anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
In addition to symptomatic treatment, if applicable, the management of adverse reactions of OFEV may require dose reduction or temporary interruption until the specific adverse reaction resolves to levels that allow continuation of therapy. OFEV treatment may be resumed at the full dosage (150 mg twice daily), or at the reduced dosage (100 mg twice daily), which subsequently may be increased to the full dosage. If a patient does not tolerate 100 mg twice daily, discontinue treatment with OFEV [see Warnings and Precautions (5.2, 5.3, 5.5, 5.7) and Adverse Reactions (6.1)].

Elevated Liver Enzymes

Dose modifications or interruptions may be necessary for liver enzyme elevations. Conduct liver function tests (aspartate aminotransferase (AST), alanine aminotransferase (ALT), and bilirubin) prior to initiation of treatment with OFEV, at regular intervals during the first three months of treatment, and periodically thereafter or as clinically indicated. Measure liver tests promptly in patients who report symptoms that may indicate liver injury, including fatigue, anorexia, right upper abdominal discomfort, dark urine or jaundice. Discontinue OFEV in patients with AST or ALT greater than 3 times the upper limit of normal (ULN) with signs or symptoms of liver injury and for AST or ALT elevations greater than 5 times the upper limit of normal. For AST or ALT greater than 3 times to less than 5 times the ULN without signs of liver damage, interrupt treatment or reduce OFEV to 100 mg twice daily. Once liver enzymes have returned to baseline values, treatment with OFEV may be reintroduced at a reduced dosage (100 mg twice daily), which subsequently may be increased to the full dosage (150 mg twice daily) [see Warnings and Precautions (5.2) and Adverse Reactions (6.1)].

In patients with mild hepatic impairment (Child Pugh A), consider treatment interruption, or discontinuation for management of adverse reactions.
NEW MATERIAL:Neutral L-lysine.L-malate crystals. USE:Useful as a crystalline amino acid transfusion solution, particularly for preparing a transfusion solution with reduced or eliminated chlorine ion content. The L-malic acid is useful for preventing ammoniemia and capable of supplying L-lysine as well as efficacy of the L-malic acid. PREPARATION:2mol L-lysine and 0.3-1.2mol, preferably 1mol L-malic acid are dissolved in an aqueous solvent and the quality of the solution is adjusted to 6.0-8.5pH, preferably 6.5-7.5pH to give an aqueous solution containing a neutral salt. Crystals of the neutral salt are then deposited by a method for adding methanol, etc., thereto. The resultant crystals are stable to moisture, tasteless and odorless and most suited for oral administration with very high solubility in water.
Treatment with potassium citrate extended-release tablets should be added to a regimen that limits salt intake (avoidance of foods with high salt content and of added salt at the table) and encourages high fluid intake (urine volume should be at least two liters per day). The objective of treatment with potassium citrate extended-release tablets is to provide potassium citrate in sufficient dosage to restore normal urinary citrate (greater than 320 mg/day and as close to the normal mean of 640 mg/day as possible), and to increase urinary pH to a level of 6.0 to 7.0. 

In patients with severe hypocitraturia (urinary citrate of less than 150 mg/day), therapy should be initiated at a dosage of 60 mEq/day (20 mEq three times/day or 15 mEq four times/day with meals or within 30 minutes after meals or bedtime snack). In patients with mild-moderate hypocitraturia (>150 mg/day), potassium citrate extended-release tablets should be initiated at a dosage of 30 mEq/day (10 mEq three times/day with meals). Twenty-four hour urinary citrate and/or urinary pH measurements should be used to determine the adequacy of the initial dosage and to evaluate the effectiveness of any dosage change. In addition, urinary citrate and/or pH should be measured every four months.

Doses of potassium citrate extended-release tablets greater than 100 mEq/day have not been studied and should be avoided. 

Serum electrolytes (sodium, potassium, chloride and carbon dioxide), serum creatinine, and complete blood count should be monitored every four months. Treatment should be discontinued if there is hyperkalemia, a significant rise in serum creatinine, or a significant fall in blood hematocrit or hemoglobin.
Patients post liver transplant (LT) with progressive familial intrahepatic cholestasis type 1 (PFIC-1) often develop progressive graft steatohepatitis, intractable diarrhea, and growth failure. A total internal biliary diversion (TIBD) during an LT may prevent or reverse these adverse events. Children with PFIC-1 who underwent an LT at our institute were divided into 2 groups, A and B based on the timeline where we started offering a TIBD in association with LT. Pre-LT parameters, intraoperative details, and posttransplant complications like graft steatosis and diarrhea were also analyzed between the 2 groups, and their growth velocity was measured in the follow-up period. Of 550 pediatric LT performed between 2011 and 2022, 13 children underwent LT for PFIC-1. Group A had 7 patients (A1-A7) and group B had 6 (B1-B6). Patients A1, A4, B4, and B5 had a failed partial internal biliary diversion before offering them an LT. Patients A1, A2, and A6 in group A died in the post-LT period (2 early allograft dysfunction and 1 posttransplant lymphoproliferative disorder) whereas A3, A4, and A5 had graft steatosis in the follow-up period. A4 was offered a TIBD 4 years after LT following which the graft steatosis fully resolved. In group B, B1, B2, B5, and B6 underwent TIBD during LT, and B3 and B4 had it 24 and 5 months subsequently for intractable diarrhea and graft steatosis. None of the patients in group B demonstrated graft steatosis or diarrhea and had good growth catch-up during follow-up. We demonstrate that simultaneous TIBD in patients undergoing LT should be a standard practice as it helps dramatically improve outcomes in PFIC-1 as it prevents graft steatosis and/or fibrosis, diarrhea, and improves growth catch-up.
Data from a controlled clinical trial conducted in pediatric patients provided evidence supporting the safety and efficacy of UNASYN for the treatment of skin and skin structure infections. Of 99 pediatric patients evaluable for clinical efficacy, 60 patients received a regimen containing intravenous UNASYN, and 39 patients received a regimen containing intravenous cefuroxime. This trial demonstrated similar outcomes (assessed at an appropriate interval after discontinuation of all antimicrobial therapy) for UNASYN- and cefuroxime-treated patients:

Most patients received a course of oral antimicrobials following initial treatment with intravenous administration of parenteral antimicrobials. The study protocol required that the following three criteria be met prior to transition from intravenous to oral antimicrobial therapy: (1) receipt of a minimum of 72 hours of intravenous therapy; (2) no documented fever for prior 24 hours; and (3) improvement or resolution of the signs and symptoms of infection.

The choice of oral antimicrobial agent used in this trial was determined by susceptibility testing of the original pathogen, if isolated, to oral agents available. The course of oral antimicrobial therapy should not routinely exceed 14 days.
BACKGROUND: Identifying the culprit during inferior myocardial infarction (MI) is still challenging. We determined the diagnostic effect of electrocardiographic (ECG) indices in identifying the culprit vessel of acute MI and the impact of coronary artery dominance on it.
METHODS: This cross-sectional study included patients with acute inferior MI who presented to Imam Khomeini Hospital and Tehran Heart Center and underwent primary PCI within 12 h of the onset of symptoms. A standard 12‑lead ECG was recorded and interpreted by two cardiologists. Based on the coronary angiography, the patients were divided into two groups of LCX or RCA involvement and were compared for general variables and ECG indices. The diagnostic values of the ECG indices for predicting the culprit vessel were then calculated.
RESULTS: We evaluated 411 patients with inferior STEMI (321 [77.5%] male, age 58.1 ± 11.1 years). RCA was the culprit vessel in 286 patients (69.1%) and LCX in 128 patients (30.9%). 321 patients (77.5%) were right dominant, 40 (9.7%) patients were left dominant, and 53 patients (12.8%), were codominant. Coronary dominance had minimal impact on the ECG indices regarding culprit identification even after adjustment for confounders. STE in lead III > lead II had the highest sensitivity for detecting RCA as the culprit (sensitivity: 89.2% and specificity: 57.8%). STE ≥0.1 mV in V5 or V6 leads had the highest sensitivity for detecting LCX as the culprit (sensitivity: 51.6, specificity: 93.7%).
CONCLUSION: In inferior STEMI, ECG indices can predict the culprit vessel with acceptable sensitivity and specificity independent of coronary artery dominance.
Participants in the eMST-group will follow a 10-week program of Enriched Music-Supported Therapy. The program comprises 3 individual self-training sessions and 1 group session per week (total program duration: 40 hours).
Set dose of nivolumab and BMS-986148 intravenous injection at or below maximum tolerated dose on specific days. Five cancers will be studied in this part: mesothelioma, pancreatic, ovarian, gastric, and non-small cell lung cancer.
Remifentanil is increased step-by-step according to the study protocol. After ensuring a steady-state period of remifentanil infusion of at least 5 minutes, the standardized painful stimuli consisting of the intracutaneous pain model and tetanic stimulation for the time period of 30 s with 80 milliampere, 50 Hz are applied. All stimulations are accompanied by the measurement of the analgesic monitoring-devices (PhysioDoloris®, SPI® and AlgiScan®). Moreover the investigators measure and inspect changes in heart rate and blood pressure as well as occurrence of defensive movements of the patients.
The intervention break starts as soon as 70 - 80 % of the target phoneme / target consonant cluster can be pronounced correctly in spontaneous speech situations during therapy. The intervention break will last for 12 weeks.
Drug: Methylphenidate (MPH) Participants will be tested twice, approximately one month apart. In one of the sessions, they will be given 10mg of MPH an hour and a half before the testing session is set to begin, to account for the time taken for the effects of the drug to start.
Women assigned to the sexual counseling group based on the BETTER model will receive four sessions in total, once a week. Each session will consist of 30 minutes on average. Better model consists of Bring up the topic, Explain, Telling, Timing, Education and Recording steps. The sessions will be conducted online as individual counselling sessions.
The safety and effectiveness of LIPITOR as an adjunct to diet to reduce LDL-C have been established pediatric patients 10 years of age and older with HeFH. Use of LIPITOR for this indication is based on a double-blind, placebo-controlled clinical trial in 187 pediatric patients 10 years of age and older with HeFH. In this limited controlled trial, there was no significant effect on growth or sexual maturation in the males or females or on menstrual cycle length in females.

The safety and effectiveness of LIPITOR as an adjunct to other LDL-C-lowering therapies to reduce LDL-C have been established pediatric patients 10 years of age and older with HoFH. Use of LIPITOR for this indication is based on a trial without a concurrent control group in 8 pediatric patients 10 years of age and older with HoFH [see Clinical Studies (14)].

The safety and effectiveness of LIPITOR have not been established in pediatric patients younger than 10 years of age with HeFH or HoFH, or in pediatric patients with other types of hyperlipidemia (other than HeFH or HoFH).
<P>PROBLEM TO BE SOLVED: To provide a system that normalizes healthcare data in various formats and exchange the data between those concerned.  <P>SOLUTION: The system comprises a first computer system 10, a second computer system and a rules engine. The first computer system 10 has healthcare data stored therein. The second computer system is in operable communication with, and is configured to extract the healthcare data from the first computer system 10. The rules engine normalizes the extracted healthcare data to a predefined format. The rules engine defines a plurality of healthcare data fields in the predefined format, as well as a plurality of relationships between fields of normalized data.  <P>COPYRIGHT: (C)2008,JPO&INPIT
BACKGROUND: The morbidity and mortality among hospital inpatients with AECOPD and CVDs remains unacceptably high. Currently, no risk score for predicting mortality has been specifically developed in patients with AECOPD and CVDs. We therefore aimed to derive and validate a simple clinical risk score to assess individuals' risk of poor prognosis.
STUDY DESIGN AND METHODS: We evaluated inpatients with AECOPD and CVDs in a prospective, noninterventional, multicenter cohort study. We used multivariable logistic regression analysis to identify the independent prognostic risk factors and created a risk score model according to patients' data from a derivation cohort. Discrimination was evaluated by the area under the receiver-operating characteristic curve (AUC), and calibration was assessed by the Hosmer-Lemeshow goodness-of-fit test. The model was validated and compared with the BAP-65, CURB-65, DECAF and NIVO models in a validation cohort.
RESULTS: We derived a combined risk score, the ABCDMP score, that included the following variables: age > 75 years, BUN > 7 mmol/L, consolidation, diastolic blood pressure ≤ 60 mmHg, mental status altered, and pulse > 109 beats/min. Discrimination (AUC 0.847, 95% CI, 0.805-0.890) and calibration (Hosmer‒Lemeshow statistic, P = 0.142) were good in the derivation cohort and similar in the validation cohort (AUC 0.811, 95% CI, 0.755-0.868). The ABCDMP score had significantly better predictivity for in-hospital mortality than the BAP-65, CURB-65, DECAF, and NIVO scores (all P < 0.001). Additionally, the new score also had moderate predictive performance for 3-year mortality and can be used to stratify patients into different management groups.
CONCLUSIONS: The ABCDMP risk score could help predict mortality in AECOPD and CVDs patients and guide further clinical research on risk-based treatment.
CLINICAL TRIAL REGISTRATION: Chinese Clinical Trail Registry NO.:ChiCTR2100044625; URL: http://www.chictr.org.cn/showproj.aspx?proj=121626 .
A medical monitoring system generates notification messages indicating that a patient being monitored may have a condition that requires attention. The system then wirelessly transfers the notification messages to a portable electronic device. The portable electronic device may include a processing circuit configured to receive the notification messages. The processing circuit may also be configured to implement an organizer function such as a task list or schedule information, and may be configured to facilitate transfer of wireless data using a wireless transceiver. The portable device may also include an identification device coupled to the processing circuit and configured to input data representative of an identity of a subject of interest from an information source at a distance from the identification device. The identification device may be a barcode scanner or may be an RFID circuit.
The present invention relates to a medicine for treating hyperplasia of mammary glands, which belongs to the technical field of traditional Chinese medicines. The medicine is prepared from traditional Chinese medicines of 5 to 15 weight portions of bupleurum root, 10 to 20 weight portions of curcuma root, 8 to 16 weight portions of green tangerine peel, 25 to 35 weight portions of tangerine seed, 25 to 35 weight portions of calcined oyster shell, 15 to 25 weight portions of cowherb seed, 8 to 12 weight portions of prepared pinellia tuber, 15 to 25 weight portions of deglued antler, 15 to 25 weight portions of spina gleditsiae, 15 to 25 weight portions of epimedium herb and 4 to 6 weight portions of liquorice. The medicine has the efficacy of soothing the liver, rectifying qi, eliminating phlegm, relieving pain, resolving phlegm and removing hard stasis. The reflection of the medicine from patients is good for many years, and the treatment effect of the medicine can be similar to that of Chinese patent medicines on the market, such as Rukangpian, Rupixiao, Ruzengning, Ruhesanjiepian, etc. 2000 patients are treated by the medicine up to now. The clinical observation proves that the product of the present invention has unique treatment effect on various kinds of hyperplasia of mammary glands and has good social and economic benefits.
The present invention discloses medicine for treating obesity fatty liver, which is prepared from seven kinds of the traditional Chinese medicine, such as giant knotweed rhizome, processed pinellia tuber, water plantain, zedoary, peach kernels, fructus polygoni orientalis and liquorice, as raw materials. The present invention also discloses a method for preparing the medicine. The medicine of the present invention has the efficiency of removing dampness, reducing phlegm, activating blood circulation and eliminating abdominal mass. The present invention mainly treats the obesity fatty liver caused by body obesity, distention and stuffiness in chests and hypochondrium, nausea, vomit, dizziness, heavy limbs, abdominal distention, anorexia, unctuous furred tongues and thready and slippery pulse. According to the authentication of Chinese medicine, the present invention treats patients caused by wetness phlegm stasis. After being used in clinic, the present invention has the advantages of quick action, conspicuous effects and no adverse reaction.
The present invention relates to a liver cancer-testis specific antigen protein and an antigen peptide. The liver cancer-testis specific antigen protein is a protein with an amino acid sequence shown in figure 1 and a protein derived from the protein with the amino acid sequence. An amino acid sequence of the antigen peptide is from AA108 to AA191 in a sequence shown in figure 1. The liver cancer-testis specific antigen protein and the antigen peptide provided by the present invention can be used as a blocking agent of the activity of E2F, and perform an antagonistic function to an isogeny analogue TFDP-1. The protein or the peptide can be used as a CT antigen or an antigen gene to be made into vaccines. The tumor antigen protein is decomposed intracellularly, and can generate a peptide fragment combined with main histocompatibility compound(MHC)-I molecules, wherein the peptide fragment can be recognized by T cells in a combination state so as to achieve the goal of treating cancers by activating immune reaction. Consequently, the present invention can be applied to the preparation of medicine for treating cancers particularly for treating liver cancer.
Tumor hypoxia has been associated with resistance to chemotherapy and radiotherapy (Brown et al, 2004; Boyle 2006). TH-302, a hypoxia activated prodrug (HAP), exploits the hypoxic nature of tumors while having little or no effect on normal tissue. TH-302 belongs to a class of alkylating agents called oxazaphosphorines which have major experimental and clinical activity (Brock 1989). Since TH-302 is selectively targeted to the hypoxic microenvironment, this agent may represent an improvement over other agents in this class. Preclinical data support the hypothesis that TH-302 targets hypoxic regions of tumors and also is able to kill other tumor cells in normoxic regions as a result of cytotoxin diffusion, leading to significant effects on tumor growth. Preclinical data has shown that TH-302 has anti-tumor activity in multiple myeloma cells in vivo and in vitro.

Additional preclinical data demonstrated the marked expansion of the hypoxic bone marrow areas in diseased mice with ALL. These results suggest that this agent may be useful in treating advanced leukemias. The drug is stable in plasma and liver, does not appear to be at risk for drug-drug interactions, and has mild, reversible toxicities. In this dose-escalation study, patients with advanced leukemias will receive infusions of TH-302 to determine the maximum tolerated dose.
AIDS patients may not tolerate or respond to sulfamethoxazole and trimethoprim in the same manner as non-AIDS patients. The incidence of adverse reactions, particularly rash, fever, leukopenia and elevated aminotransferase (transaminase) values, with sulfamethoxazole and trimethoprim therapy in AIDS patients who are being treated for P. jiroveciipneumonia has been reported to be increased compared with the incidence normally associated with the use of sulfamethoxazole and trimethoprim in non-AIDS patients. If a patient develops skin rash, fever, leukopenia or any sign of adverse reaction, reevaluate benefit-risk of continuing therapy or re-challenge with sulfamethoxazole and trimethoprim (see WARNINGS). 

Avoid coadministration of sulfamethoxazole and trimethoprim and leucovorin during treatment of P. jiroveciipneumonia (see WARNINGS). 

Electrolyte Abnormalities

Hyperkalemia: High dosage of trimethoprim, as used in patients with P. jiroveciipneumonia, induces a progressive but reversible increase of serum potassium concentrations in a substantial number of patients. Even treatment with recommended doses may cause hyperkalemia when trimethoprim is administered to patients with underlying disorders of potassium metabolism, with renal insufficiency, or if drugs known to induce hyperkalemia are given concomitantly. Close monitoring of serum potassium is warranted in these patients. 

Hyponatremia: Severe and symptomatic hyponatremia can occur in patients receiving sulfamethoxazole and trimethoprim, particularly for the treatment of P. jiroveciipneumonia. Evaluation for hyponatremia and appropriate correction is necessary in symptomatic patients to prevent life-threatening complications. 

Crystalluria: During treatment, ensure adequate fluid intake and urinary output to prevent crystalluria. Patients who are “slow acetylators” may be more prone to idiosyncratic reactions to sulfonamides.
There will be 12 50-minute individual sessions conducted at weekly intervals. Booster sessions will be conducted one, three and six months after treatment. Sessions include change of safety behavior, exposition (in sensu and in vivo), and response prevention.