anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
PROBLEM TO BE SOLVED: To form an excellent water repellent and oil repellent film by using a polymer containing a specific amount of a repeating unit derived from a fluorine-based (meth)acrylate and a repeating unit derived from a silicon- containing polymerizable compound. SOLUTION: A copolymer of the present invention comprises 5-99 pts.wt. of a repeating unit derived from a fluorine-based (meth)acrylate, 95-1 pts.wt. of a repeating unit derived from at least one silicon-containing polymerizable compound selected from a mercapto-modified silicone, an azo group-containing silicone and a polymerizable silane and 1-50 pts.wt. of a repeating unit derived from at least one non-fluorine-based monomer selected from a polyalkylene glycol (meth)acrylate, an alkyl (meth)acrylate and an macromonomer thereof. The fluorine-based (meth)acrylate is a monomer represented by formula I (Rf is a 6-16C polyfluoroalkyl or the like; A is a 1-4C alkylene, formula II (R<1> is a 1-4C alkyl; R<2> is a 1-4C alkylene) or the like).
* Mannitol Injection is for intravenous use only, preferably into a large central vein [see Warnings and Precautions (5.6), Description (11)].
  * Prior to administration of Mannitol Injection, evaluate renal, cardiac and pulmonary status of the patient and correct fluid and electrolyte imbalances [see Dosage and Administration (2.2)].
  * Do not administer Mannitol Injection simultaneously with blood products through the same administration set because of the possibility of pseudoagglutination or hemolysis. If it is essential that blood be given simultaneously, at least 20 mEq of sodium chloride should be added to each liter of mannitol solution to avoid pseudoagglutination.



Preparation

  1. Tear overwrap and remove solution container.
  2. Visually inspect the container. The closure system has two ports; the one for the administration set has a tamper evident plastic protector and the other is a medication addition site. Use only if solution is clear and container and seals are intact. 
     * Check for minute leaks by squeezing inner bag firmly. If leaks are found, discard solution as sterility may be impaired. 
     * Invert container and carefully inspect the solution in good light for cloudiness, haze, or particulate matter. Any container which is suspect should not be used.
  3. Admixing Mannitol Injection with other medications is not recommended. The addition of sodium chloride to 20% mannitol solution may result in precipitation of mannitol.
  4. Inspect Mannitol Injection visually for particulate matter and discoloration prior to administration and periodically during administration. If particulates or discoloration are present, discard the bag.
  5. Solutions of mannitol may crystallize when exposed to low temperatures. Concentrations greater than 15% have a greater tendency to crystallization. Inspect for crystals prior to administration. If crystals are observed, the container should be warmed by appropriate means to not greater than 60°C, shaken, then cooled to body temperature before administering. If all crystals cannot be completely redissolved, the container must be discarded. 



Administration

  1. Administer intravenously using sterile, filter-type administration set. It is recommended that Mannitol Injection be administered through a blood filter set to ensure against infusion of mannitol crystals.

  2. When administered peripherally, infuse slowly through a small bore needle, placed well within the lumen of a large vein to minimize venous irritation. Carefully avoid infiltration. 
  3. Do not admix with other drugs. The use of supplemental additive medication is not recommended. 
  4. To prevent air embolism, use a non-vented infusion set or close the vent on a vented set, avoid multiple connections, do not connect flexible containers in series, fully evacuate residual gas in the container prior to administration, do not pressurize the flexible container to increase flow rates, and if administration is controlled by a pumping device, turn off pump before the container runs dry.
  5. For single use only; discard unused portion.
Gamma-aminobutyric acid (GABA) is the predominant amino acid in litchi pulp, known for its neuroregulatory effects and anti-inflammatory properties. Although previous research has highlighted the pro-inflammatory characteristics of litchi thaumatin-like protein (LcTLP), interplay between GABA and LcTLP in relation to inflammation remains unclear. This study aims to explore the hepatoprotective effects of the litchi pulp-derived GABA extract (LGE) against LcTLP-induced liver inflammation in mice and LO2 cells. In vivo experiments demonstrated that LGE significantly reduced the levels of aspartate transaminase and alanine transaminase, and protected the liver against infiltration of CD4+ and CD8+ T cells and histological injury induced by LcTLP. Pro-inflammatory cytokines including interleukin-6, interleukin-1β, and tumor necrosis factor-α were also diminished by LGE. The LGE appeared to modulate the mitogen-activated protein kinase (MAPK) signaling pathway to exert its anti-inflammatory effects, as evidenced by a reduction of 47%, 35%, and 31% in phosphorylated p38, JNK, and ERK expressions, respectively, in the liver of the high-dose LGE group. Additionally, LGE effectively improved the translocation of gut microbiota by modulating its microbiological composition and abundance. In vitro studies have shown that LGE effectively counteracts the increase in reactive oxygen species, calcium ions, and pro-inflammatory cytokines induced by LcTLP. These findings may offer new perspectives on the health benefits and safety of litchi consumption.
The present invention addresses the problem of providing a fusion protein that is for use in treatment or diagnosis of cancer and that is formed between a molecule recognizing a cancer cell or the like and a streptavidin variant. According to the present invention, provided is a fusion protein in which an antigen-binding molecule having a molecular weight of 20,000 or less is bound to, via a linker sequence, the N-terminal side and/or the C-terminal side of a streptavidin variant, said streptavidin variant containing an amino acid sequence derived from the amino acid sequence of core streptavidin described in SEQ ID NO: 17 (wherein the amino acid sequence of Pro-Ser-Ala-Ala-Ser at the C-terminal may be partially or totally deleted) by the following mutations (1) to (6) and having reduced immunogenicity compared to wild-type streptavidin. (1) A mutation in which tyrosine at the 10th amino acid residue is replaced by serine or threonine. (2) A mutation in which tyrosine at the 71st amino acid residue is replaced by alanine or serine. (3) A mutation in which arginine at the 72nd amino acid residue is replaced by lysine. (4) A mutation in which glutamic acid at the 89th amino acid residue is replaced by aspartic acid. (5) A mutation in which arginine at the 91st amino acid residue is replaced by lysine. (6) A mutation in which glutamic acid at the 104th amino acid residue is replaced by glutamine or asparagine.
Fusobacterium nucleatum, a gram-negative anaerobic bacterium abundantly found in the human oral cavity, is widely recognized as a key pathobiont responsible for the initiation and progression of periodontal diseases due to its remarkable aggregative capabilities. Numerous clinical studies have linked F. nucleatum with unfavorable prognostic outcomes in various malignancies. In further research, scholars have partially elucidated the mechanisms underlying F. nucleatum's impact on various types of cancer, thus gaining a certain comprehension of the role played by F. nucleatum in cancer. In this comprehensive review, we present an in-depth synthesis of the interplay between F. nucleatum and different cancers, focusing on aspects such as tumor initiation, metastasis, chemoresistance, and modulation of the tumor immune microenvironment and immunotherapy. The implications for cancer diagnosis and treatment are also summarized. The objective of this review is to enhance our comprehension of the intricate relationship between F. nucleatum and oncogenic pathogenesis, while emphasizing potential therapeutic strategies.
The moderate exercise condition will involve participants waking briskly (equivalent to moderate intensity) on a treadmill for 10 minutes. Moderate intensity exercise is defined as 40-68% of heart rate reserve (HRR). Heart rate (HR) will be monitored using a Polar RS100 Heart Rate monitor to serve as a guide for participants to attain the appropriate intensity.
Given the rapidly aging trend worldwide and in Taiwan, the disease burden and economic impact of dementia on families, healthcare systems, and society are expected to increase unprecedentedly. It is estimated that interventions that could delay the clinical onset of dementia by a modest one year would significantly reduce the prevalence of dementia. Mild cognitive impairment (MCI) presents an early stage of cognitive impairment with a much higher risk of progression to dementia and a unique stage, potentially amenable to intervention, preventing further decline to dementia.

The microbiota-gut-brain axis is one of the most-studied gut-organ systems, and accumulating evidence shows gut microbiota might play a critical role in the pathogenesis of Alzheimer's disease (AD). However, the role of gut microbiota in the early stage of the AD spectrum, such as MCI, is unclear. Also, the effects of the probiotic supplements on cognition in patients with AD or MCI from several small randomized-controlled trials were inconsistent. Fixed regimens of probiotics were used in all these trials, and patients with MCI diagnosed by diverse research frameworks were included. As a result, the overarching goal of this proposal is to investigate the role and mechanism of the microbiota-gut-brain axis in MCI. Investigators will use data from a well-characterized cohort and a randomized controlled trial with a "precision" probiotic supplementation, i.e., a probiotic supplement based on individual gut probiotic profile, in a group of MCI due to AD, i.e., MCI with positive amyloid biomarkers.
Background and Objectives: Sepsis, a leading global health challenge, accounts for around 20% of deaths worldwide. The complexity of sepsis, especially the difference between bacterial and viral etiologies, requires an effective assessment of microcirculation during resuscitation. This study aimed to evaluate the impact of infusion therapy on microcirculation in patients with sepsis, focusing on bacterial- and COVID-19-associated sepsis using remote photoplethysmography (rPPG) and the automated capillary refill time (aCRT). Materials and Methods: This single-center prospective study was conducted in the ICU of Pauls Stradins Clinical University Hospital, including 20 patients with sepsis/septic shock. The patients were selected based on hemodynamic instability and divided into COVID-19 and Bacterial Septic Shock groups. Fluid responsiveness was assessed using the Passive Leg Raising Test (PLRT). Systemic hemodynamics and microcirculation were monitored through MAP CRT, rPPG, and serum lactate levels. Statistical analyses compared responses within and between the groups across different stages of the protocol. Results: The Bacterial group exhibited higher initial serum lactate levels and more pronounced microcirculatory dysfunction than the COVID-19 group. rPPG was more sensitive in detecting perfusion changes, showing significant differences between the groups. The automated CRT demonstrated greater sensitivity compared to the manual CRT, revealing significant differences during PLRT stages between bacterial- and COVID-19-associated sepsis. Both groups had a transient hemodynamic response to PLRT, with subsequent stabilization upon fluid infusion. Conclusions: When managing patients with sepsis in intensive care, monitoring microcirculation is of paramount importance in infusion therapy. Our study highlights the potential of rPPG and aCRT as tools for this purpose. These techniques can be used in conjunction with routine parameters, such as lactate levels and systemic hemodynamic parameters, to provide a comprehensive assessment of a patient's condition.
Disclosed are fluorinated materials for use in dental uses and non-dental uses, e.g., adhesives or coatings. Multifunctional monomers and prepolymers with pendant (meth)acrylate groups were prepared from epoxide ring-opening reactions. Resins based on the fluorinated monomers and prepolymers with diluent comonomers, were photocured as composites with particulate fillers. Fluorine contents of the prepolymers ranged from 15 to 65%. Composites with high transverse strength (up to 120 MPa), low water sorption (as low as 0.11 mass %) and extremely low polymerization shrinkage (as low as 3.4% by volume) were obtained. The fluorinated resins may be employed to produce hydrophobic dental composite materials with high strength and low polymerization shrinkage.
The present invention relates to a third refined peptide for non-finger odor frogs, a gene, a variant and applications thereof in pharmacy, which belongs to the technical field of biomedicine. The third refined peptide for non-finger odor frogs is an annular polypeptide; the molecular weight of the polypeptide is 2188.68 daltons, and the isoelectric point is 10.07. The third refined peptide has the activity of the serine protease inhibitor and has no enzyme activity. The total sequence of the third refined peptide for non-finger odor frogs is NH2-AALKGCWTKSIPPKPCFGKR-COOH, wherein the cysteine in the sixth bit and the cysteine in the sixteenth bit form an intramolecular disulfide bond. The encoding gene is composed of 304 nucleotides; the mature encoding parts are the nucleotides from the 130th bit to the 189th bit. The variant is generated by the deletion of one or more amino acids in the primitive sequence of the third refined peptide for non-finger odor frogs. The artificially-synthesized third refined peptide for non-finger odor frogs, and the variant thereof have strong inhibitory activity of serine proteinase; improved characteristics are shown in the inhibitory roles of the third refined peptide and the variant thereof. The third refined peptide for non-finger odor frogs and the variant thereof are used for preparing medicines for treating tumors, gastritis and pancreatitis, and have the advantages of simple sequence, convenient synthesis, etc.
Elevated levels of ammonia in breath can be linked to medical complications, such as chronic kidney disease (CKD), that disturb the urea balance in the body. However, early stage CKD is usually asymptomatic, and mass screening is hindered by high instrumentation and operation requirements and accessible and reliable detection methods for CKD biomarkers, such as trace ammonia in breath. Enabling methods would have significance in population screening for early stage CKD patients. We herein report a method to effectively immobilize transition metal selectors in close proximity to a single-walled carbon nanotube (SWCNT) surface using pentiptycene polymers containing metal-chelating backbone structures. The robust and modular nature of the pentiptycene metallopolymer/SWCNT complexes creates a platform that accelerates sensor discovery and optimization. Using these methods, we have identified sensitive, selective, and robust copper-based chemiresistive ammonia sensors that display low parts per billion detection limits. We have added these hybrid materials to the resonant radio frequency circuits of commercial near-field communication (NFC) tags to achieve robust wireless detection of ammonia at physiologically relevant levels. The integrated devices offer a noninvasive and cost-effective approach for early detection and monitoring of CKD.
One injection of 68Ga-NOTA-AE105 followed by PET/CT and on a separate day one injection of 18F-FDG followed by PET/MRI. Both scans will be evaluated for possible regional lymph node metastases.
PURPOSE: To obtain a bacterial preparation for treating and preventing cancers, and to provide a method therefor. CONSTITUTION: This bacterial preparation for treating and preventing cancers comprises at least one kind of pharmaceutically acceptable diluent, at least one kind of pharmaceutically acceptable carrier or adjuvant, and an active ingredient selected from the following microorganisms (1) and (2). (1) At least three strains of microorganisms having antitumor activities and selected from at least two kinds of microorganisms. The microorganisms are obtained from human intestinal bacteria. (2) At least one strain of microorganism having an antitumor activity and selected from Escherichia coli A.T.C.C. 55373, Escherichia coli A.T.C.C. 55374, Escherichia coli A.T.C.C. 55375 and Streptococcus faecalis G35 A.T.C.C. 55376.
The development of new targeted therapies for alcoholic hepatitis (AH) is one of the more urgent needs in clinical hepatology. To reach this goal, large multidisciplinary networks are required. The proposed initiative "Integrated Approaches for Identifying Molecular Targets in Alcoholic Hepatitis" (InTeam) will coordinate a multidisciplinary group composed of clinicians, physician-scientists, basic scientists and bioinformatics experts. The overarching hypothesis of InTeam is that the most rational way to provide a useful framework for future clinical trials in (AH) consists of the (i) determination of key drivers of the disease process, (ii) classification of molecular profiles and subtypes of AH, and (iii) identification of "druggable" targets based on both key drivers and molecular classification. Moreover, mouse models for AH are lacking making it impossible to evaluate promising targets in preclinical mouse studies in a meaningful manner. For this purpose, InTeam will integrate data obtained from molecular pathology studies in human AH and functional studies of key pathways in animal models. The proposed InTeam consortium includes three research projects, ten clinical centers, a Human Biorepository and a Mouse Models Core. The Human Biorepository Core will generate the to-date largest collection of samples from patients with AH from 10 academic liver centers and a comprehensive database that will serve as a basis for the proposed translational studies and be a valuable asset for the broader scientific community. The Mouse Models core will conduct murine studies after establishing and evaluating mouse models of AH based on the pathophysiology and molecular drivers of human AH determined by this consortium.
VXX-401 900mcg administered by intramuscular (IM) injection at Week 0. VXX-401 100 mcg administered by intramuscular (IM) injection at Week 4 and Week 12.
BACKGROUND: Pulmonary vein stenosis (PVS) is a rare condition in which neointimal proliferation leads to venous and arterial hypertension. Little is known about PVS after heart transplant (HTx) in children. We sought to describe the characteristics and outcomes of children who develop PVS after HTx.
METHODS: We performed a retrospective review of patients ≤18 years old who underwent HTx at two HTx centers between April 2012 and October 2023. Patients with PVS were identified via database queries. Cardiac diagnosis, PVS location and extent, and outcomes were recorded.
RESULTS: Over 11.5 years, 422 patients underwent HTx across both centers. Nineteen patients with PVS (10 male) were identified, 15 with de novo PVS. Sixteen had underlying congenital heart disease (CHD), two with anomalous pulmonary venous return. PVS was diagnosed at a median of 2 months (range 2 weeks to 14 years) after HTx. At time of initial diagnosis, 13 patients had one-vessel PVS. At final follow-up, 7/19 (37%) had increases in the number of vessels involved. Six patients underwent surgery, and nine patients had stent or balloon angioplasty. Two patients were treated for pulmonary hypertension following PVS diagnosis. Three patients died from right heart failure secondary to PVS.
CONCLUSIONS: This is the largest study to describe the characteristics of post-HTx PVS in children. PVS occurs in 4.5% of HTx, and underlying CHD is a strong risk factor. Multiple vessels can be involved and may require catheter-based or surgical intervention. Clinicians must be vigilant in monitoring the development of PVS in this population.
In forensic psychiatric clinics, patients who have committed a criminal offense on the basis of intellectual disability are also treated in according to Sect. 63 of the German Criminal Code. This group of patients has above-average lengths of stay and specific difficulties in treatment and in transition to aftercare systems are reported from practice. The present study is based on a content-analytical evaluation of ten structured interviews with practitioners of different professions who are familiar with the treatment of this patient group in forensic psychiatry. The aim was to identify treatment experiences and challenges of inpatient forensic care for this group as well as needs for change and suggestions for improvement. Respondents confirmed the specific treatment needs and person- and diagnosis-related challenges known from other studies, which were considered to be causally related to prolonged hospital stay and problems at discharge. Numerous structural and systemic barriers were also identified that impede the shortest possible forensic inpatient care and seamless transition to the non-forensic aftercare system. At the structural level, these included the need for human resources (both quantitative and qualitative) and adapted treatment concepts. Professional aftercare was considered very important for this group of patients. In this regard, the non-availability of suitable institutions, long waiting lists and reservations on the part of these institutions towards former forensic patients were identified as problems. The fact that patients with intellectual disability were less able to make their needs known than other patients and thus often received less attention from the treatment providers can be described as a systemic obstacle. This also applies to the rather high demands that the forensic system, with its goal of "improvement" through treatment, also places on people with intellectual disability. The findings of this study can contribute to improvement of the forensic inpatient care of people with intellectual disability at systemic and structural levels.