

    I also do archery, which is also a great upper body workout. I usually shoot about 4 times a week with a recurve bow. It’s also a lot of fun. My bow weighs about 36 pounds, so I’m fairly strong. Possibly, more accurately, “fairly strong for someone living with multiple chronic illnesses.”

    Although I get tired quickly. Part of the reason I want to do a good resistance training program is to get stronger for archery so I can shoot longer and have longer archery sessions. To build my endurance and increase my strength. If it’s easier to pull back a 36-pound bow, I can do it longer. Maybe I can even go every day.

    So that was the idea.

    I started two weeks ago and created a very simple program for myself.

    This is what I did.

    Upper body exercises

    All exercises consist of 3 sets of 10 repetitions.

    Bench press – 15kg

    Curved dumbbell rows – 8 kg

    Seated shoulder press – 3 kg

    Biceps curls – 5 kg

    Overhead Triceps Extension – 5kg Plate

    Lateral raises – 3 kg

    Lower body exercises

    Goblet squats body weight to sitting level and stands up

    Dumbbell lunges bodyweight

    Romanian deadlifts 20kg

    Calf increases body weight

    Dumbbell increases body weight

    My upper body was fine. I hardly had any pain anymore. But it’s a very easy, lightweight start. That’s what I was aiming for, and I got it right for my upper body.

    Now my lower body was something completely different.

    I woke up that night around 1am in terrible pain. And I mean *terrible*. It was an electric, diffuse, terrible pain through my legs. I’ve heard others call it an “electric storm in my muscles” and that’s a good description. A painful electrical storm.

    I had no control over my legs, they wouldn’t do what I wanted. Or they would…eventually. The response was slow. Talk about ‘delay’. Standing was almost impossible and walking was almost impossible used to be impossible, until I discovered that my legs were responding, just very slowly.

    I sat on the steps and lowered myself onto my butt. I didn’t feel safe walking down. I scooted on my butt, but it was the slowest scoot you’ve ever seen! It was more of a painful, slow lowering of my body, step by step, with most of my weight on my arms.

    Thank the gods you still have good upper body strength!

    This was all a big shock to me. I didn’t expect to react this way…I guess this is what happens when you do it too much when you have CIDP. I know how inflammatory arthritis responds to exercise, and too much exercise. But this neuropathic pain? This is new. A surprise. And not a nice one. But it’s all a learning experience, right?

    I took my usual painkillers, opioids, and the pain subsided a bit. But it was still unbearable. I took another dose.

    Long story short, I was in pain all day and couldn’t do anything. The next day things got better, but I still spent most of the day lying down. I couldn’t work or deliver my orders. It was the first time that I received NO orders within 24 hours. I pride myself on getting my orders FAST, so that was a big hit for me. I will NOT do that again!

    Day 3 my legs started to feel more normal. I walked normally; my legs responded in the normal time. Previously I felt like my upper body was leaning forward and my legs were catching up, way back. Very strange sensation and very unpleasant. Now I felt like I was walking normally, albeit a little slower.

    Please note, this is NOT muscle pain due to overdoing it, due to a heavy training. I’ve been a gym junkie my entire adult life. I know what sore muscles in the gym feel like. I’ve had DOMs and the cliche ‘can’t lower yourself onto the toilet because it hurts too much’. I know what it feels like when you’ve been working hard in the gym and overtraining your muscles.

    This was NOT that.

    This was something completely different. Something I’ve never felt before.

    And it took three days for me to feel vaguely normal.

    Those three statements were incredibly painful, and I was completely disabled for most of that time. It was a wake-up call.

    I made a big mistake.

    So.

    Solution? Lighten the weight. Reduce the reps. And try again.

    I’ve tried. I have failed. I felt terrible. I felt depressed.

    So.

    I went to my physio because I need support with this. The whole experience was very disappointing, disturbing even. Frustrating too. And even though I knew what to do, I knew how to do it, I didn’t do it right.

    I realized I needed some advice, with a dose of support and encouragement. Quality advice. I knew my physio would give me all that.

    He gave me two options: do it the easy way. Return it immediately to a small load. Try to do 5 reps, one set of everything. And only increased once every two weeks. And then increase the tax by 10%.

    Or do it the hard way. Start with 5 reps, but do 2 sets. If that goes well, increase by 10-20% every week. Whatever makes sense with the weights I use. If things aren’t going well, reduce the weight. And look what happens.

    Option one has the advantage that it causes absolutely NO pain. Because I can certainly do very light loads. I know it won’t leave me on the couch for two to three days, it won’t disable me and it won’t hurt. But the downside is that it will be very slow. Working slowly to find my baseline could take weeks from now. Many weeks.

    As we know, I am a very impatient person.

    Option 2 can cause pain. It might be too much. It may mean that you have to lie on the couch again for a day or two. While this would be very disappointing, my natural optimism (and perhaps my habit of overestimating my abilities) tells me I want to do it this way. If it’s too much, I wait until the pain goes away and reduce it by 20%. And try again.

    So today I’m starting over.

    I’m going to do the same upper body. It was fine. I might even increase it a bit.

    However, the lower body will be much, much less. There will be 2 sets of each.

    Squats – 5 reps

    Lunges – 5 reps per leg

    Romanian deadlifts – 10 kg

    Calf raises – 5 reps

    Step-ups – 5 per leg

    And then I’ll see how I can handle it. This is about a quarter of what I was doing before, even less. So I hope this doesn’t cause me any severe pain. A little pain is fine. And to be expected. Maybe even appreciated as a sign of progress.

    But we’ll see.

    I keep notes on what’s happening and how I’m going. It should be interesting.

    Above all, I will be honest. This is a challenge, and I’ve messed up before. And now I’m trying again, with the support of my physiotherapist.

    I don’t want people to think this is a walk in the park, it’s not. It’s a serious undertaking and I hope it will help me maintain muscle strength in my arms and legs. It will take a lot of energy, it will reduce my upright hours, hours of which I currently have too little. And it may not help. But in the worst case even if it doesn’t help. At least I’ll feel like I did everything I could to avoid muscle wasting and further disability.

    In four weeks I will go back to the physio to see how I am doing. I will also post progress reports here.

    I don’t want people to think this is easy. It’s not. But it IS feasible. And it IS worth it.

    Buy me a coffee

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  • How to Increase Glutathione to Protect Your Bones and Improve Your Health

    How to Increase Glutathione to Protect Your Bones and Improve Your Health

    Antioxidants play a crucial role in protecting our cells from damage. That includes the cells responsible for healthy bone remodeling.

    Today we’ll take a closer look at the Master Antioxidant known as glutathione. As the impressive title suggests, glutathione is a uniquely powerful antioxidant.

    The studies we will review have shown that it also offers special benefits for building and maintaining strong and healthy bones. You will learn how to increase your glutathione levels and why it is so important to prevent breakages.

    Glutathione: the master antioxidant

    Glutathione was first accurately described in 1935, but it wasn’t until the 1980s that research into the molecule’s function began to reveal its incredible abilities. At the molecular level, glutathione is a tripeptide, meaning it is composed of three amino acids – glutamate, cysteine ​​and glycine – linked by peptide bonds.

    These components combine to form a unique molecule that helps maintain cellular homeostasis or balance. It supports cell homeostasis largely by protecting against oxidative damage. This protective property makes glutathione exceptionally powerful.

    Many diseases and conditions are associated with decreased glutathione levels, including Alzheimer’s disease, cancer, chronic liver disease, cognitive disorders, diabetes, Parkinson’s disease, bone loss and more.1

    Since glutathione protects cells throughout the body, it makes sense that a deficiency could be linked to several health problems.

    Short content

    Glutathione is a molecule consisting of three amino acids: glutamate, cysteine ​​and glycine. Combined, they form a molecule that helps maintain cell homeostasis throughout the body. Low glutathione levels have been linked to a wide variety of diseases and conditions.

    Where glutathione comes from

    Maintaining optimal glutathione levels is essential for good health. Fortunately, every cell has the ability to produce glutathione in a cellular fluid called cytosol, provided it has access to the required precursor amino acids: glutamic acid (glutamate), cysteine ​​and glycine.

    The process occurs in two steps and requires special enzymes to complete. Glutathione is then pumped into the mitochondria, the organelles that create the energy that fuels every cell in our body. Glutathione protects the mitochondria against oxidative damage caused by radical oxygen species.

    Your body naturally knows how much glutathione is needed to ward off oxidative damage to your cells. But certain obstacles may prevent her from achieving that production.

    Without the building blocks of glutathione and the enzymes that enable its production, your body cannot maintain healthy levels of this powerful antioxidant.

    Short content

    Glutathione, synthesized from its constituent amino acids in a cellular fluid known as cytosol, is then transported to the mitochondria, the energy-producing organelles of the cell. Glutathione protects the mitochondria against oxidative damage.

    How to increase glutathione levels

    In order for our cells to function optimally and prevent oxidative damage, it is imperative to ensure an ample supply of glutathione in our body. The antioxidant effect directly benefits the health and quality of our bones and our bone remodeling process.

    Recent research indicates that glutathione plays an even broader role by maintaining a balanced relationship between osteoclasts and osteoblast cells responsible for bone resorption and formation respectively – mainly by inhibiting osteoclast production. This action naturally increases bone mass.2

    These strategies can help us maintain healthy levels of the Master Antioxidant.

    • Eat sulfur-rich vegetables – Glutathione production requires sulfur, which is found in plant foods such as broccoli, Brussels sprouts, kale, cauliflower, watercress and mustard greens. Studies have linked a diet high in cruciferous vegetables to reduced oxidative stress and increased glutathione levels.
    • Eat glutathione-rich foods – Foods naturally rich in glutathione, such as spinach, avocados, asparagus and okra, all reduce oxidative stress. Our digestive system is not adept at absorbing glutathione from food, so the glutathione in these foods is not likely to get into our cells. However, because they reduce oxidative stress, they help keep glutathione levels high.
    • Increase vitamin C – Vitamin C has a similar effect as the glutathione-rich foods mentioned above. It’s a powerful antioxidant itself, so an abundance of vitamin C takes the pressure off glutathione, keeping levels robust. Additionally, studies have shown that vitamin C helps replenish glutathione molecules.3
    • Eat selenium-rich foods – Glutathione needs selenium to function. Include selenium-rich foods in your diet, such as chicken, fish, brown rice and Brazil nuts. Selenium is a basic supplement in the Osteoporosis Reversal Program.
    • Include foods high in cysteine – Cysteine, one of the three amino acids that make up glutathione, is found in foods such as whey protein, tuna, lean chicken, lentils, oatmeal, yogurt, carrots, shiitake mushrooms, almond butter and sunflower seeds. Using this building block allows your body to generate more of the master antioxidant.3
    • Turmeric extract curcumin Curcumin is an extract of the spice turmeric. Studies in animals have shown that curcumin has the ability to increase glutathione levels. Curcumin can be found in a supplement form.4
    • Take milk thistle – Milk thistle is a plant that contains a collection of compounds called silymarin. Silymarin is known for its antioxidant properties and studies have shown that it increases glutathione levels. 5
    • Get high-quality sleep – Glutathione, like all antioxidants, fights oxidative stress. Poor sleep quality can increase oxidative stress, making it harder for glutathione to be produced. Prioritize consistent, high-quality sleep to increase and maintain healthy glutathione levels.6
    • Regular exercise – Exercise helps our body maintain and increase antioxidant levels. Research has shown that combining cardio training with strength training has the most beneficial effect on glutathione levels. 7

    Short content

    Keep glutathione levels high to protect your bone remodeling process. See the list of strategies above, which includes dietary changes, supplements, sleep quality, and regular exercise.

    What this means for you

    You have the ability to equip your body with the essentials to protect itself from oxidative damage. Every cell in your body is ready and able to produce the Master Antioxidant if you provide the right materials and conditions.

    For tips on incorporating foods rich in sulfur, selenium, vitamin C and glutathione into your diet, try Bone Appétit, the Save Institute’s pH-balanced cookbook and meal planner. For help building a regular exercise routine you love, try SaveTrainer, the Save Institute’s online video training platform.

    You’re not the only one making healthy changes to improve your health. Find the support you need, in whatever form it takes, and celebrate that you have the wisdom to use the resources available to you!

    References

    1 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6770193/

    2 https://www.sciencedirect.com/science/article/pii/S0753332220304972

    3 https://www.ncbi.nlm.nih.gov/pubmed/12499341

    4 https://pubmed.ncbi.nlm.nih.gov/29484396/

    5 https://pubmed.ncbi.nlm.nih.gov/2353930/

    6 https://www.ncbi.nlm.nih.gov/pubmed/25945148

    7 https://pubmed.ncbi.nlm.nih.gov/17925621/



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