anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
ZINGO ® (lidocaine hydrochloride monohydrate) powder intradermal injection system contains 0.5 mg of sterile lidocaine hydrochloride monohydrate. 

The chemical name is 2-diethylamino-2',6'-acetoxylidide, monohydrochloride, monohydrate. The molecular formula is C 14H 22N 2O · HCl · H 2O with a molecular weight of 288.8 Da. Lidocaine hydrochloride monohydrate, a local anesthetic of the amide class, has the following structural formula: 

Lidocaine hydrochloride monohydrate is freely soluble in water, soluble in alcohol and chloroform, insoluble in ether, and melts at around 74–79°C.

ZINGO is a ready-to-use, sterile, single-use, disposable, needle-free delivery system. ZINGO consists of the following components: a drug reservoir cassette filled with 0.5 mg lidocaine hydrochloride monohydrate as a powder with a nominal particle size of 40 µm, a pressurized helium gas cylinder, and a safety interlock. The safety interlock prevents inadvertent actuation of the device. Once ZINGO is pressed against the skin, the interlock is released, allowing the button to be depressed to actuate the device. A sound similar to that of a popping balloon is emitted at the time ZINGO is actuated.
Immunoglobulin E (IgE) is important in the development of allergic responses and may determine asthma severity. Omalizumab is a man-made monoclonal antibody that directly blocks the cause of allergic reactions. There are three main objectives to this study. The first is to gain an understanding of how omalizumab affects cells involved in the immune response. The second objective is to determine whether response to omalizumab is influenced by exposure to environmental factors, including allergens and viral infections. The third objective is to determine what clinical markers can be used to determine which patients would most benefit from omalizumab therapy. This study will evaluate the immune and allergic responses of inner-city children with moderate to severe asthma who are receiving omalizumab or placebo as part of a parallel study (Inner-City Anti-IgE Therapy for Asthma, ICAC-08, NCT00377572).

Nasal secretions will be collected from all participants at the beginning of this study, toward the middle of the study, and with each asthma exacerbation requiring a clinical visit. Some participants will participate in either the basophil or T-cell studies and associated procedures. These studies require blood collection at five study visits. Sputum collection will occur at four study visits. Those participants involved in the basophil studies will also undergo skin testing at three study visits.
Patients who select NG tube treatment will be randomized into experimental and control groups. The experimental groups will have 100 cc of WSC administered in the NG tube within 2 hours of NG tube placement.
Disentangling the molecular underpinnings of major depressive disorder (MDD) is necessary for identifying new treatment and prevention targets. The functional impact of depression-related transcriptomic changes on the brain remains relatively unexplored. We recently developed a novel transcriptome-based polygenic risk score (tPRS) composed of genes transcriptionally altered in MDD. Here, we sought to investigate effects of tPRS on brain structure in a developmental cohort (Adolescent Brain Cognitive Development study; n = 5124; 2387 female) at baseline (9-10 years) and 2-year follow-up (11-12 years). We tested associations between tPRS and Freesurfer-derived measures of cortical thickness, cortical surface area, and subcortical volume. Across the whole sample, higher tPRS was significantly associated with thicker left posterior cingulate cortex at both baseline and 2-year follow-up. In females only, tPRS was associated with lower right hippocampal volume at baseline and 2-year follow-up, and lower right pallidal volume at baseline. Furthermore, regional subcortical volume significantly mediated an indirect effect of tPRS on depressive symptoms in females at both timepoints. Conversely, tPRS did not have significant effects on cortical surface area. These findings suggest the existence of a sex-specific neurodevelopmental signature associated with shifts towards a more depression-like brain transcriptome, and highlight novel pathways of developmentally mediated MDD risk.
Adenosine injection is indicated for the following. 

Conversion to sinus rhythm of paroxysmal supraventricular tachycardia (PSVT), including that associated with accessory bypass tracts (Wolff-Parkinson-White Syndrome). When clinically advisable, appropriate vagal maneuvers (e.g., Valsalva maneuver), should be attempted prior to adenosine administration. 

It is important to be sure the adenosine solution actually reaches the systemic circulation (see DOSAGE AND ADMINISTRATION). 

Adenosine does not convert atrial flutter, atrial fibrillation, or ventricular tachycardia to normal sinus rhythm. In the presence of atrial flutter or atrial fibrillation, a transient modest slowing of ventricular response may occur immediately following adenosine administration.
This is a randomized, double-blind, active-comparator (metformin) controlled study in drug-naïve patients with T2DM who have an HbA1c ≥ 7.5%. The duration of the study is 55 weeks, which will include a 1-week screening period (Visit 1 to Visit 2) and a 54 week double-blind, active treatment period. At Visit 2/Day 1 patients who meet all enrollment criteria will be randomized in a 1:1 ratio to one of two active treatment groups: 1. JANUMET™ (fixed-dose combination sitagliptin/metformin) or 2. metformin. The starting fixed-dose combination of sitagliptin/metformin will be 50/500 mg administered twice-daily and then up-titrated to a dose of 50/1000 mg b.i.d. over 4 weeks. The starting dose of metformin will be 500 mg twice-daily and then up-titrated to a dose of 1000 mg b.i.d. over 4 weeks. Patients who can not tolerate JANUMET™ at a dose of at least 50/500 mg b.i.d. or metformin at a dose of at least 500 mg b.i.d. 6 weeks after randomization and throughout the study will be discontinued. During the double-blind treatment period patients will remain on the study medication, but investigators are allowed to add other antihyperglycemic agents to improve glycemic control as necessary. The investigator can schedule additional visits to initiate additional antihyperglycemic agents or monitor glycemic control at any time during the study period. There will be no fixed visit schedule, but 7 clinical visits are recommended. It is also recommended to perform the first visit on active treatment 6 weeks after randomization and after this visit to schedule visits every 3 months. All clinical and lab data can be obtained using the "Clalit health care information system".
Participants received a combination of MK-1966 (Days 1 and 21) and SD-101 (Days 1, 8, 15 and Day 22) in Part A of the study (approximately 21 days). Participants were to continue in one of two expansion cohorts (Part B or C) and receive up to 8 cycles of treatment (approximately 24 weeks). Each cycle was 21 days.
<P>PROBLEM TO BE SOLVED: To provide an LPS-derived IgM production potentiator having immunological enhancement effects for animals through oral administration.  <P>SOLUTION: The LPS-derived IgM production potentiator contains a squeezed juice component of premature green leaves of wheat and barley plants as an effective component. The premature green leaves of wheat and barley plants, preferably the green leaves (including stems and leaves collectively) at the tillering to full heading stages of e.g. barley, hulless barley, oats and tear grass plants are used. Preferably, the squeezing is made by a mechanical means without causing thermal denaturalization. The green vegetable juice obtained by removing the coarse solids in it is used as the squeezed juice component. The LPS-derived IgM production potentiator may be used for an oral administration medicine or a functional food.  <P>COPYRIGHT: (C)2009,JPO&INPIT
PURPOSE: A pharmaceutical composition containing exosomal ADAM15 is provided to suppress cell adhesion, proliferation, and migration and to be used as a novel anticancer agent. CONSTITUTION: A pharmaceutical composition for preventing or treating cancer contains human cell-derived exosomal ADAM15 as an active ingredient. The human cell is immunocytes or macrophage. The macrophage is derived from human monocytes and is treated with an immunoadjuvant. The immunoadjuvant is liposome, lipopolysaccharide, or immunostimulant oligonucleotide. The composition suppresses cell adhesion, migration, and proliferation.
Elevated concentrations of TNFα have been found in involved tissues and fluids of patients with rheumatoid arthritis, Crohn's disease, ulcerative colitis, ankylosing spondylitis, psoriatic arthritis and plaque psoriasis. In rheumatoid arthritis, treatment with infliximab products reduced infiltration of inflammatory cells into inflamed areas of the joint as well as expression of molecules mediating cellular adhesion [E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1)], chemoattraction [IL-8 and monocyte chemotactic protein (MCP-1)] and tissue degradation [matrix metalloproteinase (MMP) 1 and 3]. In Crohn's disease, treatment with infliximab products reduced infiltration of inflammatory cells and TNFα production in inflamed areas of the intestine, and reduced the proportion of mononuclear cells from the lamina propria able to express TNFα and interferon. After treatment with infliximab products, patients with rheumatoid arthritis or Crohn's disease exhibited decreased levels of serum IL-6 and C-reactive protein (CRP) compared to baseline. Peripheral blood lymphocytes from infliximab product-treated patients showed no significant decrease in number or in proliferative responses to in vitro mitogenic stimulation when compared to cells from untreated patients. In psoriatic arthritis, treatment with infliximab products resulted in a reduction in the number of T-cells and blood vessels in the synovium and psoriatic skin lesions as well as a reduction of macrophages in the synovium. In plaque psoriasis, treatment with infliximab products may reduce the epidermal thickness and infiltration of inflammatory cells. The relationship between these pharmacodynamic activities and the mechanism(s) by which infliximab products exert their clinical effects is unknown.
An alpha-dialdehyde-containing composition comprises alpha-dialdehyde(s), and ammonium salt(s) of bronsted acid.  Alpha-dialdehyde-containing composition comprises alpha-dialdehyde(s) of formula (I), and ammonium salt(s) of bronsted acid.  A  =  Aromatic or non-aromatic carbocyclic, monocylic or polycyclic group with fused or non-fused rings having 6-50C, or 5-30 membered aromatic or non-aromatic carbocyclic, monocylic or polycyclic group with fused or non-fused rings optionally combined with carbocyclic, monocyclic or polycyclic group with fused or non-fused rings having 5-30C. It is provided that the heteroatoms of heterocyclic group are nitrogen, sulfur, oxygen, and/or phosphorus. The carbocyclic or heterocyclic groups optionally bears halo, 1-6C alkyl, hydroxyl, 1-6C alkoxy, thiol, carboxylic acid, nitro, sulfo, or nitrogen-containing heterocyclic substituents. Independent claims are also included for: (1) a process for dyeing keratin fibers comprising preparing an alpha-dialdehyde-containing composition immediately before use, applying the composition to the keratin fibers, leaving the composition in contact with the keratin fibers for action time to obtain the desired coloration, and rinsing the keratin fibers; and (2) a kit for dyeing keratin fibers comprising at least2 compartments containing alpha-dialdehyde, and ammonium salt(s) of bronsted acid.
A compound of formula (I) or a pharmaceutically acceptable salt thereof: wherein ring A is a pyrrole or pyrazole ring and when ring A is a pyrrole X is C(R4) and when ring A is a pyrazole X is N(R5) and one of R1 and R5 is absent; L1 is absent or a linker selected from alkylene, O, NR6 and S; R2 is phenyl, naphthyl, heteroaryl, heterocycloalkyl or cycloalkyl; R3 is C(O)OH, or C(O)OM wherein M is a group 1 cation; and R1, R4, R5 and R6 are as defined herein. Exemplified compounds include 1-methyl-2-phenyl-4-sulfamoyl-pyrrole-3-carboxylic acid; 2-(6-amino-3-pyridyl)-1-methyl-4-sulfamoyl-pyrrole-3-carboxylic acid; and 1-methyl-3-phenyl-5-sulfamoyl-pyrazole-4-carboxylic acid. A pharmaceutical composition comprising a compound of formula (I) is also disclosed. The compounds of the invention are enzyme inhibitors, particularly metallo-β-lactamase inhibitors, for use in treating a disease or disorder caused by aerobic or anaerobic Gram-positive, or aerobic or anaerobic Gram-negative bacteria. The compounds of the invention may be used to treat bacterial infection. The compounds of formula (I) may be used in combination with an antibacterial agent, preferably a carbapenem, to treat a bacterial infection.
The inventive cosmetic preparation of active substances, as such as well as in combination with other active substances, protects the skin against free radical aggression in a particularly effective manner. The preparation consists of a bark extract of  quebracho blanco  which contains at least 90 wt. % of proanthocyanidine oligomers, a silkworm extract which contains the peptide cecropine, amino acids and a vitamin mixture, a non-ionic, cationic or anionic hydro-gel, phopholipids, a yeast disintegration product and cyclodextrines. The inventive preparation can contain additional active substances such as plant extracts of acerola, sea weed, citrus, bitter orange, cherry, papaya, tea, coffee beans, skin tree and angelica. The preparations have synergistically increased radical protection factors of up to 10,000. Cosmetic compositions containing said preparations have radical protection factors of between 40 and 400 according to the portion of the preparation.
In Part B, HCV GT3-infected NC TN participants will take 2 MK-3682B FDC tablets (each containing grazoprevir 50 mg + uprifosbuvir 225 mg + ruzasvir 30 mg) q.d. by mouth for 12 weeks.
PROBLEM TO BE SOLVED: To obtain the subject new compound having a treatment and/or prophylax is action for pathologies such as inflammation caused by autoimmune diseases, e.g. rheumatics, nephritis and asthma, and various kinds of circulatory diseases, e.g. arteriosclerosis and restenosis after PTCA, and useful as a highly safe medicine. SOLUTION: A naphthalene derivative of the formula (the semidouble bond is a single bond or a double bond; R1 -R3 are each H, a 1-4C alkyl, a halogen, hydroxyl, etc.; R4 is carboxyl, a 1-4C alkylthiocarbonyl, etc.) and its pharmacologically aceptable salt. For example, (Z)-3-(2-naphthyl)-2-(phenylthio) propenoic acid. The compound of the formula is obtained e.g. by reacting a naphthalene aldehyde derivative with a phenylthioacetic acid derivative (preferably in an equivalent ratio of 1:1) in the presence of acetic anhydride and triethylamine preferably at 80-160 deg.C with stirring.
Opioids are the gold standard for the treatment of chronic pain but are limited by adverse side effects. In our earlier work, we showed that Heat shock protein 90 (Hsp90) has a crucial role in regulating opioid signaling in spinal cord; Hsp90 inhibition in spinal cord enhances opioid anti-nociception. Building on these findings, we injected the non-selective Hsp90 inhibitor KU-32 by the intrathecal route into male and female CD-1 mice, showing that morphine anti-nociceptive potency was boosted by 1.9-3.5-fold in acute and chronic pain models. At the same time, tolerance was reduced from 21-fold to 2.9 fold and established tolerance was rescued, while the potency of constipation and reward was unchanged. These results demonstrate that spinal Hsp90 inhibition can improve the therapeutic index of morphine. However, we also found that systemic non-selective Hsp90 inhibition blocked opioid pain relief. To avoid this effect, we used selective small molecule inhibitors and CRISPR gene editing to identify 3 Hsp90 isoforms active in spinal cord (Hsp90α, Hsp90β, and Grp94) while only Hsp90α was active in brain. We thus hypothesized that a systemically delivered selective inhibitor to Hsp90β or Grp94 could selectively inhibit spinal cord Hsp90 activity, resulting in enhanced opioid therapy. We tested this hypothesis using intravenous delivery of KUNB106 (Hsp90β) and KUNG65 (Grp94), showing that both drugs enhanced morphine anti-nociceptive potency while rescuing tolerance. Together, these results suggest that selective inhibition of spinal cord Hsp90 isoforms is a novel, translationally feasible strategy to improve the therapeutic index of opioids.
PURPOSE:To obtain a cosmetic having excellent hair producing effect, removing effects on stain on the skin by blending a solution of components of aloe or aloe and Japanese angelica tree in an organic solvent with a glutamate. CONSTITUTION:Aloe or aloe and Japanese angelica tree are immersed in an organic solvent as they are or cut into a proper size, ground and immersed in the organic solvent to give an extract or fermented as they are to give a fermentation product. A glutamate is dissolved in a solution containing the extract or the fermentation product as an active ingredient to give a cosmetic. 90-70wt.% organic solvent (e.g. low-class distilled spirits) is used based on 10-30wt.% aloe and Japanese angelica tree. The ratio of aloe and Japanese angelica tree is 1-99wt.% and 99-1wt.%.
Long-term morphine use leads to tolerance and hyperalgesia in patients with chronic pain, with neuroinflammation playing a key role, but its underlying mechanisms remain elusive. This study determines that repeated intrathecal morphine injections increase double-stranded RNA (dsRNA) production in spinal neurons, due to downregulated adenosine deaminase RNA specific 1 (ADAR1) expression. Lentivirus-induced ADAR1 elevation decreases the high levels of intracellular dsRNA and attenuates morphine tolerance and hyperalgesia. dsRNA is released into cerebrospinal fluid via exosomes (Exos) after repeated morphine injections and is taken up by microglia for TLR3-TRIF-IL-6 signaling activation. Blocking Exos release with GW4869 or inhibition of TLR3 signaling mitigates neuroinflammation, preventing the development of morphine tolerance and hyperalgesia. Intrathecal injection of TLR3 inhibitor alone shows analgesic effects in neuropathic pain, and co-administration with morphine amplifies the analgesic efficacy of morphine. These findings demonstrate that targeting dsRNA-TLR3 signaling to mitigate neuroinflammation could be a promising treatment for morphine tolerance.
BACKGROUND: Rhizoctonia solani Kühn is a pathogenic fungus causing tobacco target spot disease, and leads to great losses worldwide. At present, resistant varieties and effective control strategy on tobacco target spot disease are very limited. Host-induced gene silencing (HIGS) as well as the exogenous dsRNA can be used to suppress disease progression, and reveal the function of crucial genes involved in the growth and pathogenesis of the fungus.
RESULTS: The silencing of endoPGs or RPMK1 in host plants by TRV-based HIGS resulted in a significant reduction in disease development in Nicotiana benthamiana. In vitro analysis validated that red fluorescence signals were consistently observed in the hyphae treated with Cy3-fluorescein-labeled dsRNA at 12, 24, 48 and 72 h postinoculation (hpi). Additionally, application of dsRNA-endoPGs, dsRNA-RPMK1 and dsRNA-PGMK (fusion of partial endoPGs and RPMK1 sequences) effectively inhibited the hyphal growth of R. solani YC-9 in vitro and suppressed disease progression in the leaves, and quantitative real-time PCR confirmed that the application of dsRNAs significantly reduced the expression levels of endoPGs and RPMK1.
CONCLUSION: These results provide theoretical basis and new direction for RNAi approaches on the prevention and control of disease caused by R. solani. © 2024 Society of Chemical Industry.
Cardiovascular disease (CVD) and cancer are the leading causes of mortality worldwide. Although generally thought of as distinct diseases, the intersectional overlap between CVD and cancer is increasingly evident in both causal and mechanistic relationships. The field of cardio-oncology is largely focused on the cardiotoxic effects of cancer therapies (e.g., chemotherapy, radiation). Furthermore, the cumulative effects of cardiotoxic therapy exposure and the prevalence of CVD risk factors in patients with cancer lead to long-term morbidity and poor quality of life in this patient population, even when patients are cancer-free. Evidence from patients with cancer and animal models demonstrates that the presence of malignancy itself, independent of cardiotoxic therapy exposure or CVD risk factors, negatively impacts cardiac structure and function. As such, the primary focus of this review is the cardiac pathophysiological and molecular features of therapy-naïve cancer. We also summarize the strengths and limitations of preclinical cancer models for cardio-oncology research and discuss therapeutic strategies that have been tested experimentally for the treatment of cancer-induced cardiac atrophy and dysfunction. Finally, we explore an adjacent area of interest, called "reverse cardio-oncology," where the sequelae of heart failure augment cancer progression. Here, we emphasize the cross-disease communication between malignancy and the injured heart and discuss the importance of chronic low-grade inflammation and endocrine factors in the progression of both diseases.
A system comprises a teleoperational assembly including an operator input system and a teleoperational manipulator configured for operation by the operator input system. The teleoperational manipulator is coupled to a medical instrument in a surgical environment. The system also comprises a processing unit including one or more processors. The processing unit is configured to retrieve a user profile for a user, the user profile including a parameter established during a prior teleoperational procedure. The parameter includes an ergonomic setup for an input device of the operator input system. The input device is configured to operate the teleoperational manipulator. The processing unit is also configured to provide instructions to configure an operation of the teleoperational assembly based upon the parameter. The operation includes adjusting the operator input system based on the at least one of the ergonomic setup for the operator input system.