anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
PROBLEM TO BE SOLVED: To obtain a skin preparation for external use, excellent in preventing and reducing effects on pigmentation in skin such as blackening, dermal stains or ephelides of the skin after sunburn and having high safety by including an extract from a specific crude drug plant having suppressing activities for melanogenesis and produced in Peru of South America therein. SOLUTION: This skin preparation for external use comprises an extract from Chinchilcuma as an active ingredient. Mutisia hirsuta Meyen is especially preferred as the Chinchilcuma. The extract is preferably extracted with a polar solvent. The content of the extract is 0.001-20wt.%, based on the total amount of the preparation for external use and expressed in terms of dry solids. The dosage form of the skin preparation for external use is preferably a cream, a milky lotion, an oil, etc.
The invention discloses a dexamethasone acetate local film-forming gel compound, comprising the following weight-percentage components: 0.5 to 7 percent of hydroxyalkyl fibrin, 1 to 10 percent of esterifying agent, 0.5 to 5 percent of crosslinking agent, 75 to 90 percent of menstruum and 0.01 to 3 percent of dexamethasone acetate; wherein, the crosslinking agent is a saturated fat polyol or alkydwhich has the chemical general equation of CnH2n+2-m-l (OH) m (COOH) l, and n, m and l are whole numbers and n is more than or equal to m which is more than or equal to 2, and l is more than or equalto 0, and m plus 1 is from 4 to 8 and n plus 1 is from 4 to 8. The dexamethasone acetate local film-forming gel compound of the invention is used for treating ulcer of mouth or skin. When the invention is spread onto an ulcer surface, a smooth, tough, wear-resistant and durable waterproof protection film can be formed. The dexamethasone acetate can be released to the ulcer surface through the film to promote the cure of ulcer. The formed film can be preserved for about 5 hours on the surface of oral mucosa, so as to shield outer stimulants to the ulcer and the existence of film cannot be feltin the oral cavity. And the film can be preserved for more than 7 hours on the skin surface and the adherence of the film is durable.
Abnormalities in the modulation of the glutamate system have been reported by multiple investigators studying animal models, post-mortem brains, and single gene disorders that have overlapping phenotypes with autism. Abnormalities in glutamatergic function have been reported in disorders affecting a variety of behavioral and neurological domains, from mood stability, to cognitive flexibility, memory, and motor function. Numerous studies have reported a variety of memory and motor deficits in children with autism. Whereas the neurobiology of such deficits is an area of active research, there is a paucity of intervention research for such deficits in autism. This study will attempt to study the effect of an N-methyl-D-aspartate receptor (NMDA) inhibitor, memantine, on memory, and motor praxis/expressive language skills in children with autism.

Methods: Children ages 6-12 years who are verbal and meet criteria for Autism Spectrum Disorder will be recruited across 2 sites. After consent, the children will be assessed for memory function, expressive language output and motor skills/praxis. They will then be randomized 1:1 to memantine versus placebo for 6 months. The effects of this medication on the above mentioned symptoms domains as well as its safety in this population will be studied over the 6 month period.
Obstructive sleep apnea (OSA) is a common multisystem disorder, affecting up to 10% of the pediatric population. There is scant data about OSA and adenotonsillectomy (AT) outcomes in the very young (ages 1-3). Young children with moderate/severe OSA are often underprivileged, low socioeconomic status (SES) minorities with limited access to care. Further complicating the problem is that African American children may suffer a higher preoperative and post-AT burden of disease, with greater negative consequences to these vulnerable children. Up to 75% of children with OSA continue to have sequelae of the disease post-AT. These include poor school performance, delayed speech, inattention, and long term neurocognitive dysfunction. It has been demonstrated that younger patients (below the age of 3) have larger tonsils and stunted growth on presentation for AT. More telling is that younger children face greater morbidity from the procedure, including respiratory complications, postoperative bleeding, and perioperative anoxic/hypoxic injury as validated by multiple studies. A recent study studied watchful waiting versus early AT in two groups of patients aged 5-9 without severe OSA. The findings indicated that early AT improved respiratory and quality of life indices without corresponding improvement in attention or cognitive function as assessed by neuropsychological testing 7 months post intervention. So it leads to the further question of whether children with severe OSA truly benefit from the procedure at all, and whether there maybe a trend towards harm. In this particular scenario, the investigators are hypothesizing that serum based biomarkers in the form of cytokines are of significant diagnostic benefit in demonstrating ongoing inflammation.

Therefore, the surgical stimulus and consequent stress response in the form of centrally mediated cytokines and inflammatory mediators demands study. These has been well analyzed with adult acute and chronic pain, and have been associated with neurocognitive impairment, but have not been studied as a neurocognitive biomarker in the pediatric population. Children from lower SES, with less stable social environments, or other cultural/linguistic barriers are higher risk and urgently require study.
The present invention relates to a crystalline form, solvate and hydrate of N-((1-(3-(1,2,3-triazol-1-yl)propyl)piperidine-4-yl)methyl)-4-amino-5-chloro-2-methoxybenzamide derivatives and preparation method thereof indicated by chemical formula 1 below. A crystalline form refers to a crystalline sold that does not include a fixed molecular rate of solvent molecules within the crystalline lattice, in other words, a crystalline sold, not solvate. The present invention clearly indicates solvate or more specifically hydrate. According to a specific example of the present invention, solvate refers to a compound or condensation material formed by one or more solvent molecules, in other words, N-((1-(3-(1,2,3-triazol-1-yl)propyl)piperidine-4-yl)methyl)-4-amino-5-choloro-2-methoxybenzamide derivatives or one or more solvent molecules. The solvate is a typical crystalline sold having a fixed mole rate of solvent or solute. The most well-known solvent can include water, methanol, ethanol, isopropanol or acetate acid. If the solvent is water, the formed solvate is called hydrate.
This study was designed to explore the expression changes of P2Y1 receptors in the distal colonic myenteric layer of rats. An opioid induced constipation(OIC) rat model was generated by intraperitoneal (i.p) injection of loperamide. At 7 days post-treatment, the model rats were assessed by calculating the fecal water content and the gastrointestinal transit ratio. The immunofluorescence (IF)-based histochemical study was used to observe the distribution of P2Y1 receptors in the distal colonic myenteric plexus. Western blotting (WB) was performed to evaluate the expression changes of P2Y1 proteins in the myenteric layer, and the electrophysiological approaches were carried out to determine the regulatory roles of P2Y1 receptors on distal colonic motor function. IF showed that P2Y1 receptors are co-expressed MOR in the enteric nerve cells of the distal colonic myenteric plexus. Moreover, the WB revealed that the protein levels of P2Y1 were significantly decreased in the distal colonic myenteric layer of OIC rats. In vitro tension experiments exhibited that the P2Y1 receptor antagonist MRS2500 enhanced the spontaneous contraction amplitude, adding EM2 and β-FNA did not have any effect on MRS2500. Therefore, P2Y1 receptor expression could be associated with the occurrence of OIC in this rat model and the regulation of colonic motility by MOR may be related to the release of purine neurotransmitters such as ATP in the colonic nervous system.
A remote carcinogen exposure can predispose to breast cancer onset decades later, suggesting that carcinogen-induced mutations generate long-lived premalignant clones. How subsequent events influence the progression of specific premalignant clones remains poorly understood. Herein, multistage mouse models of mammary carcinogenesis were generated by combining chemical carcinogen exposure [using 7,12-dimethylbenzanthracene (DMBA)] with transgenes that enable inducible expression of one of two clinically relevant mammary oncogenes: c-MYC (MYC) or PIK3CAH1047R (PIK). In prior work, DMBA exposure generated mammary clones bearing signature HrasQ61L mutations, which only progressed to mammary cancer after inducible Wnt1 oncogene expression. Here, after an identical DMBA exposure, MYC versus PIK drove cancer progression from mammary clones bearing mutations in distinct Ras family paralogs. For example, MYC drove cancer progression from either Kras- or Nras-mutant clones, whereas PIK transformed Kras-mutant clones only. These Ras mutation patterns were maintained whether oncogenic transgenes were induced within days of DMBA exposure or months later. Completing a full-term pregnancy (parity) failed to protect against either MYC- or PIK-driven tumor progression. Instead, a postpartum increase in mammary tumor predisposition was observed in the context of PIK-driven progression. However, parity decreased the overall prevalence of tumors bearing Krasmut, and the magnitude of this decrease depended on both the number and timing of pregnancies. These multistage models may be useful for elucidating biological features of premalignant mammary neoplasia.
A 6-month partially supervised walking exercise training using a tapered approach. Participants begin with exercising (walking) in person, on-site one time per week and 3 times per week at home for a minimum exercise dosage of 30 minutes of accumulated exercise per session during month 1. During month 2, participants will exercise on-site once every other week and 3-4 times per week at home a minimum exercise dosage of 30 minutes of accumulated exercise per session. During months 2-6, participants will exercise at home 4 times per week for a minimum exercise dosage of 30 minutes of accumulated exercise per session and they will receive a phone call every two weeks to help coach and address any problems. Participants will receive a Fitbit fitness tracker that will be used to deliver their personalized exercise program, exercise monitoring, feedback, and motivational messages.
This is a multicenter, randomized, double-blind, double-dummy, active drug-parallel-controlled, phase 2 clinical study to evaluate the efficacy and safety of Anaprazole Sodium 40 mg QD and 60 mg QD versus Rabeprazole Sodium 20 mg QD in the treatment of reflux esophagitis in Chinese subjects with reflux esophagitis. The target population for this study was subjects with endoscopically confirmed reflux esophagitis. All potential participants will provide informed consent, and those who provide informed consent will enter the Screening Period (Day -7 to Day -1) and be assessed for screening eligibility according to the inclusion and exclusion criteria. The study is expected to enroll approximately 156 subjects with reflux esophagitis (LA classification grades A-D) who meet enrollment criteria (and none of the exclusion criteria), and eligible subjects will be randomized into 3 groups (Anaprazole Sodium 40 mg QD, 60 mg QD, and Rabeprazole Sodium 20 mg QD) in a 1:1: 1 ratio according to a predefined randomization table, with 52 subjects in each group. All subjects take the corresponding study drug within 30-60 minutes before breakfast for 4 or 8 consecutive weeks (subjects were followed up at Week 4 of treatment, and if the subject'endoscopy indicated that the reflux esophagitis was healed, the healed subject ended study treatment and entered safety follow-up. Subjects who were not cured were to continue treatment until 8 weeks if endoscopy at 4 weeks of treatment indicated that reflux esophagitis was not cured.). All subjects complete treatment at 4 or 8 weeks of treatment and were followed for safety. At the end of the study, statistical analysis will be performed on the efficacy and safety indicators of the study drug to compare the efficacy and safety of Anaprazole sodium and rabeprazole sodium in the treatment of reflux esophagitis. Participants will primarily be assessed for the cure rate of reflux esophagitis based on endoscopy of 3 groups. Participants' safety will be monitored throughout the study.
RYZNEUTA (efbemalenograstim alfa-vuxw) injection is a clear, colorless, preservative-free solution supplied in a prefilled single-dose syringe with a 27-gauge, 1/2-inch needle and an UltraSafe Passive™ Needle Guard, containing 20 mg of efbemalenograstim alfa-vuxw.

Caution: This product contains natural rubber latex which may cause allergic reactions. The needle cap of the prefilled syringe contains natural rubber; persons with latex allergies should not administer this product.

RYZNEUTA is provided in a dispensing pack containing one 20 mg/mL prefilled syringe (NDC 73491-627-01).

RYZNEUTA prefilled syringe does not bear graduation marks and is intended only to deliver the entire contents of the syringe (20 mg/mL) for direct administration to adult patients.

Store refrigerated at 2° to 8°C (36° to 46°F) in the carton to protect from light. Do not shake. Discard syringes stored at room temperature for more than 48 hours. Do not freeze. Discard syringe if frozen.
Safety and effectiveness in pediatric patients 3 years of age and older have been established for the treatment of acute iron intoxication and for the treatment of transfusional iron overload in patients with chronic anemia. Safety and effectiveness in pediatric patients under the age of 3 years have not been established. 

Iron mobilization with deferoxamine mesylate is relatively poor in patients under the age of 3 years with relatively little iron overload. Deferoxamine mesylate is not recommended for use. The drug should ordinarily not be given to these patients unless significant iron mobilization (e.g., 1 mg or more of iron per day) can be demonstrated. 

High doses of deferoxamine mesylate and concomitant low ferritin levels have been associated with growth suppression in pediatric patients. Monitor weight and height in pediatric patients receiving deferoxamine mesylate every 3 months  [see Warnings and Precautions (5.5), Adverse Reactions (6.1)].
The present teaching relates to automated trocar/robot base location determination. An input related to a surgical operation includes a three-dimensional (3D) model for an organ with cut points on the organ forming a surgical trajectory. A surgical instrument is controlled by a robot to reach the cut points to carry out the operation. An insertion location for inserting the surgical instrument is identified. Based on the identified insertion location, a robot base location is determined with respect to the identified insertion location to deploy the robot for controlling the surgical instrument to reach the cut points. Signals for configuring the surgical setting are then generated based on the insertion location for the surgical instrument and the base location for the robot.
Loss of synapses between spiral ganglion neurons and inner hair cells (IHC synaptopathy) leads to an auditory neuropathy called hidden hearing loss (HHL) characterized by normal auditory thresholds but reduced amplitude of sound-evoked auditory potentials. It has been proposed that synaptopathy and HHL result in poor performance in challenging hearing tasks despite a normal audiogram. However, this has only been tested in animals after exposure to noise or ototoxic drugs, which can cause deficits beyond synaptopathy. Furthermore, the impact of supernumerary synapses on auditory processing has not been evaluated. Here, we studied mice in which IHC synapse counts were increased or decreased by altering neurotrophin 3 (Ntf3) expression in IHC supporting cells. As we previously showed, postnatal Ntf3 knockdown or overexpression reduces or increases, respectively, IHC synapse density and suprathreshold amplitude of sound-evoked auditory potentials without changing cochlear thresholds. We now show that IHC synapse density does not influence the magnitude of the acoustic startle reflex or its prepulse inhibition. In contrast, gap-prepulse inhibition, a behavioral test for auditory temporal processing, is reduced or enhanced according to Ntf3 expression levels. These results indicate that IHC synaptopathy causes temporal processing deficits predicted in HHL. Furthermore, the improvement in temporal acuity achieved by increasing Ntf3 expression and synapse density suggests a therapeutic strategy for improving hearing in noise for individuals with synaptopathy of various etiologies.
A system for rehabilitation is disclosed. The system for rehabilitation includes a monitoring device that includes a memory device storing instructions and a network interface card. The monitoring device is configured to detect information from a body part of a user. The system for rehabilitation further includes one or more processing devices operatively coupled to the monitoring device. The one or more processing devices are configured to execute the instructions to receive configuration information specified in a treatment plan for rehabilitating the body part of the user. The one or more processing devices are configured to execute the instructions for receiving the information from the monitoring device. The one or more processing devices are further configured to execute the instructions to transmit the configuration information and the information to a computing device controlling an electromechanical device, via the network interface card.
Antioxidants given concurrently with chemotherapy offer an effective strategy for reducing the negative effects of the drug. One remaining obstacle to the use of doxorubicin (DOX) in chemotherapy is cardiotoxicity. Using vitamin E (Vit. E) as a reference standard, our study focuses on the potential preventive benefits of oxyresveratrol (ORES) and/or dapagliflozin (DAPA) against DOX-induced cardiac injury. Acute cardiotoxicity was noticed after a single intravenous injection of a male rat's tail vein with 10 mg/kg of DOX. Oral doses of ORES (80 mg/kg), DAPA (10 mg/kg), and Vit. E (1 g/kg) were given, respectively. Pretreatment of animals with Vit. E, ORES and/or DAPA revealed a considerable alleviation of heart damage, as evidenced by histopathological change mitigation and a notable drop in serum AST, LDH, CK, CK-MB, and cardiac contents of MDA and NO2-. Also, serum TAC, tissue GSH, and SOD showed substantial increases. Additionally, tissue caspase-3, serum IL-6, and TNF-α were considerably reduced. Moreover, a downregulation in cardiac gene expression of ATG-5, Keap-1, and NF-κB in addition to an upregulation of Bcl-2 gene expression and HO-1, Nrf-2, and PPAR-γ protein expression clearly appeared. Ultimately, ORES and/or DAPA have an optimistic preventive action against severe heart deterioration caused by DOX.
Proteins of the uncoupling protein (UCP) family or fragments thereof used as active ingredients in cosmetic or dermatological compositions, are new. Independent claims are also included for: (1) cosmetic, dermatological or pharmaceutical composition comprising a peptide as above; (2) cosmetic care method for reducing, eliminating or preventing excess subcutaneous fat and/or combating cellulite and/or combating the orange peel effect, comprising applying a composition as above to the skin. ACTIVITY : Dermatological; Anorectic. No biological data given. MECHANISM OF ACTION : Lipogenesis inhibitor. Pro-Leu-Asp-Thr-Ala-Lys-Val-Arg-Leu-Gln (0.5% of a 50 ppm solution) was added to cultures of 3T3-L1 pre-adipocyte cells before differentiation. On staining with oil red, the cells showed lower levels of lipid vesicles than control cells. No effect was observed if the peptide was added after differentiation.
Functional tricuspid regurgitation (TR) develops due to functional and structural alterations related to heart failure (HF), mitral valve disease and atrial fibrillation. An increase in cardiac filling pressure due to left ventricular (LV) systolic or diastolic dysfunction leads to left atrial, right atrial (RA) and right ventricular (RV) remodeling, which causes tricuspid annular dilatation and TR. The development of significant functional TR causes RV dysfunction and further dilation of RV, which deteriorates TR. Functional TR may occur with HF with preserved or reduced ejection fraction (EF), and the prevalence of moderate-to-severe functional TR is around 19% in patients with HF. Regardless of LVEF or pulmonary artery pressure, presence of moderate or severe functional TR is associated with more symptoms, reduced cardiac output, and worse renal function. A vicious cycle of significant TR, RV volume overload, adverse remodeling of RA, RV, and tricuspid annulus, and consequent aggravation of TR is suggested as a pathophysiologic mechanism of the poor clinical outcomes of patients with TR, and the presence of moderate or severe functional TR is a strong independent determinant of mortality in patients with HF. Because functional TR has a strong prognostic impact and plays an important pathophysiologic role in patients with HF, functional TR is suggested as a therapeutic target in HF. However, there have been no proven medical therapies for TR and only loop diuretics are cautiously recommended for relief of congestive symptoms in patients with severe TR and signs of RV failure. In patients with functional TR associated with systolic dysfunction, medical therapy for HF with a reduced EF may diminish functional TR by improving LV systolic function. Otherwise, the morbidity and mortality of patients with functional TR remain high and a novel therapeutic agent is needed to improve clinical outcomes of HF patients with functional TR and a preserved LV ejection fraction.

Sodium-glucose co-transporter 2 (SGLT2) inhibitors induce urinary excretion of glucose and sodium by blocking the SGLT2 transporter in the proximal tubule (8). SGLT2 inhibitor-induced natriuresis lower cardiac preload and reduce pulmonary congestion and systemic edema. SGLT2 inhibitors also restore tubuloglomerular feedback and lower the intraglomerular pressure by vasoconstriction of the afferent arterioles and consequently reduce hyperfiltration-related renal damage. The beneficial effects of SGLT2 inhibitors on the heart and kidneys may halt the vicious cardiorenal cycle in patients with functional TR (9), which results in deterioration of renal function, hospitalization for heart failure, and cardiovascular mortality.

Accordingly, the Enavogliflozin Outcome Trial in Functional Tricuspid Regurgitation (EVENT) will test the hypothesis that, compared with placebo, therapy with the SGLT2 inhibitor enavogliflozin for 18 months would improve clinical and echocardiographic outcomes in HF patients with functional TR and preserved LVEF.