anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Administer Promethazine VC with Codeine Oral Solution by the oral route only.

Always use an accurate milliliter measuring device when administering Promethazine VC with Codeine Oral Solution to ensure that the dose is measured and administered accurately. A household teaspoon is not an accurate measuring device and could lead to overdosage [ see Warnings and Precautions ( 5.7) ]. For prescriptions where a measuring device is not provided, a pharmacist can provide an appropriate measuring device and can provide instructions for measuring the correct dose. Do not overfill. Rinse the measuring device with water after each use. 

Advise patients not to increase the dose or dosing frequency of Promethazine VC with Codeine Oral Solution because serious adverse events such as respiratory depression may occur with overdosage [ see Warnings and Precautions ( 5.1)  and Overdosage ( 10) ]. The dosage of Promethazine VC with Codeine Oral Solution should not be increased if cough fails to respond; an unresponsive cough should be reevaluated for possible underlying pathology [ see Dosage and Administration ( 2.3)  and Warnings and Precautions ( 5.6) ].
BACKGROUND: Brain tumor surgery is routinely supported by several intraoperative techniques, such as fluorescence, brain mapping and neuronavigation, which are often used independently. Efficacy of navigation is limited by the brain-shift phenomenon, particularly in cases of large or deep-sited lesions. Intraoperative imaging was introduced also to update neuronavigation data, to try and solve the brain-shift phenomenon-related pitfalls and increase overall safety. Nevertheless, each intraoperative imaging modality has some intrinsic limitations and technical shortcomings, making its clinical use challenging. We used a multimodal intraoperative imaging protocol to update neuronavigation, based on the combination of intraoperative Ultrasound (i-US) and intraoperative Computed Tomography (i-CT) integrated with 5-ALA fluorescence and neuromonitoring-guided resection.
METHODS: This is a pilot study on 52 patients (29 men), including four children, with a mean age of 57.67 years, suffering from brain low- (N.=10) or high-grade (N.=34) glioma or metastasis (N.=8), prospectively and consecutively enrolled. They underwent 5-ALA fluorescence-guided microsurgical tumor resection and neuromonitoring was used in cases of lesions located in eloquent areas, according to preoperative clinical and neuroradiological features. Navigated B-mode ultrasound acquisition was carried out after dural opening to identify the lesion. After tumor resection, i-US was used to identify residual tumor. Following further tumor resection or in cases of unclear US images, post-contrast i-CT was performed to detect and localize small tumor remnants and to allow further correction for brain shift. A final i-US check was performed to verify the completeness of resection. Clinical evaluation was based on comparison of pre- and postoperative Karnofsky Performance Score (KPS) and assessment of overall survival (OS) and progression-free survival (PFS). Extent of tumor resection (EOTR) was evaluated by volumetric postoperative Magnetic Resonance performed within 48 h after surgery.
RESULTS: Forty-one of the 52 (78.8%) patients were alive and still under follow-up in December 2017. 5-ALA was strongly or vaguely positive in 45 cases (86.5%). Seven lesions (four low-grade glioma, one high-grade glioma, and two metastases) were not fluorescent. i-US visualized residual tumor after resection of all fluorescent or pathological tissue in 22 cases (42.3%). After i-US guided resection, i-CT documented the presence of further residual tumor in 11 cases (21.1%). Mean EOTR was 98.79% in the low-grade gliomas group, 99.84% in the high-grade gliomas group and 100% in the metastases group. KPS changed from 77.88, preoperatively, to 72.5, postoperatively. At the last follow-up, mean KPS was 84.23.
CONCLUSIONS: The combination of different intraoperative imaging modalities may increase brain tumor safety and extent of resection. In particular, i-US seems to be highly sensitive to detect residual tumors, but it may generate false positives due to artifacts. Conversely, i-CT is more specific to localize remnants, allowing a more reliable updating of navigation data.
Participants will be administered two 60 micrograms sublingual films of IGLMI following start of an autonomic crises. The maximum amount for the study is four oral films of 60 micrograms in 24 hours, two at the beginning of the crises and if needed, two additional within two hours.
PURPOSE: To investigate the impact of lateral lymph node metastasis in papillary thyroid microcarcinoma (PTMC).
METHODS: 5241 PTMC patients with follow-up information were enrolled in the current study. These patients underwent primary surgery in our situation from January 1997 to December 2016. Additionally, a validation cohort consisting of 274 PTMC patients who underwent primary surgery between January 2020 and December 2021 was also included. Univariable and multivariate logistic analyses were conducted to identify the association between clinicopathologic features and lateral lymph node metastasis (LLNM). Kaplan-Meier survival curve analysis was used to calculate the disease-free survival (DFS) rate. The fitting curve was generated to identify the quantitative relationship between central lymph node metastases (CLNM) and LLNM.
RESULTS: Of 5241 PTMC patients, cervical lymph node metastasis was detected in 1494 (28.5%) cases, including 1364 (26.0%) with CLNM only and 130 (2.5%) with LLNM. With a median follow-up time of 60 months (interquartile range [IQR], 44-81), recurrence was detected in 114 patients (2.2%). Multivariate Cox regression analyses showed that LNM was the only independent risk factor for recurrence, with HR values of 3.03 in CLNM and 11.14 in LLNM, respectively. Tumor diameter >0.5 cm (hazard ratio [HR]:1.80), multifocality (HR:2.59), bilaterality (HR:2.13), extrathyroidal invasion (HR:2.13), and CLNM (HR:5.11) were independent risk factors for LLNM. The prevalence of LLNM escalated significantly with increasing number of lymph node involvement in CLNM when stratified by the number of metastatic lymph nodes and trend was observed similarly in the validation cohort. The fitting curve showed that the incidence of LLNM could be as high as 20.7% when the number of CLNM ≥ 5.
CONCLUSIONS: By analyzing a large database with follow-up information, our study provides evidence that LLNM is significantly correlated with tumor recurrence in patients with PTMC. Tumor size (>0.5 cm), multifocality, bilaterality, extrathyroidal extension (ETE) and CLNM are independent risk factors for LLNM.
Gene silencing of BcDCL genes improves gray mold disease control in the cultivated strawberry. Gene silencing technology offers new opportunities to develop new formulations or new pathogen-resistant plants for reducing impacts of agricultural systems. Recent studies offered the proof of concept that the symptoms of gray mold can be reduced by downregulating Dicer-like 1 (DCL1) and 2 (DCL2) genes of Botrytis cinerea. In this study, we demonstrate that both solutions based on dsRNA topical treatment and in planta expression targeting BcDCL1 and BcDCL2 genes can be used to control the strawberry gray mold, the most harmful disease for different fruit crops. 50, 70 and 100 ng μL-1 of naked BcDCL1/2 dsRNA, sprayed on plants of Fragaria x ananassa cultivar Romina in the greenhouse, displayed significant reduction of susceptibility, compared to the negative controls, but to a lesser extent than the chemical fungicide. Three independent lines of Romina cultivar were confirmed for their stable expression of the hairpin gene construct that targets the Bc-DCL1 and 2 sequences (hp-Bc-DCL1/2), and for the production of hp construct-derived siRNAs, by qRT-PCR and Northern blot analyses. In vitro and in vivo detached leaves, and fruits from the hp-Bc-DCL1/2 lines showed significantly enhanced tolerance to this fungal pathogen compared to the control. This decreased susceptibility was correlated to the reduced fungal biomass and the downregulation of the Bc-DCL1 and 2 genes in B. cinerea. These results confirm the potential of both RNAi-based products and plants for protecting the cultivated strawberry from B. cinerea infection, reducing the impact of chemical pesticides on the environment and the health of consumers.
A liposomal vaccine composition comprises a beta-amyloid (a β) -derived peptide antigen displayed on the surface of liposomes. The vaccine composition further comprises a peptide comprising a universal T cell epitope encapsulated within the liposome. The vaccine composition further comprises an adjuvant, which may form part of the liposome and may be at least partially displayed on the surface of the liposome. These vaccine compositions are used to treat, prevent, induce or alleviate symptoms associated with: amyloid-beta related diseases or disorders characterized by or associated with impaired cognitive memory. The vaccine composition may be provided as a kit. Related methods of producing the liposomal vaccine composition are also provided.
Participants will receive a five-minute phone call from one physician 3 to 4 days after a fresh or frozen embryo transfer. The physician will not have access to patient specific IVF cycle details. The phone call will follow scripted questions and utilize scripted phrases to help minimize variation.
A cleansing composition including a sarcosine based surfactant is disclosed. Desirably, the cleansing composition contains a sarcosinate surfactant. Additional cleansing surfactants that are nonionic, anionic, cationic, amphoteric, zwitterionic, or combinations thereof, may also be incorporated into the cleansing composition. The cleansing composition may be used in combination with a product, such as a personal care product, to improve aesthetic properties of that product such as glide across the skin. As such, the cleansing product has a coefficient of friction of less than about 0.40. More particularly, cleansing compositions may be incorporated into or onto a substrate, such as a wipe substrate, an absorbent substrate, a fabric or cloth substrate, or a tissue substrate, among others.
Safety and efficacy of guanfacine extended-release in pediatric patients less than 6 years of age have not been established. The efficacy of guanfacine extended-release was studied for the treatment of ADHD in five controlled monotherapy clinical trials (up to 15 weeks in duration), one randomized withdrawal study and one controlled adjunctive trial with psychostimulants (8 weeks in duration) in children and adolescents ages 6 to 17 who met DSM-IV® criteria for ADHD [see Adverse Reactions (6) and Clinical Studies (14)].

Animal Data

In studies in juvenile rats, guanfacine alone produced a slight delay in sexual maturation in males and females at 2 to 3 times the maximum recommended human dose (MRHD). Guanfacine in combination with methylphenidate produced a slight delay in sexual maturation and decreased growth as measured by a decrease in bone length in males at a dose of guanfacine comparable to the MRHD and a dose of methylphenidate approximately 4 times the MRHD.

In a study where juvenile rats were treated with guanfacine alone from 7 to 59 days of age, development was delayed as indicated by a slight delay in sexual maturation and decreased body weight gain in males at 2 mg/kg/day and in females at 3 mg/kg/day. The No Adverse Effect Level (NOAEL) for delayed sexual maturation was 1 mg/kg/day, which is equivalent to the MRHD of 4 mg/day, on a mg/m2 basis. The effects on fertility were not evaluated in this study.

In a study where juvenile rats were treated with guanfacine in combination with methylphenidate from 7 to 59 days of age, a decrease in ulna bone length and a slight delay in sexual maturation were observed in males given 1 mg/kg/day of guanfacine in combination with 50 mg/kg/day of methylphenidate. The NOAELs for these findings were 0.3 mg/kg of guanfacine in combination with 16 mg/kg/day of methylphenidate, which are equivalent to 0.3 and 1.4 times the MRHD of 4 mg/day and 54 mg/day for guanfacine and methylphenidate, respectively, on a mg/m2 basis. These findings were not observed with guanfacine alone at 1 mg/kg/day or methylphenidate alone at 50 mg/kg/day.
The present invention relates to antibodies or fragments thereof that specifically bind FcγRIIB, particularly human FcγRIIB, more particularly the extracellular domain of FcγRIIB with greater affinity than said antibodies or fragments thereof bind FcγRIIA, particularly human FcγRIIA, and block the Fc binding site of FcγRIIB. The present invention also encompasses the use of an anti-FcγRIIB antibody or an antigen-binding fragment thereof, as a single agent therapy for the treatment, prevention, management, or amelioration of a cancer, preferably a B-cell malignancy, particularly, B-cell chronic lymphocytic leukemia or non-Hodgkin's lymphoma, an autoimmune disorder, an inflammatory disorder, an IgE-mediated allergic disorder, or one or more symptoms thereof. The present invention also encompasses the use of an anti-FcγRIIB antibody or an antigen-binding fragment thereof, in combination with other cancer therapies. The present invention provides pharmaceutical compositions comprising an anti-FcγRIIB antibody or an antigen-binding fragment thereof, in amounts effective to prevent, treat, manage, or ameliorate a cancer, such as a B-cell malignancy, an autoimmune disorder, an inflammatory disorder, an IgE-mediated allergic disorder, or one or more symptoms thereof. The invention further provides methods of enhancing the therapeutic effect of therapeutic antibodies by administering the antibodies of the invention to enhance the effector function of the therapeutic antibodies. The invention also provides methods of enhancing efficacy of a vaccine composition by administering the antibodies of the invention with a vaccine composition. The invention further provides methods of treating cancer and/or regulating immune complex-mediated cell activation by administering the antibodies of the invention to enhance an immune response. The invention also provides methods of breaking tolerance to an antigen by administering an antigen-antibody complex and an antibody of the invention.
The present invention relates to methods and systems for brain sex phenotype score prediction according to application of artificial intelligence algorithms to scalp electroencephalography data. Whether male- or female-born, each person does not necessarily abide by biologically predetermined sex for the brain. The human brain is sexually dimorphic, which matters when a decision on mental health and treatment selection is made. A brain sex phenotype score is introduced to address the need to measure the current brain sex. The score estimation method relies on the deep learning algorithm that integrates the feature extraction and classification processes into a single automated architecture. The method uses novel algorithms for scalp electroencephalogram data augmentation and channel rolling, allowing the claimed network to be more precise and converge faster. A SAAS-based framework for brain sex phenotype score calculation is disclosed in one or more embodiments.
Patients receive pembrolizumab IV over 30 minutes on day 1. Courses repeat every 3 weeks for up to 2 years (6 months for patients achieving CR) in the absence of disease progression or unacceptable toxicity.
Lifetime studies in animals have not been conducted to evaluate the carcinogenic potential of linezolid. Neither mutagenic nor clastogenic potential was found in a battery of tests including: assays for mutagenicity (Ames bacterial reversion and CHO cell mutation), an in vitro unscheduled DNA synthesis (UDS) assay, an in vitro chromosome aberration assay in human lymphocytes, and an in vivo mouse micronucleus assay.  
  
Linezolid did not affect the fertility or reproductive performance of adult female rats given oral doses of up to 100 mg/kg/day for 14 days prior to mating through Gestation Day 7. It reversibly decreased fertility and reproductive performance in adult male rats when given at doses ≥50 mg/kg/day, with exposures approximately equal to or greater than the expected human exposure level (exposure comparisons are based on AUCs). The reversible fertility effects were mediated through altered spermatogenesis. Affected spermatids contained abnormally formed and oriented mitochondria and were non-viable. Epithelial cell hypertrophy and hyperplasia in the epididymis was observed in conjunction with decreased fertility. Similar epididymal changes were not seen in dogs.  
  
In sexually mature male rats exposed to drug as juveniles, mildly decreased fertility was observed following treatment with linezolid through most of their period of sexual development (50 mg/kg/day from days 7 to 36 of age, and 100 mg/kg/day from days 37 to 55 of age), with exposures up to 1.7 times greater than mean AUCs observed in pediatric patients aged 3 months to 11 years. Decreased fertility was not observed with shorter treatment periods, corresponding to exposure in utero through the early neonatal period (gestation day 6 through postnatal day 5), neonatal exposure (postnatal days 5 to 21), or to juvenile exposure (postnatal days 22 to 35). Reversible reductions in sperm motility and altered sperm morphology were observed in rats treated from postnatal day 22 to 35.
Risk Summary   
Available data from postmarketing experience with use of atovaquone in pregnant women are insufficient to identify a drug-associated risk for major birth defects, miscarriage, or adverse maternal or fetal outcomes. Pregnant women with HIV who are infected with PCP are at increased risk of adverse pregnancy outcomes (see Clinical Considerations).Atovaquone given orally by gavage to pregnant rats and rabbits during organogenesis did not cause fetal malformations at plasma concentrations up to 3 times and 0.5 times, respectively, the estimated human exposure based on steady-state plasma concentrations (see Data).   
The estimated background risk of major birth defects and miscarriage for the indicated population is unknown. All pregnancies have a background risk of birth defect, loss, or other adverse outcomes. In the U.S. general population, the background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively.   
Clinical Considerations    
Disease-Associated Maternal and/or Embryo/Fetal Risk:Pregnant women with HIV who are infected with PCP are at increased risk of severe illness and maternal death associated with PCP compared with non-pregnant women.   
Data Animal Data:Atovaquone administered in oral doses of 250, 500, and 1,000 mg/kg/day to pregnant rats during organogenesis (Gestation Day [GD] 6 to GD15) did not cause maternal or embryo-fetal toxicity at doses up to 1,000 mg/kg/day corresponding to maternal plasma concentrations approximately 3 times the estimated human exposure during the treatment of PCP based on steady-state plasma concentrations. In pregnant rabbits, atovaquone administered in oral doses of 300, 600, and 1,200 mg/kg/day during organogenesis (GD6 to GD18) caused decreased fetal body length at a maternally toxic dose of 1,200 mg/kg/day corresponding to a plasma concentration that is approximately 0.5 times the estimated human exposure based on steady-state plasma concentrations. In a pre- and post-natal study in rats, atovaquone administered in oral doses of 250, 500, and 1,000 mg/kg/day from GD15 until Lactation Day (LD) 20 did not impair the growth or developmental effects in first generation offspring at doses up to 1,000 mg/kg/day corresponding to approximately 3 times the estimated human exposure based on steady-state plasma concentrations during the treatment of PCP. Atovaquone crossed the placenta and was present in fetal rat and rabbit tissue.
Performance of a single-blinded randomized control trial to evaluate effectiveness of postoperative pain control in erector spinae plane blocks with bupivacaine with liposomal bupivacaine as the control versus bupivacaine with dexmedetomidine. Plan to randomize patients by alternating months, so that odd months' patients will receive bupivacaine 0.25% with liposomal bupivacaine in the erector spinae plane block. Even months patients will receive bupivacaine 0.25% with dexmedetomidine in the erector spinae plane block.

Block will be performed with ultrasound by the Acute Pain Service team. A time out confirming location of surgery, allergies, consents completed prior to start of the block. Patients will be monitored with 5 lead electrocardiography, non-invasive blood pressure, and pulse oximetry. After skin wheal with 1% lidocaine via 25-27 g needle and echogenic 20 g needle will be utilized to perform the block. The needle will be placed under direct ultrasound visualization into the erector spinae plane. The plane will be hydro dissected with normal saline to confirm needle tip has accessed the erector spinae plane. The local anesthetic will be given in a total of 0.2 ml/kg up to 20 mls (selected based on the study group placement) and aspiration will occur every 5 mls during the block. This will be repeated on the second side if a bilateral block is indicated in based on the surgical consent. All patients will receive 10 mg IV dexamethasone post-induction of anesthesia.

While the patient is in patient pain scores and milligrams of morphine equivalence (MMEs) will be collected every 6 hours based on charting by the nurses providing care starting from time "0" in the PACU after surgery, up until discharge. Then to obtain pain scores up to 72 hours after surgery, patients will be called at home after 72 hours and asked what their pain scores had been daily since discharge and a total of tabs taken daily.
Culprit lesion is treated initially and all other lesions with diameter stenosis angiographically \>50% and FFR \<0.80 are treated in a separate procedure within the index hospitalization. Stenoses \> 90% are treated without prior FFR.
PROBLEM TO BE SOLVED: To provide a synthesizing device capable of synthesizing an 11C-labeled compound having a sufficient radioactivity and purity in a short period of time and with a good reproducibility. SOLUTION: This synthesizing device for producing an 11C-labeled chemical is composed of an 11CH2I-preparing unit, an intermediate-synthesizing unit, an enzyme reaction unit, and a separating and purifying unit. Here, the 11CH2I- preparing unit prepares 11CH2I and includes a means for transferring it to the next intermediate synthesizing unit. The intermediate synthesizing unit reacts N-(diphenylmethylene)glycine tert-butylester with 11C-labeled methyl iodide, and then hydrolyzes to obtain 11C-labeled D, L-alanine and includes a means for removing a used solvent completely. The enzyme reaction unit carries out an enzyme reaction of 11C-labeled D, L-alanine synthesized in the above intermediate-synthesizing unit by using a suitable enzyme substrate. The separation and purification unit separates and purifies the 11C-labeled chemical obtained from the above enzyme reaction unit.