Chief of Trauma - The CORE Institute;
Orthopaedic Trauma & Upper Extremity Surgeon;
Associate Professor - University of Arizona College of Medicine Phoenix
Terrible bicondylar tibial plateau fracture with joint comminution.
These are bad injuries, with risk of compartment syndrome, wound complications, infection, and post traumatic arthritis. Studies show about 30% risk of complications.
This patient had a fasciotomy and external fixation placed. Then definitive surgery 2 days later. Fracture was fixed and wounds were closed.
You can see the joint was pretty smashed. It was fixed as best as possible, but it’s hard to make these perfect when there’s so much joint comminution. The lateral meniscus was torn which was fixed as well. And dual plate fixation for medial and lateral sides.
❗️The goal of surgery is to achieve a stable straight knee, and avoid complications (wound healing and infection). While many develope radiographic arthritis, most don’t need a knee replacement.
❗️Studies show the risk of total knee arthroplasty at 10 years post injury is about 7% (5 times higher than a matched cohort). So not as high as some people think, but not insignificant.
This one has some radiographic evidence of post traumatic arthritis, which is expected given the initial injury. But one year later patient has minimal symptoms and great range of motion.
Used with patient permission
#orthotrauma#orthopaedics#orthopedics#ortho#fracture#bone#tibialplateau#knee#tibia
📰 Once a PEP, Always a PEP? Myth vs. Reality in Compliance
Have you ever wondered: If someone is classified as a Politically Exposed Person (PEP), do they remain one for life?
The short answer: Not necessarily.
PEP status is not about the title alone — it’s about influence, risk exposure, and context. Let’s break it down:
🔹 Scenario 1 – Former Position, No Ongoing Influence
If a customer held a prominent public role in the past but stepped down, and after a review period (often 12–24 months under a risk-based approach) shows no signs of political or financial influence, they may be reclassified as non-PEP with proper review and documentation.
🔹 Scenario 2 – Legacy or Continued Influence
If the individual, even after leaving office, continues to wield influence through political networks, family ties, or powerful connections, the PEP classification should remain. Influence, not the title alone, drives the risk.
🔹 Scenario 3 – Active Role
If the person is still holding a prominent public function, the PEP flag must remain without question.
⚖️ Key Risk-Based Considerations
✅ Has the source of wealth been independently verified?
✅ Is the person linked to high-risk industries or jurisdictions?
✅ Could the classification be a false positive?
📌 Takeaway
PEP status is not automatically permanent. A risk-based approach, backed by strong documentation and periodic reviews, ensures firms balance compliance with practicality.
Get my E-book on - "Mastering Politically Exposed Persons (PEPs) Compliance: A Practical Guide for AML & KYC Professionals"
👉 https://lnkd.in/gHGWKwDG
Ever wake up just before your alarm? It might not be a coincidence…
It turns out, our brains have a natural way of keeping track of time, an inborn “clock” mechanism, which is synchronised to light in our environment.
It’s got the coolest name for such a tiny brain region: the suprachiasmatic nucleus (SCN) - literally, the group of cells (nucleus) above (supra) the optic chiasm (crossing).
The SCN is essentially your brain’s “master clock” because it is responsible for coordinating our circadian rhythms.
Light-sensitive cells in your eyes send signals to the SCN, which regulates melatonin - a hormone that makes us sleepy - via the pineal gland.
Our species evolved to be diurnal, being active in the day and sleeping at night. As a result, daylight inhibits melatonin release, making us more alert. At night, the lack of light promotes melatonin release, making us sleepy.
This is why for better sleep hygiene, experts often recommend limiting exposure to electronic devices for at least an hour before bedtime. The light from electronic devices can shift your body clock and this gets aggravated by heightened anxiety associated with doom scrolling -- neither of which helps your sleep.
Want to support your brain’s internal clock? A few simple habits can make a big difference:
👉 Get natural sunlight in the morning. This helps reset your body clock.
👉 Stick to a consistent sleep schedule, even on weekends.
👉 Limit screens at least an hour before bed.
👉 Keep your bedroom dark and cool to promote better sleep.
BTW, in teenagers melatonin starts to be produced later at night, which is why many teenagers don’t feel sleepy until much later in the evening. It’s also the reason they struggle to get up in the morning. For teens, going to school early is a bit like forcing them into a different time zone during the week and only letting them reset on weekends. When your teenager sleeps in on the weekends, bear in mind they are dealing with a genuine biological change in their circadian rhythm during the teenage years.
So when you wake right before your alarm, blame (or credit!) your suprachiasmatic nucleus for being such a good time keeper!
Understanding our biology helps us work with our natural rhythms rather than against them. How do you optimize your daily schedule around your circadian patterns?
Peer-reviewed science confirms A calcified pineal gland contributes directly to Alzheimer’s, Parkinson’s, and neurodegenerative diseases, disrupts circadian rhythm, suppresses melatonin, and—including age-related cognitive decline.
Here’s the key:
The pineal gland sits outside the blood-brain barrier, making it highly susceptible to bioaccumulation of calcium, fluoride, and aluminum—acting like a magnet for neurotoxic load.
But the breakthrough?
It’s reversible.
Over 90% of pineal calcification may be responsive to intervention.
Studies published in Nature, JAMA Neurology, and Frontiers in Neuroscience now show that with targeted detoxification, trace mineral restoration, and vibrational stimulation (light, sound, magnetics), the pineal gland’s structure and function can be measurably reactivated.
This is not fringe. It’s observable, biological, and increasingly repeatable.
And it may hold the key to restoring neuroplasticity, perception, and cognitive clarity.
Why it matters:
The pineal gland is a photoreceptive neuroendocrine transducer—sensitive to light, magnetism, and circadian rhythm.
• Synthesizes melatonin
• Regulates REM sleep
• Orchestrates glymphatic detox (brain cleansing)
• Contains retinal-like photoreceptor cells that detect light and synchronize internal timekeeping with solar cues
Yet under toxic load for majority of the world population especially western world, it calcifies— when it does:
• Sleep breaks down
• Neuroinflammation rises
• Cognitive fog deepens
• Spiritual and sensory perception narrows
Peer-reviewed studies now directly correlate pineal calcification with:
• Early-onset Alzheimer’s
• Parkinsonian tremors
• Impaired REM/glymphatic flow
• Diminished melatonin production
• Loss of intuitive, photonic, and extrasensory sensitivity
The reversal is biological and can be done with weeks to months.
Protocols under exploration include:
• Chelating agents (boron, magnesium, iodine)
• Full-spectrum & near-infrared photobiomodulation
• Acoustic resonance (Solfeggio tones, PEMF, gamma entrainment)
• Cold immersion, breathwork, pineal-activating meditation
• Circadian realignment (sunlight, sleep hygiene)
• Avoidance of fluoridated water and toothpaste
Below in the comments I will add a detailed effective routine.
Inside the pineal are piezoelectric microcrystals—biogenic calcite structures that vibrate in response to EM fields.
When they resonate, perception expands.
When they calcify, perception contracts.
This isn’t just about sleep.
It’s about sovereignty—biological, neurological, and spiritual.
“The light of the body is the eye: if therefore thine eye be single, thy whole body shall be full of light.”
— Matthew 6:22
This isn’t just belief.
It’s bioelectrical coherence.
A re-tuning of the human instrument with circadian time, rhythm, and light.
The data is clear:
The body can regenerate once in homeostasis.
The brain can realign and retune.
And the inner eye… can open—again.
Surgeon-in-Chief
The Daniel and Jane Och Spine Hospital
New York-Presbyterian/Allen Hospital
Professor & Chief of Spinal Surgery
Chief of Spinal Deformity Surgery
Columbia Univ. Dept. of Orthopedic Surgery
Minimizing the risk of neurological deficits in spinal deformity surgery is a top priority for every spine surgeon in the operating room. But despite the advancements in technology and intraoperative neuromonitoring, we are still seeing a prevalence of intraoperative neurological events as high as 23%. There is a plethora of studies in the literature that discuss a variety of different risk factors to try an anticipate these problems and potentially adjust the surgical plan accordingly, such as the Cobb measurements, deformity angular ratio (DAR), 3DCT DAR, and the spinal cord shape classification system (SCSCS) among others. However, no preoperative risk stratification tool of IONM loss exists to help delineate important preoperative factors that should be considered in the decision making process prior to deformity correction. In our newly published study in The Journal of Bone and Joint Surgery, Inc., we leveraged a machine learning approach to develop the first preoperative prediction tool for spinal cord-level IONM data loss during adult and pediatric spinal deformity surgery.
From a total of 1,106 patients, we were able to delineate 8 critical non-modifiable preoperative factors with the following scores: conus level below L2 (2 points), type 3 spinal cord (2 points), cervical UIV (2 points), preop thoracic cobb angle ≥75 degrees (2 points), sagittal-DAR ≥15 (2 points), preop lower extremity deficit (2 points), preop TK ≥ 80 degrees (1 point), and the total-DAR (1 point). Scores between 0 and 2, 3 and 6, and 7 and 12 resulted in low, moderate, and high risk of cord-level IONM data loss, respectively. The performance of our model had an AUC of 0.921 and 0.898 on our training and testing sets with over 90% accuracy! By employing predictive modeling for proper risk stratification, clinicians can engage in more informed discussions with patients and potentially adjust operative plans to optimize neurologic safety, particularly those with elevated risk factors for cord-level IONM data loss and resultant neurologic deficit.
Link to the full study:
https://lnkd.in/g3vz2_U3Nathan J. Lee, MDVarun ArvindTed ShiAlexandra DionneChidebelum NnakeAnastasia FerraroMatthew CooneyErik Lewerenz Justin L. Reyes Steven RothJustin K. ScheerTom ZervosEarl Thuet, CNIMJoseph LombardiZeeshan SardarRon Lehman, MDBenjamin Roye MD-MPHMichael VitaleFthi M. Hassan, MPH
A Harvard-led study found that delaying breakfast by 1 hour increases death risk by 8-11%.
Researchers tracked 2,945 adults aged 42-94 from the UK for up to 22 years.
They measured breakfast, lunch, and dinner times at multiple points throughout the study.
The key finding: For each hour people delayed their breakfast, their all-cause mortality risk increased by 8–11%.
Late breakfast eaters were also more likely to experience:
- Poor sleep quality
- Oral health problems
- Depression and chronic fatigue
- Difficulty with meal preparation
Over the 22-year follow-up period, this pattern held even after adjusting for age, lifestyle, and existing health conditions.
As a doctor, this seemed too drastic to be true.
So I looked deeper and found an important caveat:
The researchers themselves cautioned that this doesn't PROVE late breakfast causes early death.
It's possible that declining health makes people eat later.
Think about it:
- Depression makes you sleep in and skip meals
- Oral health problems make morning eating difficult
- Chronic fatigue shifts your entire routine later
- Physical limitations delay meal preparation
So late breakfast timing might be a warning sign of other health issues, not the root cause.
My take as a doctor:
A high-protein, high-fibre meal before work is the perfect start to your day (bonus points for black coffee).
But don’t panic about timing - what you’re eating matters much more over time.
What time do you usually have your first meal?
#healthandwellness#healthtips#lifestyle
Building The Sleep Company | Creating India’s Sleep Revolution Through comfort Technology | Ex-P&G Leadership | IIM-C | Served 2M+ Customers | ET 40U40 - 2024 | Fortune 40U40
Sleeping with lights on can give you heart disease in few years. A study on 88,905 people over 9.5 years proved it.
I've spent years obsessing over SmartGRID technology at The Sleep Company. Back pain, spinal alignment, comfort - we thought we had it figured out.
Then UK Biobank published research that changed everything.
They studied 88,905 adults over 9.5 years. The findings were shocking.
The biggest cardiovascular threat while you sleep is the light in your bedroom.
Here's what the data showed:
📍 People in moderately bright rooms had a 20% higher risk of heart attack.
📍 Those in brighter rooms faced a 27% higher risk.
📍 The brightest rooms showed a 47% increase.
The mechanism is disturbing:
→ Artificial light disrupts circadian rhythm
→ Triggers brain stress activity
→ Inflames blood vessels over time
→ Raises cardiovascular disease risk
What makes this urgent for India:
Already, cardiovascular diseases are rising at a high rate. Urban areas have constant light pollution. Most bedrooms have multiple light sources at night - phones, streetlights, electronics.
Here's what you can do to protect your heart:
→ Keep bedrooms completely dark using blackout curtains
→ Turn off all electronics 30-60 minutes before sleep
→ Use warm, dim lighting if you need a nightlight
→ Cover or remove LED indicators from devices in your room
Better sleep isn't just about comfort anymore. It's about protecting your heart by controlling your bedroom environment.
This changes how we need to think about sleep health entirely.
Internationally recognized Dementia Coach & Author | Founder of the International Caregivers Association | Creator of TDI Model | Memory Care Program Design | Team Optimization | The Psychology of the Dementia Brain
POOR SLEEP LINKED TO BRAIN'S WASTE-REMOVAL BREAKDOWN
A new study reveals that poor sleep in older adults disrupts the brain’s glymphatic system, responsible for clearing harmful waste and toxins. Researchers found that compromised sleep quality leads to dysfunction in this crucial system, potentially increasing risks for memory decline and cognitive impairments.
Using advanced brain imaging in 72 older adults, the research highlighted that poor sleep negatively impacts connections within brain networks linked to memory performance. These insights emphasize the importance of maintaining good sleep hygiene to support brain health and healthy aging.
3 Key Facts:
1. Sleep and Brain Health: Poor sleep quality impairs the brain’s glymphatic system, crucial for clearing harmful proteins.
2. Cognitive Impact: Dysfunctional glymphatic activity due to poor sleep correlates with memory decline in older adults.
3. Neural Networks: Sleep quality directly influences brain networks, affecting overall cognitive health and aging.
Source: https://lnkd.in/g4JsJS2n
The Hidden Cost of Poor Sleep on Cellular Aging
A new meta-analysis published in Sleep Medicine Reviews (2025) examining over 400,000 participants has revealed poor sleep quality is significantly associated with premature cellular aging.
Poor sleepers showed 24% higher odds of accelerated telomere shortening.
Telomeres are like the plastic tips on shoelaces, protecting our genetic material from damage. Each time our cells divide, these telomeres naturally shorten, acting as a kind of biological countdown timer.
When they become too short, cells can no longer divide properly, contributing to aging and disease. and they are a key marker of biological aging.
Wake time after sleep onset was strongly linked to cellular aging.
Also they found daytime impairments from poor sleep were significantly associated with shorter telomeres.
Sleep like your life depends on it, because it does!
Link to paper https://lnkd.in/gHz-Ghpc
Relationship Between Hypocalcemia and Body Condition Score (BCS) in Dairy Cows
1. Impact of Low BCS on Hypocalcemia Risk
a. Energy Deficiency and Hypocalcemia
Low BCS (2.5 or lower) indicates insufficient fat reserves, which means cows are unable to meet energy demands during early lactation.
In the weeks leading up to calving, cows with low BCS are more likely to experience a negative energy balance leading to the mobilization of body fat. Increased fat mobilization causes the release of NEFAs, which can inhibit calcium absorption and disrupt calcium homeostasis.
b. Reduced Ability to Mobilize Calcium
Low BCS cows are often in a state of nutrient deficiency, which can lead to reduced osteoclastic activity (the breakdown of bone to release calcium) and poor intestinal calcium absorption, contributing to impaired calcium mobilization during the high-demand period (early lactation).
2. Impact of High BCS on Hypocalcemia Risk
a. Increased Risk of Subclinical Hypocalcemia
High BCS (4.0 or higher) indicates overconditioned cows, with an excess of fat reserves. Excess fat can increase the levels of NEFAs, leading to a negative effect on calcium metabolism. NEFAs are thought to inhibit parathyroid hormone (PTH) secretion and disrupt the cow’s ability to mobilize calcium from bone and absorb it from the gut, further exacerbating hypocalcemia risk.
b. Impaired Response to Calcium Demand
Overconditioned cows also show a reduced sensitivity to parathyroid hormone (PTH), which is critical for regulating calcium homeostasis. PTH stimulates the release of calcium from bone stores, increases calcium absorption from the intestines, and reduces calcium excretion by the kidneys.
3. Strategies to Manage BCS and Hypocalcemia
a. Ideal BCS at Calving
Aim for a BCS of 3.0–3.5 at calving to ensure cows have adequate energy reserves without being overconditioned or underconditioned.
This optimal BCS allows cows to meet the calcium demand for lactation while reducing the risk of energy deficiencies and calcium mobilization issues.
b. Avoid Sudden Weight Loss Pre-Calving
Cows with low BCS should be gradually improved before calving by providing a balanced diet that supports weight gain without causing excess fat deposition.
Cows with high BCS should be managed to prevent excessive weight gain during the dry period, which can lead to fatty liver syndrome and calcium metabolism disruptions.
c. Calcium Supplementation
Provide calcium supplementation to cows, particularly during the transition period, to prevent milk fever and subclinical hypocalcemia.
d. Monitor Blood Calcium Levels
Regularly monitor blood calcium levels, especially in cows at high risk (e.g., cows with low or high BCS, or those with a history of milk fever), and provide appropriate calcium therapy (oral or intravenous) as needed.
#dairy_farming#animal_nutrition#cow_welfare#cow_comfort#dairy#ruminant#livestock#harafiee_nutrition#calf#heat_stress#transition_cow