anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Group TAPB (transverse abdominis plane block): 20 ml of 0.25% bupivacaine will be used each time for plane block on both sides. Patients will be sedated with 1 mg midazolam and 50 mcg fentanyl intravenously in the preoperative preparation room in the operating room and 20 ml of 0.25% bupivacaine was administered bilaterally on each side under ultrasound guidance. After the block application, the patient was taken to the operating room and standard general anaesthesia was applied.
Ssample of 40 healthy pregnant women Two referees will perform four successive measurements of the diameter of the right portal vein (RPV) during the same ultrasound examination at the third trimester. Each operator will qualify the appearance of the right portal vein as normal or collapsed using an evaluation grid, and will independently performe a series of two measurements using the same method.
PURPOSE:The titled drug that contains an aminobenzoic acid derivative or its salt as an active ingredient, thus permitting long-term administration, because of its low toxicity. CONSTITUTION:An agent for preventing ishemic cardiopathy is obtained by using 0.01-100wt% of a compound of formula (R is glycoside) or its salt such as p-aminobenzoic acid-N-L-arabinoside as an active ingredient and mixing it with diluents such as extender, binder humectant or disintegrator. It is effective to coronary ateriosclerosis, acute or chronic myocardiac infarction, stable and unstable stenocardia, arrhythmia, cardiac insufficiency and so on. The drug is orally administered 0.1-1,000mg/kg/day, parenterally 0.01-200mg/kg/day once to 4 times in portions a day. Since the compound has no antibiotic activity, there is no anxiety of disturbing intestional flora. Further, it exerts no influence on mutagenecity, cellular and humoral immunities, thus being a very safe drug.
BACKGROUND: Multiple sclerosis is a neurodegenerative disease that damages the myelin sheath within the central nervous system. Axonal demyelination, particularly in the corpus callosum, impacts communication between the brain's hemispheres in persons with multiple sclerosis (PwMS). Changes in interhemispheric communication may impair gait coordination which is modulated by communication across the corpus callosum to excite and inhibit specific muscle groups. To further evaluate the functional role of interhemispheric communication in gait and mobility, this study assessed the ipsilateral silent period (iSP), an indirect marker of interhemispheric inhibition and how it relates to gait adaptation in PwMS.
METHODS: Using transcranial magnetic stimulation (TMS), we assessed interhemispheric inhibition differences between the more affected and less affected hemisphere in the primary motor cortices in 29 PwMS. In addition, these same PwMS underwent a split-belt treadmill walking paradigm, with the faster paced belt moving under their more affected limb. Step length asymmetry (SLA) was the primary outcome measure used to assess gait adaptability during split-belt treadmill walking. We hypothesized that PwMS would exhibit differences in iSP inhibitory metrics between the more affected and less affected hemispheres and that increased interhemispheric inhibition would be associated with greater gait adaptability in PwMS.
RESULTS: No statistically significant differences in interhemispheric inhibition or conduction time were found between the more affected and less affected hemisphere. Furthermore, SLA aftereffect was negatively correlated with both average percent depth of silent period (dSP%AVE) (r = -0.40, p = 0.07) and max percent depth of silent period (dSP%MAX) r = -0.40, p = 0.07), indicating that reduced interhemispheric inhibition was associated with greater gait adaptability in PwMS.
CONCLUSION: The lack of differences between the more affected and less affected hemisphere indicates that PwMS have similar interhemispheric inhibitory capacity irrespective of the more affected hemisphere. Additionally, we identified a moderate correlation between reduced interhemispheric inhibition and greater gait adaptability. These findings may indicate that interhemispheric inhibition may in part influence responsiveness to motor adaptation paradigms and the need for further research evaluating the neural mechanisms underlying the relationship between interhemispheric inhibition and motor adaptability.
Subjects will continue exclusive/ predominant breastfeeding for 6 weeks. Breastmilk may be consumed directly from the breast or breast milk may be expressed and fed through infant feeding bottle.
Porphyromonas gingivalis (P. gingivalis), the main pathogen responsible for periodontitis, is linked to systemic disorders via the oral-gut axis. Short-chain fatty acids (SCFAs) are vital for gut health, but their role in P. gingivalis-induced gut disorders remains unclear. This study utilized metabolomics and 16 S rRNA sequencing to explore gut microbiota and SCFAs levels in P. gingivalis-induced periodontitis mouse models. Significant changes were observed in gut, including a reduction in SCFAs-producing bacteria, such as Lactobacillus, Ligilactobacillus, Allobucalum, and a notable decrease in Firmicutes and Actinobacteriota. The intestinal permeability tests and histological analyses revealed that periodontitis led to epithelial inflammation, reduced mucin secretion, and compromised gut barrier integrity. In vitro experiments with Caco-2 cells co-cultured with P. gingivalis showed that the bacterium disrupted cellular junctions by impairing autophagy, specifically through the ATG5-LC3 pathway, leading to decreased expression of tight junction proteins and reduced SCFA absorption. Remarkably, rapamycin treatment both in vitro and in vivo restored gut barrier function by enhancing autophagy, increasing tight junction protein expression, and promoting SCFAs absorption via MCT1 and SMCT1, alongside GPR43/GPR109a pathway activation. These findings reveal autophagy's novel role in regulating SCFAs metabolism in P. gingivalis-induced gut dysbiosis, offering insights for preventing and treating periodontitis-related systemic diseases.
Systems and methods for multi-modality data processing are provided. Some embodiments are particularly directed to labeling and indexing multi-modality medical data. In one embodiment, a method for labeling medical data received by a multi-modality medical processing system includes receiving, by the medical processing system, medical data to be labeled. A reference set of labels corresponding to the medical data is presented at a display device. A selection of a first label from the reference set of labels is received from an interface device. A target set of labels corresponding to the medical data is presented at the display device, the target set of labels based on the first label. A selection of a second label from the target set of labels is received from the interface device. The medical data is then labeled based on the first and second labels.
This is a randomized controlled prospective study looking at the effect of using a pedometer with graduated step-count goals following radical cystectomy on rate of ileus, return of bowel function and post-operative narcotic use. Subjects will be randomized into a control group or study group. The control group will receive standard of care, with information provided regarding the importance of ambulation following surgery. The study group will receive a pedometer with graduated step-count goals from post-operative day 0 to post-operative day 21. Both groups will be given a standardized post-operative narcotic regimen, and will be asked to record initial passage of flatus and first bowel movement. Subjects will remain on the study until post-operative day 21.
Clofarabine Injection is supplied in single-dose flint vials containing 20 mg of clofarabine in 20 mL of solution. Each box contains one Clofarabine Injection vial. The 20 mL flint vials contain 20 mL (20 mg) of solution. The pH range of the solution is 4.5 to 7.5. The solution is sterile, clear and practically colorless, is preservative-free, and is free from foreign matter.

Vials containing undiluted Clofarabine Injection should be stored at 25°C (77°F); excursions permitted to 15°C to 30°C (59°F to 86°F). Do not freeze. Retain in carton until contents are used.

Clofarabine is a cytotoxic drug. Follow applicable special handling and disposal procedures.1
PURPOSE: Ventral hernias are a common complication of laparotomy, posing challenges particularly when primary fascial closure is unattainable. Although chemical component separation using preoperative botulinum toxin A (BTX) injections has emerged as a promising adjunct, objective evidence of its efficacy remains limited. This study aimed to objectively assess the effect of preoperative BTX on traction force during ventral hernia repair.
METHODS: A prospective, single-blind study was conducted on patients with midline incisional hernias following liver transplantation. BTX was administered unilaterally, and the traction force required to medially advance the anterior rectus sheath was measured intraoperatively. Pre- and post-injection CT scans were analyzed for changes in hernia size and LAW muscle measurements. Statistical analyses were performed to evaluate traction force differences between BTX-injected and uninjected sides.
RESULTS: Ten patients underwent hernia repair with primary fascial closure achieved in all cases. Comparison of pre- and post-injection CT scans showed no significant changes in hernia size. LAW muscle length increased by 1.8 cm, while thickness decreased by 0.2 cm. Intraoperative traction force measurements revealed a significant reduction on the BTX-injected side compared to the uninjected side (p < 0.0001). The traction force ratio on the BTX-injected to the uninjected side averaged 57%, indicating the efficacy of BTX in reducing tension.
CONCLUSION: Preoperative BTX significantly reduces traction force during ventral hernia repair, highlighting its potential as an adjunctive therapy in complex cases. While challenges remain in patient selection and outcome assessment, BTX offers a promising avenue for enhancing abdominal wall reconstruction outcomes and reducing surgical complications.
NEW MATERIAL:The compound of formula I (R1 and R2 are 1 to 10C alkyl or alkenyl; (m) is 1 to 3; A is acid group of inorganic or organic acid). EXAMPLE:2',3'-O-dibutanoyl-S-adenosylmethlonine methyl ester. USE:A treating agent for cerebral apoplexy effective in suppressing necrocytosis after ischemia, improving the availability of glucose in the brain, suppressing cerebral edema, improving electroencephalogram, improving evoked potential, ameliorating kinetic function, etc. It has high fat-solubility and is capable of easily releasing S-adenosylmethionine. PREPARATION:The objective compound can be produced by reacting S-adenosyl- L-homocysteine of formula II with trichloroethyloxycarbonyl chloride, reacting the product with an alcohol of formula R1-OH to obtain an ester compound of formula III, reacting the ester with an active derivative of a fatty acid of formula R2-COOH. removing the protecting groups from the product and reacting the resultant compound of formula IV with a methylation agent.
### Pregnancy Category C

In studies conducted in rats and rabbits, methylphenidate was administered orally at doses of up to 75 and 200 mg/kg/day, respectively, during the period of organogenesis. Teratogenic effects (increased incidence of fetal spina bifida) were observed in rabbits at the highest dose, which is approximately 40 times the maximum recommended human dose (MRHD) on a mg/m2 basis. The no effect level for embryo-fetal development in rabbits was 60 mg/kg/day (11 times the MRHD on a mg/m2 basis). There was no evidence of specific teratogenic activity in rats, although increased incidences of fetal skeletal variations were seen at the highest dose level (7 times the MRHD on a mg/m2 basis), which was also maternally toxic. The no effect level for embryo-fetal development in rats was 25 mg/kg/day (2 times the MRHD on a mg/m2 basis). When methylphenidate was administered to rats throughout pregnancy and lactation at doses of up to 45 mg/kg/day, offspring body weight gain was decreased at the highest dose (4 times the MRHD on a mg/m2 basis), but no other effects on postnatal development were observed. The no effect level for pre- and postnatal development in rats was 15 mg/kg/day (equal to the MRHD on a mg/m2 basis).

Adequate and well-controlled studies in pregnant women have not been conducted. Methylphenidate should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
The primary goal will be to perform continuous stepping while maintaining HR within 70-85% maximum predicted HR (if patients are deconditioned, PTs will gradually increase intensity to desired levels as tolerated). We will also record Ratings of Perceived Exertion (RPE) every 3-5 minutes, with goals of 15-18. Sessions will be divided into \~10 minute increments (\~25% of sessions) between speed-dependent treadmill training (described above for treadmill stepping), skill-dependent treadmill training, overground training, and stair climbing.
Glioma represents a notoriously aggressive and malignant tumor that targets the central nervous system, with a poor prognosis for patients. In this research, we set out to examine the role of hydroxyacyl-CoA dehydrogenase trifunctional multienzyme complex subunit alpha (HADHA) in glioma, its clinical significance, as well as its potential biological mechanisms. In this study, we used immunohistochemistry staining to assess the expression level of HADHA in glioma tissues. We also evaluated the correlation between HADHA expression and patient survival using the Kaplan-Meier method. To determine the role of HADHA in glioma cells, we conducted loss-of-function assays in vitro and in vivo. Additionally, we utilized co-immunoprecipitation and protein stability assays to investigate the potential mechanisms involving HADHA, MDM2, and p53 in glioma. Our research findings indicate that gliomas exhibit high levels of HADHA. Clinically, high expression of HADHA suggests an increased risk of malignant tumors, recurrence, and reduced survival rates. Functionally, knocking down HADHA can lead to decreased proliferation, enhanced apoptosis, and inhibited migration of glioma cells. Mechanistically, HADHA accelerates MDM2-mediated p53 ubiquitination through interaction with MDM2. Consistently, MDM2 knockdown or overexpression of p53 can attenuate the promoting effect of HADHA overexpression on the malignant progression of glioma. We have discovered a novel role of HADHA in promoting MDM2-mediated p53 ubiquitination, which contributes to the progression of glioma. This finding provides a new perspective to understand the pathogenesis of glioma and offers a potential target for developing innovative therapeutic strategies.
First questionnaire (spiegel questionnaire) will allow a score on 30. If the score is \> 18, the patient will be in the control group.
Children receive speech-language services in the community. Children are assessed at baseline, 4 months after baseline, 10 months after baseline, and 16 months after baseline.
A superoxide dismutase fusion polypeptide, a preparation method thereof and application thereof in preparing anti-aging products relate to the technical fields of genetic engineering and synthetic biology. The amino acid sequence of the recombinant SOD enzyme fusion polypeptide is shown as SEQ ID NO. 3, and the fusion expression is carried out on mPeSOD2-1 with strong heat resistance and the humanized cell repair polypeptide with high function but instability. The mPeSOD2-1 is used as a partner protein to protect repair polypeptide, resist high temperature and degradation and retain the biological activity of the two. After high-temperature incubation, the fusion polypeptide has strong oxidation resistance, is beneficial to removing excessive harmful oxygen free radicals, protecting and repairing cells, and also has the effects of maintaining cells, promoting cell proliferation and repairing organism injury. The fusion polypeptide has strong stability, high activity and strong industrial practicability, and has wide application prospect in the fields of anti-aging cosmetics, health-care foods and the like for delaying the aging of organisms and promoting the regeneration of organisms and skin.
Chronic fatigue (ME/CFS) and fibromyalgia syndrome (FM) are a chronic musculoskeletal pain disorder that predominantly afflicts women. Frequently associated insomnia, cognitive abnormalities, and fatigue may lead to early disability. No consistent soft tissue abnormalities have been identified so far in these patients. The cause of these disorders is unknown, no highly effective treatment is available and the current methods of diagnosis are imprecise and unreliable. The Investigators previously used quantitative sensory testing to improve upon diagnoses of these disorders by supplementing the current procedure of manipulating defined pressure points by hand and noting the presence or absence of pain. The quantitative methods of evaluation involve repetitive application of brief, non-injurious thermal/mechanical stimulation that normally produces a moderate degree of temporal summation of sensation intensity. The patients and normal control subjects will verbally rate the magnitude of late sensations elicited by each stimulus, using a numerical scale. Chronic pain in these patients results, at least partially, from exaggerated activation of central N-methyl-D-aspartate (NMDA) receptors as a result of enhanced input from unmyelinated peripheral afferent nerve fibers supplying deep tissues. Temporal summation of second pain can lead to central sensitization with subsequent signs of hyperalgesia and allodynia. Functional brain imaging of ME/CFS and FM patients, as proposed in this study, will be used to document their ratings of repetitive experimental stimuli and the resulting pain augmentation. Successful completion of this study will provide a new method for the evaluation of chronic pain/fatigue mechanism and their response to therapy.
A method for determining the pathogenicity/benign nature of genomic variations associated with a given disease is described. The method comprises the following steps: accessing genomic data (D) comprising a list of a plurality of genomic variations of the patient, and then for each variation detected, verifying (S1) by the electronic computing device whether the variation meets each of a plurality of predefined pathogenicity/benign criteria. Each of these pathogenicity/benign criteria is a proposition, which may be true or false, related to the variation, the proposition being related to a first condition or a second condition, and wherein at least one of the foregoing criteria relates to the first condition and at least another of the criteria relates to the second condition. The "first condition" includes statistical conditions and/or previously known conditions. "second condition" includes patient-specific conditions. Each pathogenicity/benign criterion is associated with a level of evidence that is indicative of a pathogenic or benign condition or level. The method then provides: input information (I) is prepared (S2) for a trained algorithm (a) which is trained using artificial intelligence techniques and/or machine learning techniques. The input information (I) includes, for each variation and for each level of evidence, information concerning the number of pathogenicity/benign criteria associated with the level of evidence that the variation meets. Finally, the method comprises processing the aforementioned input information by means of a trained algorithm (a) to obtain output information (O) indicative of the pathogenicity/benign nature of each of the considered plurality of genomic variations. The algorithm (a) is trained based on a training dataset of known cases in a preliminary training step (S0) which provides in input the calculated input information (I0) for the known cases and based on knowledge of the pathogenicity/benign nature of the respective known cases.
Abiraterone acetate, the active ingredient of abiraterone acetate tablets USP is the acetyl ester of abiraterone. Abiraterone is an inhibitor of CYP17 (17α-hydroxylase/C17,20-lyase). Each abiraterone acetate tablet USP contains 250 mg or 500 mg of abiraterone acetate. Abiraterone is designated chemically as 17-(Pyridin-3-yl)androsta-5,16-dien-3β-yl acetate and its structure is:

Abiraterone acetate is a white to off-white, non-hygroscopic, crystalline powder. Its molecular formula is C26H33NO2 and it has a molecular weight of 391.55. Abiraterone acetate is a lipophilic compound with an octanol-water partition coefficient of 3.57 (Log P) and Freely soluble in methylene chloride, in tetrahydrofuran, and in toluene, soluble in methanol, in ethanol, in ethyl acetate, in isobutyl methyl ketone, in N,N-dimethyl formamide and in acetone, sparingly soluble in acetonitrile and in dimethyl sulfoxide, slightly soluble in hexane, very slightly soluble in 0.1N hydrochloride and practically insoluble in water. The pKa value of abiraterone Acetate is 3.06.  
Abiraterone acetate tablets USP are available in 250 mg and 500 mg film-coated tablets and 250 mg uncoated tablets with the following inactive ingredients:

  * 250 mg film-coated tablets: colloidal silicon dioxide, croscarmellose sodium, hydroxypropyl methylcellulose, lactose monohydrate, magnesium stearate, microcrystalline cellulose and sodium lauryl sulfate. The film-coating contains iron oxide red, iron oxide yellow, polyethylene glycol, polyvinyl alcohol, talc, and titanium dioxide.
  * 500 mg film-coated tablets: colloidal silicon dioxide, croscarmellose sodium, hydroxypropyl methylcellulose, lactose monohydrate, magnesium stearate, microcrystalline cellulose and sodium lauryl sulfate. The film-coating contains iron oxide black, iron oxide red, polyethylene glycol, polyvinyl alcohol, talc, and titanium dioxide.
  * 250 mg uncoated tablets: colloidal silicon dioxide, croscarmellose sodium, lactose monohydrate, magnesium stearate, microcrystalline cellulose, povidone, and sodium lauryl sulfate.



250 mg uncoated tablets: FDA approved dissolution test specifications differ from USP.  
250 mg and 500 mg film-coated tablets: Meets USP dissolution test 3.