anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Diabetes mellitus with its systemic complications has been an enormous health treat to the world population today. In the US, the ophthalmic related complications has been estimated to cause up to 4.2 million (28.5%) people in 2005 till 2008 to suffer from blindness. One of the most common causes of visual acuity loss in patients with diabetes mellitus is diabetic macular edema (DME).

The gold standard of treatment for clinically significant macular edema (CSME), a form of DME, is through focal and grid laser as shown by the Early Treatment Diabetic Retinopathy Study. The development of newer drugs such as anti vascular endothelial growth factors anti (VEGFs), an alternative to laser treatment, has become a topic of interest in the recent years. Other alternative to treatment of DME is steroid such as triamcinolone injection and dexamethasone injections. However, both anti VEGFs and steroids are expensive and not readily available in all centres. Both types of medications require repeated treatment and the route of administration through intravitreal also poses risk of endophthalmitis, lens injury, retinal detachment, vitreous hemorrhage, increase in intraocular pressure and cataract.

The pathophysiology of DME is not fully understood yet. It was suggested that it is likely to be a chronic low-grade inflammation. Through this theory, topical non-steroidal anti-inflammatory drugs (NSAIDs) have been used to treat DME. The investigators postulate that the addition of topical NSAIDs in patients receiving standard treatment of laser therapy may help to improve the outcome of patients with DME. It has the advantage of no needles involved, convenient, easy to use and minimal side effects. The aim of this study is to evaluate the outcome of visual acuity and macular thickness at 3 months post treatment between laser monotherapy and combination of laser and topical nepafenac in DME.
Rheumatoid arthritis (RA) is an autoimmune disease involving T and B lymphocytes. Autoantibodies contribute to joint deterioration and worsening symptoms. Adenosine deaminase (ADA), an enzyme in purine metabolism, influences adenosine levels and joint inflammation. Inhibiting ADA could impact RA progression. Intracellular ATP breakdown generates adenosine, which increases in hypoxic and inflammatory conditions. Lymphocytes with ADA play a role in RA. Inhibiting lymphocytic ADA activity has an immune-regulatory effect. Synovial fluid levels of ADA are closely associated with the disease's systemic activity, making it a useful parameter for evaluating joint inflammation. Flavonoids, such as quercetin (QUE), are natural substances that can inhibit ADA activity. QUE demonstrates immune-regulatory effects and restores T-cell homeostasis, making it a promising candidate for RA therapy. In this review, we will explore the impact of QUE in suppressing ADA and reducing produced the inflammation in RA, including preclinical investigations and clinical trials.
The investigators will acquire de-novo brain MRI and time-of-flight MRA in randomly selected surviving Northern Manhattan Study (NOMAS) participants. The investigators aim to include at 20 participants with dementia and 40 participants without (as determined by the ongoing NOMAS procedures). In addition to MRI, participants in this group will have three PET studies.
Pterostilbene (PTE), a naturally occurring phenolic compound primarily found in blueberries, demonstrates neuroprotective properties. However, the role of PTE in Parkinson's disease (PD) remains unclear. This study aimed to investigate the neuroprotective role of PTE in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD animal model. Our findings demonstrate that administering PTE effectively reversed the diminished levels of dopamine in the striatum, thereby ameliorating motor impairments in the MPTP model. Moreover, PTE administration mitigated the loss of dopaminergic (DA) neurons and reduced the upregulation of α-synuclein (α-syn) induced by MPTP. Mechanistic analysis revealed that PTE administration inhibited the activation of microglia and astrocytes, as well as pro-inflammatory factors such as TNF-α and IL-1β in the MPTP model. Additionally, PTE administration decreased MPTP-induced levels of reactive oxygen species (ROS) and malondialdehyde (MDA), while increasing total antioxidant capacity (TAOC) and superoxide dismutase (SOD) activity, thereby attenuating oxidative stress. Collectively, these findings demonstrate that PTE exerts neuroprotective effects in the MPTP mouse model of PD by suppressing neuroinflammation and oxidative stress. Thus, PTE holds promise as a therapeutic agent for PD.
Alzheimer's disease (AD) is a global medical challenge. Studies have shown that neurotoxicity caused by pathological aggregation of β-amyloid (Aβ) is an important factor leading to AD. Therefore, inhibiting the pathological aggregation of Aβ is the key to treating AD. The recombinant human HspB5-ACD structural domain protein (AHspB5) prepared by our group in the previous period has been shown to have anti-amyloid aggregation effects, but its inability to penetrate biological membranes has limited its development. In this study, we prepared a recombinant fusion protein (T-AHspB5) of TAT and AHspB5. In vitro experiments showed that T-AHspB5 inhibited the formation of Aβ1-42 protofibrils and had the ability to penetrate the blood-brain barrier; in cellular experiments, T-AHspB5 prevented Aβ1-42-induced oxidative stress damage, apoptosis, and inflammatory responses in neuronal cells, and its mechanism of action was related to microglia activation and mitochondria-dependent apoptotic pathway. In animal experiments, T-AHspB5 improved memory and cognitive dysfunction and inhibited pathological changes of AD in APP/PS1 mice. In conclusion, this paper is expected to reveal the intervention mechanism and biological effect of T-AHspB5 on pathological aggregation of Aβ1-42, provide a new pathway for the treatment of AD, and lay the foundation for the future development and application of T-AHspB5.
INTRODUCTION AND OBJECTIVES: Recent studies have indicated a potential association of hypertension with Hashimoto's thyroiditis (HT) and other autoimmune diseases, yet the impact of antihypertensive drugs on HT risk is not well understood.
METHODS: We employed a drug-target Mendelian randomization approach to investigate the prolonged impact of 9 classes of antihypertensive medications on HT susceptibility in European and Asian populations. Genetic variants close to or within genes associated with the drug targets and systolic blood pressure (SBP) were utilized to mimic the effects of antihypertensive medications. We focused on drugs linked to a lower risk of coronary artery disease for our main analysis. We gathered genetic data on SBP and HT risk from comprehensive genome-wide association studies available for European and Asian groups. For a supplementary analysis, we used expression quantitative trait loci (eQTLs) related to drug target genes as proxies.
RESULTS: Our analysis revealed that the use of calcium channel blockers (CCBs) is linked to a reduced risk of HT in both European (OR [95% CI]: 0.96 [0.95 to 0.98] per 1 mmHg decrease in SBP; p = 3.51×10-5) and Asian populations (OR [95% CI]: 0.28 [0.12, 0.66]; p = 3.54×10-3). Moreover, genetically mimicking the use of loop diuretics (OR [95% CI]: 0.94 [0.91, 0.97]; p = 3.57×10-5) and thiazide diuretics (0.98 [0.96, 0.99]; p = 3.83×10-3) showed a significant association with a decreased risk of HT only in European population. These outcomes were confirmed when eQTLs were employed to represent the effects of antihypertensive medications.
CONCLUSION: The study suggests that CCBs and diuretics could potentially reduce the risk of HT in different populations. Additional research is needed to assess the feasibility of repurposing antihypertensive medications for the prevention of HT.
OBJECTIVE: This study aimed to investigate the changes of follicular helper T (TFH) and follicular regulatory T (TFR) cell subpopulations in patients with non-small cell lung cancer (NSCLC) and their significance.
METHODS: Peripheral blood was collected from 58 NSCLC patients at different stages and 38 healthy controls. Flow cytometry was used to detect TFH cell subpopulation based on programmed death 1 (PD-1) and inducible co-stimulator (ICOS), and TFR cell subpopulation based on cluster determinant 45RA (CD45RA) and forkhead box protein P3 (FoxP3). The levels of interleukin-10 (IL-10), interleukin-17a (IL-17a), interleukin-21 (IL-21), and transforming growth factor-β (TGF-β) in the plasma were measured, and changes in circulating B cell subsets and plasma IgG levels were also analyzed. The correlation between serum cytokeratin fragment antigen 21-1 (CYFRA 21-1) levels and TFH, TFR, or B cell subpopulations was further explored.
RESULTS: The TFR/TFH ratio increased significantly in NSCLC patients. The CD45RA+FoxP3int TFR subsets were increased, with their proportions increasing in stages II to III and decreasing in stage IV. PD-1+ICOS+TFH cells showed a downward trend with increasing stages. Plasma IL-21 and TGF-β concentrations were increased in NSCLC patients compared with healthy controls. Plasmablasts, plasma IgG levels, and CD45RA+FoxP3int TFR cells showed similar trends. TFH numbers and plasmablasts were positively correlated with CYFRA 21-1 in stages I-III and negatively correlated with CYFRA 21-1 in stage IV.
CONCLUSION: Circulating TFH and TFR cell subpopulations and plasmablasts dynamically change in different stages of NSCLC, which is associated with serum CYFRA 21-1 levels and reflects disease progression.
People with Multiple Sclerosis (MS) face numerous physical and mental symptoms as well as emotional and social challenges. The fact that the disease usually occurs in young adulthood, when individuals are most productive, causes disability, its unpredictable and variable nature, and the lack of a known treatment make it difficult to live with MS and accept the disease. The physical, cognitive, behavioral and social changes that occur with the disease affect daily life activities, well-being. and greatly affects the quality of life. There are various interventions developed to improve the adaptation processes of individuals diagnosed with a chronic disease such as MS, to prevent and reduce psychiatric symptoms, and to increase quality of life and well-being. One of the intervention approaches is positive psychological interventions from the field of positive psychology. Positive psychological interventions are a psychosocial intervention method based on the systematic completion of certain activities aimed at increasing positive emotions, thoughts and behaviors. Since the interventions focus on strengthening positive mental states rather than reducing psychological symptoms, they also have an advantage over traditional interventions in that they can be applied to both sick and non-patients. However, it appears that positive psychological intervention studies have just begun to be implemented in patients with MS. In our country, no study has been found using positive psychological intervention in MS patients. This study aims to determine the effectiveness of positive psychological interventions on the quality of life and well-being levels of patients with multiple sclerosis.
The prevalence of chronic kidney disease (CKD) is increasing worldwide, making the disease an urgent clinical challenge. Caloric restriction has various anti-aging and organ-protective effects, and unraveling its molecular mechanisms may provide insight into the pathophysiology of CKD. In response to changes in nutritional status, intracellular nutrient signaling pathways show adaptive changes. When nutrients are abundant, signals such as mechanistic target of rapamycin complex 1 (mTORC1) are activated, driving cell proliferation and other processes. Conversely, others, such as sirtuins and AMP-activated protein kinase, are activated during energy scarcity, in an attempt to compensate. Autophagy, a cellular self-maintenance mechanism that is regulated by such signals, has also been reported to contribute to the progression of various kidney diseases. Furthermore, in recent years, ketone bodies, which have long been considered to be detrimental, have been reported to play a role as starvation signals, and thereby to have renoprotective effects, via the inhibition of mTORC1. Therefore, in this review, we discuss the role of mTORC1, which is one of the most extensively studied nutrient-related signals associated with kidney diseases, autophagy, and ketone body metabolism; and kidney energy metabolism as a novel therapeutic target for CKD.
Patients receive cabozantinib S-malate PO QD on days 1-21 and pembrolizumab IV over 30 minutes on day 1. Cycles repeat every 21 days for up to 2 years in the absence of disease progression or unacceptable toxicity.
Neck-specific exercise with digital web-based support and four visits to a physiotherapist. Neck-specific exercise will be performed based on a well-structured framework of neck-specific exercise for facilitation of deep neck muscles, increased muscle coordination, improved neck posture and increased neck muscle endurance. Plus additional convergence dialogue meeting as treatment arm no 1.
Psoriasis is a chronic inflammatory skin disease commonly accompanied by joint involvement known as psoriatic arthritis (PsA) \[1\]. PsA is a subgroup of spondyloarthritis and is characterized by peripheral arthritis, dactylitis, enthesitis and spondylitis. Axial involvement, which occurs in approximately 40% of PsA patients may affect the entire spine, particularly the sacroiliac joint, leading to reduced cervical rotation, lateral flexion and anterior flexion of the spine \[2,3\]. Exercise interventions in PsA primarily aim to relieve pain, improve mobility and enhance functional capacity \[4\]. Mat Pilates exercises have been demonstrated as a safe and beneficial intervention in various rheumatic diseases, exhibiting significant improvements in functional status, fatigue, disease activity, pain, and overall quality of life \[5-7\]. Additionally, Pilates has been reported as effective in maintaining and enhancing spinal mobility \[8,9\]. However, despite these favorable outcomes, the efficacy of Pilates exercises in PsA remains unexplored.

The aim of this study is to investigate the effectiveness of mat pilates exercises in psoriatic arthritis patients with axial involvement.
INTRODUCTION: Brain atrophy is a well-established MRI outcome for predicting clinical progression and monitoring treatment response in persons with multiple sclerosis (pwMS) at the group level. Despite the important progress made, the translation of brain atrophy assessment into clinical practice faces several challenges.
AREAS COVERED: In this review, the authors discuss technical- and subject-related barriers for implementing brain atrophy assessment as part of the clinical routine at the individual level. Substantial progress has been made to understand and mitigate technical barriers behind MRI acquisition. Numerous research and commercial segmentation techniques for volume estimation are available and technically validated, but their clinical value has not been fully established. A systematic assessment of subject-related barriers, which include genetic, environmental, biological, lifestyle, comorbidity, and aging confounders, is critical for the interpretation of brain atrophy measures at the individual subject level. Educating both medical providers and pwMS will help better clarify the benefits and limitations of assessing brain atrophy for disease monitoring and prognosis.
EXPERT OPINION: Integrating brain atrophy assessment into clinical practice for pwMS requires overcoming technical and subject-related challenges. Advances in MRI standardization, artificial intelligence, and clinician education will facilitate this process, improving disease management and potentially reducing long-term healthcare costs.
The current invention discloses novel approaches to help individuals defend against headaches and body pains with orally-delivered cyanocobalamin, methylcobalamin, adenosylcobalamin, and combinations thereof. Original clinical research conducted by the inventor on almost 2,000 humans yielded surprising and unexpected results showing differences in the frequency and severity of pains in the head and the body favoring cyanocobalamin patients over placebo. In one FDA-approved Phase III study on 1,551 patients, 4.4 percent of headaches and body pains were rated as "Severe" in the cyanocobalamin group versus 11.5 percent in the placebo group. Once inside the body cyanocobalamin is converted to methylcobalamin and adenosylcobalamin, but not to hydroxocobalamin. One preferred embodiment of the current invention is a once daily dissolving medication that is placed on the tongue and swallowed, and contains combinations of cyanocobalamin, methylcobalamin, and adenosylcobalamin in amounts that are effective in defending the individual against headache and body pain. The current invention provides the patient's mitochondria with sufficient concentrations of essential micronutrients to survive, increase in number and manufacture the chemical energy (ATP) that is required to prevent the brief vasoconstriction followed by vasodilation associated with headache and body pain.
Renal Toxicity

Long-term administration of NSAIDs has resulted in renal papillary necrosis and other renal injury. Renal toxicity has also been seen in patients in whom renal prostaglandins have a compensatory role in the maintenance of renal perfusion. In these patients administration of an NSAID may cause a dose-dependent reduction in prostaglandin formation and, secondarily, in renal blood flow, which may precipitate overt renal decompensation. Patients at greatest risk of this reaction are those with impaired renal function, dehydration, hypovolemia, heart failure, liver dysfunction, salt depletion, those taking diuretics and angiotensin-converting enzyme (ACE) inhibitors or ARBs, and the elderly. Discontinuation of NSAID therapy is usually followed by recovery to the pretreatment state. 

Sumatriptan and naproxen sodium tablets should be discontinued if clinical signs and symptoms consistent with renal disease develop or if systemic manifestations occur. 

Sumatriptan and naproxen sodium tablets are not recommended for use in patients with severe renal impairment (creatinine clearance [CrCl] <30 mL/min) unless the benefits are expected to outweigh the risk of worsening renal function [see Use in Specific Populations (8.6), Clinical Pharmacology (12.3)]. If sumatriptan and naproxen sodium tablets are used in patients with advanced renal disease, monitor patients for signs of worsening renal function. Monitor renal function in patients with mild (CrCl = 60 to 89 mL/min) or moderate (CrCl = 30 to 59 mL/min) renal impairment, preexisting kidney disease, or dehydration. 

The renal effects of sumatriptan and naproxen sodium tablets may hasten the progression of renal dysfunction in patients with preexisting renal disease. 

Correct volume status in dehydrated or hypovolemic patients prior to initiating sumatriptan and naproxen sodium tablets. Monitor renal function in patients with renal or hepatic impairment, heart failure, dehydration, or hypovolemia during use of sumatriptan and naproxen sodium tablets [see Drug Interactions (7)]. Avoid the use of sumatriptan and naproxen sodium tablets in patients with advanced renal disease unless the benefits are expected to outweigh the risk of worsening renal function. If sumatriptan and naproxen sodium tablets are used in patients with advanced renal disease, monitor patients for signs of worsening renal function. 

Hyperkalemia

Increases in serum potassium concentration, including hyperkalemia, have been reported with the use of NSAIDs, even in some patients without renal impairment. In patients with normal renal function, these effects have been attributed to a hyporeninemic-hypoaldosteronism state.
Arteries and veins develop different types of occlusive diseases and respond differently to injury. The biological reasons for this discrepancy are not well understood, which is a limiting factor for the development of vein-targeted therapies. This study contrasts human peripheral arteries and veins at the single-cell level, with a focus on cell populations with remodeling potential. Upper arm arteries (brachial) and veins (basilic/cephalic) from 30 organ donors were compared using a combination of bulk and single-cell RNA sequencing, proteomics, flow cytometry, and histology. The cellular atlases of six arteries and veins demonstrated a 7.8× higher proportion of contractile smooth muscle cells (SMCs) in arteries and a trend toward more modulated SMCs. In contrast, veins showed a higher abundance of endothelial cells, pericytes, and macrophages, as well as an increasing trend in fibroblasts. Activated fibroblasts had similar proportions in both types of vessels but with significant differences in gene expression. Modulated SMCs and activated fibroblasts were characterized by the upregulation of MYH10, FN1, COL8A1, and ITGA10. Activated fibroblasts also expressed F2R, POSTN, and COMP and were confirmed by F2R/CD90 flow cytometry. Activated fibroblasts from veins were the top producers of collagens among all fibroblast populations from both types of vessels. Venous fibroblasts were also highly angiogenic, proinflammatory, and hyper-responders to reactive oxygen species. Differences in wall structure further explain the significant contribution of fibroblast populations to remodeling in veins. Fibroblasts are almost exclusively located outside the external elastic lamina in arteries, while widely distributed throughout the venous wall. In line with the above, ECM-targeted proteomics confirmed a higher abundance of fibrillar collagens in veins vs. more basement ECM components in arteries. The distinct cellular compositions and transcriptional programs of reparative populations in arteries and veins may explain differences in acute and chronic wall remodeling between vessels. This information may be relevant for the development of antistenotic therapies.
The invention discloses attapulgite/jasmine flower/green tea toothpaste and a production method thereof. The technical proposal is that: the production method comprises the following steps: steaming for enzyme deactivation, preparing ingredients, low-speed stirring, pulverization and pulping, milling, high-speed stirring, vacuum degassing and packaging. Through the steps, finished products of attapulgite/jasmine flower/green tea toothpaste are obtained. The attapulgite/jasmine flower/green tea toothpaste contains pasty attapulgite clay, fresh green tea, fresh jasmine flower, fresh magnolia flower, sodium dodecylsulfate, potassium sorbate, borneol and deionized water. The invention utilizes pasty attapulgite clay as a major ingredient, has no addition of abrasives, adhesives and humectant, and can improve toothpaste quality while reducing production cost. Pulverized and milled Plant fibers can not only increase the viscosity of the toothpaste but also improve the abrasion effect and stability of the toothpaste. The inventive mothed is suitable for the production of attapulgite/jasmine flower/green tea toothpaste, herbal toothpaste and other medicinal toothpaste.