anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
SYMBICORT 80/4.5 and SYMBICORT 160/4.5 each contain micronized budesonide and micronized formoterol fumarate dihydrate for oral inhalation only. 

Each SYMBICORT 80/4.5 and SYMBICORT 160/4.5 canister is formulated as a hydrofluoroalkane (HFA 227; 1,1,1,2,3,3,3-heptafluoropropane)-propelled pressurized metered dose inhaler containing either 60 or 120 actuations [see Dosage Forms and Strengths (3) and How Supplied/Storage and Handling (16)]. After priming, each actuation meters either 91/5.1 mcg or 181/5.1 mcg from the valve and delivers either 80/4.5 mcg, or 160/4.5 mcg (budesonide micronized/formoterol fumarate dihydrate micronized) from the actuator. The actual amount of drug delivered to the lung may depend on patient factors, such as the coordination between actuation of the device and inspiration through the delivery system. SYMBICORT also contains povidone K25 USP as a suspending agent and polyethylene glycol 1000 NF as a lubricant. 

SYMBICORT should be primed before using for the first time by releasing two test sprays into the air away from the face, shaking well for 5 seconds before each spray. In cases where the inhaler has not been used for more than 7 days or when it has been dropped, prime the inhaler again by shaking well for 5 seconds before each spray and releasing two test sprays into the air away from the face. 

One active component of SYMBICORT is budesonide, a corticosteroid designated chemically as (RS)-11β, 16α, 17,21-Tetrahydroxypregna-1,4-diene-3,20-dione cyclic 16,17-acetal with butyraldehyde. Budesonide is provided as a mixture of two epimers (22R and 22S). The empirical formula of budesonide is C25H34O6 and its molecular weight is 430.5. Its structural formula is:

Budesonide is a white to off-white, tasteless, odorless powder which is practically insoluble in water and in heptane, sparingly soluble in ethanol, and freely soluble in chloroform. Its partition coefficient between octanol and water at pH 7.4 is 1.6 x 103.

The other active component of SYMBICORT is formoterol fumarate dihydrate, a selective beta2-agonist designated chemically as (R*,R*)-(±)-N-[2-hydroxy-5-[1-hydroxy-2-[[2-(4-methoxyphenyl)-1-methylethyl]amino]ethyl]phenyl]formamide, (E)-2-butendioate(2:1), dihydrate. The empirical formula of formoterol is C42H56N4O14 and its molecular weight is 840.9. Its structural formula is:

Formoterol fumarate dihydrate is a powder which is slightly soluble in water. Its octanol-water partition coefficient at pH 7.4 is 2.6. The pKa of formoterol fumarate dihydrate at 25°C is 7.9 for the phenolic group and 9.2 for the amino group.
This is a a real world registry study. All patients with hypertension in community hospitals in China will be eligible . Patient demographics, medical history, clinical characteristics, physical examination, laboratory tests (including UCAR, blood routine, urine routine, blood biochemistry, and ECG), antihypertensive drugs (including: ACEI/ ARB, thiazide diuretics, CCB, beta-blockers, alpha-blockers, and other antihypertensive drugs used in real-life clinical practice in other communities.) will be recorded. All patients are anticipated to be followed up for 12-month. Effectiveness of different antihypertensive medications on Urine Albumin-to-Creatinine Ratio (UACR) will be evaluted.
ALDARA Cream should be applied 5 times per week for a full 6 weeks to a biopsy-confirmed sBCC. An example of a 5 times per week application schedule is to apply ALDARA Cream, once per day, Monday through Friday. ALDARA Cream should be applied prior to normal sleeping hours and left on the skin for approximately 8 hours, after which time the cream should be removed by washing the area with mild soap and water. The prescriber should demonstrate the proper application technique to maximize the benefit of ALDARA Cream therapy. 

It is recommended that patients wash their hands before and after applying ALDARA Cream. The patient should wash the treatment area with mild soap and water before applying the cream, and allow the area to dry thoroughly.

The target tumor should have a maximum diameter of 2 cm and be located on the trunk (excluding anogenital skin), neck, or extremities (excluding hands and feet). The treatment area should include a 1 cm margin of skin around the tumor. Sufficient cream should be applied to cover the treatment area, including 1 cm of skin surrounding the tumor. ALDARA Cream should be rubbed into the treatment area until the cream is no longer visible.

Contact with the eyes, lips, and nostrils should be avoided.

Local skin reactions in the treatment area are common [see Adverse Reactions (6.2, 6.5)]. A rest period of several days may be taken if required by the patient's discomfort or severity of the local skin reaction. 

Early clinical clearance cannot be adequately assessed until resolution of local skin reactions (e.g., 12 weeks post-treatment). Local skin reactions or other findings (e.g., infection) may require that a patient be seen sooner than the post-treatment assessment for clinical clearance. If there is clinical evidence of persistent tumor at the post-treatment assessment for clinical clearance, a biopsy or other alternative intervention should be considered. Lesions that do not respond to therapy should be carefully re-evaluated and management reconsidered; the safety and efficacy of a repeat course of ALDARA Cream treatment have not been established. If any suspicious lesion arises in the treatment area at any time after a determination of clinical clearance, the patient should seek a medical evaluation [see Clinical Studies (14.2)] . 

ALDARA Cream is packaged in single-use packets, with 12 packets supplied per box. Patients should be prescribed no more than 36 packets for the 6-week treatment period. Unused packets should be discarded. Partially used packets should be discarded and not reused.
Patients head and neck CT scans performed as standard of care done prior to radiation treatment and approximately 12 weeks following treatment, will be acquired in the dual-energy computed tomography (DECT) mode. Participants will have one additional scan, also in the DECT mode, 2 to 3 weeks after the start of their radiation treatment.
The invention discloses a new pharmaceutical application of schisanhenol and a preparation method of a homogenized suspension of schisanhenol. The homogenized suspension is used for treating Parkinson disease and expanding the application range of schisanhenol, and also provides a potential drug candidate for the treatment of Parkinson disease. A new preparation method is adopted, which is implemented by preparing schisanhenol into a homogenized suspension, and the homogenized suspension is applied to the oral medication of experimental animals. Animal experiments show that in a MPTP induced parkinson rat model, the schisanhenol homogenized suspension can significantly improve the dyskinesia of experimental animals, and shows a good dose-dependent trend. Concrete embodiments are as follows: compared with a model set, the number of falling of a rat taking the schisanhenol homogenized suspension is significantly reduced, and the incubation period is obviously increased; and the climbing time of a rat detected by using a pole climbing method is significantly shortened, and the dyskinesia score is significantly reduced. The schisanhenol homogenized suspension has a good treatment effect on schisanhenol.
PCT No. PCT/US95/09702 Sec. 371 Date Apr. 28, 1997 Sec. 102(e) Date Apr. 28, 1997 PCT Filed Jul. 31, 1995 PCT Pub. No. WO96/04281 PCT Pub. Date Feb. 15, 1996The present invention provides AGT inactivating compounds such as substituted O6-benzylguanines of the formula wherein, for example, R1 is amino, hydroxy, or alkylamino, R2 is aminoalkyl, hydroxyalkyl, or alkylaminoalkyl, and R3 is halo, hydroxyalkyl, thiol or alkylthio, as well as pharmaceutical compositions comprising such compounds and a pharmaceutically acceptable carrier. The present invention further provides a method of enhancing the chemotherapeutic treatment of tumor cells in a mammal with an antineoplastic alkylating agent which causes cytotoxic lesions at the O6-position of guanine comprising administering to a mammal an effective amount of one of the aforesaid compounds and administering to the mammal an effective amount of an antineoplastic alkylating agent which causes cytotoxic lesions at the O6-position of guanine.
Polymerizable saccharide monomers are made by the reaction of a saccharose and a (meth)acrylate. Hydrophilic, hydrophobic and thermoreversible gels and foams are formed upon polymerization of the saccharide monomers. Hydrophilic sucrose monomers are synthesized by reaction of sucrose with an epoxy acrylate. Hydrophobic sucrose monomers are synthesized by reaction of sucrose with methacrylol chloride followed by acetyl chloride. Thermoreversible sucrose monomers are obtained by modifying sucrose with polymerizable substituents prepared from methacryloyl chloride and aminocarboxylic acids. The modified sucrose monomers are copolymerized with hydrophobic poly(alkyleneoxide) (meth)acrylates to produce hydrogels exhibiting inverse thermoreversible properties. The thermosensitive hydrogels are biodegradable and can be used in the area of controlled drug delivery.
According to the results of the single-dose study, it is planned to carry out multiple-dose studies in 1 to 3 dose groups. A total of 12 subjects in each dose group, of which 10 received the test drug, 2 received placebo. It is necessary to decide the multiple administration method and dosage according to the result of single administration, which is initially determined to be once a day. After the first dose, Day3, Day6, Day8 and Day12 were evaluated for tolerance, and the next group of tests was conducted under the premise that the previous group of Day12 tolerance evaluation was tolerated.
Treatment cycles will repeat until there is evidence of progressive disease (PD), toxicity, or withdrawal. If any participant experiences a dose-limiting toxicity (DLT), an additional 3 participants will be enrolled at this dose level (for a total of 6). If no further DLTs, enrollment into Cohort 2 will occur.
According to one embodiment of the present invention, an artificial intelligence-based brain information providing apparatus includes: a brain signal measurement part collecting a signal related with the brain of a user; a brain signal stimulation part for stimulating the brain of the user for a signal collection operation of the brain signal measurement part; and a diagnosis part determining a brain state of the user, based on the collected signal. The signal collection operation of the brain signal measurement part is performed in a state in which the user is moving, and the diagnosis part determines the brain state of the user based on at least one brain activation area extracted consecutively for a predetermined period. The apparatus also includes: an image collection part collecting a medical image related with the user; and a user data collection part collecting body information related with the user. The diagnosis part determines the brain state of the user using the at least one brain activation area, the body information related with the user and the medical image related with the user. The diagnosis part determines a brain disease of the user. The brain disease includes dementia, mild cognitive impairment (MCI), parkinsonism, a depression, a stroke, epilepsy, a brain tumor and a developmental disorder. The apparatus also includes a management part providing information for improving the brain state of the user in response to the brain state of the user determined by the diagnosis part. Therefore, the present invention is capable of helping to develop the brain in a healthy way by avoiding the use of anesthetic drugs.
BACKGROUND: Chronic nonspecific low back pain (CNLBP) is a common disorder in people of active ages and significantly affects their quality of life. Different structures in the lumbar area can cause LBP. The lumbar muscle disorders, including the psoas major (PM) muscles, have an essential role in LBP. Magnetic Resonance Imaging (MRI) has been introduced as a safe and useful instrument for investigating the morphological properties of skeletal muscle. In general, PM morphology changes may be one reason for the pain and disability experienced in CNLBP patients. Thus, this study aimed to assess the relationship among the PM's Cross-sectional area (CSA), medial-lateral (ML), and anterior-posterior (AP) diameters, with disability index and pain score in patients with CNLBP.
METHOD: One hundred twenty patients with CNLBP (60 men and 60 women) participated in this cross-sectional study. Axial MRIs were obtained from L3/L4 and L4/L5 disc levels. Then, patients filled out Rolland Morris Disability Questionnaires, demographic data forms, and the Numeric Pain Rating Scale (NPRS). Image J software was used to analyze the images. Using Linear Regression and the Pearson test, the correlation between muscle CSA and diameters, as well as data obtained from questionnaires and NPRS, was analyzed.
RESULTS: Results from the statistical analysis showed no statistically significant relationship among morphological characteristics of the psoas major muscle in L3/L4 and L4/L5 disc levels with disability index and pain score (p < 0.05).
CONCLUSIONS: There is no significant relationship between the PM morphological characteristics and disability index and pain score. Therefore, muscle CSA and diameters are insufficient to determine the cause of CNLBP.
The primary aim of this multi-site, multi-clinician randomized controlled trial is to determine if Memory and Attention Adaptation Training (MAAT), a cognitive-behavioral therapy (CBT) intervention, can improve self-reported and objectively measured cognitive functioning in breast cancer survivors who previously received chemotherapy. Breast cancer survivors (Stage I-III) who were treated with chemotherapy 1-5 years prior to enrollment and who have subjective cognitive complaints may be eligible for this study. After eligibility is confirmed, participants will complete baseline assessments of subjective and objective memory and attention functioning as well as behavioral rating scales, and will be randomized to MAAT or Supportive Therapy (ST; to control for therapist time and attention) for 8 weeks. Both treatments (MAAT and ST) will be delivered through videoconferencing using mobile (smartphone, laptop or other electronic device) in order to reduce survivor travel or time away from work or family. Data collection methods will include telephone- and web-administered measures of subjective and objective cognitive function, as well as various behavioral ratings. Outcome assessments will be conducted post-treatment and at 6-month follow-up. It is hypothesized that MAAT participants will have significantly improved scores of self-reported cognitive impairments and objective neurocognitive test scores (on verbal memory and processing speed) at post-treatment and 6-month follow-up compared to participants randomized to ST. In addition, willing and eligible participants will be asked to complete a functional MRI working memory task at baseline and post-treatment, to examine whether those who receive MAAT show greater increase in brain network activation than those who receive ST. This may advance understanding of the neural mechanisms underlying improvement of objective and self-reported cognitive function after chemotherapy. The sample size (n=100/group) will allow for a 10-15% drop out-rate and still provide 80% power to detect group differences using two (Group: MAAT vs. ST) by 3 (time: baseline, posttreatment, 6-month follow-up) ANCOVA at alpha=0.05. Potential baseline differences between MAAT and ST groups on primary outcome variables or other factors that may affect cognition (e.g., anxiety, fatigue or depression) will be evaluated as potential covariates, although such differences due to randomization are not anticipated.
The present invention provides an AD converter used to convert analog input signals into digitized digital output signals. The AD converter contains a plurality of comparators, a high-order field decision unit, a low-order field calculating unit and a low-order field decision unit. The comparators are used to compare the analog input signal with the analog threshold values corresponding to the assigned digital threshold values of each comparator. The high-order decision unit is used to decide a data value corresponding to the high-order field of digital output signal, based on different comparation results from the comparators. The low order field calculating unit utilizes the comparators to calculate candidate values of a data value corresponding to the low-order field at the lower side of the high-order field. The low-order field decision unit is to decide a data value corresponding to the low-order field according to the candidate values.
The invention describes novel formulations of nonsteroidal anti-inflammatory drugs (NSAIDS) based on complex aggregates with at least three amphipatic components suspended in a suitable, e.g. pharmaceutically acceptable, polar liquid medium. A suitably ionised NSAID is one of the two, amongst said three, components that tends to destabilise lipid membranes, the other system component with such activity being typically a surfactant. In contrast, the remaining amongst said at least three amphipatic components typically forms a stable lipid membrane on it's own. An essential characteristics of the resulting, relatively large, aggregates is an improved ability to penetrate pores, in a semi-permeable barrier, at least 30%, and often much smaller than the average diameter of the complex aggregate. This enables said aggregates to mediate NSAID transport through semi-permeable barriers including mammalian skin. As a result of the skin penetration by NSAID loaded large aggregates, the drug delivered transcutaneously with such carriers gets deeper into the tissue than the corresponding NSAID from a solution on the skin surface. This is believed to be due to the special ability of suitable large carriers to bypass the local sink of blood capillaries at the epidermal-dermal junction in the skin. The carrier-mediated delivery of locally applied NSAIDs thus allows therapy of deep tissues under the drug administration site, which is medically highly desirable.
BACKGROUND: The skeletal muscle atrophy is prevalently occurred in numerous chronic disease complications. Despite its important clinical significance, there are currently no therapeutic drugs, so new biomarkers and molecular mechanisms need to be discovered urgently.
METHODS: Transcriptome and proteome sequencing data were collected from normal and skeletal muscle atrophic mice. The differentially expressed genes (DEGs) and proteins (DEPs) were analyzed. Applying PPI analysis to obtain overlapping genes and proteins, which were next subjected to GO and KEGG enrichment analysis. Combined analysis of transcriptomics and proteomics was performed to get key genes that were simultaneously found in GO and KEGG enrichment results. Subsequently, RT-qPCR and immunofluorescence were constructed to verify the expression of screened key genes.
RESULTS: By combination of transcriptomics, proteomics and RT-qPCR results, we identified 14 key genes (Cav1, Col3a1, Dnaja1, Postn, Ptges3, Cd44, Clec3b, Igfbp6, Lamc1, Alb, Itga6, Mmp2, Timp2 and Cd9) that were markedly different in atrophic mice. Single-gene GSEA and immunofluorescence suggested Cd9 was probably the biomarker for skeletal muscle atrophy.
CONCLUSIONS: Our study hinted that Cd9 was potential biomarker and may interfere with skeletal muscle atrophy through process of aerobic respiration, oxidative phosphorylation, and metabolism of amino acids and fatty acids.
SIGNIFICANCE: The present study holds the subsequent significance: Frist, we investigated biomarkers for skeletal muscle atrophy using multi-omics approach. A total of 14 genes were markedly different in skeletal muscle atrophic mice. We finally found Cd9 is a potential biomarker for skeletal muscle atrophy. Our work presents novel biomarkers and potential regulatory mechanisms for the early detection and intervention of muscle atrophy.
OBJECTIVES: I. Determine the maximum tolerated dose, dose limiting toxicity, recommended phase II dose, and safety of BMS-214662 in patients with advanced solid tumors. II. Determine the pharmacokinetics of BMS-214662 in these patients. III. Assess the absolute oral bioavailability of BMS-214662 using a capsule and single intravenous dose in these patients. IV. Determine any preliminary evidence of antitumor activity of BMS-214662 in these patients.

OUTLINE: This is a dose escalation study. Patients receive BMS-214662 IV over 1 hour on day -7, followed by oral BMS-214662 daily on days 0-14 for course 1 only. Beginning with course 2, patients receive oral BMS-214662 twice daily for 14 days. Treatment continues every 3 weeks in the absence of disease progression or unacceptable toxicity. Cohorts of 3-6 patients receive escalating doses of BMS-214662 until the maximum tolerated dose (MTD) is determined. The MTD is defined as the dose at which fewer than 2 of 6 patients experience dose limiting toxicity. Patients are followed every 4 weeks until toxicities resolve.

PROJECTED ACCRUAL: A total of 30-40 patients will be accrued for this study within 12-18 months.
The invention relates to a brewing method for pine pollen wine. In the prior art, the brewing method for the pine pollen wine has not characteristics of simple production process, low brewing cost and good efficacy of the prepared pine pollen wine. The brewing method provided by the present invention is characterized in that: raw materials of the pine pollen wine comprise: 48.0 g of broken pine pollen, 16.0 g of medlar, 24.0 g of tuckahoe, 18.0 g of mycelium of cultured cordyceps sinensis, 1.6 g of taurine, sorghum wine having a volume percent concentration of 50% and water. The method sequentially comprises processes of immersing, blending, filtering and filling. During the dipping process and the blending process, the broken pine pollen, the medlar, the tuckahoe, the mycelium of cultured cordyceps sinensis and the taurine are placed in a immersion tank, followed by adding the sorghum wine and immersing for 20-30 days to obtain supernatant; the supernatant is filtered through a pressure filtration to obtain filtrate, followed by adding water to blend the filtrate to a volume percent of 36%. During the filtering process, the filtrate from the dipping process and the blending process is filtered again to obtain the secondary filtrate, followed by standing for 48 hours to obtain half-finished product wine. The method provided by the present invention has advantages of simple production process, low brewing cost and good efficacy of the prepared pine pollen wine.
Laparoscopic Roux-en-Y gastric bypass (LRYGB) and laparoscopic sleeve gastrectomy (LSG) are to bariatric procedure. After both procedures, a changed secretion of hormones from the gastrointestinal tract is believed to affect appetite and glucose metabolism. Studies have shown that after LRYGB, there is a significant increased secretion of GLP-1 and PYY. In contrast, a decreased secretion of ghrelin is a characteristic finding after LSG opposite post-LRYGB, where secretion of ghrelin is reported to be increased, decreased or unchanged. Ghrelin is primarily secreted from the gastric mucosa in the fasting state and decreases in response to food intake. Ghrelin stimulates food intake through appetite-regulating centers in the hypothalamus. Administration of exogenous ghrelin has been reported to stimulate appetite. In addition, ghrelin has recently been suggested also to affect glucose metabolism by inhibition of glucose-stimulated insulin secretion. Therefore the markedly decreased secretion of ghrelin could be of particular important for the decreased appetite and improved glucose tolerance seen after LSG.