Dr Kevin Lee

@dr-kevinlee.com

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Physician-Imager: endocrinology & nuclear medicine #AusMedSky https://www.linkedin.com/in/kevinleefracp/

Figure 3. Quercetin’s Enhancement of Macroautophagy for Cellular Regulation. The quercetin’s dynamic role in bolstering macroautophagy is a critical cellular process for maintaining homeostasis through the degradation and recycling of proteins and organelles. Quercetin modulates the mechanistic target of rapamycin (mTOR) pathway and activates AMP-activated protein kinase (AMPK), leading to decreased mTOR activity and the initiation of autophagy.
Schematic representation of different signaling pathways and targets by quercetin as a potential therapeutic strategy in autoimmune diseases.
Graph showing Percentage change (Δ%) in the 8 components/subscales of the SF-36 Quality of Life Scale from the beginning to eight months of this study among 88 patients with T2DM randomized to intervention (n = 42) and control (n = 46) groups.
Pie chart- 70.8% answered yes to better manage and improve quality of life since official diagnosis of POTS
Graphic abstract. Results Protocol #1: Standing heart rate was reduced (105 [99-116] beats/min vs 119 [105-130] beats/min; P < 0.001) and symptoms improved (P < 0.001), during AM-ON vs AM-OFF. Standing heart rate (P = 0.04) and symptoms (P = 0.004) increased when compression was removed after several hours. Protocol #2: Standing heart rate was reduced (84 [77-90] beats/min vs 89 [84-100] beats/min; P < 0.001), and symptoms improved (P = 0.03), during AM-ON vs AM-OFF. Standing heart rate (P = 0.02) and symptoms (P < 0.001) increased when compression was removed after several hours. Conclusions Commercially available compression tights reduced heart rate and symptoms both acutely and after several hours of use. This additional benefit persisted whether concomitant medications were used. (Compression Garments in the Community With POTS [COM-COM-POTS]; NCT04881318)
Estrogen agonist activity of luteolin and quercetin. T47D KBluc cells were treated with luteolin (circles), quercetin (squares), or vehicle for 20 h. Induction of luciferase activity by 1 nM 17β-estradiol is defined as 100 %
Simulated receptor occupancy of naltrexone at the mu (red) and kappa (blue) opioid receptor as a function the log10 of the oral dose (D) The sixfold difference in naltrexone’s affinity for MOR over KOR results in a right shift of the dose-occupancy curve. As a result, the difference in receptor occupancy between 25 and 100 mg naltrexone is only 5.5% for MOR (red arrow), but 19.6% for KOR (blue arrow). Vertical reference lines represent 25 and 100 mg doses.
This image explains the mechanism of action (MOA) of memantine in Alzheimer's disease (AD) based on the signal-to-noise hypothesis. Key Points from the Image and Caption: NMDA Receptor Dysfunction in AD: Alzheimer's pathology (e.g., Aβ, Tau, energy deficits) causes dysregulated NMDA receptor activity, leading to excessive "synaptic noise." Memantine's Role: Memantine acts as a filter blocking 'synaptic noise' by selectively blocking NMDA receptors. It helps differentiate between pathological noise and relevant synaptic signals. Restoration of Synaptic Plasticity: By filtering excessive noise, memantine allows synaptic plasticity to be restored and improves neuronal communication. Voltage-Dependent Action: Memantine preferentially blocks NMDA receptors under pathological conditions (e.g., excessive glutamate) without disrupting normal synaptic activity.
Methods: A comprehensive search was conducted on the Scopus, Medline, ClinicalTrials.gov, and Cochrane Library databases up until May 20th, 2024. This review incorporates RCTs that examine the comparison between LDN and placebo in fibromyalgia patients. We employed random-effect models to analyze the odds ratio and mean difference (MD) for presentation of the outcomes. Results: A total of 4 RCTs with 222 fibromyalgia patients were incorporated. The results of our meta-analysis showed a significant reduction in pain scores (MD: –0.86, 95% confidence interval [CI]: –1.20, –0.51, P < 0.001, I2 = 33%) and higher increment in pressure pain threshold (MD: 0.17, 95% CI: 0.08, 0.25, P < 0.001, I2 = 0%) among fibromyalgia patients who received LDN than those who only received a placebo. The fibromyalgia impact questionnaire revised and pain catastrophizing scale did not differ significantly between the two groups. LDN was also associated with higher incidence of vivid dreams and nausea, but showed no significant difference with the placebo in terms of serious adverse events, headache, diarrhea, and dizziness. Conclusions: This study suggests the efficacy of LDN in mitigating pain symptoms for fibromyalgia patients with a relatively good safety profile.
This diagram illustrates the interplay between ancestral genes, environmental factors (past and modern), and how survival responses have evolved to adapt to challenges but can also become maladaptive in contemporary settings. Here’s a breakdown: Ancestral Environment • Challenges: Starvation, fear, and desperation prompted the adaptive survival response to conserve energy and enhance survival. • Adaptive Survival Response: • Physiological Outcomes: • Insulin Resistance: Maintains blood glucose during starvation. • Hyperandrogenism: Increases strength and fitness. • Enhanced Energy Storage: Boosts survival in harsh conditions. • Decreased Fertility: Increases survival of individuals under stress. Modern Environment • Challenges: Western diet, dysbiosis, sedentary lifestyle, stress, and chemical exposures activate a maladaptive survival response. • Maladaptive Survival Response: • Pathological Outcomes: • Insulin Resistance: Leads to PCOS and metabolic diseases. • Hyperandrogenism: Results in acne, hirsutism, and infertility. • Enhanced Energy Storage: Causes obesity and metabolic disorders. • Decreased Fertility: Necessitates infertility treatments. Developmental Programming and Transgenerational Transmission This concept highlights that survival responses (adaptive or maladaptive) can be passed down through generations via epigenetic mechanisms. The once advantageous adaptations to ancient environments now contribute to modern diseases when mismatched with current lifestyles. In summary, this diagram links evolutionary survival mechanisms to contemporary chronic health issues like obesity, PCOS, and infertility, emphasising the role of environmental mismatch.
This flowchart illustrates the physiological cycle triggered by simple carbohydrate intake, leading to downstream metabolic effects. Here’s a breakdown: 1. Simple Carbohydrate Intake: Initiates the cycle. 2. Hyperglycaemia: Results in elevated blood glucose levels. 3. Sustained Hyperinsulinaemia: Chronic elevation of insulin in response to hyperglycaemia. 4. Reactive Hypoglycaemia: A drop in blood glucose following the insulin spike. 5. Snacking: Increased hunger leads to frequent snacking, perpetuating the cycle. 6. Obesity & Insulin Resistance: Repeated hyperinsulinaemia contributes to obesity and insulin resistance. 7. Cortisol Secretion: Hypoglycaemia stimulates cortisol production. 8. Adrenal Androgen Secretion: Cortisol indirectly stimulates androgen production. 9. Conversion to Testosterone: Androgens convert to testosterone. 10. Hirsutism: Excess testosterone leads to male-pattern hair growth, particularly in females. Feedback Loops: • Obesity & Insulin Resistance** exacerbate sustained hyperinsulinaemia. • Adrenal androgens further reinforce the metabolic dysfunction, worsening the cycle. This diagram reflects the complex interplay of hormones and metabolism often observed in conditions such as polycystic ovarian syndrome (PCOS) or metabolic syndrome.
Figure 1. The extended autonomic system. The EAS consists of the central autonomic network (CAN)/stress system, Langley’s autonomic nervous system (ANS), neuroendocrine systems, and inflammatory/immune systems. The four components are bi-directionally inter-related, meaning 6 combinations of relationships. In the central autonomic network, the “stress system” in the Chrousos/Gold schema includes the paraventricular nucleus of the hypothalamus (PVN), which is the source of arginine vasopressin (AVP) and corticotrophin-releasing hormone that drive the hypothalamic-pituitary-adrenocortical axis (HPA), and the pontine locus ceruleus (LC), the main source of norepinephrine in the brain. Abbreviations: Abbreviations: A5 = A5 noradrenergic cell group; AMY = amygdala; ANP = atrial natriuretic peptide; ANS = autonomic nervous system; AP = area posterma; BNP = brain-derived neurotrophic factor; CING = cingulate cortex; CVLM = caudal ventrolateral medulla; DDA = DOPA-dopamine autocrine-paracrine system; DMNX = dorsal motor nucleus of the vagus nerve; ENS = enteric nervous system; GHE = ghrelin; HACER = hypothalamic area controlling emotional responses; Hippo = hippocampus; INS = insulin; LEP = leptin; NA = nucleua ambiguus; NO = nitric oxide; NTS = nuclear of the solitary tract; PACAP = pituitary adenyl cyclase-activating polypeptide; PAG = periaqueductal grey region; PNS = parasympathetic nervous system; Pre-Bötz = pre-Bötzinger complex; RAS = renin-angiotensin-aldosterone system; RPG = respiratory pattern generator; RTN = retrotrapezoid nucleus; RVLM = rostral ventrolateral medulla; SAS = sympathetic adrenergic system; SNS = sympathetic noradrenergic system; THY = thyroid; VTA = ventral tegmental area.
This image compares two doctors, Dr Bob and Dr Carol, appointment slots using coloured bars, along with total amounts of $1005 for Dr Bob and $616.20 for Dr Carol, former with shorter consultations, latter filled with longer appointments
The image illustrates the inhibitory role of quercetin on enzymes involved in carbohydrate digestion, particularly α-amylase and α-glucosidase. Here’s a breakdown of the information: Key Points from the Diagram: 1. Carbohydrate Digestion Process: • Starch: Broken down by α-amylase into maltose, which is further hydrolysed into glucose. • Sucrose: Cleaved into glucose and fructose by α-glucosidase. 2. Effect of Quercetin: • Quercetin inhibits both α-amylase and α-glucosidase, reducing the breakdown of starch and sucrose. • This slows the release of glucose into the bloodstream, effectively lowering the glycaemic index of foods.
Imagine it’s Christmas time in a little town, and everyone is excited about a big family party. In this town, when you get sick, you need to give special presents to the doctor to help you feel better. You don’t keep these presents yourself—you give them to a big, green, grumpy business called Grinch Care Co. because they promise, “If you get sick, we will use these presents to pay the doctor!” But guess what? Grinch Care Co. doesn’t like to share these presents. When someone gets sick, Grinch Care Co. might take a very long time before giving any presents to the doctor. Sometimes, they say, “No! We won’t give any presents!” And if people say, “That’s not fair!” Grinch Care Co. tries to make excuses and pretend they did nothing wrong. By doing this, Grinch Care Co. keeps more presents for themselves, instead of using them to help sick people feel better.
Neuroinflammation and dysbiosis. During local nasal inflammation (chronic rhinosinusitis and allergic rhinitis), the count and type of microbial communities change significantly (there is a loss of key symbiotic species, while pathobionts often overgrow). Dysbiotic conditions result in alterations in immune responses, cerebral metabolism, endocrine signaling, and neuronal physiology due to epithelial barrier disruption. Thus, an increase in the production of proinflammatory mediators by the host (cytokines, oxidative stress, exosomes, etc.) and bacteria (exosomes, LPS, peptidoglycans), which can penetrate directly into the CNS through the olfactory pathway or the vessel-rich nasal mucosa, causing neuroinflammation. The anatomical relationship of the nasal cavity with olfactory pathways and the CNS (particularly the limbic system) and, therefore, with monoaminergic brainstem neurons may underlie several pathophysiological changes in emotions (depression), memory, hormonal, and autonomic dysfunctions, and may lead to neurodegeneration
https://thyroidpatients.ca/2022/07/17/can-normal-tsh-rule-out-thyroid-disease/amp/ The image compares the distribution of TSH (thyroid-stimulating hormone) levels in a healthy population to the distribution of TSH levels for a healthy individual over time. It highlights that population-level TSH has a wider range, while an individual’s TSH tends to fluctuate within a much narrower range. Key points from the reference (Hoermann & Midgley, 2012): • Population TSH levels: These represent the variability across many individuals and follow a broader distribution. • Individual TSH levels: For a single healthy individual, TSH levels are more stable and confined to a tighter range.
Figure 1. Melatonin originated 2.5 billion years ago, and it is present in all organisms from bacteria to humans; its structure has never been changed. https://www.mdpi.com/2076-3921/11/1/140
The image visually highlights the relationship between life expectancy and health expenditure per capita across various countries. In the chart, the United States is an outlier, spending significantly more on healthcare per capita compared to other countries, yet achieving a lower life expectancy. Here's a breakdown of what this graph suggests: Key Observations: High Spending, Low Return (US): The US spends substantially more on healthcare (over $10,000 per capita annually), far exceeding other countries. Despite this, life expectancy in the US is considerably lower than in nations with much lower health expenditures. Other Countries' Performance: Countries like Japan, Australia, Switzerland, and Norway achieve higher life expectancy with lower spending. Most OECD countries cluster along a curve where incremental increases in healthcare spending correspond to modest life expectancy gains.
The image compares vehicle size evolution over the years: 1840, 1980, and 2022, showcasing the increase in width and space vehicles occupy on roads. It highlights the trend towards larger and heavier cars, like SUVs, over time. This is referred to as "autobesity," where cars increasingly encroach on public spaces, reducing room for pedestrians and cyclists, while impacting safety and the environment.
Figure 1 Illustration of the targets of clomiphene citrate in the HPG axis in males. The hypothalamus secretes GnRH, which is delivered to the pituitary gland to stimulate the biosynthesis of the gonadotropins LH and FSH. LH functions within Leydig cells and results in the secretion of testosterone. Testosterone can be modified via aromatase for estradiol and acts as a negative feedback signal in the HPG axis. Clomiphene citrate can reduce this signal and weaken the negative feedback loop to improve testosterone synthesis
Possible Impact of Microglia on Personality and Social Behaviors. Early-life environmental experiences such as psychological stress and traumatic events may activate human microglia, establish a certain neuro-synaptic-microglial connection, which is memorized unconsciously as a primer for an extended period, and this formation in the human brain determines each human’s personality and personality- oriented social behaviors in later life. In sum, neuronal networks with active microglia may induce noisy-decision-making, which is equivalent to personality- oriented behaviors (A). On the other hand, decision-making with neuronal dominant networks may induce straightforward behaviors, which are less affected by personality (B). In the present study, the control group’s personality- oriented behaviors could be formulated by microglial priming effects (A), and the minocycline group’s situation- oriented behaviors may be induced by suppressing microglial contribution to social behaviors (B).
A step-wise approach as a pyramid to managing NBD is shown in Figure 1.
The image illustrates the physiological responses to lower body negative pressure (LBNP) with decreasing venous return. It highlights percentage changes in three parameters: Mean Arterial Pressure (MAP): Remains relatively stable, showing minimal change. Cerebral Blood Flow (CBF): Decreases progressively, measured using MRI. Cardiac Output (CO): Drops significantly with increasing negative pressure, reflecting reduced venous return and overall circulation.
A graph depicting Frank-Starling relationship between ventricular end-diastolic volume and stroke volume in the normal heart, and in preload impairment secondary to venous obstruction
Graphic abstract . Highlights • The TLRs/MyD88/NF-κB axis is the key pathway involved in PM2.5 associated injury. • Metformin reduces PM2.5-induced generation of IL-6 by inhibits TLRs/MyD88/NF-κB pathway. • Metformin protects against PM2.5-induced macrophages mitochondrial damage and cytotoxicity in an AMPKα2 independent manner.
FT3 level of normal health subjects across 24 hour period, showing highest fT3 levels early hours after midnight, lowest in the afternoon
This is a clinical decision flowchart for managing Bertolotti syndrome. But highlight the normal & normal branches to SPECT Key Steps in the Flowchart: 1. Initial Assessment: • Determine if pain occurs with activity. • If no pain, likely no further intervention is needed. 2. Physical Therapy (PT): • First-line management for pain. • If symptoms improve or resolve, follow-up as needed. 3. Imaging (if PT fails): • MRI: Evaluate for structural abnormalities. • SPECT: Assess for inflammation or abnormal bone activity. 4. Selective Injection: • If inflammation is confirmed, perform a targeted injection. • Follow with additional physical therapy to monitor for improvement. 5. Radiofrequency Ablation (RFA): • If injections and PT fail, consider RFA to manage chronic pain. 6. Surgical Intervention: • If all non-surgical options fail, proceed to resection or spinal fusion. This structured pathway ensures progressive, evidence-based interventions tailored to the severity and persistence of symptoms. Let me know if you’d like further insights or clarification!
The things people asked me as a child seem so obsolete; my husband and I don't say to each other "What do you think Gideon will be when he grows up?" Instead, we ask "How do we make sure Gideon grows up without a life-limiting disability?"
English: Mosaic medallion in the floor of the main hall of the Jordan Hall of Science, University of Notre Dame. Bears the quotation from Theodosius Dobzhansky (1900-1975), "Nothing in Biology makes sense except in the light of evolution."
Thr92-DIO2 localizes in the ER where, with the support of appropriate cofactors, it is able to convert T4 into T3 for transcriptional regulation in the nucleus. DIO2 is recycled through the Golgi. Ala92-DIO2 causes ER stress and impairs the recycling of DIO2, which aberrantly accumulates in the Golgi, where it is not active. ER stress and decreased T3 production exert biological effects on glial cells and neurons, affecting neurological function.
Consequences of the Availability Heuristic For Patients: Patients experiencing vaccine injuries may feel dismissed or invalidated if doctors or institutions under-recognise their symptoms. Delayed diagnosis and treatment may worsen outcomes for affected individuals. For Public Trust: If vaccine injuries are consistently under-recognised or poorly addressed, public trust in vaccination programs and health institutions may erode, ironically increasing vaccine hesitancy. For Research and Policy: Rare vaccine injuries may not receive adequate attention in research or policy development, leading to insufficient monitoring, treatment protocols, or compensation frameworks. Mitigating the Availability Heuristic in Vaccine Injury Recognition Education and Training: Provide healthcare professionals with updated information on the signs, symptoms, and reporting protocols for rare vaccine injuries. Incorporate vaccine injury scenarios into continuing medical education to keep these cases "available" in clinical memory. Improved Surveillance: Strengthen systems for reporting and monitoring adverse events, ensuring better data collection and analysis to make rare cases more visible. Balanced Communication: Public institutions should acknowledge vaccine injuries transparently while continuing to emphasise the overwhelming safety and benefits of vaccines. Frame discussions with evidence-based comparisons, highlighting the rarity of severe adverse events in relation to the risks of vaccine-preventable diseases. Patient-Centred Care: Encourage healthcare providers to listen empathetically to patients' concerns and investigate potential vaccine injuries thoroughly, even if the probability is low.
This is a forest plot summarising a meta-analysis of acetazolamide’s efficacy in managing sleep apnoea, categorised into primary and secondary subgroup analyses. The key metrics include the standardised mean difference (SMD) with 95% confidence intervals (CIs), the number of studies included in each subgroup, and the p-value for subgroup differences (P). Key Observations: 1. Overall Effect: • Acetazolamide significantly favours improvement over control (SMD: -0.70; 95% CI: -0.83 to -0.58). 2. Primary Subgroup Analysis: • Dose: Both low (<500 mg/day) and high (≥500 mg/day) doses show efficacy, with higher doses trending towards greater effect. • Sleep Apnoea Type: • Central Sleep Apnoea (CSA) showed a stronger effect (SMD: -0.80; 95% CI: -1.00 to -0.61) than Obstructive Sleep Apnoea (OSA) (SMD: -0.63; 95% CI: -0.80 to -0.47). • CSA Subtypes: • CSA due to heart failure (CSA-CHF) and idiopathic CSA had the strongest responses. • CSA caused by opioids had a smaller effect. 3. Secondary Subgroup Analysis (focusing on significant factors): • Altitude: Greater efficacy at high altitudes. • Study Design: Randomised controlled trials (RCTs) demonstrated a larger effect compared to observational studies. • Placebo Control: Studies with a placebo control showed a stronger effect size. • Risk of Bias: Studies with low/unclear risk of bias had better outcomes than those with high risk. • Study Location: Asian studies demonstrated a smaller effect size compared to non-Asian studies.
Figure 2: Hemodynamic changes following CPAP, acetazolamide, and acetazolamide plus CPAP treatments. Individual data of office mean arterial pressure (top panels) and aortic augmentation index (bottom panels) at baseline and follow-up in the CPAP, acetazolamide, and acetazolamide plus CPAP groups. Mean values at baseline and follow-up are indicated by the solid black bars. Significance values refer to comparison within groups. CPAP = continuous positive airway pressure.
Figure 2. Acrocyanosis in the distal leg in the dependent position (A) that immediately disappears on raising the leg up against gravity (B) in a person with long COVID. She was initially misdiagnosed with functional neurologic disorder based on non-epileptic spells, which were subsequently determined to be pre-syncopal episodes caused by post-COVID-19 postural orthostatic tachycardia syndrome.
Latest updates from David Systrom During the Massachusetts ME/CFS & FM Association and Open Medicine Foundation Fall 2020 Event on Zoom, David Systrom reported on the results of iCPET in a set of ME/CFS patients. The VO_2max is lower in patients vs controls (figure 3, up). As mentioned before, VO_2max is an index that includes contributions from cardiac performances, pulmonary efficiency, and oxygen extraction rate in the periphery. In other words, a low VO_2max gives us no explanation for why it is low. This finding seems to be due to different reasons in different patients even though the common denominator among all ME/CFS patients of this cohort is low pressure in the right atrium during upright exercise (low RAP, figure 3, left). But then, if we look at the slope of Qt in function of VO_2 (figure 3, right) we find three different phenotypes. Those with a high slope are defined “high flow” (in red in figure 3). Then we have a group with a normal flow (green) and a group with a low flow (blue). If we look then at the ability to extract oxygen by muscles (figure 3, below) expressed by the ratio \frac{arterial\;O_2 - venous\;O_2}{HB} we can see that the high-flow patients reach the lowest score. In summary, all ME/CFS patients of this cohort present with poor VO_2max and preload failure. A subgroup, the high-flow phenotype, has poor oxygen extraction capacity at the level of skeletal muscles. Figure 3. The results presented by David Systrom are here displayed around a schematic representation of the circulatory system. VO_2 is a global measure of the efficiency of the circulatory system. CO, which stands for cardiac output (indicated Qt in this blog post) is related to the output of the left half of the heart. RAP is the pressure of the right atrium. By Paolo Maccallini.
Table 12. Examples of treatment methods without sufficient scientific evidence or without a medical or scientific basis in environmental medicine [5, 73, 160, 384, 512, 762]. Treatment methods without sufficient scientific evidence Antifungal treatment not in line with guidelines Detoxification therapy, e.g., with cholestyramine (CSM therapy) Dietary changes Homeopathic treatments Symbiosis control Treatment methods without a medical or scientific basis Bioresonance therapy (Moratherapy) Autologous blood and urine treatment Holistic intestinal cleansing Salt therapy Clinical ecology procedures (e.g., provocation and neutralization test (PN test))
Venn diagram 1. POTS (Postural Orthostatic Tachycardia Syndrome): • Overall prevalence: 0.17% • Overlap with ME/CFS: 11–40% 2. Hashimoto’s Thyroiditis: • Overall prevalence: 0.8% • Overlap with ME/CFS: 17–20% 3. Fibromyalgia: • Overall prevalence: 5.4% • Overlap with ME/CFS: 30–77% 4. Family History of Autoimmune Diseases: • No specific prevalence percentage listed for the general population. • Overlap with ME/CFS: 18–41% 5. ME/CFS (Myalgic Encephalomyelitis/Chronic Fatigue Syndrome): • Overall prevalence: 0.2–0.3%
FIGURE 1. Benefits of Metformin and Potential Mechanism of Improved Responses to Influenza and SARS-CoV-2 infections. The multiple mechanisms by which metformin can improves outcomes after infection with influenza (flu) or SARS-CoV-2 (COVID-19 virus). Metformin can directly impact T cells, B cells, monocytes, and macrophages to control inflammatory responses and promote immune-mediated protection. Metformin also acts on numerous aging pathways, such as nutrient sensing, mitochondrial dysfunction, loss of proteostasis, epigenetic alterations, telomere attrition, senescence, and inflammation, that are dysregulated with aging and lead to decreased resilience in older adults. Retrospective and prospective studies have shown that metformin improves certain outcomes after infection with flu or SARS-CoV-2. More specifically, metformin leads to reduced hospitalization and mortality, decreased SARS-CoV-2 viral load, reduced incidence of long-COVID, and better control of inflammatory responses to infection. Additionally, after flu vaccination, metformin was shown to increase flu specific antibodies in diabetics and circulating T follicular helper cells (cTfh) in non-diabetic older adults. Further, individuals vaccinated against COVID while taking metformin had reduced complications post-infection. Thus, the cumulative benefits of metformin have the potential to improve infection outcomes and overall immunological resilience in older adults.
Figure 1. Possible pathobiological mechanisms whereby neuroglia may become reactive in ME/CFS. Note the possible contribution of immune processes (including autoimmunity to GPCR), metabolic dysfunction(s), endothelial/vascular dysfunction and oxidative/nitrosative stress.
The chart appears to show the percentage change in COMPASS-31 scores for two groups: those treated with IVIG (Intravenous Immunoglobulin, n=15) and those treated with Albumin (n=12). Key observations: 1. COMPASS-31 Score Changes: • A positive percentage indicates worsening symptoms, as marked with a red upward arrow. • A negative percentage indicates improvement, as marked with a green downward arrow. 2. Group Comparison: • The IVIG group has a wider spread of changes, with some individuals showing worsening symptoms while others improve significantly. • The Albumin group appears to show more consistent improvement, with most data points below the 0% line, suggesting better outcomes in reducing COMPASS-31 scores. 3. Thresholds: • The green dotted line at -20% highlights a clinically meaningful improvement threshold.
Gastrointestinal transit times measures by wireless motil- ity capsule. Wireless motility capsules were performed in 20 female patients with postural orthostatic tachycardia syndrome (POTS) and 20 age-matched controls without POTS. All patients had formal autonomic testing to confirm or exclude POTS. Gastric transit times (GTT), small bowel transit times (SBTT), and colonic transit times (CTT) are plotted in the graph, with each patient represented by a cir- cle. The dashed lines represent the upper limit of normal, or in the case of GTT, both the upper and lower limit of normal. The percent- age with abnormal transit were compared among patients with and without POTS using Fisher’s exact test. p < 0.05 is indicated as an asterisk (*)
Table 1 https://pmc.ncbi.nlm.nih.gov/articles/PMC11348541/table/T1/
Graphic abstract Here’s a textual description of the key components: 1. Population: • Sample size: 100 individuals suspected of idiopathic MCAS. • The diagram shows a split between self-evaluations via the internet and physician-diagnosed cases. 2. Study Design: • Diagnostic MCAS criteria: 1. Medical history, signs, and symptoms. 2. Increase in serum tryptase during symptomatic episodes. 3. Response to treatment. • Duration: 12 weeks. 3. Symptoms: • Chronic continuous symptoms in the cohort: • Fatigue (57%) • Musculoskeletal pain (53%) • Abdominal pain (43%) • Pruritus (34%) • Diarrhoea (34%). 4. Diagnostic Findings: • Increased tryptase levels were detected in 2 patients. • Criteria used: a >20% increase and a rise of ≥2 ng/mL during episodes. 5. Outcomes: • Patient-reported outcome measures (PROMs) controlled complete responders to MC-mediator targeted treatment. • Results assessed with: • HADS (Hospital Anxiety and Depression Scale). • HADS+ (HADS with additional outcome measures for disease control). 6. Conclusion: • MCAS was confirmed in 2% of the suspected cases.
Response to mast cell mediator-targeted treatment based on the patient-reported outcome measures (PROMs), SAS (Symptom Activity Score), MC-QoL (Mastocytosis Quality of Life Questionnaire), and SCT (Symptom Control Test) in the study population (n = 83). The values before initiation of treatment (visit 2) and after a 6-week mast cell mediator-targeted treatment (visit 3) were compared. Nonresponse in SAS and MC-QoL means less than 30% improvement, partial response means at least 30% but less than 90% improvement, and complete response means at least 90% improvement. For SCT values less than 12 before and at least 12 points after treatment were attributed to partial response (controlled disease), SCT values of 16 points after treatment were considered complete response. Rates of patients that achieved complete, partial, and nonresponse in all three PROMs and in at least one PROM are displayed
P-PEM: individuals with ME and CFS with post-exertional malaise; P-No PEM: individuals with ME and CFS without post-exertional malaise; C-PEM: controls with post-exertional malaise; C-No PEM: controls without post-exertional malaise; log(OR): log (odds ratio).
Figure 2. Proportion of (A) post-exertional malaise (PEM) and (B) orthostatic intolerance (OI) for men and women who had PEM or OI and who were SARS-CoV-2 positive and not living with post-COVID-19 condition (PnL-PCC), SARS-CoV-2 positive and living with post-COVID-19 condition (PL-PCC), and negatives.
https://avant.org.au/resources/updated-telehealth-guidelines-new-requirements
The image shows two panels. In the first panel, a group of men are sitting around a table inside what appears to be a private jet. The table is set with McDonald’s fast food items, including burgers, fries, and drinks. Recognisable logos and packaging can be seen on the table. One of the individuals holds a box of fries while others are holding burgers or drinks. In the second panel, a closer view focuses on one man holding a McDonald’s burger box in his hands with a Coca-Cola bottle placed in front of him.
https://cvphysiology.com/blood-pressure/bp017