anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Erlotinib, a kinase inhibitor, is a quinazolinamine with the chemical name N-(3-ethynylphenyl)-6,7-bis(2-methoxyethoxy)-4-quinazolinamine. Erlotinib tablets contains erlotinib as the hydrochloride salt that has the following structural formula:

Erlotinib hydrochloride has the molecular formula C22H23N3O4∙HCl and a molecular weight of 429.90. The molecule has a pKa of 5.42 at 25°C. Erlotinib hydrochloride is very slightly soluble in water, slightly soluble in methanol and practically insoluble in acetonitrile, acetone, ethyl acetate and hexane.

Aqueous solubility of erlotinib hydrochloride is dependent on pH with increased solubility at a pH of less than 5 due to protonation of the secondary amine. Over the pH range of 1.4 to 9.6, maximal solubility of approximately 0.4 mg/mL occurs at a pH of approximately 2.

Erlotinib tablets for oral administration are available in three dosage strengths containing erlotinib hydrochloride (27.3 mg, 109.3 mg and 163.9 mg) equivalent to 25 mg, 100 mg and 150 mg erlotinib and the following inactive ingredients: hypromellose, lactose monohydrate, microcrystalline cellulose, PEG, sodium lauryl sulfate, sodium starch glycolate, sodium stearyl fumarate and titanium dioxide.
Peripheral blood transcriptomes from 383 patients with newly diagnosed melanoma were subjected to differential gene expression analysis. The hypotheses were that impaired systemic immunity is associated with poorer prognosis (thicker tumors and fewer tumor-infiltrating lymphocytes) and evidence of systemic inflammation (high-sensitivity CRP and fibrinogen levels). Higher fibrinogen levels were associated with thicker primary tumors. In single-gene analysis, high-sensitivity CRP levels were significantly associated with higher blood CD274 expression (coding for PD-L1), but each was independently prognostic, with high-sensitivity CRP associated with increased mortality and higher CD274 protective, independent of age. Pathway analysis identified downregulation of immune cell signaling pathways in the blood of people with thicker tumors and notable upregulation of signal transducer and activator of transcription 1 gene STAT1 in people with brisk tumor-infiltrating lymphocytes. Transcriptomic data provided evidence for increased NF-kB signaling with higher inflammatory markers but with reduction in expression of HLA class II molecules and higher CD274, suggesting that aberrant systemic inflammation is a significant mediator of reduced immune function in melanoma. In summary, transcriptomic data revealed evidence of reduced immune function in patients with thicker tumors and fewer tumor-infiltrating lymphocytes at diagnosis. Inflammatory markers were associated with thicker primaries and independently with death from melanoma, suggesting that systemic inflammation contributes to that reduced immune function.
Diclofenac potassium capsules are a nonsteroidal anti-inflammatory drug, available as liquid-filled capsules of 25 mg for oral administration. Diclofenac potassium, USP is a white to slightly yellowish crystalline powder. It is sparingly soluble in water at 25°C. The chemical name is 2-[(2,6-dichlorophenyl) amino] benzeneacetic acid monopotassium salt. The molecular weight is 334.24. Its molecular formula is C 14H 10Cl 2NKO 2, and it has the following chemical structure. 

The inactive ingredients in diclofenac potassium capsules include: lactic acid, polyethylene glycol, polysorbate 80, povidone, and water. The capsule shells contain bovine hydrolyzed collagen, gelatin, lecithin, medium chain triglycerides, sorbitans, sorbitol, and water. The capsules are printed with black ink composed of black iron oxide, polyvinyl acetate phthalate, polyethylene glycol and propylene glycol.
The controlled trials only allowed treatment of one eye per patient. In patients who present with eligible lesions in both eyes, physicians should evaluate the potential benefits and risks of treating both eyes concurrently. If the patient has already received previous Visudyne therapy in one eye with an acceptable safety profile, both eyes can be treated concurrently after a single administration of Visudyne. The more aggressive lesion should be treated first, at 15 minutes after the start of infusion. Immediately at the end of light application to the first eye, the laser settings should be adjusted to introduce the treatment parameters for the second eye, with the same light dose and intensity as for the first eye, starting no later than 20 minutes from the start of infusion.

In patients who present for the first time with eligible lesions in both eyes without prior Visudyne therapy, it is prudent to treat only one eye (the most aggressive lesion) at the first course. One week after the first course, if no significant safety issues are identified, the second eye can be treated using the same treatment regimen after a second Visudyne infusion. Approximately 3 months later, both eyes can be evaluated and concurrent treatment following a new Visudyne infusion can be started if both lesions still show evidence of leakage.
Cosmetic composition comprises polyurethane urea. The polyurethane urea is terminated with a copolymer unit of polyethylene oxide and polypropylene oxide and contains at least one hydroxyl group-containing polycarbonate polyol. An independent claim is also included for preparing the cosmetic composition, comprising: (i) producing at least one polycarbonate polyol, at least one aliphatic, cycloaliphatic or aromatic polyisocyanate or mixtures of such polyisocyanates, at least one monofunctional mixed polyoxyalkylene ether of polyethylene oxide and polypropylene oxide or a mixture of such polyether, and optionally at least one short-chain aliphatic polyols, optionally diluted with an inert solvent which is miscible with water and reactive against isocyanate group; (ii) heating the composition obtained from the step (i) at 50-120[deg] C; (iii) dosing at least one monofunctional mixed polyoxyalkylene ether of polyethylene oxide and polypropylene oxide or a mixture of such polyether, and at least one short-chain aliphatic polyol, optionally diluted with an inert solvent which is miscible with water and reactive against isocyanate group, which are not added, optionally at the beginning of the reaction; (iv) dissolving the prepolymer obtained by using aliphatic ketone; (v) adding at least one aliphatic or cycloaliphatic diamine and at least one amino alcohol as a chain extender or mixtures of such compounds as component (d) for chain elongation; (vi) adding water for dispersion; and (vii) removing the aliphatic ketone, preferably by distillation. ACTIVITY : Dermatological. No biological data given. MECHANISM OF ACTION : None given.
###  Teratogenic Effects

Dextroamphetamine sulfate has been shown to have embryotoxic and teratogenic effects when administered to A/Jax mice and C57BL mice in doses approximately 41 times the maximum human dose. Embryotoxic effects were not seen in New Zealand white rabbits given the drug in doses 7 times the human dose nor in rats given 12.5 times the maximum human dose. While there are no adequate and well-controlled studies in pregnant women, there has been 1 report of severe congenital bony deformity, tracheoesophageal fistula, and anal atresia (VATER association) in a baby born to a woman who took dextroamphetamine sulfate with lovastatin during the first trimester of pregnancy. Dextroamphetamine sulfate extended-release capsules should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

###  Nonteratogenic Effects

Infants born to mothers dependent on amphetamines have an increased risk of premature delivery and low birth weight. Also, these infants may experience symptoms of withdrawal as demonstrated by dysphoria, including agitation, and significant lassitude.
Patients undergo RT as Arm I. Patients also receive ADT consisting of leuprolide, goserelin, buserelin, histrelin, triptorelin, degarelix, or relugolix at the discretion of the treating physician, for 6 months in the absence of disease progression or unacceptable toxicity. Patients may also receive bicalutamide or flutamide for 0, 30 or 180 days.
Adult Growth Hormone Deficiency (GHD)

Either of two approaches to Norditropin dosing may be followed: a non-weight-based regimen or a weight-based regimen.

Non-weight based — based on published consensus guidelines, a starting dose of approximately 0.2 mg/day (range, 0.15-0.30 mg/day) may be used without consideration of body weight. This dose can be increased gradually every 1-2 months by increments of approximately 0.1-0.2 mg/day, according to individual patient requirements based on the clinical response and serum insulin-like growth factor I (IGF-I) concentrations. The dose should be decreased as necessary on the basis of adverse events and/or serum IGF-I concentrations above the age- and gender-specific normal range. Maintenance dosages vary considerably from person to person, and between male and female patients.

Weight-based — based on the dosing regimen used in the original adult GHD registration trials, the recommended dosage at the start of treatment is not more than 0.004 mg/kg/day. The dose may be increased to not more than 0.016 mg/kg/day after approximately 6 weeks according to individual patient requirements. Clinical response, side effects, and determination of age- and gender-adjusted serum IGF-I concentrations should be used as guidance in dose titration.

A lower starting dose and smaller dose increments should be considered for older patients, who are more prone to the adverse effects of somatropin than younger individuals. In addition, obese individuals are more likely to manifest adverse effects when treated with a weight-based regimen. In order to reach the defined treatment goal, estrogen-replete women may need higher doses than men. Oral estrogen administration may increase the dose requirements in women.
INTRODUCTION: The early diagnosis of kidney injury in type 2 diabetes (T2DM) is important to prevent the long-term damaging effects of kidney loss and is decisive for patient outcomes. While SIRT2 is implicated in diabetes pathogenesis, its correlation with diabetic nephropathy remains unexplored. This study was designed to evaluate the association of urine SIRT2 levels with diabetic kidney injury, as well as potential underlying mechanisms.
METHODS: In T2DM patients, db/db mice, and high glucose plus palmitic acid treated HK2 cell models, ELISA, Immunoturbidimetry, Immunohistochemistry, Western blot, and Quantitative real-time polymerase chain reaction were used to detect SIRT2 levels and kidney damage. According to urinary albumin/creatinine ratio (UACR), 163 T2DM patients were divided into three groups. Spearman correlation analysis was used to investigate the relationship between urinary sirtuin2/creatinine ratio (USCR) and biomarkers of kidney injury. The influencing factors of albuminuria in T2DM patients were analyzed by logistic regression model.
RESULTS: In our findings, the Macro group exhibited the highest USCR levels as UACR increased. There was a positive association between USCR and UACR, α1-microglobulin/creatinine ratio (UαCR), β2-microglobulin/creatinine ratio (UβCR), and retinol-binding protein/creatinine ratio (URCR), with a negative correlation observed with eGFR. Logistic ordered multiclassification regression analysis, adjusting for confounding variables, confirmed that USCR remained a significant risk factor for the severity of albuminuria in T2DM patients. In the db/db mice kidney SIRT2 protein level increased significantly. Increased SIRT2 protein levels were also observed in renal tubular epithelial cells treated with high glucose plus palmitic acid. Moreover, SIRT2 promotes the expression of proinflammatory factors TNF-α and IL-6 by modulating the phosphorylation of p38 MAPK and p-JNK in renal tubular cells induced by high glucose and palmitic acid.
CONCLUSION: Urinary SIRT2 is closely related to eGFR, renal tubule injury, and urinary albumin excretion in T2DM patients, which is expected to be an important indicator to comprehensively reflect renal injury.
The prevalence of diabetes and chronic kidney disease (CKD) is increasing worldwide. Diabetic kidney disease is a chronic condition characterized by a gradual increase in urinary albumin excretion, blood pressure, cardiovascular risk, and a decline in glomerular filtration rate (GFR) that can progress to end-stage kidney disease (ESKD). Individuals with diabetes should be screened for CKD annually. Screening should include both measurement of albuminuria and estimation of GFR (eGFR). The structural changes in diabetic kidney disease in individuals with type 1 diabetes are rather uniform, but the histological picture in those with type 2 diabetes and CKD is on the contrary a mix of changes ranging from minor abnormalities to severe glomerulosclerosis, tubulointerstitial fibrosis, and arteriolohyalinosis. Scarring of the kidneys is closely related to the kidney function. Individuals with diabetes often require multiple therapies to prevent progression of CKD and its associated comorbidities and mortality. Management of cardiorenal risk factors, including lifestyle modification, control of blood glucose, blood pressure, and lipids, use of renin-angiotensin-aldosterone system (RAAS) blockers, use of sodium-glucose co-transporter 2 (SGLT2) inhibitors, and the non-steroidal mineralocorticoid receptor antagonist finerenone in individuals with T2D are the cornerstones of therapy. Primary care physicians (PCPs) play a critical role in identifying individuals with CKD, managing early stages of CKD, and referring those with moderate to severe CKD or rapidly declining kidney function to a nephrologist. Referral to a nephrologist should be considered when certain thresholds for eGFR, albuminuria, proteinuria, hematuria, or hypertension are exceeded. This review summarizes current guidelines for the management of CKD and its complications and highlights the role of PCPs in the care of individuals with CKD.
PURPOSE: Ultrasound is the imaging modality of choice for preoperative diagnosis of lymph node metastasis (LNM) in thyroid cancer (TC), yet its efficacy remains suboptimal. As radiomics gains traction in tumor diagnosis, its integration with ultrasound for LNM differentiation in TC has emerged, but its diagnostic merit is debated. This study assesses the accuracy of ultrasound-integrated radiomics in preoperatively diagnosing LNM in TC.
METHODS: Literatures were searched in PubMed, Embase, Cochrane, and Web of Science until July 11, 2023. Quality of the studies was assessed by the radiomics quality score (RQS). A meta-analysis was executed using a bivariate mixed effects model, with a subgroup analysis based on modeling variables (clinical features, radiomics features, or their combination).
RESULTS: Among 27 articles (16,410 TC patients, 6356 with LNM), the average RQS was 16.5 (SD:5.47). Sensitivity of the models based on clinical features, radiomics features, and radiomics features plus clinical features were 0.64, 0.76 and 0.69. Specificities were 0.77, 0.78 and 0.82. SROC values were 0.76, 0.84 and 0.81.
CONCLUSION: Ultrasound-based radiomics effectively evaluates LNM in TC preoperatively. Adding clinical features does not notably enhance the model's performance. Some radiomics studies showed high bias, possibly due to the absence of standard application guidelines.
Cardiac relaxation is a complex process that involves various interconnected characteristics and, along with contractile properties, determines stroke volume. Perioperative ischemia-reperfusion injury and left ventricular diastolic dysfunction (DD) are characterized by the left ventricle's inability to receive a sufficient blood volume under adequate preload. Baseline DD and perioperative DD have an impact on postoperative complications, length of hospital stay, and major clinical outcomes in a variety of cardiac pathologies. Several baseline and perioperative factors, such as age, female sex, hypertension, left ventricle hypertrophy, diabetes, and perioperative ischemia-reperfusion injury, contribute to the risk of DD. The recommended diagnostic criteria available in guidelines have not been validated in the perioperative settings and still need clarification. Timely diagnosis of DD might be crucial for effectively treating postoperative low cardiac output syndrome. This implies the need for an individualized approach to fluid infusion strategy, cardiac rate and rhythm control, identification of extrinsic causes, and administration of drugs with lusitropic effects. The purpose of this review is to consolidate scattered information on various aspects of diastolic dysfunction in cardiac surgery and provide readers with well-organized and clinically applicable information.
A critical event notification system continuously monitors patient statistics and lab data to detect critical events, and automatically pages a responsible physician or physicians, each having an alphanumeric pager. In particular, a computer is used to continually access real-time data and multiple hospital databases which are periodically updated. These databases include patient chart databases, databases corresponding to patient history and databases maintained by various labs. The computer, preferably a clinical information system, is automatically provided with certain data, or periodically extracts it from other, relational databases. The computer automatically reviews this data, makes the critical event determination, and formulates an alphanumeric message that is informative as to the patient's condition and the reasons why a critical event was detected. After automatically retrieving from a database a personal identification number ("PIN") for a remote pager of each physician responsible for the patient, the computer automatically establishes modem contact with a paging network, and causes the network to page each responsible physician and transmit to them the alphanumeric message. The alphanumeric message preferably indicates patient name, diagnosis, the event prompting the page, and the name and return telephone number of medical personnel at the hospital who are attending the particular patient. The system also has widespread applications outside medicine.
A new approach to immune system transplantation and other organ transplantation is described below. The invention describes the novel use of human tissues, or products derived from human tissues including but not limited to antigens, proteins, glycoproteins, and carbohydrates, taken from an individual patient, group or group of patients, to induce immunological tolerance to human antigens in other mammals. Mammals thus rendered tolerant to human antigens can subsequently serve as immune system donors, and as donors of other biological systems, to recipient humans. The invention also uniquely integrates experimentally documented observations from diverse fields of biological and medical research. The invention provides novel treatments for all cancers; for hereditary and acquired immunodeficiency disorders including AIDS; for failures of host immunological defenses including infectious diseases; for hereditary end acquired bone marrow failure syndromes; and for autoimmune diseases. In addition, the invention provides a novel method for achieving successful organ transplantation in humans, without graft rejection or graft-versus-host disease.
Many patients admitted to intensive care units (ICUs) are at high risk of dying. We hypothesize that focused training sessions for ICU providers by palliative care (PC) certified experts will decrease aggressive medical interventions at the end of life. We designed and implemented a 6-session PC training program in communication skills and goals of care (GOC) meetings for ICU teams, including house staff, critical care fellows, and attendings. We then reviewed charts of ICU patients treated before and after the intervention. Forty-nine of 177 (28%) and 63 of 173 (38%) patients were identified to be at high risk of death in the pre- and postintervention periods, respectively, and were included based on the study criteria. Inpatient mortality (45% vs 33%; P = .24) and need for mechanical ventilation (59% vs 44%, P = .13) were slightly higher in the preintervention population, but the difference was not statistically significant. The proportion of patients in whom the decision not to initiate renal replacement therapy was made because of poor prognosis was significantly higher in the postintervention population (14% vs 67%, P = .05). There was a nonstatistically significant trend toward earlier GOC discussions (median time from ICU admission to GOC 4 vs 3 days) and fewer critical care interventions such as tracheostomies (17% vs 4%, P = .19). Our study demonstrates that directed PC training of ICU teams has a potential to reduce end of life critical care interventions in patients with a poor prognosis.
A nonaqueous ointment for the treatment of persons who are identified by their ophthalmologist to have an infection of common parasites in and around the follicles of the eyelash. The invention is a highly viscous mixture of inert components and antiparasitic powder, as well as a method of application considering the unique composition's qualities. The unique ointment and application method eradicate the pathogens entirely by taking into account their general behavior and lifecycle. Once an infection is identified using instruments readily available to eye doctors in their offices, the ointment is applied once daily to the base of the eye lashes by an ointment tube with an ophthalmic tip. The ointment is applied shortly before bed, over the course of several months. Existing methods of treatment have additional side effects and are largely ineffective, with the parasites often recovering in number after treatment has ceased. The current invention far exceeds these levels of therapeutic effectiveness and offers a permanent solution to the infection of the follicles.
Patients receive talazoparib PO daily and avelumab IV over 60 minutes on days 1 and 15. Cycles repeat every 28 days in the absence of disease progression or unacceptable toxicity.
Scars and stretch marks are extremely common. For scars, evidence of alterations of the dermal and hypodermic layers is known, while for stretch marks, less data are available, and they are considered purely aesthetic conditions. The intra- and inter-subject variability of the skin makes the comparison between these two particularly complex. This study presents the case of a 54-year-old man who had both stretch marks and a surgical scar on his abdomen. We performed ultrasound and elastosonographic investigations for both to analyse the structural alteration of the skin and subcutaneous layers. Their structures were also compared to the structure of intact skin. The two skin conditions appeared substantially morphologically different and different from intact skin. The alterations detected, particularly of the connective structures, allow us to state that both scars and stretch marks are alterations of both the dermis and the hypodermis and stretch marks differ from scars.