anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
The primary objective for this study was to measure the reduction in GERD symptoms as evidenced by analysis of the GERD-HRQL questionnaire at 3-months post-procedure with an objective of achieving a 50% or greater improvement. The trial was powered to detect a 50% reduction in mean GERD-HRQL at 3-months using a one-sided t-test with an α of .05 and a β level of .10, testing versus the equality of means. The calculation referenced above includes the added assumption that the standard deviation will be no more than 20 percent. The null hypothesis stated that the mean percent reduction in GERD symptoms was less than or equal to 50 percent at 3-months versus the alternate hypothesis that it was greater. The device treatment was considered a success if the statistical test rejected the null hypothesis at a one-sided p-value of 0.05 or less. Primary endpoint success was thus related to the statistical conclusion that the mean percent reduction was greater than 50%. A one-sided 95 percent confidence interval was constructed for the percent reduction in GERD symptoms. In order to assess the data with an "Intent to Treat" spirit, the number of patients who achieved a 50% reduction was analyzed as a fraction of the total number of patients who received the treatment.

For secondary endpoint measures, statistical tests for medians were based on a Wilcoxon sign rank test of the percent improvement in a given study measure. This was based on the paired patient data of the pre-treatment scores versus the 6-month scores. The issue of multiple statistical tests of hypothesis being performed on data arising from individual patients was addressed in the following way. The comparison of GERD-HRQL scores was taken as the main results for which no correction of significance level was necessary. To recognize multiple testing using the method of Bonferroni, statistical significance was claimed for the secondary results only if, for a single test, the nominal p-value was \<.01. Given that some patients, during the course of the clinical study, were lost to follow-up, all outcomes were examined using the method of last visit carried forward, provided that at least one follow-up visit had been completed. It should be noted that using this method had little impact on the results; as compared to an analysis of the data of just those patients who completed follow-up, excluding those who missed the visit or were lost to follow up. However, this method was employed to account for those patients who were lost to follow-up, with specific consideration to those who had been lost to follow-up due to unsatisfactory treatment effect. Means and standard deviations are reported using the mean (SD) format, medians and interquartile ranges are reported using the median (IQR) format.
BACKGROUND: Huntington's disease (HD) is marked by a CAG-repeat expansion in the huntingtin gene that causes neuronal dysfunction and loss, affecting mainly the striatum and the cortex. Alterations in the neurovascular coupling system have been shown to lead to dysregulated energy supply to brain regions in several neurological diseases, including HD, which could potentially trigger the process of neurodegeneration. In particular, it has been observed in cross-sectional human HD studies that vascular alterations are associated to impaired cerebral blood flow (CBF). To assess whether whole-brain changes in CBF are present and follow a pattern of progression, we investigated both resting-state brain perfusion and vascular reactivity longitudinally in the zQ175DN mouse model of HD.
METHODS: Using pseudo-continuous arterial spin labelling (pCASL) MRI in the zQ175DN model of HD and age-matched wild-type (WT) mice, we assessed whole-brain, resting-state perfusion at 3, 6 and 9 and 13 months of age, and assessed hypercapnia-induced cerebrovascular reactivity (CVR), at 4.5, 6, 9 and 15 months of age.
RESULTS: We found increased perfusion in cortical regions of zQ175DN HET mice at 3 months of age, and a reduction of this anomaly at 6 and 9 months, ages at which behavioural deficits have been reported. On the other hand, under hypercapnia, CBF was reduced in zQ175DN HET mice as compared to the WT: for multiple brain regions at 6 months of age, for only somatosensory and retrosplenial cortices at 9 months of age, and brain-wide by 15 months. CVR impairments in cortical regions, the thalamus and globus pallidus were observed in zQ175DN HET mice at 9 months, with whole brain reactivity diminished at 15 months of age. Interestingly, blood vessel density was increased in the motor cortex at 3 months, while average vessel length was reduced in the lateral portion of the caudate putamen at 6 months of age.
CONCLUSION: Our findings reveal early cortical resting-state hyperperfusion and impaired CVR at ages that present motor anomalies in this HD model, suggesting that further characterization of brain perfusion alterations in animal models is warranted as a potential therapeutic target in HD.
<P>PROBLEM TO BE SOLVED: To provide a home health management system for reducing the burden on a doctor by automatically diagnosing health based on health data of an assignor who entrusts home health management and association data, and sharing the data by individual medical institutes, and quickly utilizing the data when the illness symptom of the assignor is developed.  <P>SOLUTION: Measurement equipment 2 for measuring data on health of an assignor 1 at home and home side terminal equipment 3 equipped with a storage device 3a in which the data are stored are connected through the Internet to a host computer 4a of a health management center 4. Response data from the health management center 4 are output to the home side terminal equipment 3. Each assignor 1 at home is registered in the file of the storage device of the host computer 4a. Basic data configured of the data stored in the storage device 3a of the home side terminal equipment 3 of each assignor 1 at home the principal specification data and the response data are stored in a database 4b of the host computer 4a. The server of the host computer 4a is connected through a communication line to an individual medical institute 5.  <P>COPYRIGHT: (C)2009,JPO&INPIT
Disclosed is a process for processing ginseng honey date, which is characterized in that the processing approaches comprises that 1) a red date is served as the carrier, and a ginseng is served as the main medicine, and the haw, banksia rose, radix adenophorae, codonopsis pilosula, astragalus root, salvia miltiorrhizae, motherwort, kudzuvine root, pericarpium, white mustard seed, root bark of tree peony, tuckahoe, turtle, cordyceps sinensis and honey are compounded according to the proportion. 2) The materials are put into the water pan to be cooked for one hour. 3) The red date is fished out to be dried and securely packed by food bags. The invention has the advantages that the ginseng honey date can enhance the organism immunity and corporeity, and the medicine is contained in the food as a whole. After eating, the ordinary people can strengthen the bodies, and the weak people can be nourished. The eating is convenient, and the storage is easy.
Each 5 mL (one teaspoonful), for oral administration contains: Promethazine hydrochloride 6.25 mg; codeine phosphate 10 mg in a flavored oral solution base with a pH between 4.7 and 5.2. Alcohol 7%. 

Inactive Ingredients: Artificial raspberry flavor, ascorbic acid, citric acid anhydrous, D&C Red #33, dehydrated alcohol, edetate disodium, FD&C Blue #1, glycerin, liquid sugar, methylparaben, purified water, saccharin sodium, sodium benzoate, sodium citrate dihydrate and sodium propionate. 

Codeine is one of the naturally occurring phenanthrene alkaloids of opium derived from the opium poppy; it is classified pharmacologically as a narcotic analgesic. Codeine phosphate may be chemically designated as 7,8-Didehydro-4,5α-epoxy-3-methoxy-17-methylmorphinan-6α-ol phosphate (1:1)(salt) hemihydrate. 

The phosphate salt of codeine occurs as white, needle-shaped crystals or white crystalline powder. Codeine phosphate is freely soluble in water and slightly soluble in alcohol. It has a molecular weight of 406.37, a molecular formula of C 18H 21NO 3•H 3PO 4•½H 2O, and the following structural formula: 

Promethazine hydrochloride, a phenothiazine derivative, is chemically designated as (±)-10-[2-(Dimethylamino)propyl] phenothiazine monohydrochloride.

Promethazine hydrochloride occurs as a white to faint yellow, practically odorless, crystalline powder which slowly oxidizes and turns blue on prolonged exposure to air. It is soluble in water and freely soluble in alcohol. It has a molecular weight of 320.88, a molecular formula of C 17H 20N 2S•HCl, and the following structural formula:
PURPOSE:To obtain an agent for the prevention or treatment of absorptive bone diseases such as malignant hypercalcemia, Paget's disease of bone and osteoporosis by using a naphthalene derivative as an active component. CONSTITUTION:This agent for the prevention and treatment of bone diseases contains a naphthalene derivative of the formula (R<1> and R<2> are H or OH; R<3> is H or methyl) as an active component. The compound of formula is e.g. podophyllotoxin, desoxypodophyllotoxin, 4'-demethylpodophyllotoxin, alpha-peltatin and beta-peltatin. The compound of formula has an action to suppress the isolation of calcium and inorganic phosphoric acid from the calvaria of cultured neonatal mouse induced by PTHrp(1-34) which is a peptide relating to parathyroid hormone. It suppresses the calcium concentration in blood in PTHrp(1-34)-induced hypercalcemia by the premedication in an in vivo experiment.
PURPOSE: A composition containing a crude extract of Zingiber zerumbet is provided to enhance radiation treatment effect for cancer or radioresistant cancer. CONSTITUTION: A composition for enhancing radiation treatment for cancer contains a crude extract of Zingiber zerumbet or non-polar solvent soluble extract of the crude extract as an active ingredient. The crude extract is extract of water, C1-C4 alcohol or mixture solvent thereof. The non-polar solvent soluble extract is extract solubilized in n-hexane, dichloromethane, chloroform, or ethyl acetate. A composition for enhancing radiation treatment for cancer contains humulene derivatives of chemical formula 1 or 2 or pharmaceutically acceptable salt thereof as an active ingredient. The compound of chemical formula 1 is isolated from Zingiber zerumbet.
Endothelial glycocalyx (eGC) covers the inner surface of the vessels and plays a role in vascular homeostasis. Syndecan is considered the "backbone" of this structure. Several studies have shown eGC shedding in sepsis and its involvement in organ dysfunction. Matrix metalloproteinases (MMP) contribute to eGC shedding through their ability for syndecan-1 cleavage. This study aimed to investigate if doxycycline, a potent MMP inhibitor, could protect against eGC shedding in lipopolysaccharide (LPS)-induced sepsis and if it could interrupt the vascular hyperpermeability, neutrophil transmigration, and microvascular impairment. Rats that received pretreatment with doxycycline before LPS displayed ultrastructural preservation of the eGC observed using transmission electronic microscopy of the lung and heart. In addition, these animals exhibited lower serum syndecan-1 levels, a biomarker of eGC injury, and lower perfused boundary region (PBR) in the mesenteric video capillaroscopy, which is inversely related to the eGC thickness compared with rats that only received LPS. Furthermore, this study revealed that doxycycline decreased sepsis-related vascular hyperpermeability in the lung and heart, reduced neutrophil transmigration in the peritoneal lavage and inside the lungs, and improved some microvascular parameters. These findings suggest that doxycycline protects against LPS-induced eGC shedding, and it could reduce vascular hyperpermeability, neutrophils transmigration, and microvascular impairment.
Low back pain (LBP) is a common issue that negatively affects a person's quality of life and imposes substantial healthcare expenses. In this study, we introduce the (Back-pain Movement) BackMov test, using inertial motion capture (MoCap) to assess lumbar movement changes in LBP patients. The test includes flexion-extension, rotation, and lateralization movements focused on the lumbar spine. To validate its reproducibility, we conducted a test-retest involving 37 healthy volunteers, yielding results to build a minimal detectable change (MDC) graph map that would allow us to see if changes in certain variables of LBP patients are significant in relation to their recovery. Subsequently, we evaluated its applicability by having 30 LBP patients perform the movement's test before and after treatment (15 received deep oscillation therapy; 15 underwent conventional therapy) and compared the outcomes with a specialist's evaluations. The test-retest results demonstrated high reproducibility, especially in variables such as range of motion, flexion and extension ranges, as well as velocities of lumbar movements, which stand as the more important variables that are correlated with LBP disability, thus changes in them may be important for patient recovery. Among the 30 patients, the specialist's evaluations were confirmed using a low-back-specific Short Form (SF)-36 Physical Functioning scale, and agreement was observed, in which all patients improved their well-being after both treatments. The results from the specialist analysis coincided with changes exceeding MDC values in the expected variables. In conclusion, the BackMov test offers sensitive variables for tracking mobility recovery from LBP, enabling objective assessments of improvement. This test has the potential to enhance decision-making and personalized patient monitoring in LBP management.
Participants from central Mississippi are provided with 24 months of interpregnancy care. The results from this arm are compared to a historical control group (who were not given interpregnancy care) from the same geographical area in Mississippi.
The aim of this protocol is to allow genetic-related evaluations for patients with a variety of known or suspected genetic disorders.) If not eligible for a specific NICHD research protocol, patients with genetic-related conditions may be evaluated under the auspices of this protocol to provide stimuli for new clinical research initiatives. Standard medically-indicated laboratory or radiological studies may be performed to confirm a diagnosis or to aid in the management of the patient. Clinical data and excess biospecimens collected as part of clinical care will be analyzed for research purposes. In some cases, the subjects may receive medical or surgical treatment for their disorder at the NIH CC according to current clinical practice. The overall purpose of genetic evaluations under this protocol is to support our research missions, generate hypotheses bank specimens for analysis or future use as controls. Family members of subjects evaluated on this protocol (who have informative meiotic inheritance relationships to the proband or index case) may also be enrolled.
The invention comprises compounds of the general formula: <FORM:0863546/IV (b)/1> and acid addition salts thereof, wherein R1 is a methyl group, each of R2 and R3 are hydrogen atom or an alkyl group (up to 4 carbon atoms) and R4 is a hydrogen atom, and the preparation thereof by condensing a phenthiazine of the general formula:  <FORM:0863546/IV (b)/2> with a halo alkyl amine of the general formula:  <FORM:0863546/IV (b)/3> wherein X is a chlorine or a bromine atom, if desired in the presence of an alkaline condensation and a solvent. Specifications 802,725, 802,726 and 863,547 are referred to.  Reference has been directed by the Comptroller to Specification 802,725.ALSO:Pharmaceutical compositions comprise compounds of the general formula <FORM:0863546/VI/1> or their acid addition salts wherein R1 is a methyl group, each of R2 and R3 is a hydrogen atom or a C1-4 alkyl group and R4 is a hydrogen atom, and an inert carrier. Compositions include tablets and solutions for parenteral or local application.  Acid addition salts include the hydrochlorides, hydrobromides, sulphates, citrates, tartrates, succinates, maleates, acetates, benzoates and hexahydrobenzoates. Specifications 802,725, 802,726 and 863,547 are referred to.  Reference has been directed by the Comptroller to Specification 802,725.
Methylphenidate hydrochloride extended-release tablets, USP are a central nervous system (CNS) stimulant. Methylphenidate hydrochloride extended-release tablets, USP are available in four tablet strengths. Each extended-release tablet for once-a-day oral administration contains 18 mg, 27 mg, 36 mg, or 54 mg of methylphenidate hydrochloride, USP and is designed to have a 12-hour duration of effect. Chemically, methylphenidate hydrochloride, USP is d,l (racemic) methyl α-phenyl-2-piperidineacetate hydrochloride. Its molecular formula is C14H19NO2•HCl. Its structural formula is: 

Methylphenidate hydrochloride, USP is a white, odorless crystalline powder. Its solutions are acid to litmus. It is freely soluble in water and in methanol, soluble in alcohol, and slightly soluble in chloroform and in acetone. Its molecular weight is 269.77. 

Methylphenidate hydrochloride extended-release tablets, USP also contain the following inert ingredients: colloidal silicon dioxide, fumaric acid, hypromellose 2208, hypromellose 2910, lactose monohydrate, magnesium stearate, methacrylic acid copolymer Type A, methacrylic acid copolymer Type B, talc, titanium dioxide, and triethyl citrate. The 18 mg strength also contains iron oxide red, iron oxide yellow, polyethylene glycol 3350, and polyvinyl alcohol. The 27 mg strength also contains FD&C Blue #2/Indigo Carmine Aluminum Lake, iron oxide black, iron oxide yellow, polyethylene glycol 3350, and polyvinyl alcohol. The 36 mg strength also contains triacetin. The 54 mg strength also contains iron oxide red, polyethylene glycol 3350, and polyvinyl alcohol. The imprinting ink contains ammonium hydroxide, iron oxide black, propylene glycol, and shellac.

Meets USP Dissolution Test 11.
A food product. Minimum of 2 minutes of chew time prior to salivary sample being obtained.
BSg group comprised 20 procedures performed in patients OAT. At the moment of surgery, the contents of an anestube (1.8 ml) were mixed with a sufficient amount of BS powder to obtain a paste similar in consistency to tooth-paste (29). A thin layer of the paste was applied on the bone ridge, and buccal and palatal-lingual flaps were then repositioned and sutured as in the Cg. compression on the wound with a dry gauze for 30 minutes, after which a new dry gauze was placed for another two hours.
OBJECTIVE: Glucagon-like peptide-1 (GLP1) and leptin (Lep) are afferent signals that regulate energy metabolism. Lactational hypernutrition results in hyperphagia and adiposity in adult life, and these events can be prevented by exercise. We evaluated the effects of swimming training on hypothalamic (GLP1-R) and Lep receptor (Lep-R) gene expressions in lactational hypernutrition-induced obesity.
METHODS: On the 3rd postnatal day, the litter sizes of lactating dams were adjusted to small litters (SL; 3 pups/dams) or normal litters (NL; 9 pups/dams). After weaning (21 days), NL and SL male rats were randomly distributed to sedentary (Sed) and exercised (Exe) groups. Exercised mice swam (30 min/3 times/week) for 68 days. Food intake and body weight gain were registered. At 92 days, intraperitoneal glucose and insulin tolerance tests were performed and rats were euthanized at 93 days; adipose tissue depots were weighed, and blood counts and plasma biochemical analyses performed. Hypothalamus were isolated to evaluate Lep-R and GLP1-R gene expressions.
RESULTS: Small litters sedentary rats presented increased body weight gain, adiposity, insulin sensibility and higher fasting values of glucose and triglycerides, besides higher hypothalamic gene expressions of Lep-R and GLP1-R, compared to NLSed animals. SLExe rats did not develop obesity or metabolic abnormalities and Lep-R and GLP1-R hypothalamic gene expressions were normalized.
CONCLUSION: Lactational hypernutrition induces obesity and metabolic dysfunction in adult life, in association with higher hypothalamic expressions of the Lep-R and GLP1-R genes. Exercise prevented obesity and improved metabolic state in SL overnourished rats, and normalized their hypothalamic Lep-R and GLP1-R gene expressions.
There will be no virtual reality application. Sleep quality and mental well-being scale will be applied every 6 weeks.
Participants will be administered GSK1795091 100 ng IV on Days 1 and 8 followed by once weekly administration of GSK1795091 100 ng IV in combination with GSK3174998 24 mg administered at Q3W via the IV route until Week 12. From Week 12 onwards, GSK1795091 100 ng IV will be administered in combination with GSK3174998 24 mg at Q3W interval.
AIM: Gastric emptying scintigraphy is used to assess patients with symptoms of dyspepsia or gastroparesis. An alteration of fundus accommodation may explain these symptoms. The aim of this study was to determine the accommodation in gastric emptying scintigraphy studies performed in our institution.
MATERIAL AND METHODS: 50 patients (43 children) referred for gastric emptying assessment were evaluated. After fasting for 8 h, and following international guidelines, egg labeling was performed with 37 mBq of [99mTc]Tc-DTPA and administration of standardized food. Areas of interest were defined in the stomach at different times, and the corresponding retention percentages were calculated. Considering the image at time zero, gastric accommodation was qualitatively and quantitatively assessed, calculating the ratio between proximal stomach counts and total counts.
RESULTS: Of the 50 patients studied, 32 had normal emptying, 10 had slowed emptying and 8 had accelerated emptying. Within the group of patients with normal emptying, 8 had altered accommodation (25%) and another 8 in the group with abnormal emptying (44%). Applying the ROC curve analysis to quantitative values, the most appropriate cut-off value was 0.785 with p < 0.001, sensitivity 82.4% and specificity 100%.
CONCLUSION: Gastric emptying scintigraphy in addition to determining motility, made it possible to assess both qualitatively and quantitatively the distribution of the radiotracer in the stomach and thus, indirectly, the accommodation in the fundus. It provided added diagnostic information in a simple manner, without protocol changes and allowing more specific treatments to be assessed.
While the manifestations of many inherited retinal disorders are limited to loss of vision, others are part of a syndrome that affects multiple tissues, particularly the nervous system. Most syndromic retinal disorders are thought to be recessively inherited. Two dogs out of a litter of Cirneco dell' Etna dogs, both males, showed signs of retinal degeneration, along with tremors and signs described as either atypical seizures or paroxysmal dyskinesias, while the other two male littermates were normal. We named this oculo-neurological syndrome CONS (Cirneco oculo-neurological syndrome), and undertook homozygosity mapping and whole-genome sequencing to determine its potential genetic etiology. Notably, we detected a 1-bp deletion in chromosome 6 that was predicted to cause a frameshift and premature stop codon within the canine AMPD2 gene, which encodes adenosine monophosphate deaminase, an enzyme that converts adenosine 5'-monophosphate (AMP) to inosine 5'-monophosphate (IMP). Genotyping of the available Cirneco population suggested perfect segregation between cases and controls for the variant. Moreover, this variant was absent in canine genomic databases comprised of thousands of unaffected dogs. The AMPD2 genetic variant we identified in dogs presents with retinal manifestations, adding to the spectrum of neurological manifestations associated with AMPD2 variants in humans.
All subjects will receive a single IV injection of unfiltered sulfur colloid radiolabeled with 8 mCi Tc99m on study day 0. All subjects will receive a single IV injection of 200 mcg tilmanocept radiolabeled with 8 mCi Tc99m on study day 3.