anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
One aspect of the invention is a kind of novel foam having and being suspended in granule therein. Another aspect of the present invention is the foamed assembly (15,209,220,222) for foam tuner (10,70,150,180,200,201,205). Foamed assembly includes air sparging element (34,224,236), mixing chamber (32,210,228) and air chamber (35,226). Mixing chamber is positioned at the side of air sparging element and which defines a part for mixing chamber. Air chamber is positioned at the opposite side of air sparging element and which defines a part for air chamber. Air chamber (226) has air intake (230). Mixing chamber (228) has liquid inlet (232) and outlet (234), and outlet is positioned at the downstream of entrance. Foamed assembly also becomes a part for novel foam tuner. Foamed assembly and foam tuner have many foams being suspended in granule therein for manufacturing.
PURPOSE:To obtain a remedy for autoimmune diseases such as rheumarthritis, SLE, etc., by treating a monoclonal antibody to be selectively and specifically linked to an autoantigen with a treatment such as a protease, etc., removing a complement fixation site from it to give a part, using the part as the remedy. CONSTITUTION:A monoclonal antibody to be selectively and specifically linked to a body component to become an autoantigen is treated with a protease, etc., a complement fixation site is removed from it to give a part such as Fab, F(ab')2, Fab', etc., and autoimmune diseases are remedied by using a drug containing it as a main component. By an extraordinary immune adjusting mechanism, a body component of its own is used as an anitgen to prepare an autoantibody, an antigen-antibody reaction, activation of complement, migration of leukocyte, etc. are produced to cause tissue disorder, etc. The part from which complement fixation site is removed is linked to the autoantigen, to inhibit the antigen-antibody reaction. Namely, only production of harmful autoantibody is inhibited, useful immune reaction is not influenced, so this remedy is more advantageous than existing immunosuppressive agents.
The present invention relates to a modified botulinum neurotoxin A (BoNT/A) for use in treating limb spasticity, wherein the modified BoNT/A is administered by intramuscular injection to a plurality of affected muscles of a subject, wherein the modified BoNT/A is administered by way of a unit dose of 53 Units to 948 Units of modified BoNT/A at the plurality of affected muscles, and wherein 1 Unit is an amount of the modified BoNT/A that corresponds to the calculated median lethal dose (LD50) in mice, wherein the plurality of affected muscles are selected from: a first group comprising: the flexor digitorum superficialis, the flexor digitorum profundus, the flexor carpi radialis, the flexor carpi ulnaris, the brachioradialis, the pronator teres, the biceps brachii, the gastrocnemius medial head, the gastrocnemius lateral head, the flexor digitorum longus, the flexor hallucis longus, the gastrocnemius, the deltoid, the levator scapulae, the pronator quadratus, the flexor policis longus, the adductor policis, the flexor policis brevis, the palmaris longus, the lumbricales, the opponens policis, the adductor magnus, the adductor longus, the adductor brevis, the gracilis, the medial hamstrings, the lateral hamstrings, the tensor fascia lata, the rectus femoris, the vastus lateralis, the vastus medialis, the vastus intermedius, the gluteus maximus, the tibialis anterior, the flexor digitorum brevis, the extensor hallucis longus, and the flexor hallucis brevis; and a second group comprising: the triceps brachii (long head), the subscapularis, the pectoralis (e.g. the pectoralis major), the latissimus dorsi, the biceps brachii, the brachialis, the soleus, the tibialis posterior, the brachioradialis, the teres major, the iliopsoas, and the gastrocnemius; and wherein a single unit dose is administered at an affected first group muscle and/or multiple unit doses are administered at an affected second group muscle, and wherein the total dose administered during the treatment is up to 14,220 Units, and wherein the modified BoNT/A comprises: a modification at one or more amino acid residue(s) selected from: ASN 886, ASN 905, GLN 915, ASN 918, GLU 920, ASN 930, ASN 954, SER 955, GLN 991, GLU 992, GLN 995, ASN 1006, ASN 1025, ASN 1026, ASN 1032, ASN 1043, ASN 1046, ASN 1052, ASP 1058, HIS 1064, ASN 1080, GLU 1081, GLU 1083, ASP 1086, ASN 1188, ASP 1213, GLY 1215, ASN 1216, GLN 1229, ASN 1242, ASN 1243, SER 1274, and THR 1277, wherein the modification is selected from: i. substitution of an acidic surface exposed amino acid residue with a basic amino acid residue; ii. substitution of an acidic surface exposed amino acid residue with an uncharged amino acid residue; iii. substitution of an uncharged surface exposed amino acid residue with a basic amino acid residue; iv. insertion of a basic amino acid residue; and v. deletion of an acidic surface exposed amino acid residue; or wherein the modified BoNT/A comprises a BoNT/A light-chain and translocation domain, and a BoNT/B receptor binding domain (Hc domain). Also provided are corresponding methods of treatment and uses, as well as unit dosage forms, and kits.
Allergen preparations useful as vaccines or desensitizing agents for the treatment of allergies caused by pollen are prepared by cultivating a microorganism (which is specific to pollen of a species causing allergies) in a sterilized aqueous extract from the pollen species in question until the resulting suspension of microorganisms in the pollen extract has allergen activity, separating the microorganisms from the pollen extract which is collected as an allergen preparation, and optionally extracting with water the microorganisms separated off for the recovery of a further allergen preparation.  Said microorganisms are defined as those which live on the pollen grains and can be isolated therefrom.  They may be either bacteria or fungi.  In an example, the fungus Aureobasidum pullulans isolated from birch pollen is cultivated in a birch pollen extract. The culture obtained is filtered, and the residue is freeze-dried. In another example the fungus Sporobolomyces pararoseus, isolated from timothy pollen, is cultivated in a timothy pollen extract.  The culture is filtered, the filtrate is put into amoules and the residue is freeze-dried.  Aqueous extracts of the freeze-dried residue show allergen activity.  Allergen preparations may also be prepared using several different microorganisms from one and the same pollen species.  Specificed microorganisms include Cladosporium herbarum, Penicillium eyclopium, Cryptococcus laurentii, Rodotorula minuta, Cladosporium cladosporioides and Cryptococcus albidus, all being isolated from, e.g. timothy pollen.
Embodiments may include a method for reducing a solvent concentration in a plurality of microparticles. The method may involve contacting a mixture including the plurality of microparticles and the solvent with water to form an aqueous suspension. A first portion of the solvent may dissolve into the water of the aqueous suspension to reduce the solvent concentration in the plurality of microparticles from a first solvent concentration in the mixture to a second solvent concentration in the aqueous suspension. The method may also include transferring the aqueous suspension to a concentration unit that may further reduce the solvent concentration from the second solvent concentration to a third solvent concentration. The method may further include transferring a microparticle concentrate with the third solvent concentration to a washing unit to form an amalgam of washed microparticles with a fourth solvent concentration. The method may also include drying the amalgam of washed microparticles.
Hepatocellular carcinoma (HCC) is a disease of high unmet medical need that has become a global health problem. The development of targeted therapies for HCC has been hindered by the incomplete understanding of HCC pathogenesis and the limited number of relevant preclinical animal models. We recently unveiled a previously uncharacterized YES kinase (encoded by YES1)-dependent oncogenic signaling pathway in HCC. To model this subset of HCC, we established a series of syngeneic cell lines from liver tumors of transgenic mice expressing activated human YES. The resulting cell lines (referred to as HepYF) were enriched for expression of stem cell and progenitor markers, proliferated rapidly, and were characterized by high SRC family kinase (SFK) activity and activated mitogenic signaling pathways. Transcriptomic analysis indicated that HepYF cells are representative of the most aggressive proliferation class G3 subgroup of HCC. HepYF cells formed rapidly growing metastatic tumors upon orthotopic implantation into syngeneic hosts. Treatment with sorafenib or the SFK inhibitor dasatinib markedly inhibited the growth of HepYF tumors. The new HepYF HCC cell lines provide relevant preclinical models to study the pathogenesis of HCC and test novel small-molecule inhibitor and immunotherapy approaches.
Currently, there is an increase in the aging of the population, which represents a risk factor for many diseases, including sarcopenia. Sarcopenia involves progressive loss of mass, strength, and function of the skeletal muscle. Some mechanisms include alterations in muscle structure, reduced regenerative capacity, oxidative stress, mitochondrial dysfunction, and inflammation. The zebrafish has emerged as a new model for studying skeletal muscle aging because of its numerous advantages, including histological and molecular similarity to human skeletal muscle. In this study, we used fish of 2, 10, 30, and 60 months of age. The older fish showed a higher frailty index with a value of 0.250 ± 0.000 because of reduced locomotor activity and alterations in biometric measurements. We observed changes in muscle structure with a decreased number of myocytes (0.031 myocytes/μm2 ± 0.004 at 60 months) and an increase in collagen with aging up to 15% ± 1.639 in the 60-month group, corresponding to alterations in the synthesis, degradation, and differentiation pathways. These changes were accompanied by mitochondrial alterations, such as a nearly 50% reduction in the number of intermyofibrillar mitochondria, 100% mitochondrial damage, and reduced mitochondrial dynamics. Overall, we demonstrated a similarity in the aging processes of muscle aging between zebrafish and mammals.
AKTEN® (lidocaine hydrochloride ophthalmic gel) 3.5% is a sterile, preservative-free, single-patient use ophthalmic gel preparation for topical ocular anesthesia. Lidocaine hydrochloride is designated chemically as acetamide, 2-(diethylamino)-N-(2,6-dimethylphenyl) monohydrochloride with a molecular formula of C14H22N2O • HCl and molecular weight of 270.8. The structural formula of the active ingredient is: 

AKTEN® contains 35 mg of lidocaine hydrochloride per mL as the active ingredient. AKTEN® also contains Hypromellose, Sodium Chloride, and Water for Injection as inactive ingredients in the 1 mL tube configuration. AKTEN® contains Hypromellose, Sodium Chloride, and Water for Injection as inactive ingredients in the 5 mL in 10 mL bottle configuration. The pH may be adjusted to 5.5 to 7.5 with Hydrochloric Acid and/or Sodium Hydroxide.
Control arm: Usual Pediatric Care. The control condition is usual care delivered by pediatricians at 1, 2, 4, and 6 month well child visits.
INTRODUCTION: Lung ischemia/reperfusion injury (LIRI) is a pathological process caused by the deficiency and subsequent reperfusion of oxygen and blood to the lung. Literature reports that the catalytic activity and expression of HDAC6 can be induced in response to IRI. HDAC6 inhibition confers protective effects against a series of IRI and also exerts pulmonary protection against various lung damage. The present study was formulated to investigate the functional role of HDAC6 inhibitor in LIRI and to probe into the intrinsic mechanisms underlying the protective role of HDAC6 inhibitor against LIRI.
METHODS: Lung epithelial cell line MLE-12 cells were subjected to H/R injury to construct in vitro cell culture model of LIRI. For functional experiments, MLE-12 cells were pre-treated with various concentrations of selective HDAC6 inhibitor ACY-1215 (1, 5, 10 μM) to evaluate the biological role of HDAC6 in LIRI. For rescue experiments, MLE-12 cells were pre-treated with Nrf2 inhibitor ML385 (10 μM) or ERK activator LM22B-10 (50 μM) to discuss the molecular mechanisms.
RESULTS: It was verified that HDAC6 inhibition repressed H/R-induced apoptosis, oxidative stress, inflammation and mitochondrial dysfunction of MLE-12 cells. HDAC6 inhibition activated Nrf2/HO-1 signaling pathway and inactivated ERK/NF-κB signaling pathway in MLE-12 cells. The repressing effects of HDAC6 inhibition on H/R-induced apoptosis, oxidative stress, inflammation and mitochondrial dysfunction of MLE-12 cells were partially abolished upon pre-treatment with Nrf2 inhibitor ML385 or ERK activator LM22B-10.
CONCLUSION: HDAC6 inhibition may mitigate H/R-induced lung epithelial cell injury depending on activation of Nrf2/HO-1 signaling pathway and inactivation of ERK/NF-κB signaling pathway.
Hypersensitivity to carboplatin has been reported in 2% of the patients. These allergic reactions have been similar in nature and severity to those reported with other platinum-containing compounds, i.e., rash, urticaria, erythema, pruritus, and rarely bronchospasm and hypotension. Anaphylactic reactions have been reported as part of post-marketing surveillance (see WARNINGS). These reactions have been successfully managed with standard epinephrine, corticosteroid, and antihistamine therapy.

There have been reports of hypersensitivity reactions which progressed to Kounis syndrome (acute allergic coronary arteriospasm that can result in myocardial infarction). Kounis syndrome can develop in patients with and without cardiac risk factors, and may present with cardiac and allergic symptoms. Coronary vasospasm may be eliminated with steroids, antihistamines, and spasmolytics treatment.
Spinal cord injury (SCI) is a catastrophic accidence with little effective treatment, and inflammation played an important role in that. Previous studies showed photobiomodulation (PBM) could effectively downregulate the process of inflammation with modification of macrophage polarization after SCI; however, the potential mechanism behind that is still unclear. In the presented study, we aimed to investigate the effect of PBM on the expression level of versican, a matrix molecular believed to be associated with inflammation, and tried to find the mechanism on how that could regulate the inflammation process. Using immunofluorescence technique and western blot, we found the expression level of versican is increased after injury and markedly downregulated by irradiation treatment. Using virus intrathecal injection, we found the knock-down of versican could produce the effect similar to that of PBM and might have an effect on inflammation and macrophage polarization after SCI. To further verify the deduction, we peptide the supernatant of astrocytes to induce M0, M1, and M2 macrophages. We found that the versican produced by astrocytes might have a role on the promotion of M2 macrophages to inflammatory polarization. Finally, we investigated the potential pathway in the regulation of M2 polarization with the induction of versican. This study tried to give an interpretation on the mechanism of inflammation inhibition for PBM in the perspective of matrix regulation. Our results might provide light on the inflammation regulation after SCI.
Observational (no investigational intervention) arm. Children (6-17 years) with any type of OI who are already receiving bisphosphonate treatment as standard of care treatment for orthopedic symptoms. Changes in hearing, quality of life, and bone density will be observed for the duration of the study.
Patients with HR+/HER2- metastatic/locally advanced BC whose treatment decision with palbociclib has been made by their treating physician and who meet the eligibility criteria will be invited to participate in the study. Patients who initiate treatment with palbociclib plus letrozole/aromatase inhibitor or palbociclib plus fulvestrant in line with the licensed indication(s), as first or second line therapy for metastatic/locally advanced BC at enrollment may be included in the study.

The variables assessed in this study will be patient demographics, clinical characteristics, comorbid conditions and concomitant medications, HR+ HER2-locally advanced and metastatic BC treatment history, current BC treatment, performance status (Eastern Cooperative Oncology Group (ECOG), clinical outcomes, and QoL. All assessments described in this protocol are performed as part of normal clinical practice or standard practice guidelines for the patient population and healthcare provider specialty in the countries where this non-interventional study is being conducted. All data collected in this study are intended to capture the real-world treatment patterns and outcomes for patients with HR+/HER2- metastatic/locally advanced BC. An electronic case report form (eCRF) will be used for data collection. Investigators will be trained with an initial on-site visit to the clinic on the protocol, electronic data capture (EDC) system (i.e., eCRF), investigator site master file (ISMF), documentation, and any applicable study processes. Any new information relevant to the performance of this non-interventional study (NIS) will be forwarded to the medical staff during the study. Remote data monitoring will be conducted during the life of the study to ensure timely reporting of safety data, data integrity and consistency.
BACKGROUND: Despite recent advances the prognosis of pulmonary hypertension remains poor and warrants novel therapeutic options. Extensive studies, including ours, have revealed that hypoxia-induced pulmonary hypertension is associated with high oxidative stress. Cerium oxide nanozyme or nanoparticles (CeNPs) have displayed catalytic activity mimicking both catalase and superoxide dismutase functions and have been widely used as an anti-oxidative stress approach. However, whether CeNPs can attenuate hypoxia-induced pulmonary vascular oxidative stress and pulmonary hypertension is unknown.
RESULTS: In this study, we designed a new ceria nanozyme or nanoparticle (AuCeNPs) exhibiting enhanced enzyme activity. The AuCeNPs significantly blunted the increase of reactive oxygen species and intracellular calcium concentration while limiting proliferation of pulmonary artery smooth muscle cells and pulmonary vasoconstriction in a model of hypoxia-induced pulmonary hypertension. In addition, the inhalation of nebulized AuCeNPs, but not CeNPs, not only prevented but also blunted hypoxia-induced pulmonary hypertension in rats. The benefits of AuCeNPs were associated with limited increase of intracellular calcium concentration as well as enhancement of extracellular calcium-sensing receptor (CaSR) activity and expression in rat pulmonary artery smooth muscle cells. Nebulised AuCeNPs showed a favorable safety profile, systemic arterial pressure, liver and kidney function, plasma Ca2+ level, and blood biochemical parameters were not affected.
CONCLUSION: We conclude that AuCeNPs is an improved reactive oxygen species scavenger that effectively prevents and treats hypoxia-induced pulmonary hypertension.
A non-contact and non-invasive apparatus and method for monitoring of health characteristics of a user. The apparatus includes one or more cameras and processor for real-time video of the user and for processing at least each frame from the obtained real-time video. One or more facial regions are from each processed frame to extract one or more regions of interest present therein. The extracted regions of interest are at least one image based physiological monitoring model along with one or more Photo plethysmography imaging (iPPG) and Optical Coherence Tomography (OCT) variations to process one or more extracted regions of interest and obtain at least one result indicative of the health characteristics of the of user based on the real-time video by using Convolutional Neural Network algorithm. The method can be implemented as an AI based software or a platform. A report can be generated for warning for any abnormal range.
The immediate intervention group will take part in the online parent training program called the Parent Web (PW). This immediate intervention group are parents of PATHS children who took part in a social emotional curriculum (PATHS) at age 4 to 5 years old and during the PW trial will be 11 to 13 years old. Parents are participating in the Parent Web.
Patients receiving combination therapy for chronic hepatitis C virus (HCV) infection (standard or pegylated interferon alfa \[PEG-IFN\] in combination with ribavirin \[RBV\]) frequently develop moderate to severe anemia. In large, prospective, clinical trials of PEG-IFN alfa-2b and PEG-IFN alfa-2a, the reported mean decreases in hemoglobin (Hb) were 2.5 g/dL, and 3.7 g/dL, respectively. Furthermore, in a retrospective study, 54% of standard interferon/RBV-treated patients had hemoglobin decreases of at least 3 g/dL. It is important to understand the causes, natural history, and risk factors associated with HCV therapy-induced anemia, because such decreases in hemoglobin can result in RBV dose reduction or discontinuation, which may decrease the likelihood of a virologic response by patient. Erythropoietin is an endogenous hormone that acts in the bone marrow to increase the number of erythroid progenitor cells (red blood cells). Normally, a decrease in the hemoglobin level is accompanied by an increase in the serum erythropoietin (sEPO) level, which will ultimately normalize the Hemoglobin level. The relationship between hemoglobin and serum erythropoietin is less apparent in patients with chronic diseases such as cancer and human immunodeficiency virus (HIV) infection. It is not known whether HCV/HIV co-infected patients receiving combination PEG-IFN/RBV therapy have a similarly diminished erythropoietic response to anemia. The objective of this study is to document the pattern of hemoglobin changes and erythropoietic response (from baseline to final assessment) in HCV/HIV co-infected patients receiving combination therapy with IFN / RBV. N/A