anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
A composition that includes an activatable aggregate is described herein. The aggregate has a core and a shell. In some embodiments, when the aggregate is exposed to acoustic energy, the core of the aggregate includes a hydrogel that is capable of absorbing a relatively large amount of water. The core of the aggregate is covalently bound to a shell of linear aliphatic moieties. The aggregate is synthesized to minimize the amount of water in the core, prior to exposure to acoustic energy. Methods of hydrating using the compositions are also provided.
Age-related differences in sustained attention may be related to the prevalence and content of task unrelated thought or mind-wandering. Older adults report less mind-wandering in sustained tasks than younger adults, something that is surprising due to the reduced performance on tasks. It is clear that both cognitive and emotional processes underlie comprehension and sustained attention and relate to prevalence of task unrelated thought and performance. A complex process such as reading comprehension presents a challenge for improvement because of the wide range of changes that occur with age. Pharmacological therapies can target only a limited number of the many changes believed to underlie functional decline. One way that may mitigate these declines in performance in a broad way is mindfulness training. Thus, the investigators conducted a randomized study to assess the effects of mindfulness training relative to an active health education control group on mind wandering and controlled processing abilities in older adults. All individuals that contact the Clinical Neuroscience Laboratory (CNLab) with interest underwent a phone screening assessing inclusion/exclusion criteria.Those participants meeting I/E criteria were invited to participate in the study. During the first assessment session, written informed consent was obtained; additional inclusion/exclusion measures were administered; and self-report questionnaires and assessment measures were completed. Following the first assessment session, four training sessions took place. Participants were randomized into either the a mindfulness training intervention or a health education intervention. Subsequently, all participants were invited back for post-assessment session.
We report a case of a woman in her early 80s with antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis presented as myalgia mimicking polymyalgia rheumatica (PMR). She had positive results for the Neer and Hawkins-Kennedy impingement tests, and a normal serum creatine kinase (CK) concentration. At first, we suspected PMR; however, the patient did not strictly meet the classification criteria. Electromyography revealed an abnormal myogenic pattern, and muscle MRI revealed intramuscular and fascial hyperintensity. Moreover, chest CT revealed interstitial lung disease, and test results for ANCAs were positive. We diagnosed the patient with ANCA-associated vasculitis based on the criteria and treated her with corticosteroids and rituximab. Thus, ANCA-associated vasculitis can cause muscle involvement without elevation of the CK concentration and mimic PMR.
Participants inadequately controlled on background MET were randomised to receive, in addition to MET, a sulfonylurea (SU) (glibenclamide, gliclazide, or glimepiride). The SU was gradually increased to the maximum permitted dose (glibenclamide 15 mg per day or miconizied equivalent of 10.5 mg per day; gliclazide 240 mg per day; glimepiride 4 mg per day) as required to achieve a target HbA1c of less than or equal to 7.0 percent.
Spinal cord is the cylindrical structure of nerve fibers and tissues that is enclosed in the spine and provides connection between the brain and all parts of the body. The spinal cord is particularly prone to injury. The spinal cord does not have the ability to repair other parts of the body, if it is damaged. A spinal cord injury happens when the spinal cord is affected by trauma, loss of its normal blood flow, or tumor or infection compression. Lesions in the spinal cord are described as either complete or incomplete.In a complete spinal cord injury, the body suffers complete loss of sensation and muscle control below the injury stage. In an incomplete injury to the spinal cord, there is a certain stay behind feature below injury point. In most cases all sides of the body are similarly affected. Neck injuries to the upper portion of the spinal cord can cause quadriplegia-paralysis of both arms and legs. If the spinal cord injury occurs lower in the back then it can only induce paraplegia-paralysis of both legs. The incidence of SCI to be between 13 and 33 cases per million per year, and their estimate of the incidence of SCI was between 110 and 1120 per million populations. Quadriplegia term refers to the motor and sensory function of cervical spinal cord because neurons inside the neuron damaged the spinal canal. Quadriplegia can cause in the arms, trunk, legs and pelvic organs. Not including brachial plexus or peripheral nervous injury.Trauma is the principal cause of spinal cord injury. Nearly half of the incidents are attributed to accidents involving motor vehicles. Certain forms of trauma include: falling to the spine from a height, stabbing or gunshot wound and sports injuries. Spinal cord damage may also be caused by tumor, infection, or inflammation caused by compression of the spinal cord. Many patients have normal backbone canal and a higher risk of spinal cord injurySome prognostic factors are related to survival, includes demographic, injury, and psychosocial variables. The most important prognostic factors are age and severity of injury including the level of the nervous system, the degree of damage integrity, and ventilator dependence Patients with spinal cord injury (SCI), especially those with higher levels of disease, rely on care and assistance in their daily activities, most of which are provided by informal caregivers. Where home caregivers are involved, low usage of home services is observed. Provides care based on a doctor's prescription based on care needs, assessed by a qualified service provider using standardized procedures.
Peptides comprising a fragment of SEQ ID NO 2 or SEQ ID NO 8 are disclosed. The fragment comprises at least 8 contiguous amino acids of SEQ ID NO. 8, including at least one of positions 121 and 135 of SEQ ID NO. 8. Alternatively, the fragment comprises positions 6 to 13 of SEQ ID NO. 3 and the peptide comprises NO more than 21 amino acids, the fragment comprises positions 7 to 22 of SEQ ID NO. 3 and the peptide comprises NO more than 40 amino acids, or the fragment comprises positions 18 to 33 of SEQ ID NO. 3 and the peptide comprises NO more than 33 amino acids. Alternatively, the fragment comprises the amino acid sequence of SEQ ID NO 29 and the peptide comprises NO more than 21 amino acids and is for use in the treatment and/or prevention of cancer. The peptides are capable of inducing an immune response against the TGF-beta R2-1a frameshift mutein.
Pembrolizumab 200 mg will be administered as an approximately 30 minute (-5/+10 mins) IV infusion every 3 weeks. Sites should make every effort to target infusion timing to be as close to 30 minutes as possible. Patients will be followed with DCE perfusion MRI done at baseline and every 9 weeks (+/- 7 days). Patients will be allowed to stay on treatment in spite of increase in tumor size, provided the patient has no, or manageable, new neurologic symptoms, and at the discretion of treating physician. In that situation, tumor resection should be encouraged for the distinction between tumor progression and immunologic reactions. Patients undergoing surgical resection will have tissue collected for collateral studies. All collected tissue will be stored in the Pathology Core Tissue bank at MSK.
AIM: Given estrogen's recognized regulatory influence on diverse metabolic and immune functions, this study sought to explore its potential impact on fibrosis and elucidate the underlying metabolic regulations.
METHODS: Female mice underwent ovary removal surgery, followed by carbon tetrachloride (CCl4) administration to induce liver injury. Biochemical index analysis and histopathological examination were then conducted. The expression levels of alpha-smooth muscle actin (α-SMA), transforming growth factor-β (TGF-β), and collagen type 1 alpha 1 chain (COL1A1) were assessed using western blotting to further elucidate the extent of liver injury. Finally, metabolite extraction and metabolomic analysis were performed to evaluate metabolic changes.
RESULTS: Ovary removal exacerbated CCl4-induced liver damage, while estrogen supplementation provided protection against hepatic changes resulting from OVX. Furthermore, estrogen mitigated liver injury induced by CCl4 treatment in vivo. Estrogen supplementation significantly restored liver damage induced by OVX and CCl4. Comparative analysis revealed significant alterations in pathways including aminoacyl-tRNA biosynthesis, glycine, serine, and threonine metabolism, lysine degradation, and taurine and hypotaurine metabolism in estrogen treatment.
CONCLUSION: Estrogen supplementation alleviates liver injury induced by OVX and CCl4, highlighting its protective effects against fibrosis and associated metabolic alterations.
One of the probable hypotheses for the onset of autoimmunity is molecular mimicry. This study aimed to determine the HLA-II risk alleles for developing Hashimoto's thyroiditis (HT) in order to analyze the molecular homology between candidate pathogen-derived epitopes and potentially self-antigens (thyroid peroxidase, TPO) based on the presence of HLA risk alleles. HLA-DRB1/-DQB1 genotyping was performed in 100 HT patients and 330 ethnically matched healthy controls to determine the predisposing/protective alleles for HT disease. Then, in silico analysis was conducted to examine the sequence homology between epitopes derived from autoantigens and four potentially relevant pathogens and their binding capacities to HLA risk alleles based on peptide docking analysis. We identified HLA-DRB1*03:01, *04:02, *04:05, and *11:04 as predisposing alleles and DRB1*13:01 as a potentially predictive allele for HT disease. Also, DRB1*11:04 ~ DQB1*03:01 (Pc = 0.002; OR, 3.97) and DRB1*03:01 ~ DQB1*02:01 (Pc = 0.004; OR, 2.24) haplotypes conferred a predisposing role for HT. Based on logistic regression analysis, carrying risk alleles increased the risk of HT development 4.5 times in our population (P = 7.09E-10). Also, ROC curve analysis revealed a high predictive power of those risk alleles for discrimination of the susceptible from healthy individuals (AUC, 0.70; P = 6.6E-10). Analysis of peptide sequence homology between epitopes of TPO and epitopes derived from four candidate microorganisms revealed a homology between envelop glycoprotein D of herpes virus and sequence 151-199 of TPO with remarkable binding capacity to HLA-DRB1*03:01 allele. Our findings indicate the increased risk of developing HT in those individuals carrying HLA risk alleles which can also be related to herpes virus infection.
A process is disclosed for treating cancer by the process of indirect targeted immunocytolysis, which comprises conjugating an immunogenic sensitizing agent to a targeting agent which is capable of binding to aberrant cells, such as cancer cells in a human or animal host. The conjugate is then introduced into the body of an animal or human which has previously been actively immunized against the sensitizing agent or concomitantly treated with the appropriate antibody (passive immunization). Binding of the conjugate to the object cells occurs and is accompanied by the binding of antibodies produced against the sensitizing agent. This results in triggering of a complement cascade and/or an antibody-dependent T-cell-mediated response leading to cell destruction. Also disclosed are the novel targeting agent/sensitizing agent conjugates for use in the process. Agents comprise autocrine differentiation-inhibiting factor/toxoid conjugates.
Desmopressin nasal spray solution 0.01% dosage must be determined for each individual patient and adjusted according to the diurnal pattern of response. Response should be estimated by two parameters: adequate duration of sleep and adequate, not excessive, water turnover. Patients with nasal congestion and blockage have often responded well to intranasal desmopressin acetate. The usual dosage range in adults is 0.1 mL to 0.4 mL daily, either as a single dose or divided into two or three doses. Most adults require 0.2 mL daily in two divided doses. The morning and evening doses should be separately adjusted for an adequate diurnal rhythm of water turnover. For children aged 3 months to 12 years, the usual dosage range is 0.05 mL to 0.3 mL daily, either as a single dose or divided into two doses. About 1/4 to 1/3 of patients can be controlled by a single daily dose of desmopressin acetate administered intranasally. Fluid restriction should be observed. (See WARNINGS, PRECAUTIONS, Pediatric Use and Geriatric Use.)  
  
The nasal spray pump can only deliver doses of 0.1 mL (10 mcg) or multiples of 0.1 mL. If doses other than these are required, the rhinal tube delivery system may be used.  
  
The spray pump must be primed prior to the first use. To prime pump, press down five (5) times. The bottle will now deliver 10 mcg of drug per spray. Discard desmopressin nasal spray solution 0.01% 

after 50 sprays since the amount delivered thereafter per spray may be substantially less than 10 mcg of drug.
Leucovorin is indicated to diminish the toxicity and counteract the effect of inadvertently administered overdosages of methotrexate. Leucovorin administration should begin as promptly as possible. As the time interval between methotrexate administration and leucovorin initiation increases, the effectiveness of leucovorin in counteracting toxicity decreases. Monitoring of the serum methotrexate concentration is essential in determining the optimal dose and duration of treatment with leucovorin.

In cases of massive overdosage, hydration and urinary alkalinization may be necessary to prevent the precipitation of methotrexate and/or its metabolites in the renal tubules. Generally speaking, neither hemodialysis nor peritoneal dialysis has been shown to improve methotrexate elimination. However, effective clearance of methotrexate has been reported with acute, intermittent hemodialysis using a high-flux dialyzer (Wall, SM et al:  Am J Kidney Dis 28(6):846-854, 1996). 

Accidental intrathecal overdosage may require intensive systemic support, high-dose systemic leucovorin, alkaline diuresis and rapid CSF drainage and ventriculolumbar perfusion.

In post-marketing experience, overdose with methotrexate has generally occurred with oral and intrathecal administration, although intravenous and intramuscular overdose have also been reported.

Reports of oral overdose often indicate accidental daily administration instead of weekly (single or divided doses). Symptoms commonly reported following oral overdose include those symptoms and signs reported at pharmacologic doses, particularly hematologic and gastrointestinal reaction. For example, leukopenia, thrombocytopenia, anemia, pancytopenia, bone marrow suppression, mucositis, stomatitis, oral ulceration, nausea, vomiting, gastrointestinal ulceration, gastrointestinal bleeding. In some cases, no symptoms were reported. There have been reports of death following overdose. In these cases, events such as sepsis or septic shock, renal failure, and aplastic anemia were also reported.

Symptoms of intrathecal overdose are generally central nervous system (CNS) symptoms, including headache, nausea and vomiting, seizure or convulsion, and acute toxic encephalopathy. In some cases, no symptoms were reported. There have been reports of death following intrathecal overdose. In these cases, cerebellar herniation associated with increased intracranial pressure, and acute toxic encephalopathy have also been reported.

Glucarpidase is indicated for the treatment of toxic methotrexate concentrations in patients with delayed methotrexate clearance due to impaired renal function (refer to the glucarpidase prescribing information). If glucarpidase is used, do not administer leucovorin within two hours before or after a dose of glucarpidase because leucovorin is a substrate for glucarpidase. There are published case reports of intravenous and intrathecal glucarpidase treatment to hasten clearance of methotrexate in cases of overdose.
Anemia is a major complication of chronic kidney disease (CKD). Its prevalence increases with advancing age and progression of kidney disease. The main cause of anemia linked to CKD is represented by the reduction erythropoietin secretion. The increase in cardiovascular risk and mortality is strongly associated with the presence of anemia, and grows with the severity of the anemia, as described in numerous studies. The main therapies for the control of anemia have so far been represented by iron supplementation, the use of synthetic erythropoietin and blood transfusions. Despite the availability of adequate therapies, the prevalence of anemia in CKD continues to be significant. Drugs that inhibit the enzyme prolyl hydroxylase of hypoxia inducible factor (HIF-PHi) are able to mimic a condition of hypoxia and increase the production of endogenous erythropoietin. HIF-PHi therefore represents an important therapeutic alternative for the control of anemia linked to CKD. Numerous studies have confirmed the ability of HIF-PHi to correct anemia and maintain hemoglobin at adequate values; they also highlighted other potential beneficial pleiotropic factors on cholesterol control and iron homeostasis. Further studies are needed to confirm the safety of the drug, especially regarding cardiovascular risk, vascular thrombosis and neoplastic growth. This document highlights the mechanism of action, effects and pharmacological characteristics of HIF-PHi.
PROBLEM TO BE SOLVED: To obtain a hair treatment agent capable of improving residue-related problems without lowering its hairdressing capacity and producing no static electricity on the hair by including a fluorinated acid to neutralize a polymer having a basic group as one of the ingredients of the agent. SOLUTION: This hair treatment agent contains (A) a fluorinated acid to neutralize (B) a polymer having a basic group as one of the ingredients of the agent, in particular hairdressing. The preferable component A is shown by the formula A-(CH2 )x -(CF2 )y -(CH2 )z -B (X and Z are each 0 to 5; Y is 1 to 21; A is an acidic group; B is an acidic group or F; wherein Z is 0 when B is F, and preferable acidic groups A and B are each COOH, SO3 H, OPO2 H or OPO3 H2 ), e.g. perfluoropentanoic acid. The compound shown by the formula is preferably soluble in an aqueous or water/ethanol solution containing at least 10 wt.% of water. The component B is a (co)polymer synthesized from one or more types of monomers containing a basic group, in particular basic nitrogen atom(s).
Medicine (A), in a formulation that is delivered to the apical membrane of mucosal epithelial cells through the respiratory tract, contains at least one peptide (I) that activates guanylate cyclase C (GCC). Independent claims are also included for the following: (1) Inhalation device containing (A); and (2) Diagnosing diseases that are accompanied by breathing disorders or disorders of mucus secretion in the respiratory tract, by detecting at least one (I). ACTIVITY : Antiasthmatic; Antiinflammatory. No details of tests for these activities are given. MECHANISM OF ACTION : Stimulation or activation of GCC, a G protein-coupled receptor that catalyzes conversion of guanosine triphophate to cyclic guanosine monophosphate (cGMP) and is present on the apical (air) side of respiratory epithelial cells but not on the basolateral (blood) side. cGMP activates membrane-associated type II protein kinase which in turn activates the regulatory domain of the cystic fibrosis transmembrane conductance regulator, resulting in secretion of chloride ions and water from the cells, causing fluidization of the mucus. No biological data given.
The following information on adverse reactions is based on data from both oral and IV administration of melphalan as a single agent, using several different dose schedules for treatment of a wide variety of malignancies. 

Hematologic: The most common side effect is bone marrow suppression leading to leukopenia, thrombocytopenia, and anemia. White blood cell count and platelet count nadirs usually occur 2 to 3 weeks after treatment, with recovery in 4 to 5 weeks after treatment. Irreversible bone marrow failure has been reported. 

Gastrointestinal: Gastrointestinal disturbances such as nausea and vomiting, diarrhea, and oral ulceration occur infrequently. Hepatic disorders ranging from abnormal liver function tests to clinical manifestations such as hepatitis and jaundice have been reported. Hepatic veno-occlusive disease has been reported. 

Hypersensitivity: Acute hypersensitivity reactions including anaphylaxis were reported in 2.4% of 425 patients receiving Melphalan hydrochloride for Injection for myeloma (see WARNINGS). These reactions were characterized by urticaria, pruritus, edema, skin rashes, and in some patients, tachycardia, bronchospasm, dyspnea, and hypotension. These patients appeared to respond to antihistamine and corticosteroid therapy. If a hypersensitivity reaction occurs, IV or oral melphalan should not be readministered since hypersensitivity reactions have also been reported with oral melphalan. Cardiac arrest has also been reported rarely in association with such reports. 

Miscellaneous: Other reported adverse reactions include skin hypersensitivity, skin ulceration at injection site, skin necrosis rarely requiring skin grafting, maculopapular rashes, vasculitis, alopecia, hemolytic anemia, allergic reaction, pulmonary fibrosis (including fatal outcomes), and interstitial pneumonitis. Temporary significant elevation of the blood urea has been seen in the early stages of therapy in patients with renal damage. Subjective and transient sensation of warmth and/or tingling. 

To report SUSPECTED ADVERSE REACTIONS, contact Meitheal Pharmaceuticals Inc. at 1-844-824-8426 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.