anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
A system for identifying a patient device location of a patient stimulation device within the heart of a patient. The system receives a patient electrocardiogram that is collected while the patient stimulation device is activated and while cardiac tissue is not captured. The electrocardiogram reflects current through blood within the heart resulting from the activation. The system determines a device location based on an association between library electrocardiograms and library device locations and based on similarity between the library electrocardiograms and the patient electrocardiogram. A library electrocardiogram represents an electrocardiogram that would be collected when a stimulation device is activated within the heart of a patient at the associated library device location. The system outputs an indication of the determined device location to indicate the patient device location of the patient stimulation device when the patient electrocardiogram was collected.
<P>PROBLEM TO BE SOLVED: To provide an oral composition having high retentivity in the oral cavity, preventing the oral cavity from being dried and highly safe to a human body.  <P>SOLUTION: The oral composition is used in the oral cavity and prevents the interior of the oral cavity from being dried. The composition contains honey and a sugar fatty acid ester of an ester of sugar and a fatty acid. The content of the honey in the oral composition is preferably 10-50 wt.%. The content of the sugar fatty acid ester in the oral composition is preferably 0.05-5 wt.%. The sugar of the sugar fatty acid ester is preferably constituted of pentose and/or hexose.  <P>COPYRIGHT: (C)2009,JPO&INPIT
Dyskeratosis Congenita (DC) is a multisystem disorder intrinsically associated with telomere dysfunction, leading to bone marrow failure (BMF). Although the pathology of DC is largely driven by mutations in telomere-associated genes, the implications of gene fusions, which emerge due to telomere-induced genomic instability, remain unexplored. We meticulously analyzed gene fusions in RNA-Seq data from DC patients to provide deeper insights into DC's progression. The most significant DC-specific gene fusions were subsequently put through in silico assessments to ascertain biophysical and structural attributes, including charge patterning, inherent disorder, and propensity for self-association. Selected candidates were then analyzed using deep learning-powered structural predictions and molecular dynamics simulations to gauge their potential for forming higher-order oligomers. Our exploration revealed that genes participating in fusion events play crucial roles in upholding genomic stability, facilitating hematopoiesis, and suppressing tumors. Notably, our analysis spotlighted a particularly disordered polyampholyte fusion protein that exhibits robust higher-order oligomerization dynamics. To conclude, this research underscores the potential significance of several high-confidence gene fusions in the progression of BMF in DC, particularly through the dysregulation of genomic stability, hematopoiesis, and tumor suppression. Additionally, we propose that these fusion proteins might hold a detrimental role, specifically in inducing proteotoxicity-driven hematopoietic disruptions.
Overdosage with FOTIVDA can cause severe hypertension and hypertensive crisis that may result in death [see WARNINGS AND PRECAUTIONS (5.1)] . 

During clinical studies, three patients inadvertently received doses ≥ 2.68 mg (≥ 2 times the recommended dose) of FOTIVDA. One patient who received two daily doses of 8.9 mg of FOTIVDA experienced hypertensive crisis with severe hypertensive retinopathy; a second patient who received three doses of 1.34 mg in one day experienced fatal uncontrolled hypertension; and a third patient who received two doses of 1.34 mg FOTIVDA in one day experienced persistent hypertension lasting over 5 days.

There is no specific treatment or antidote for FOTIVDA overdose.

In cases of suspected overdose, withhold FOTIVDA, closely monitor patients for hypertension and hypertensive crisis and other potential adverse reactions. Immediately manage signs or symptoms of hypertension and provide other supportive care as clinically indicated.
PROBLEM TO BE SOLVED: To obtain the subject solution capable of suppressing its bitter taste by masking the bitter taste remaining in the mouth and peculiar to bromhexine or salts thereof without damaging the stability of bromhexine or salts thereof, by including thaumatin. SOLUTION: This solution is obtained by including thaumatin. Bromhexine or a salt thereof is generally included at 0.001-0.1 wt.%, based on the whole weight of the solution. The thaumatin is preferably used at 0.1-1 pt.wt., as pure thaumatin, based on 1 pt.wt. of the bromhexine or the salt thereof. Further compounding with sugar alcohol (s) is preferable because of its being capable of completely masking the bitter taste of this solution. As the sugar alcoholism, erythritol and/or xylitol is (are) preferable. One pt.wt. of bromhexine is preferably compounded with >=600 pts.wt. of the sugar alcohol(s). The sugar alcohol(s) is (are) preferably used at 2-20 wt.%, normally, based on the whole weight of this solution. This solution is preferably pH 2.5-4.8.
FIELD: cosmetics. SUBSTANCE: invention relates to cosmetic compositions containing at least one mahogany extract as coloration agent and can also include dihydroxyacetone. Invention also relates to cosmetic compositions containing at least one compound represented by formula I (given in description), in which R 1 , R 2 , R 3 , R 6  and R 9 , same or different, independently denote hydrogen atom or C1-C4-alkyl, and R 4 , R 5 , R 7  and R 8 , same or different, independently denote hydrogen atom, hydroxyl, or C1-C4-alkoxy. Employment of these compositions is also a subject of invention. EFFECT: enabled rapid coloration close to naturally produced sunburn. 27 cl, 2 tbl, 2 ex
Provided is a novel antibody that will bind with fibrin but will not bind with fibrinogen, and also provided is a use for the novel antibody. Specifically, provided is an antibody or antigen-binding fragment thereof that binds with human fibrin and comprises: (a) H strand CDR1 formed from the amino acid sequence of sequence No. 1, or an amino acid sequence in which the same amino acid sequence contains one or several conservative amino acid substitutions; (b) H strand CDR2 formed from the amino acid sequence of sequence No. 2, or an amino acid sequence in which the same amino acid sequence contains one or several conservative amino acid substitutions; (c) H strand CDR3 formed from the amino acid sequence of sequence No. 3, or an amino acid sequence in which the same amino acid sequence contains one or several conservative amino acid substitutions; (d) L strand CDR1 formed from the amino acid sequence of sequence No. 4, or an amino acid sequence in which the same amino acid sequence contains one or several conservative amino acid substitutions; (e) L strand CDR2 formed from the amino acid sequence of sequence No. 5, or an amino acid sequence in which the same amino acid sequence contains one or several conservative amino acid substitutions; and (f) L strand CDR3 formed from the amino acid sequence of sequence No. 6, or an amino acid sequence in which the same amino acid sequence contains one or several conservative amino acid substitutions.
PURPOSE:To provide the titled crystallized glass most suitable as an artificial bone and a dental material by composing the glass of the oxide of Cu, Li, La, Gd, Ti, Sm, Nb, Zr, or Ru and specified calcium phosphate, vitrifying, and then crystallizing the material. CONSTITUTION:The glass consists of 0.1-30wt% >=1 kind of oxide selected from the oxide of Cu, Li, La, Gd, Ti, Sm, Nb, Zr, and Ru and the remainder of calcium phosphate whose atomic ratio of calcium to phosphorus is regulated to 0.35-1.7, and the material is vitrified, then heat-treated and crystallized. When the content of the oxide is regulated to <0.1wt%, the effect is not fully exhibited, because the crystallization proceeds mostly with devitrification on the surface. Meanwhile, when the content is regulated to >=30wt%, the m.p. is gradually increased, the viscosity is also increased, and the moldability is unfavorably effected. When said atomic ratio exceeds the value of 1.7, the m.p. is raised, and the material is not vitrified. Meanwhile, when the ratio is lower than 0.35, crystallization becomes difficult, and the material is unfavorably made chemically unstable.
Methods and compositions for treating ovarian failure are provided. In one embodiment, the method includes administering stem cells into the ovary of a female subject in need of such treatment. The stem cells are preferably bone marrow derived stem cells (BMSC). In other embodiments, the stem cells are embryonic stem cells, adult stem cells, induced stem cells, induced pluripotent stem cells, umbilical cord blood cells, or combinations thereof. The stem cells can be autologous or heterologous. In one embodiment, the stem cells have the following surface marker profile: CD105 positive, CD166 positive, CD90 positive, and CD73 positive as well as CD14 negative, CD34 negative, CD45 negative, HLA-DR negative, and CD 19 negative. The stem cells are administered in an amount effective to restore ovarian hormone production and promote folliculogenesis.
2 DOSAGE AND ADMINISTRATION

2.1 General Instructions Carefully consider the potential benefits and risks of MOBIC and other treatment options before deciding to use MOBIC. Use the lowest effective dose for the shortest duration consistent with individual patient treatment goals [see Warnings and Precautions  (5.4)]. After observing the response to initial therapy with MOBIC, adjust the dose to suit an individual patient's needs. In adults, the maximum recommended daily oral dose of MOBIC is 15 mg regardless of formulation. In patients with hemodialysis, a maximum daily dosage of 7.5 mg is recommended [see Warnings and Precautions  (5.6), Use in Specific Populations  (8.7), and Clinical Pharmacology ( 12.3)]. MOBIC oral suspension 7.5 mg/5 mL or 15 mg/10 mL may be substituted for MOBIC tablets 7.5 mg or 15 mg, respectively. Shake the oral suspension gently before using. MOBIC may be taken without regard to timing of meals.   


2.2 Osteoarthritis For the relief of the signs and symptoms of osteoarthritis the recommended starting and maintenance oral dose of MOBIC is 7.5 mg once daily. Some patients may receive additional benefit by increasing the dose to 15 mg once daily.   


2.3 Rheumatoid Arthritis For the relief of the signs and symptoms of rheumatoid arthritis, the recommended starting and maintenance oral dose of MOBIC is 7.5 mg once daily. Some patients may receive additional benefit by increasing the dose to 15 mg once daily.   


2.4 Juvenile Rheumatoid Arthritis (JRA) Pauciarticular and Polyarticular Course To improve dosing accuracy in smaller weight children, the use of the MOBIC oral suspension is recommended. MOBIC oral suspension is available in the strength of 7.5 mg/5 mL. For the treatment of juvenile rheumatoid arthritis, the recommended oral dose of MOBIC is 0.125 mg/kg once daily up to a maximum of 7.5 mg. There was no additional benefit demonstrated by increasing the dose above 0.125 mg/kg once daily in these clinical trials. Juvenile Rheumatoid Arthritis dosing using the oral suspension should be individualized based on the weight of the child: 

0.125 mg/kg
Ischemia-reperfusion (I/R) injury, a prevalent pathological condition in medical practice, presents significant treatment challenges. Hydrogen sulfide (H2S), acknowledged as the third gas signaling molecule, profoundly impacts various physiological and pathophysiological processes. Extensive research has demonstrated that H2S can mitigate I/R damage across multiple organs and tissues. This review investigates the protective effects of H2S in preventing I/R damage in the heart, brain, liver, kidney, intestines, lungs, stomach, spinal cord, testes, eyes, and other tissues. H2S provides protection against I/R damage by alleviating inflammation and endoplasmic reticulum stress; inhibiting apoptosis, oxidative stress, and mitochondrial autophagy and dysfunction; and regulating microRNAs. Significant advancements in understanding the mechanisms by which H2S reduces I/R damage have led to the development and synthesis of H2S-releasing agents such as diallyl trisulfide-loaded mesoporous silica nanoparticles (DATS-MSN), AP39, zofenopril, and ATB-344, offering a new therapeutic avenue for I/R injury.
AIMS: The prevalence of gestational diabetes mellitus (GDM) has spurred investigations into various interconnected factors, among which gut dysbiosis is notably prominent. Although gut dysbiosis is strongly associated with GDM, the specific role of the gut microbiome in the pathogenesis of GDM remains unknown. This study aims to explore the pathogenesis of GDM from gut microbiota.
MATERIALS AND METHODS: In our study, we constructed two GDM mice models: one induced by a high-fat diet (HFD) and the other through fecal microbiota transplantation (FMT) from GDM patients. In vitro, we used a co-culture system of RAW264.7 and 3T3-L1 adipocytes.
KEY FINDINGS: We induced a GDM-like state in pregnant mice by FMT from GDM patients, which was consistent with the HFD model. A potential mechanism identified involves the diminished abundance of SCFA-producing microbiota, which reduces SCFAs, particularly propionic acid and butyric acid. In vitro, butyric and propionic acids were observed to alleviate LPS-induced TLR4-NF-κB activation, thereby reducing inflammation levels and inhibiting adipose insulin resistance via the PI3K/AKT signaling pathway. This reduction appears to trigger the polarization of adipose tissue macrophages toward M1 and promote insulin resistance in adipose tissue.
SIGNIFICANCE: Our study fills this knowledge gap by finding that alterations in gut microbiota have an independent impact on hyperglycemia and insulin resistance in the GDM state. In vivo and in vitro, gut dysbiosis is linked to adipose tissue inflammation and insulin resistance via the bacterial product SCFAs in the GDM state, providing new insights into the pathogenesis of GDM.
BACKGROUND AND OBJECTIVES: Incidental diffuse-weighted imaging (DWI)-positive subcortical and cortical lesions, or acute incidental cerebral microinfarcts (CMIs), are a common type of brain ischemia, which can be detected on magnetic resonance DWI for approximately 2 weeks after occurrence. Acute incidental CMI was found to be more common in patients with cancer. Whether acute incidental CMI predicts future ischemic stroke is still unknown. We aimed to examine the association between acute incidental CMI in patients with cancer and subsequent ischemic stroke or transient ischemic attack (TIA).
METHODS: This is a retrospective cohort study. We used Clalit Health Services records, representing over half of the Israeli population, to identify adults with lung, breast, pancreatic, or colon cancer who underwent brain MRI between January 2014 and April 2020. We included patients who underwent scan between 1 year before cancer diagnosis and 1 year after diagnosis. Primary outcome was ischemic stroke or TIA using International Classification of Diseases, Ninth Revision codes. Secondary outcomes were intracranial hemorrhage (ICH) and mortality. Records were followed from first MRI until primary outcome, death, or end of follow-up (January 2023). Cox proportional hazards models were used to calculate hazard ratio (HR) for patients with and without acute incidental CMI, as a time-dependent covariate.
RESULTS: The study cohort included 1,618 patients with cancer, among whom, 59 (3.6%) had acute incidental CMI on at least 1 brain MRI. The median (interquartile range) time from acute incidental CMI to stroke or TIA was 26 days (14-84). On multivariable analysis, patients with acute incidental CMI had a higher stroke or TIA risk (HR 2.97, 95% CI 1.08-8.18, p = 0.035) compared with their non-CMI counterparts. Acute incidental CMIs were also associated with mortality after multivariable analysis (HR 2.76, 95% CI 2.06-3.71, p < 0.001); no association with ICH was found.
DISCUSSION: Acute incidental CMI on brain MRI in patients with active cancer is associated with an increased risk of near-future ischemic stroke or TIA and mortality. This finding might suggest that randomly detected acute incidental CMI in patients with cancer may guide primary cerebrovascular risk prevention and etiologic workup.
The invention discloses a method for preparing pure hair and toenail ectodermal dysplasia model pig nuclear transplantation donor cells and a special gene editing system thereof. The invention provides a method for preparing recombinant porcine cells, which comprises the following steps: co-transfecting the HOXC13-gRNA1, the HOXC13-gRNA4 and the NCN protein to a pig cell to obtain a recombinant pig cell. The recombinant pig cell is a recombinant cell with a mutant HOXC13 gene. The present invention provides a polypeptide comprising SEQ ID NO:16 HOXC13-gRNA1, SEQ ID NO:17, a kit of HOXC13-gRNA4 and NCN proteins. The application of the kit is as follows: preparing a recombinant porcine cell; preparing a pure hair and toenail type ectodermal dysplasia model pig; preparing a pure hair and toenail type ectodermal leaf dysplasia cell model or a pure hair and toenail type ectodermal leaf dysplasia tissue model or a pure hair and toenail type ectodermal leaf dysplasia organ model. The invention has great application value for researching and developing the pure hair and toenail type ectodermal dysplasia medicament and disclosing the pathogenesis of the disease.
1,117,948. Extracting medicinal protein. TEIKOKU HORMONE MFG. CO. Ltd. 3 March, 1966 [3 March, 1965], No. 9396/66. Heading A5B. An active material having biological activity with respect to the nervous system is obtained from the submaxillary glands of ungulate mammals, e.g. cattle, horses and swine, by extraction with an aqueous medium e.g. water or 2% saline, precipitating the protein therefrom, redissolving the precipitate and separating the active fraction from the large amount of inactive mucoid present therein. This may be achieved by fractional precipitation of the mucoid by addition of a salt, acid or watermiscible organic solvent or by adding a watersoluble zinc salt which forms a complex with the active material, which may be precipitated free from mucoid by addition of acetone or ethanol. The active material is separable into two fractions e.g. by treating an aqueous saline solution thereof with a weakly basic solution of acrinol, a protein/acrinol complex effective with respect to the proliferation of glial cells is precipitated and a protein effective with respect to the growth of neurons and the regeneration of axons remains in solution. Both may be purified by ion-exchange techniques.
Carcinogenicity studies have not been conducted with panobinostat.

Panobinostat was mutagenic in the Ames assay, and caused endo-reduplication (increased number of chromosomes) in human peripheral blood lymphocytes in vitro and DNA damage in an in vitro COMET assay in mouse lymphoma L5178Y cells.

FARYDAK may impair male and female fertility. In an oral fertility study conducted in rats, 10, 30, or 100 mg/kg doses of panobinostat were administered to females 3 times weekly (Days 1, 3, and 5) for 2 weeks prior to mating, then during the mating period, and on gestation Days 0, 3, and 6. An increase in early resorption and/or post-implantation loss in female rats were observed at doses ≥10 mg/kg. Number of pregnancies was reduced at doses ≥30 mg/kg. Prostate atrophy accompanied by reduced secretory granules, and testicular degeneration, oligospermia and increased epididymal debris were observed in repeated dose oral toxicity studies in dogs, e.g., in the 4-week study at the dose of 1.5 mg/kg. These effects were not completely reversed following a 4-week nondosing period.
Maternal obesity and/or high-fat diet (HF) consumption can disrupt appetite regulation in their offspring, contributing to transgenerational obesity and metabolic diseases. As fatty acids (FAs) play a role in appetite regulation, we investigated the maternal and fetal levels of FAs as potential contributors to programmed hyperphagia observed in the offspring of obese dams. Female mice were fed either a control diet (CT) or HF prior to mating, and fetal and maternal blood and tissues were collected at 19 days of gestation. Elevated levels of linoleic acid were observed in the serum of HF dams as well as in the serum of their fetuses. An increased concentration of eicosadienoic acid was also detected in the hypothalamus of female HF-O fetuses. HF-O male fetuses showed increased hypothalamic neuropeptide Y (Npy) gene expression, while HF-O female fetuses showed decreased hypothalamic pro-opiomelanocortin (POMC) protein content. Both male and female fetuses exhibited reduced hypothalamic neurogenin 3 (NGN-3) gene expression. In vitro experiments confirmed that LA contributed to the decreased gene expression of Pomc and Ngn-3 in neuronal cells. During lactation, HF female offspring consumed more milk and had a higher body weight compared to CT. In summary, this study demonstrated that exposure to HF prior to and during gestation alters the FA composition in maternal serum and fetal serum and hypothalamus, particularly increasing n-6, which may play a role in the switch from POMC to NPY neurons, leading to increased weight gain in the offspring during lactation.
Lipin proteins including Lipin 1-3 act as transcriptional co-activators and phosphatidic acid phosphohydrolase enzymes, which play crucial roles in lipid metabolism. However, little is known about the function of Lipin3 in triglyceride (TG) metabolism. Here, we identified a novel mutation (NM_001301860: p.1835A>T/p.D612V) of Lipin3 in a large family with hypertriglyceridemia (HTG) and obesity through whole-exome sequencing and Sanger sequencing. Functional studies revealed that the novel variant altered the half-life and stability of the Lipin3 protein. Hence, we generated Lipin3 heterozygous knockout (Lipin3-heKO) mice and cultured primary hepatocytes to explore the pathophysiological roles of Lipin3 in TG metabolism. We found that Lipin3-heKO mice exhibited obvious obesity, HTG, and non-alcoholic fatty liver disorder. Mechanistic study demonstrated that the haploinsufficiency of Lipin3 in primary hepatocytes may induce the overexpression and abnormal distribution of Lipin1 in cytosol and nucleoplasm. The increased expression of Lipin1 in cytosol may contribute to TG anabolism, and the decreased Lipin1 in nucleoplasm can reduce PGC1α, further leading to mitochondrial dysfunction and reduced TG catabolism. Our study suggested that Lipin3 was a novel disease-causing gene inducing obesity and HTG. We also established a relationship between Lipin3 and mitochondrial dysfunction.