anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Persistent type (T) 2 airway inflammation plays an important role in the development of severe asthma. However, the molecular mechanisms leading to T2 severe asthma have yet to be fully clarified. Human normal lung epithelial cells (BEAS-2B cells) were transfected with LINC00158/BCL11B plasmid/small interfering RNA (siRNA). Levels of epithelial-mesenchymal transition (EMT)-related markers were measured using real-time qPCR (RT-qPCR) and western blot. A dual luciferase reporter assay was used to validate the targeting relationship between LINC00158 and BCL11B. The effects of LINC00158-lentivirus vector-mediated overexpression and dexamethasone on ovalbumin (OVA)/lipopolysaccharide (LPS)-induced severe asthma were investigated in mice in vivo. Our study showed that overexpression of LINC00158/BCL11B inhibited the levels of EMT-related proteins, apoptosis, and promoted the proliferation of BEAS-2B cells. BCL11B was a direct target of LINC00158. And LINC00158 targeted BCL11B to regulate EMT, apoptosis, and cell proliferation of BEAS-2B cells. Compared with severe asthma mice, LINC00158 overexpression alleviated OVA/LPS-induced airway hyperresponsiveness and airway inflammation, including reductions in T helper 2 cells factors in lung tissue and BALF, serum total- and OVA-specific IgE, inflammatory cell infiltration, and goblet cells hyperplasia. In addition, LINC00158 overexpression alleviated airway remodeling, including reduced plasma TGF-β1 and collagen fiber deposition, as well as suppression of EMT. Additionally, overexpression of LINC00158 enhanced the therapeutic effect of dexamethasone in severe asthmatic mice models. LINC00158 regulates BEAS-2B cell biological function by targeting BCL11B. LINC00158 ameliorates T2 severe asthma in vivo and provides new insights into the clinical treatment of severe asthma.
Frailty status is linked with a poorer clinical outcome, and patients with frailty are often less revascularized, even with percutaneous coronary intervention (PCI). We therefore sought to assess the impact of frailty on the clinical outcome of older patients with non-ST elevation acute myocardial infarction (NSTEMI) who underwent PCI. We prospectively enrolled 141 consecutive older patients (>75 years) admitted for NSTEMI; 104 patients underwent PCI (35 with frailty, 69 without frailty), and 37 were not revascularized (22 with frailty, 15 without). Patients with frailty were older, less frequently male, more affected by dementia and severe left ventricular dysfunction, and less treated with PCI; patients treated with PCI were younger and less affected by dementia. Thirty-day mortality rates were proportionally higher, from 3% in patients without frailty treated with PCI, to 7% in patients without frailty not treated with PCI, 17% in patients with frailty treated with PCI, and 48% in patients with frailty not treated with PCI (p <0.05). Similarly, 6-month mortality rates were proportionally higher (12%, 29%, 37%, and 71%). At multivariable analysis, frail status was associated to a sixfold increased risk of mortality at 30 days; at 6 months, frail status was associated to a 3.4-fold risk of death (p <0.01), but PCI was also associated to a lower risk of mortality (odds ratio 0.2, p <0.01). In an observational study in older patients with NSTEMI, frail status is associated to a poorer outcome, whereas PCI is associated to a better long-term outcome. A careful selection of patient suitable for revascularization by PCI may be useful in improving outcomes of older patients with frailty with NSTEMI.
Disclosed is a compound capable of specifically binding with β amyloid protein. The compound has thereon a nuclide having a large cross section for capturing thermal neutrons and the compound is capable of specifically binding with β amyloid protein. The nature of the compound allows same to be used in conjunction with a neutron capturing therapeutic apparatus to eliminate β amyloid protein. Similarly, when the compound is marked using radioactive element 11C, the compound can also be used in conjunction with PET/CT for determining the part of the brain at where β amyloid protein is deposited, thus being used for diagnosing Alzheimer's disease. Also disclosed is a preparation method for the compound. The beneficial effect of the present invention is such that the compound capable of specifically binding with β amyloid protein is provided, thus making the treatment and diagnosis of Alzheimer's disease more targeted.
Deficiency of adenosine deaminase 2 (DADA2) is an inborn error of immunity caused by loss-of-function mutations in the adenosine deaminase 2 (ADA2) gene. Clinical manifestations of DADA2 include vasculopathy and immuno-hematological abnormalities, culminating in bone marrow failure. A major gap exists in our knowledge of the regulatory functions of ADA2 during inflammation and hematopoiesis, mainly due to the absence of an ADA2 orthologue in rodents. Exploring these mechanisms is essential for understanding disease pathology and developing new treatments. Zebrafish possess two ADA2 orthologues, cecr1a and cecr1b, with the latter showing functional conservation with human ADA2. We establish a cecr1b-loss-of-function zebrafish model that recapitulates the immuno-hematological and vascular manifestations observed in humans. Loss of Cecr1b disrupts hematopoietic stem cell specification, resulting in defective hematopoiesis. This defect is caused by induced inflammation in the vascular endothelium. Blocking inflammation, pharmacological modulation of the A2r pathway, or the administration of the recombinant human ADA2 corrects these defects, providing insights into the mechanistic link between ADA2 deficiency, inflammation and immuno-hematological abnormalities. Our findings open up potential therapeutic avenues for DADA2 patients.
High blood pressure, or hypertension, is a serious problem in the African-American (AA) population which affects nearly 7 of every 10 AAs in our area. Previously the investigators showed that a significant number of AAs held onto or retained salt during mental stress (sodium retainers). The investigators believe that the increased salt load and resulting blood pressure load contributes to the eventual development of hypertension in these individuals. The purpose of this study is to find out if this response is due to the direct stimulation of the kidney (the organ that controls salt levels in the body, by the brain). To do this, the investigators will determine if a drug that stops the connection between the brain and the kidney during mental stress will prevent sodium retention in sodium retainers. Prazosin is an alpha adrenergic receptor blocker that has been approved by the Food and Drug Administration (FDA). None of the subjects who participate in this study have high blood pressure. The subjects will not know which testing week is the drug week and which is the placebo week. Participants will test twice during this study, one of the weeks they will take Prazosin daily and the other week of testing they will take a placebo (sugar pill) daily in order to see if Prazosin changes how their body handles salt during stress. The participants will not be informed as to which of the testing weeks is the Prazosin week or the placebo week. This study will involve a screening visit, two first dose visits and two testing weeks over an approximate 5 week period (this include a one week "washout" period). Each testing week will have a 3 day salt-controlled diet prior to testing and an approximate 3-hour testing period on Day 4. The 3-hour testing period will include 10 minutes of a baseline rest, 45 minutes of mild stress (competitive video game), and 45 minutes of a recovery rest. A total of 4 blood and 4 urine samples will be collected during the 3-hour period. Each blood draw will consist of about 4 teaspoons for a total of 16 teaspoons. If the participants are female, a pregnancy test will be performed at the beginning of each testing visit (screening, first dose-1, test day-1, first dose-2 and test day-2) to confirm that they are not pregnant. Muscle sympathetic nerve activity will be measured during testing through the insertion of electrodes just below the knee on the outer part of the right leg. Additionally, an IV infusion will be administered for the phenylephrine challenge to insure total blockade of the sympathetic nervous system.
The invention relates to a traditional Chinese medicine compound preparation, and discloses an immunity-enhancing capsule. The capsule is prepared from the following components in parts by weight: 230-260 parts of grape skin extract, 15-30 parts of vitamin C, 50-70 parts of magnesium stearate and 50-70 parts of mannitol. The immunity enhancing capsule has the advantages of good immunity regulating effect, no toxic or side effect and high safety. Resveratrol which is contained in grape skin and is richer than that in grape pulp and grape seeds is a polyhydroxyphenol compound, is capable of preventing cardiovascular and cerebrovascular diseases, and has an extremely strong cancer resistance. The invention further discloses a method for preparing the immunity-enhancing capsule. The preparation method is easy to operate, is environmentally friendly, economic, effective and non-toxic, and has a wide application prospect.
Patients receive recombinant Flt3 ligand (CDX-301) SC on days -7 to -1, 1-3, and 22-28 of cycle 1 and only on days 1-3 of cycle 2. Patients also receive CDX-1401 SC or ID on day 1 of each cycle and poly-ICLC SC on days 1-2 of each cycle. Treatment repeats every 28 days for 4 cycles in the absence of disease progression or unacceptable toxicity.
Autoimmune diseases of the nervous system are a type of disease in which the human immune system mistakenly attacks its own nervous system, causing damage to the structure and function of the nervous system. Its main pathogenic mechanism is that autoimmune cells, autoantibodies and other immune molecules directly or indirectly attack the nervous system. Autoimmune diseases of the nervous system can affect the central nervous system, peripheral nervous system and neuromuscular junction, leading to pathological changes such as neuronal or axonal damage, demyelination, and destruction of neuromuscular junction. Autoimmune diseases of the nervous system are relatively rare, with a wide range of damage and complex and diverse clinical manifestations. They have the characteristics of complexity of immune diseases and high mortality and disability of nervous system diseases. At present, the understanding of the disease is limited, and some diseases are difficult to diagnose. Globally, it is a major cause of disability in young and middle-aged people and can cause huge social and economic burdens. However, due to the lack of a series of relatively reliable prognostic predictors, it is impossible to carry out personalized immunotherapy to achieve the best therapeutic effect, and serious adverse events may occur. Proteomics, metabolomics, intestinal microorganisms and intestinal high-throughput targeted metabolomics, exosomes, miRNA sequencing, single-cell transcriptome sequencing and other detection methods and lymphocyte subsets have been hot topics in the study of various diseases in recent years. It has been found that abnormalities in the expression and function of certain genes, proteins, metabolites, miRNAs, intestinal flora and lymphocyte subsets are closely related to the occurrence and development of many diseases and the functional disability of patients, and have a good suggestive effect on prognosis judgment.
A process for isolating substantially pure natural L-.beta.-3-indolylalanine (L-.beta.-3) from a mixture of amino acids, such as a protein hydrolysate, is described. A protein hydrolysate, for example of casein or soy protein, is passed over a polymeric resin attractive to aromatic amino acids but not attractive to aliphatic amino acids. The aromatic amino acids are retained on the resin while the aliphatic amino acids pass over the resin and are collected. The resin is then washed with water to displace any residual aliphatic acids which may be physically associated with but not bound to the resin. Thereafter, the resin is eluted with a dilute acid to displace L-phenylalanine and L-tyrosine and provide a solution thereof while allowing L-.beta.-3 to be retained on the resin. The resin is then further eluted with a dilute base to displace L-.beta.-3 from the resin and provide a solution of L-.beta.-3. Substantially pure natural L-.beta.-3 is recoverable from this solution.
Primary aldosteronism (PA), a significant and curable cause of secondary hypertension, is seen in 5-10% of hypertensive patients, with its prevalence contingent upon the severity of the hypertension. The principal aetiologies of PA include bilateral idiopathic hypertrophy (BIH) and aldosterone-producing adenomas (APAs), while the less frequent causes include unilateral hyperplasia, familial hyperaldosteronism (FH) types I-IV, aldosterone-producing carcinoma, and ectopic aldosterone synthesis. This condition, characterised by excessive aldosterone secretion, leads to augmented sodium and water reabsorption alongside potassium loss, culminating in distinct clinical hallmarks: elevated aldosterone levels, suppressed renin levels, and hypertension. Notably, hypokalaemia is present in only 28% of patients with PA and is not a primary indicator. The association of PA with an escalated cardiovascular risk profile, independent of blood pressure levels, is notable. Patients with PA exhibit a heightened incidence of cardiovascular events compared to counterparts with essential hypertension, matched for age, sex, and blood pressure levels. Despite its prevalence, PA remains frequently undiagnosed, underscoring the imperative for enhanced screening protocols. The diagnostic process for PA entails a tripartite assessment: the aldosterone/renin ratio (ARR) as the initial screening tool, followed by confirmatory and subtyping tests. A positive ARR necessitates confirmatory testing to rule out false positives. Subtyping, achieved through computed tomography and adrenal vein sampling, aims to distinguish between unilateral and bilateral PA forms, guiding targeted therapeutic strategies. New radionuclide imaging may facilitate and accelerate such subtyping and localisation. For unilateral adrenal adenoma or hyperplasia, surgical intervention is optimal, whereas bilateral idiopathic hyperplasia warrants treatment with mineralocorticoid antagonists (MRAs). This review amalgamates established and emerging insights into the management of primary aldosteronism.
The study is a two center 12-week double-blind, placebo-controlled trial of adalimumab in patients with moderate to severely active axial spondyloarthritis (without radiological sacroiliitis) who have had an inadequate response to who are or intolerant to NSAID therapy. Patients may have been treated in the past with concomitant DMARDs. For these patients a washout period of at least 4 weeks is necessary. If Leflunomide was discontinued, it should be stopped at least 3 months or should be washed out within 4 weeks before study start. Patients who have been treated previously with approved biologics are allowed to enter the study if they failed due to lack of efficacy and/or intolerance. The placebo-controlled treatment period of 12 weeks will be followed by an open-label maintenance therapy up to Week 52. Following screening and baseline evaluations, patients will be assessed at Weeks 2, 4, 8, and 12. During the maintenance therapy visits will be performed at Weeks 16, 20 and every eight weeks thereafter.Efficacy and safety measurements will be recorded throughout the entire 52 weeks study.Non-responders (fail to reach ASAS 40) at and after week 12 of open label therapy (at week 24), will be eligible for adalimumab dose escalation to 40 mg weekly.The study will be followed by a 24 weeks follow up phase. During this period the patients will be assessed every eight weeks.
The patient will undergo NIF-guided RAMIE using ICG dye using the standard Ivor-Lewis approach. This will be a two-stage operation involving a first stage through a 5-port robotic approach through the abdomen to achieve a proximal gastrectomy and D2 nodal dissection. A feeding jejunostomy would not be inserted, as per the enhanced recovery pathway for esophagectomy. In addition, the vascularization of the conduit can be confirmed using the near-infrared camera of the robot with the ICG dye. The second stage of the operation will involve a 4-port robotic approach through the right chest to achieve thoracic nodal dissection, esophagectomy, and a hand-sewn anastomosis between the residual esophagus and the gastric conduit at the level of the azygous vein. During this second stage of the operation, NIF with ICG dye will be used to visualize the vascular supply of the gastric conduit, and assess the gastric conduit for any perfusions to potentially reduce anastomotic leaks.
AIMS: The ultimate goal is to personalize brain stimulation for stroke so outcomes of the upper limb can be maximized for each individual patient. Even though stimulation is one of the most well studied methods to augment plasticity and boost recovery, it is still not approved for outpatient therapy. Benefits of stimulation are weak and variable especially in patients who suffer from greater damage and disability. The key limitation of the standard approach is its generic assumptions about plasticity. The current standard assumes that ipsilesional primary motor cortex (iM1) can impact recovery for patients in all ranges of severity, and intact, contralesional cortices always compete with iM1 to inhibit recovery. But, these long-standing assumptions fail to consider that iM1 or its pathways are damaged in a majority (58-83%) of patients. As such, the potential of iM1 would be weak and variable, and patients will have little option but to rely on plasticity of intact, contralesional cortices that are more likely to survive. Of all surviving cortices, contralesional dorsal premotor cortex (cPMd) expresses plasticity most consistently. cPMd is activated in movement of the paretic limb when activating iM1 is less likely. cPMd even reduces its competition with iM1 and offers its ipsilateral pathways instead to support recovery of the proximal paretic limb when pathways from iM1 are largely damaged.

Several groups including the investigator have recently theorized that personalizing stimulation so as to selectively stimulate iM1 in mild, and cPMd in patients with greater severity would help generalize benefits of stimulation. These theoretical claims, however, remain untested since several gaps exist. For instance, what is the cut-off level of severity that stratifies those who respond to stimulation of iM1 from those who respond to stimulation of cPMd? Even then, are substrates for 'personalized' stimulation same as the substrates that express plasticity in recovery, i.e. if patients benefit from stimulation of cPMd, do they express contralesional plasticity in recovery? Here, the investigator premise that variances in expressions of plasticity can explain how to best stratify patients for robust, personalized stimulation.
Problem is to provide the agent of keratotic plug Regeneration, keratotic plug Regeneration method and the keratotic plug Regeneration kit that can not cause pachylosis and effectively suppress the regeneration of keratotic plug. Solution: a kind of keratotic plug Regeneration agent, it is characterized in that, contain: (a) specific acid (for example, lactic acid, butanedioic acid, citric acid etc.) or the specific surfactant of its salt, (b) is (for example, fatty acid alkali, high alkyl sulfate salt, polyoxy alkylidene phytosterol etc.) and (c) specific anti-pachylosis improver (for example, POEPOP dimethyl ether, tranexamic acid, pantothenyl ethyl ether, trimethylglycine, glycylglycine etc.). Skin used to the keratotic plug Regeneration method of the keratotic plug Regeneration agent that after the skin cleaner that comprises POE fatty acid ester, dermal administration is comprised to specific acid (for example, lactic acid, butanedioic acid, citric acid etc.) or its salt and comprised aforementioned skin cleaner and the keratotic plug Regeneration kit of keratotic plug Regeneration agent.
Primary phase of the transition from the fetal to post-natal period is the most important, vulnerable and stressful phase in human life. Hence, care methods that facilitate better adaptation of neonates with early post¬natal environment have an important role in growth of newborns. Attachment is a unique relationship between the parents and their infants that begins during pregnancy when fetus grows in uterus and continues to the postnatal period with the relationship of mother and baby. This reciprocal parent-infant relationship is an essential element of the attachment process that helps relaxation of both mother and the infant. Kangaroo mother care has facilitated infant growth and decreased morbidities and hospital stay. Adding massage therapy may potentiate the kangaroo mother care benefits and better growth in preterm low birth weight infants admitted in neonatal intensive care unit. However, there is a very few published studies from Bangladesh regarding this. The objective of this study is to evaluate whether kangaroo mother care plus massage therapy is associated with better growth of preterm low birth weight infants.

This study will be conducted in the department of Neonatology in Bangabandhu Sheikh Mujib Medical University over a period of eighteen months. After detailed history taking and thorough general and systemic examination the newborn will enter in to intervention or control group after taking informed written consent. Randomization will be done by random allocation software (version 2.0 developed by Mahmood Saghaei, Iran). Patient will be enrolled according to the inclusion and exclusion criteria. Thereafter control group will receive standard kangaroo mother care and intervention group will get massage therapy along with kangaroo mother care, up to discharge both group will be meticulously monitored by the investigator. Data will be collected by structured questionnaire and analysis will be done by The Statistical Package for Social Sciences (SPSS), version 25.
Disclosed are a method for enhancing capacity to kill an abnormal cell, a pharmaceutical composition and a method for enhancing ADCC in a patient undergoing an antibody drug therapy. The method of treating a patient comprises a step of administering to the patient an NK cell in combination with an antibody drug. The NK cell comprises an HANK cell. Acquisition of the HANK cell comprises: using an empty cell envelope carrying a cytokine to perform in vitro activation of an in vivo NK cell. The NK cell comprising the HANK cell is administered to the patient in combination with the antibody drug. The HANK cell and the antibody drug can mutually enhance their capacities to kill abnormal cells, thereby significantly enhancing treatment effect.
CBT: This is the control arm of the study. This included 5 weekly sessions of CBT therapy via telephone.
Lotrafilcon B multifocal soft contact lenses with comfort additive worn in both eyes on an extended wear basis. Extended wear is defined as up to 6 days continuous wear (including while sleeping/overnight).
Participants who completed 96 weeks of CAB 30 mg + ABC/3TC QD regimen in Maintenance Period transitioned to Extension Period and received an optimized loading dose of CAB LA 600 mg+RPV LA 900 mg IM at Week 100 and Week 104 followed by CAB LA 600 mg+RPV LA 900 mg IM-Q8W in the Extension Phase. Participants were followed up until end of Extension Period.
An ultrasound guided Femoral Nerve catheter will be inserted. 20ml of 1.5% lidocaine will be administered.
The standard of care at the University of Virginia Medical Center for liver transplantation patients is a 3.375 gram dose of piperacillin / tazobactam (Zosyn®) at the time of induction of anesthesia, though this dose may be adjusted for renal insufficiency. This dose is repeated during the operation every six hours.