anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
On the basis of experience with a group of subjects with severely impaired renal function treated with ranitidine, the recommended dosage in patients with a creatinine clearance <50 mL/min is 150 mg or 10 mL of syrup (2 teaspoonfuls of syrup equivalent to 150 mg of ranitidine) every 24 hours. Should the patient's condition require, the frequency of dosing may be increased to every 12 hours or even further with caution. Hemodialysis reduces the level of circulating ranitidine. Ideally, the dosing schedule should be adjusted so that the timing of a scheduled dose coincides with the end of hemodialysis.

Elderly patients are more likely to have decreased renal function, therefore caution should be exercised in dose selection, and it may be useful to monitor renal function (see and ). CLINICAL PHARMACOLOGY: Pharmacokinetics: GeriatricsPRECAUTIONS: Geriatric Use
Deferasirox can cause hepatic injury, fatal in some patients. In Study 1, 4 patients (1.3%) discontinued deferasirox because of hepatic toxicity (drug-induced hepatitis in 2 patients and increased serum transaminases in 2 additional patients). Hepatic toxicity appears to be more common in patients greater than 55 years of age. Hepatic failure was more common in patients with significant comorbidities, including liver cirrhosis and multi-organ failure [see Adverse Reactions (Error! Hyperlink reference not valid.)]. Acute liver injury and failure, including fatal outcomes, have occurred in pediatric deferasirox-treated patients. Liver failure occurred in association with acute kidney injury in pediatric patients at risk for overchelation during a volume depleting event. Interrupt deferasirox therapy when acute liver injury or acute kidney injury is suspected and during volume depletion. Monitor liver and renal function more frequently in pediatric patients who are receiving deferasirox in the 20 to 40 mg/kg/day range and when iron burden is approaching normal. Use the minimum effective dose to achieve and maintain a low iron burden [see Dosage and Administration (Error! Hyperlink reference not valid.), Warnings and Precautions (Error! Hyperlink reference not valid.), Adverse Reactions (Error! Hyperlink reference not valid.)].

Measure transaminases [aspartate transaminase (AST) and alanine transaminase (ALT)] and bilirubin in all patients before the initiation of treatment, and every 2 weeks during the first month and at least monthly thereafter. Consider dose modifications or interruption of treatment for severe or persistent elevations.

Avoid the use of deferasirox in patients with severe (Child-Pugh C) hepatic impairment. Reduce the starting dose in patients with moderate (Child-Pugh B) hepatic impairment [see Dosage and Administration (Error! Hyperlink reference not valid.), Use in Specific Populations (Error! Hyperlink reference not valid.)]. Patients with mild (Child-Pugh A) or moderate (Child-Pugh B) hepatic impairment may be at higher risk for hepatic toxicity.
<P>PROBLEM TO BE SOLVED: To overcome or at least ameliorate problems associated with production and handling of clostridial toxin.  <P>SOLUTION: A single chain polypeptide is provided which comprises first and second domains. The first domain is a clostridial neurotoxin light chain or a fragment or a variant thereof, wherein the first domain is capable of cleaving one or more vesicles or plasma membranes associated proteins essential to exocytosis. The second domain is a clostridial neurotoxin heavy chain H<SB>N</SB>portion or a fragment or a variant thereof, wherein the second domain is capable of translocating the polypeptide into a cell or increasing the solubility of the polypeptide compared to the solubility of the first domain on its own or both translocating the polypeptide into a cell and increasing the solubility of the polypeptide compared to the solubility of the first domain on its own. The second domain is a molecular clamp peptide sequence which forms a noncovalent linkage with a molecular clamp peptide complementary sequence existing on another peptide, thereby the second domain is coupled with another peptide.  <P>COPYRIGHT: (C)2011,JPO&INPIT
Electrocardiogram (ECG) is the main criterion for arrhythmia detection. As a means of identification, ECG leakage seems to be a common occurrence due to the development of the Internet of Medical Things. The advent of the quantum era makes it difficult for classical blockchain technology to provide security for ECG data storage. Therefore, from the perspective of safety and practicality, this article proposes a quantum arrhythmia detection system called QADS, which achieves secure storage and sharing of ECG data based on quantum blockchain technology. Furthermore, a quantum neural network is used in QADS to recognize abnormal ECG data, which contributes to further cardiovascular disease diagnosis. Each quantum block stores the hash of the current and previous block to construct a quantum block network. The new quantum blockchain algorithm introduces a controlled quantum walk hash function and a quantum authentication protocol to guarantee legitimacy and security while creating new blocks. In addition, this article constructs a hybrid quantum convolutional neural network called HQCNN to extract the temporal features of ECG to detect abnormal heartbeats. The simulation experimental results show that HQCNN achieves an average training and testing accuracy of 94.7% and 93.6%. And the detection stability is much higher than classical CNN with the same structure. HQCNN also has certain robustness under the perturbation of quantum noise. Besides, this article demonstrates through mathematical analysis that the proposed quantum blockchain algorithm has strong security and can effectively resist various quantum attacks, such as external attacks, Entanglement-Measure attack and Interception-Measurement-Repeat attack.
The loss of the SOST gene product sclerostin leads to sclerosteosis characterized byihigh bone mass (HBM). In this report, we found that sclerostin could antagonize canonical, Wnt signaling in human embryonic kidney A293 cells and mouse osteoblastic MC3T3 cells. This sclerostin-mediated antagonism could be reversed by over-expression of Wnt coreceptor LRP5. In addition, we found that sclerostin bound to LRP5 as well as LRP6 and identified the first two YWTD-EGF repeat domains of LRP5 as being responsible for the binding. Although these two repeat domains are required for transducing canonical Wnt signals, canonical Wnt did not appear to compete with sclerostin for binding to LRP5. Examination of the expression of sclerostin and Wnt7b, an autocrine canonical Wnt, during primary calvarial osteoblast differentiation revealed that sclerostin is expressed at the late stages of osteoblast differentiation coinciding with the expression of osteogenic marker osteocalcin and trailing after the expression of Wnt7b. Given the plethora of evidence indicating that canonical Wnt signaling stimulates osteogenesis, we believe that the HBM phenotype associated with the loss of sclerostin may at least in part be attributed to an increase in canonical Wnt signaling resulting from the reduction in sclerostin-mediated Wnt antagonism.
Systems, methods, and media for laboratory testing services are disclosed. A request for an electronic form can be received from an electronic device. A customized electronic form can be sent to the electronic device. The electronic form may be customized based at least in part on a healthcare provider associated with the request. At least one laboratory test may be requested to be ordered for at least one patient associated with the healthcare provider. At least one predefined rule may be applied to the requested order to verify that the order is valid. At least one laboratory can be selected to perform the ordered laboratory tests. Specimen collection information may be sent to a collection facility and can be based at least in part on rules or preferences of a lab selected to perform a laboratory test. Customized test reports can be provided to a healthcare provider.
The NASA-NEI Dynamic Light Scattering (DLS) device detects early molecular lens changes before clinical means are able to detect any lens changes in animal and limited human studies. This ability will make it very useful in future clinical studies of cataract etiology as well as treatment. A recently concluded clinical cross sectional study of lenses (in vivo) using the DLS device showed good reproducibility and good correlation with clinical cataract grading. It also detected remarkable changes in the lens crystalline proteins with aging and with cataract formation. We therefore propose to study the characteristics of the crystalline proteins in pristine young normal lenses with DLS for comparison with aging and cataractous lens findings. We will examine 30 young normal subjects, perform undilated eye examinations, and obtain DLS measurements of their lenses. We will then use these DLS measurements for comparison with the previously obtained aging and cataract DLS measurements, to obtain normative data for future lens and cataract clinical studies.
The treating clinician will use the MAP-Knee Tool together with the adolescent. The tool includes four separate components: 1) a tool for diagnosing the most common types of non-traumatic knee pain (SMILE), 2) credible explanations of the aetiology and pathogenesis specific to the diagnosis based on multiple methods with an iterative design, 3) a presentation of prognostic factors based on an individual participant data meta-analysis(19), and 4) an option grid that presents the users of the tool with pros and cons of commonly used management options based on a systematic literature search of systematic and narrative reviews within non-traumatic adolescent knee pain. An overarching focus of all components was to support shared decision-making and base decisions on all three pillars of evidence-based medicine: patient values, clinical expertise, and relevant research. Therefore, the tool should not provide the users with definitive answers simply based on available evidence.
Craniosynostosis, the premature fusion of cranial sutures, can lead to distortion of skull shape and neurological dysfunction. We present a novel case of Horner syndrome as the presenting sign of craniosynostosis associated with elevated intracranial pressure. A 10-year-old boy presenting for strabismus follow-up was noted to have new-onset anisocoria, greater in the dark, and mild right upper eyelid ptosis. Apraclonidine testing was concerning for Horner syndrome. Neuroimaging demonstrated previously undiagnosed sagittal craniosynostosis with tortuous optic nerves and large cerebrospinal fluid spaces around both optic nerves. The patient was referred to neurosurgery and underwent a lumbar puncture with an opening pressure of 44 cm H2O. He underwent surgical cranial expansion. By six months postoperatively, his anisocoria had resolved.
In accordance with the present invention, there are provided novel receptor interacting factors, referred to herein as "SMRT", i.e., a Silencing Mediator (co-repressor) for Retionic Acid Receptor (RAR) and Thyroid hormone Receptor (TR). SMRT is anovel protein whose association with RAR and TR both in solution and on DNA response elements is destabilized by ligand. The interaction of SMRT with mutant receptors correlates with the transcriptional silencing activites of receptors. in vivo, SMRT functions as a potent co-repressor. A GAL4 DNA binding domain (DBD) fusion of SMRT behaves as a frank repressor of a GAL4-dependent reporter. Together, these data identify a novel class of cofactor which is believed to represent an important mediator of hormone action.
Malaria remains a major concern of morbidity and mortality. Despite treating infected individuals with artemisinin-based combination therapies (ACTs), cerebral and severe malaria cause enormous mortality in children and adults. The only treatment option is parenteral administration of artemisinin or quinine with supportive symptomatic therapies. However, the fatality rate remains high despite parasite clearance emphasizing the need of adjunct therapy to prevent malaria mortality. In this invention, heme synthesized in the malaria parasite is shown to be associated with parasite virulence, disease severity and cerebral pathogenesis. Parasite heme enhances the formation of hemozoin - a parasite molecule associated with cerebral and severe malaria. Griseofulvin prevents experimental cerebral malaria (ECM) by inhibiting parasite heme synthesis and hemozoin formation, without affecting parasite growth. Griseofulvin exhibits synergy with arteether - the principal component of ACTs and prevents ECM. Griseofulvin is claimed as an adjunct drug for ACTs and other antimalarials to prevent malaria mortality.
OBJECTIVE: To compare between lower permanent retainers placed in the middle of the incisal third and retainers placed in the middle of lower incisors in terms of gingival condition, lower incisors stability and retainers' failure rate.
MATERIALS AND METHODS: This is a split-mouth clinical trial. Fifty patients finished fixed orthodontic treatment and required fixed permanent retainer in the lower arch were recruited. A multistranded (0.0215 inch) retainer, with a vertical step in the midline placing half of the retainer in the incisal third and the other half in the middle of the lower incisors was attached to all the teeth in the lower labial segment. After one year, all the subjects were recalled. The primary outcome was to evaluate the plaque index (PI) and the gingival index (GI) of the lower labial segment teeth. The secondary outcome was to assess retainers' failure rate and the relapse in lower labial segment alignment.
RESULTS: The GI and the PI scores were significantly smaller on the side where the retainer was placed incisally (P = 0.004, P < 0.001, respectively). There was no statistical difference in the average Irregularity Index (IRI) and the retainer's failure rate between the two sides (P = 0.52, P = 0.76, respectively).
CONCLUSION: Placing lower fixed retainers in the incisal third will improve the lower labial segment oral hygiene and gingival health in the lingual area without affecting the efficiency or the integrity of the retainers. This trial was not registered Null Hypothesis: Placing the lower permanent retainer in the middle of the lingual surfaces of the lower labial segment' teeth or in the incisal third will not affect the gingival health of the lower incisors.
Carbamazepine coadministration with oral risperidone decreased the steady-state plasma concentrations of risperidone and 9-hydroxyrisperidone by about 50%. Plasma concentrations of carbamazepine did not appear to be affected. Coadministration of other known CYP 3A4 enzyme inducers (e.g., phenytoin, rifampin, and phenobarbital) with risperidone may cause similar decreases in the combined plasma concentrations of risperidone and 9-hydroxyrisperidone, which could lead to decreased efficacy of Risperidone for Extended-Release Injectable Suspension treatment. At the initiation of therapy with carbamazepine or other known hepatic enzyme inducers, patients should be closely monitored during the first 4 to 8 weeks, since the dose of Risperidone for Extended-Release Injectable Suspension may need to be adjusted. A dose increase, or additional oral risperidone, may need to be considered. On discontinuation of carbamazepine or other CYP 3A4 hepatic enzyme inducers, the dosage of Risperidone for Extended-Release Injectable Suspension should be re-evaluated and, if necessary, decreased. Patients may be placed on a lower dose of Risperidone for Extended-Release Injectable Suspension between 2 to 4 weeks before the planned discontinuation of carbamazepine or other CYP 3A4 enzyme inducers to adjust for the expected increase in plasma concentrations of risperidone plus 9-hydroxyrisperidone. For patients treated with the recommended dose of 25 mg Risperidone for Extended-Release Injectable Suspension and discontinuing from carbamazepine or other CYP 3A4 enzyme inducers, it is recommended to continue treatment with the 25 mg dose unless clinical judgment necessitates lowering the Risperidone for Extended-Release Injectable Suspension dose to 12.5 mg or necessitates interruption of Risperidone for Extended-Release Injectable Suspension treatment. The efficacy of the 12.5 mg dose has not been investigated in clinical trials [see also Dosage and Administration (2.5)]
The prognosis of early-onset colorectal cancer (EOCRC) is worse than that of late-onset colorectal cancer (LOCRC), and the incidence has gradually increased in recent years, so it is necessary to study the pathogenesis and explore the target of early-onset colorectal cancer patients. In this study, investigators aimed to explore the specific molecular pathologic map of EOCRC by comparing LOCRC. This study enrolled 11,344 patients with colorectal cancer treated at the Colorectal Center of the First Affiliated Hospital of Nanjing Medical University from 2003 to 2022, of whom 578 were EOCRC and 10,766 were LOCRC. The tumor-related mutation status and tumor mutation burden (TMB) of patients were detected by next-generation sequencing technology. PD-L1 expression was detected by immunohistochemistry. The microsatellite instability was detected by polymerase chain reaction (PCR) coupled with capillary electrophoresis (2B3D NCI Panel) in all patients. Among the 11,344 patients, 180 patients with EOCRC and 90 patients with LOCRC patients underwent NGS investigation. Compared with LOCRC, EOCRC patients generally presented a later TNM stage, lower tumor differentiation, and poorer histological type. In LOCRC with MSI-H stupe, TNM stage is earlier than whom with MSI-L/MSS. In addition, the frequency of MSI-H was significantly higher in EOCRC (10.2%) than LOCRC (2.2%). The frequency of 7-mutation panel (ARID1A, FANCI, CASP8, DGFRA, DPYD, TSHR, and PRKCI) were relatively higher in LOCRC. In EOCRC group, the TNM stage of MSI-H subtype patients was earlier while harbored with worse tissue differentiation and higher proportion of mucinous adenocarcinoma. Besides, among the EOCRC patients, FBXW7, FAT1, ATM, ARID1A and KMT2B mutation frequencies were significantly increased in patients with MSI-H type. Comparing with MSI-H patients of LOCRC, the EOCRC patients with MSI-H presented a higher mutation frequencies of FGFBR2, PBRM1, RNF43, LRP1B, FBXW7, ATM and ARID1A. In addition, EOCRC patients were identified with higher tumor mutation burden, especially in the MSI-H type. PD-L1 expression calculated by tumor proportion score (TPS) was also elevated in EOCRC and correlated with MSI status.
This study will be a randomized clinical trial and will be conducted at Al- Mustafa Medical and Physiotherapy Center. The study will be completed within the time duration of six months. For data collection, a convenient sampling technique will be used. The Population will be diagnosed with osteoarthritis patients. A sample size of total 24 patients will be taken in this study. The measurement tool will be Active knee extension test, Goniometer and Numeric pain rating scale. The pre-test and post-test outcome measurement will be taken. Patients will be divided into two groups. Group A will receive the Bowen technique intervention and Group B will receive the Post Isometric Relaxation technique. The interventions groups will receive three sessions per week for 4 weeks.
Technologies are described for a formulation and production of a formulation. The methods may comprise depositing a non-steroidal anti-inflammatory drug (NSAID) compound into a chamber. The methods may comprise depositing a N-methyl-D-aspartate (NMDA) receptor antagonist into the chamber. The methods may comprise respectively depositing a muscle relaxant, a local anesthetic into the chamber, depositing an anticonvulsant into the chamber, depositing an antidepressant into the chamber, and depositing a calcium channel blocking agent into the chamber. The methods may comprise milling the NSAID compound, the NMDA receptor antagonist, the muscle relaxant, the local anesthetic, the anticonvulsant, the antidepressant, and the calcium channel blocking agent into a powder. The methods may comprise adding a solvent with the powder and mixing the solvent with the powder to form a solution. The methods may comprise adding a base cream to the solution and mixing the base cream and the solution to form the formulation.
The invention relates to the method for decreasing postprandial glucose excursion in a mammal in need thereof comprising a step of administering to said mammal an effective amount of water comprising from 99.76 to 99.99 molecular % of isotopologueHO at 0 to 240 min from the start of ingestion of a meal. Preferably, the effective amount water comprising from 99.76 to 99.99 molecular % of isotopologueHO is administered orally. Preferably, the effective amount of the water comprising from about 99.76 to about 99.99 molecular % of isotopologueHO is 0.1 to 20 g/kg body weight of a mammal. Further, invention relates to the medical food for decreasing postprandial glucose excursion in a mammal in need thereof which comprises water comprising from about 99.76 to about 99.99 molecular % of isotopologueHO. Further, invention relates to use of water comprising from about 99.76 to about 99.99 molecular % of isotopologueHO for the manufacture of a medical food for decreasing postprandial glucose excursion in a mammal in need thereof. Preferably, the mammal is human.
Methylphenidate transdermal system use may result in a persistent loss of skin pigmentation at and around the application site. Loss of pigmentation, in some cases, has been reported at other sites distant from the application site. Chemical leukoderma can mimic the appearance of vitiligo, particularly when the loss of skin pigmentation involves areas distant from the application site. Individuals with a history of vitiligo and/or a family history of vitiligo may be more at risk. Skin depigmentation may persist even after methylphenidate transdermal system use is discontinued. Monitor for signs of skin depigmentation, and advise patients to immediately inform their healthcare provider if changes in skin pigmentation occur. Discontinue use of the methylphenidate transdermal system in patients with chemical leukoderma.
PURPOSE OF REVIEW: Sleep deprivation is known to affect multiple aspects of mental health, physical health, and daily functioning. With increasing reports of sleep disturbances and increasing mental health needs in adolescents, it is imperative that healthcare providers have a strong understanding of the relationship between sleep and mental health, the impact of poor sleep on the school experience, and an understanding of behavioral interventions targeting sleep practices.
RECENT FINDINGS: Recent studies have shown that the relationship between sleep and mental health is complex and multifaceted. While mental health diagnoses and symptoms can negatively influence sleep quality and quantity, so too does poor sleep increase the risk of mental health diagnoses, symptom severity, and suicide risk. Sleep likewise affects the school experience, both positively and negatively. Targeted interventions and prevention programs may be effective in treatment of sleep disturbances for adolescents.
SUMMARY: Clinicians must be aware of the above associations and their clinical implications. Patients with either mental health or sleep concerns should be screened for potential co-morbid conditions. Improving sleep hygiene practices can improve the sleep experience in adolescents, however, there remains a gap in understanding the best method to improve sleep hygiene practices in this population.