anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Fibromyalgia is one of the most common rheumatic diseases, second only to osteoarthritis. It causes chronic muscle pain and fatigue. Acupuncture functions by targeting specific nerve pathways to different organs or parts of the body. Research has shown that acupuncture is effective in decreasing or eliminating people's sensitivity to pain in targeted regions. However, some believe that the reduction in pain is due to a placebo response rather than acupuncture itself. This study will use two brain-imaging techniques to determine the brain response to acupuncture versus a simulation of acupuncture, thereby assessing whether acupuncture is actually effective in relieving pain.

Participants in this single-blind study will be randomly assigned to receive either acupuncture or a placebo treatment. The placebo will consist of a simulation of acupuncture. Functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) will be used to assess activity of brain mu-opioid receptors. These receptors are involved in the body's ability to perceive pain. All participants will be scanned twice using the fMRI scanner, once before any treatment sessions and once at the conclusion of all treatment sessions. Both fMRI sessions will involve applying pressure to the thumb to elicit a response in the brain in order to assess the corresponding fMRI blood oxygen level dependent (BOLD) signal and whether this activation changes after treatment intervention. Participants will then receive nine treatments of acupuncture or placebo outside the scanner over a 4-week period. The PET portion of this study is optional, and, if you elect to participate, your first treatment session will be performed in the PET scanner. After this first session, participants will have seven additional treatment sessions outside of the scanner over a 4-week period. The last session will be performed in the PET scanner to assess changes in mu-opioid receptor activity that may have occurred over the 4 weeks. A baseline visit to determine eligibility and a close-out visit at week 8 are also part of the participation schedule. It is very important that participants live within driving distance of Ann Arbor, MI due to the significant number of visits to our Center.
BACKGROUNDS: Platelet-to-albumin ratio (PAR) is a new systemic inflammatory prognostic indicator associated with many inflammatory diseases. However, its role in radiation cystitis (RC) is obscure. This study aimed to explore whether PAR could be used as an effective parameter for predicting the RC risk in local advanced cervical cancer (CC) treated with radiotherapy.
METHODS: A total of 319 local advanced CC patients who received radical radiotherapy at Fujian Cancer Hospital were enrolled between December 2018 and January 2021. Demographics and clinical parameters were retrospectively analyzed. Univariate and multivariate analyses were used to identify the risk factors for RC. Backward and stepwise regression was applied to construct two monograms-one with primary significant factors and the other with extra inflammatory biomarkers. A DeLong test was applied to compare the prediction abilities of two nomograms. Calibration curves and decision curve analysis (DCA) evaluated its prediction consistency, discrimination ability, and clinical net benefit.
RESULTS: Univariate analysis showed that age, tumor size, stage, total radiation dose, pelvic radiation dose, Systemic Immune-Inflammation Index (SII), platelet-to-lymphocyte ratio (PLR), and PAR were significantly associated with RC occurrence (all p < 0.05). Multivariate analyses indicated that age, tumor size, stage, total radiation dose, and PAR were independent factors (all p < 0.05). Then, the area under curve (AUC) value of the nomogramSII+PAR was higher (AUC = 0.774) compared to that of the baseline nomogram (AUC = 0.726) (pDelong = 0.02). Also, the five-cross validation confirmed the stability of the nomogramSII+PAR. Moreover, the calibration curve and DCA exhibited the nomograms' good prediction consistency and clinical practicability.
CONCLUSIONS: PAR and SII could be valued for CC patients who are treated with radiation therapy. The nomogram based on PAR and SII could stratify patients who need extra intervention and nursing care to prevent bladder radiation damage and improve patients' quality of life.
Drugs Metabolized by CYP2D6

Bupropion and its metabolites (erythrohydrobupropion, threohydrobupropion, hydroxybupropion) are CYP2D6 inhibitors. Therefore, coadministration of WELLBUTRIN SR with drugs that are metabolized by CYP2D6 can increase the exposures of drugs that are substrates of CYP2D6. Such drugs include certain antidepressants (e.g., venlafaxine, nortriptyline, imipramine, desipramine, paroxetine, fluoxetine, and sertraline), antipsychotics (e.g., haloperidol, risperidone, thioridazine), beta-blockers (e.g., metoprolol), and Type 1C antiarrhythmics (e.g., propafenone and flecainide). When used concomitantly with WELLBUTRIN SR, it may be necessary to decrease the dose of these CYP2D6 substrates, particularly for drugs with a narrow therapeutic index.

Drugs that require metabolic activation by CYP2D6 to be effective (e.g., tamoxifen) theoretically could have reduced efficacy when administered concomitantly with inhibitors of CYP2D6 such as bupropion. Patients treated concomitantly with WELLBUTRIN SR and such drugs may require increased doses of the drug [see Clinical Pharmacology (12.3)].

Digoxin

Coadministration of WELLBUTRIN SR with digoxin may decrease plasma digoxin levels. Monitor plasma digoxin levels in patients treated concomitantly with WELLBUTRIN SR and digoxin [see Clinical Pharmacology (12.3)].
A drug delivery molecule has a targeting moiety, coupled to a routing moiety and a bioactive molecule. The targeting moiety binds to a cell receptor without eliciting an agonistic effect and binding results in uptake of the drug delivery molecule into the cell. Contemplated drug delivery molecules may be employed for treatment and diagnosis. A method of selectively targeting an endothelial cell includes recognizing that presence or absence of somatostatin type II receptors on the endothelial cell correlates with a proximal position of the endothelial cell to an anomalous cell. Endothelial cells proximal to anomalous cells are then presented with a somatostatin type II receptor specific compound. In further methods, the presence of a somatostatin type II receptor on an endothelial cell proximal to a tissue is correlated with a disease of the tissue. In subsequent steps, somatostatin type II receptor specific compounds are administered to the endothelial cell.
Sulfamethoxazole and trimethoprim is rapidly absorbed following oral administration. Both sulfamethoxazole and trimethoprim exist in the blood as unbound, protein-bound and metabolized forms; sulfamethoxazole also exists as the conjugated form. The metabolism of sulfamethoxazole occurs predominately by N4-acetylation, although the glucuronide conjugate has been identified. The principal metabolites of trimethoprim are the 1- and 3-oxides and the 3’- and 4’-hydroxy derivatives. The free forms of sulfamethoxazole and trimethoprim are considered to be the therapeutically active forms. Approximately 70% of sulfamethoxazole and 44% of trimethoprim are bound to plasma proteins. The presence of 10 mg percent sulfamethoxazole in plasma decreases the protein binding of trimethoprim by an insignificant degree; trimethoprim does not influence the protein binding of sulfamethoxazole.  
  
Peak blood levels for the individual components occur 1 to 4 hours after oral administration. The mean serum half-lives of sulfamethoxazole and trimethoprim are 10 and 8 to 10 hours, respectively. However, patients with severely impaired renal function exhibit an increase in the half-lives of both components, requiring dosage regimen adjustment (see DOSAGE AND ADMINISTRATION section). Detectable amounts of sulfamethoxazole and trimethoprim are present in the blood 24 hours after drug administration. During administration of 800 mg sulfamethoxazole and 160 mg trimethoprim b.i.d., the mean steady-state plasma concentration of trimethoprim was 1.72 mcg/mL. The steady-state mean plasma levels of free and total sulfamethoxazole were 57.4 mcg/mL and 68 mcg/mL, respectively. These steady-state levels were achieved after three days of drug administration.1 Excretion of sulfamethoxazole and trimethoprim is primarily by the kidneys through both glomerular filtration and tubular secretion. Urine concentrations of both sulfamethoxazole and trimethoprim are considerably higher than are the concentrations in the blood. The average percentage of the dose recovered in urine from 0 to 72 hours after a single oral dose of sulfamethoxazole and trimethoprim is 84.5% for total sulfonamide and 66.8% for free trimethoprim. Thirty percent of the total sulfonamide is excreted as free sulfamethoxazole, with the remaining as N4-acetylated metabolite.2 When administered together as sulfamethoxazole and trimethoprim, neither sulfamethoxazole nor trimethoprim affects the urinary excretion pattern of the other.  
  
Both sulfamethoxazole and trimethoprim distribute to sputum, vaginal fluid and middle ear fluid; trimethoprim also distributes to bronchial secretion, and both pass the placental barrier and are excreted in human milk.
Idiopathic pulmonary fibrosis (IPF) is characterised by lung scarring and stiffening, for which there is no effective cure. Based on the immunomodulatory and anti-fibrotic effects of induced pluripotent stem cell (iPSC) and mesenchymoangioblast-derived mesenchymal stem cells (iPSCs-MSCs), this study evaluated the therapeutic effects of iPSCs-MSCs in a bleomycin (BLM)-induced model of pulmonary fibrosis. Adult male C57BL/6 mice received a double administration of BLM (0.15 mg/day) 7-days apart and were then maintained for a further 28-days (until day-35), whilst control mice were administered saline 7-days apart and maintained for the same time-period. Sub-groups of BLM-injured mice were intravenously-injected with 1×106 iPSC-MSCs on day-21 alone or on day-21 and day-28 and left until day-35 post-injury. Measures of lung inflammation, fibrosis and compliance were then evaluated. BLM-injured mice presented with lung inflammation characterised by increased immune cell infiltration and increased pro-inflammatory cytokine expression, epithelial damage, lung transforming growth factor (TGF)-β1 activity, myofibroblast differentiation, interstitial collagen fibre deposition and topology (fibrosis), in conjunction with reduced matrix metalloproteinase (MMP)-to-tissue inhibitor of metalloproteinase (TIMP) ratios and dynamic lung compliance. All these measures were ameliorated by a single or once-weekly intravenous-administration of iPSC-MSCs, with the latter reducing dendritic cell infiltration and lung epithelial damage, whilst promoting anti-inflammatory interleukin (IL)-10 levels to a greater extent. Proteomic profiling of the conditioned media of cultured iPSC-MSCs that were stimulated with TNF-α and IFN-γ, revealed that these stem cells secreted protein levels of immunosuppressive factors that contributed to the anti-fibrotic and therapeutic potential of iPSCs-MSCs as a novel treatment option for IPF.
Solution containing no active excipients, infused i.v. over 30 minutes as a single infusion in Part 1 or as 4 infusions administered 4 weeks apart in Part 2.
Clinical studies investigating the benefits of beta-lactam therapeutic drug monitoring (TDM) among critically ill patients are hindered by small patient groups, variability between studies, patient heterogeneity, and inadequate use of TDM. Accordingly, definitive conclusions regarding the efficacy of TDM remain elusive. To address these challenges, we propose an innovative approach that leverages data-driven methods to unveil the concealed connections between therapy effectiveness and patient data, collected through a randomized controlled trial (DRKS00011159; 10th October 2016). Our findings reveal that machine learning algorithms can successfully identify informative features that distinguish between healthy and sick states. These hold promise as potential markers for disease classification and severity stratification, as well as offering a continuous and data-driven "multidimensional" Sequential Organ Failure Assessment (SOFA) score. The positive impact of TDM on patient recovery rates is demonstrated by unraveling the intricate connections between therapy effectiveness and clinically relevant data via machine learning.
The November 13th Paris attacks were the most violent and devastating events to occur in France since World War II. A large number of persons are likely to develop PTSD or trauma-related disorders, especially victims directly involved, their families, as well as the the first responders. In this context, there is an urgent need to enhance treatment resources. Psychotherapy is known to be effective but it is costly, and require qualified professionals. Pharmacotherapy (e.g., selective serotonin reuptake inhibitor,SSRIs) is also considered effective. However, side effects often lead patients to abandon their treatment. An alternative evidence-based intervention is the use of the β-adrenergic blocker propranolol used to interfere with the reconsolidation of a recalled traumatic memory, so as to reduce its strength over time. This clinical trial will evaluate the effectiveness and cost-utility of reconsolidation blockade compared to treatment as usual. The study involves four assessments: pre- and post-treatment and 13 weeks and 1 year follow up. The outcome measures include: PTSD symptoms, socioeconomic variables, quality of life and social functioning measures. The investigators hypothesize that all patients will improve. However, patients receiving reconsolidation blockade will recover faster than treatment as usual. Finally, investigators hypothesize that reconsolidation blockade will be well accepted both by the professionals and the patients.
Immediately after completion of a 15-minute intravenous infusion of ampicillin and sulbactam for injection, peak serum concentrations of ampicillin and sulbactam are attained. Ampicillin serum levels are similar to those produced by the administration of equivalent amounts of ampicillin alone. Peak ampicillin serum levels ranging from 109 to 150 mcg/mL are attained after administration of 2000 mg of ampicillin plus 1000 mg sulbactam and 40 to 71 mcg/mL after administration of 1000 mg ampicillin plus 500 mg sulbactam. The corresponding mean peak serum levels for sulbactam range from 48 to 88 mcg/mL and 21 to 40 mcg/mL, respectively. After an intramuscular injection of 1000 mg ampicillin plus 500 mg sulbactam, peak ampicillin serum levels ranging from 8 to 37 mcg/mL and peak sulbactam serum levels ranging from 6 to 24 mcg/mL are attained. 

The mean serum half-life of both drugs is approximately 1 hour in healthy volunteers. 

Approximately 75 to 85% of both ampicillin and sulbactam are excreted unchanged in the urine during the first 8 hours after administration of ampicillin and sulbactam for injection to individuals with normal renal function. Somewhat higher and more prolonged serum levels of ampicillin and sulbactam can be achieved with the concurrent administration of probenecid. 

In patients with impaired renal function the elimination kinetics of ampicillin and sulbactam are similarly affected, hence the ratio of one to the other will remain constant whatever the renal function. The dose of ampicillin and sulbactam for injection in such patients should be administered less frequently in accordance with the usual practice for ampicillin (see DOSAGE AND ADMINISTRATION section). 

Ampicillin has been found to be approximately 28% reversibly bound to human serum protein and sulbactam approximately 38% reversibly bound. 

The following average levels of ampicillin and sulbactam were measured in the tissues and fluids listed: 

Penetration of both ampicillin and sulbactam into cerebrospinal fluid in the presence of inflamed meninges has been demonstrated after IV administration of ampicillin and sulbactam for injection. 

The pharmacokinetics of ampicillin and sulbactam in pediatric patients receiving ampicillin and sulbactam for injection are similar to those observed in adults. Immediately after a 15-minute infusion of 50 to 75 mg ampicillin and sulbactam for injection/kg body weight, peak serum and plasma concentrations of 82 to 446 mcg ampicillin/mL and 44 to 203 mcg sulbactam/mL were obtained. Mean half-life values were approximately 1 hour.
The study included a total of 96 individuals, 43 males, and 53 females, who applied to the Department of Radiology of the Karabuk University Training and Research Hospital between March-June 2019 with complaints of LBP. Individuals' sociodemographic information and medical history were recorded using the LBP assessment form. The Oswestry LBP Disability Questionnaire was used for LBP. Thickness measurements of muscle (m.) psoas major, m. multifidus, m. quadratus lumborum and m. erector spinae were taken on MRI corresponding to the L3-L4 vertebra level. Cobb Angle method was used for LLA determination. Measurements were made in three repetitions using the Radiant DICOM viewer program, and their averages were recorded.
A resin/drug compound is prepared by contacting "Amberlite" (Registered Trade Mark) IR-120 (in the hydrogen form) with an aqueous solution of dihydrocodeinone bitartrate with stirring. The compound contains about 26,22% by weight of the drug.  The resin/drug compound is dispersed in water in the presence of air and using a colloidal thixotropic suspending agent.  Compositions with specified therapeutic agents are described.ALSO:Thixotropic medicines comprise a stable aqueous suspension of a water-insoluble drug and air in a medium including a suspension of a potassium salt of a sulphuric ester of a high molecular weight polysaccharide obtained by water extraction of the seaweed Furcellaria fastigiata as thixotropic agent.  The compositions may be prepared using a conventional double chambered dispersator in which the thixotropic agent is blended into the aqueous medium by mechanical and hydraulic shearing action which also aerates the composition, the water-insoluble drug being added subsequently.  A specific example relates to a suspension of dihydrocodeinone "resinate" (see Group IV (a)), other specified drugs which may be used are: antibiotics, e.g. procaine penicillin, chloro-mycetin, erythromycin stearate; gastro-intestinal agents, e.g. aluminium hydroxide and phosphate gels, polyamine methylene resins, magnesium trisilicate, kaolin and bismuth subcarbonate; diuretics and cardiovascular agents, e.g. theophylline; vasodilators, e.g. quinidine; steroids, e.g. progesterone and testosterone and, particularly, sulpha-drugs, e.g. sulphamethazine, sulphadiazine, sulphaethyl-thiadiazole, sulphaguanidine and sulphamerazine.
OBJECTIVES: Coronary artery calcification (CorCa) identifies high cardiovascular risk in the general population. In this setting, aortic valve calcification (AoCa) showed contradictory results. Our goal has been to assess the prognostic power of CorCa and AoCa in patients with chest pain who underwent an ECG-gated cardiac multidetector CT (cardiac-MDCT).
METHODS: A total of 528 patients without previous known coronary artery disease, with chest pain who underwent a cardiac-MDCT multidetector, were retrospectively recruited. The primary endpoint included death, acute coronary syndrome, stroke, and heart failure.
RESULTS: A total of 61 patients (11.6%) had an event during a mean follow-up of almost 6 years (5.95 ± 2.98). The most frequent event was acute coronary syndrome (6.4%). Total mortality was 4.5%. Patients with CorCa > 0 had more events than those without CorCa (17.3% versus 4.3%; p < 0.001). Likewise, when only patients without AoCa were considered (n = 118), clinical events were more frequent in those with CorCa (12.7% versus 3.6%; p = 0.004). After excluding patients with coronary artery disease, events were more frequent in those with CorCa (12.6% versus 4.3%; p = 0.004). The higher the Agatston score, the more frequent the events. Patients with AoCa  > 0 had more events than those without (16.5% versus 7.3%; p < 0.001), but in patients without CorCa, no difference in events was seen (6.2% versus 3.6%; p = 0.471). A Cox regression analysis showed age, smoking, prior stroke, and CorCa but not AoCa to be independently related to events.
CONCLUSIONS: In summary, CorCa, but not AoCa, is related to cardiovascular events in patients with chest pain who undergo a cardiac-MDCT.
CLINICAL RELEVANCE STATEMENT: We show that coronary artery calcification, but not aortic valve calcification, detected in a coronary CT scan is tightly related to cardiovascular events. Although this is a message already shown by other groups in the general population, we do believe that this work is unique because it is restricted to patients with chest pain sent to coronary CT. In other words, our work deals with what we face in our routine everyday practice.
KEY POINTS: • The presence and the amount of coronary artery calcification are associated with cardiovascular events in patients with chest pain. • Aortic valve calcification is not associated with cardiovascular events in patients with chest pain.
BACKGROUND: Myasthenia gravis (MG) is a chronic autoimmune disorder characterized by fluctuating muscle weakness. Despite the availability of established therapies, the management of MG symptoms remains suboptimal, partially attributed to lack of efficacy or intolerable side-effects. Therefore, new effective drugs are warranted for treatment of MG.
METHODS: By employing an analytical framework that combines Mendelian randomization (MR) and colocalization analysis, we estimate the causal effects of blood druggable expression quantitative trait loci (eQTLs) and protein quantitative trait loci (pQTLs) on the susceptibility of MG. We subsequently investigated whether potential genetic effects exhibit cell-type specificity by utilizing genetic colocalization analysis to assess the interplay between immune-cell-specific eQTLs and MG risk.
RESULTS: We identified significant MR results for four genes (CDC42BPB, CD226, PRSS36, and TNFSF12) using cis-eQTL genetic instruments and three proteins (CTSH, PRSS8, and CPN2) using cis-pQTL genetic instruments. Six of these loci demonstrated evidence of colocalization with MG susceptibility (posterior probability > 0.80). We next undertook genetic colocalization to investigate cell-type-specific effects at these loci. Notably, we identified robust evidence of colocalization, with a posterior probability of 0.854, linking CTSH expression in TH2 cells and MG risk.
CONCLUSIONS: This study provides crucial insights into the genetic and molecular factors associated with MG susceptibility, singling out CTSH as a potential candidate for in-depth investigation and clinical consideration. It additionally sheds light on the immune-cell regulatory mechanisms related to the disease. However, further research is imperative to validate these targets and evaluate their feasibility for drug development.