anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
In a study of rodents internally contaminated with plutonium, the rate of plutonium elimination was measured after treatment with Ca-DTPA and Zn-DTPA given intravenously as a single dose of 10 to 1,000 micromol/kg (0.54-54 × maximum human dose, MHD). When treated within one hour of internal contamination, Ca-DTPA resulted in about a 10-fold higher rate of elimination of plutonium in the urine as compared to Zn-DTPA. The chelating capacity of Ca-DTPA is greatest immediately and up to approximately 24 hours after internal contamination, a time period when the radiocontaminant is still circulating and readily available for chelation. After the first dose of Ca-DTPA, maintenance treatment with either Ca-DTPA or Zn-DTPA resulted in similar rates of elimination of radioactivity. However, at comparable doses, Ca-DTPA had more toxicity (e.g., more depletion of trace metals, higher rate of mortality, the presence of kidney and liver vacuolization, and small bowel hemorrhagic lesions).

In another study, rodents contaminated with aerosolized plutonium and americium were treated with Ca-DTPA and Zn-DTPA. The treatment schedule involved inhalation of Ca-DTPA 2 micromol/kg (0.11 MHD) 30 minutes after contamination followed by inhalation of Zn-DTPA 2 micromol/kg at approximately 6 hours, 1, 2, 3, and 6 days, then twice weekly to day 26 or day 27. The treatment regime reduced the lung deposit of plutonium and americium to 1-2% of that in untreated animals. Systemic deposit in liver and skeleton were reduced by half.

Literature and U.S. Registry data in humans indicate that intravenous administration of Ca-DTPA forms chelates with radioactive contaminants found in the circulation, interstitial fluid, and tissues. When Ca-DTPA is administered by inhalation within 24 hours of internal radioactive contamination, it can chelate transuranium elements. Expectoration is expected to decrease the amount of radioactive contaminant available for systemic absorption.

The effectiveness of chelation decreases with time after internal contamination because the transuranium elements become incorporated into the tissues. Give chelation treatment as soon as possible after known or suspected internal contamination with transuranium elements has occurred. [See Dosage and Administration (2.1, 2.2)]
Participants will receive the following: Clinical Exam, Blood Tests, CT Scans (with and without contrast) or Ultrasound, Abdominal Device X-ray, and Angiography. These tests will aid in the design of the Cook Custom Aortic Endograft. The Cook Custom Aortic Endograft has a variable design such that seal and fixation may be obtained proximal and distal to pathology in the juxtarenal aorta, suprarenal or thoracoabdominal aorta. Grafts may include a combination of up to 5 fenestrations and branches.
The high prevalence of amphetamine use disorder (AUD) among men who have sex with men (MSM) leads to significant health disparities, including increased risk for HIV sero-conversion. Reducing methamphetamine use mitigates HIV risk. Currently no psychopharmacological agent exists for the treatment of AUD; innovative interventions are desperately needed. Oxytocin, a social neuropeptide, has well-studied anti-addiction effects in animal models of substance dependence. The use of intranasal oxytocin for a variety of human substance use disorders is under early investigation, although no one has studied oxytocin's effects in AUD. In other populations, oxytocin's effects are known to vary depending on social context. Psychosocial treatment alone has been shown to reduce methamphetamine and HIV risk in MSM at a community-based clinic in San Francisco, The Stonewall Project. The investigators propose a randomized, double-blind pilot study of psychopharmacological-psychosocial combination therapy, administration of intranasal oxytocin versus placebo prior to six Motivational Interviewing Group Therapy (MIGT) sessions, in 28 mixed HIV sero-status MSM initiating treatment for AUD. The investigators aim to assess: 1) tolerability, 2) feasibility for larger randomized controlled trials, and 3) exploratory measures of efficacy, including: a) urine levels of methamphetamine and metabolites, b) methamphetamine craving, c) engagement in MIGT through third-party coding of videotaped group sessions and self-reported measures of group connectedness, d) psychophysiological stress responses to group engagement, and e) sexual risk taking.
TUXARIN ER is contraindicated in patients with known or suspected gastrointestinal obstruction, including paralytic ileus [see Contraindications (4)]. The use of codeine in TUXARIN ER may obscure the diagnosis or clinical course of patients with acute abdominal conditions.

The concurrent use of anticholinergics with TUXARIN ER may produce paralytic ileus [see Drug Interactions (7.10)].

The codeine in TUXARIN ER may result in constipation or obstructive bowel disease, especially in patients with underlying intestinal motility disorders. Use with caution in patients with underlying intestinal motility disorders.

The codeine in TUXARIN ER may cause spasm of the sphincter of Oddi, resulting in an increase in biliary tract pressure. Opioids may cause increases in serum amylase [see Warnings and Precautions (5.17)]. Monitor patients with biliary tract disease, including acute pancreatitis for worsening symptoms.
* Life-threatening and fatal meningococcal infections have occurred in patients treated with complement inhibitors. Meningococcal infection may become rapidly life-threatening or fatal if not recognized and treated early.
  * Complete or update meningococcal vaccination (for serogroups A, C, W and Y, and serogroup B) at least 2 weeks prior to administering the first dose of VEOPOZ, unless the risks of delaying therapy outweigh the risk of developing a meningococcal infection. Follow the most current Advisory Committee on Immunization Practices (ACIP) recommendations for meningococcal vaccination in patients receiving a complement inhibitor.
  * Patients receiving VEOPOZ are at increased risk for invasive disease caused by N. meningitidis, even if they develop antibodies following vaccination. Monitor patients for early signs of meningococcal infections and evaluate immediately if infection is suspected [see Warnings and Precautions (5.1)].
Acute oral overdosage with inorganic salts of zinc in humans is reported rarely. In the event of overdosage, the unabsorbed zinc salt should be removed from the stomach by lavage as quickly as possible. The plasma level of zinc should be measured, and heavy metal chelation therapy should be considered if the plasma level of zinc is elevated markedly (>1000 μg/dL). In addition, any signs or symptoms of toxicity should be treated as medically indicated.

One fatality associated with overdosage of zinc sulfate has been reported. The death of this adult woman followed the accidental ingestion of approximately 28 g of zinc sulfate. Death occurred on the fifth day after ingestion and was attributed to renal failure. Hemorrhagic pancreatitis and hyperglycemic coma resulted from the overdose. The amount ingested was 500 mg/Kg of zinc sulfate, a value that is in the same order of magnitude as that found to be lethal in animals.
Patients in the dexmedetomidine group will be administered a bolus of 0.3 ug/kg intravenous dexmedetomidine over 10 min before anesthetic induction. After bolus injection, a continuous infusion of 0.3 ug/kg/hr of intravenous dexmedetomidine will be administered until the end of surgery.
Aminoacyl-tRNA synthetases are the enzymes catalyzing ligation of their cognate amino acids and tRNAs. Human glutaminyl-tRNA synthetase (QRS) consists of the unique N-terminal extension (236 aa) and the C-terminal catalytic domain (539 aa). Here, we found that the N- and C-domains of QRS interacted with pro-apoptotic mediator, Daxx, and its downstream kinase, ASK1 (apoptosis signal-regulating kinase), respectively. The experimental results suggest that QRS may inhibit the ASK1 activity via two different ways. First, its C-terminal domain made direct inhibitory interaction with ASK1. Second, it inhibited the pro-apoptotic interaction between Daxx and ASK1. QRS also blocked the Daxx-ASK1 mediated apoptosis. Thus, QRS is not only an enzyme for protein synthesis but also plays a regulatory role in apoptosis
A linker-drug represented by formula (I) or a pharmaceutically acceptable salt or solvate thereof is provided. In formula (I), C is a conjugator, L is a linker unit, D is a toxin unit, and n is an integer ranging from 1 to 4. The structure of the conjugator is represented by formula (II). In formula (II), X is a leaving group, each of R 1  and R 2  is independently a single bond or —NH—, and Z is substituted aryl, heteroaryl, linear alkyl, cycloalkyl, heterocycloalkyl, or a combination thereof. The antibody is conjugated to the linker unit through a cysteine residue of the antibody. An antibody-drug conjugate (ADC) employing the above linker-drug is also provided.
Sepsis, a life-threatening condition resulting from immune dysregulation, is typically triggered by bacterial infections and commonly coexists with diabetes mellitus. Neutrophils are the first responders to infection and require regulated activation to control pathogen and damage-associated molecular patterns. Dysregulation of neutrophil activation leads to uncontrolled inflammatory responses, often observed in both sepsis and diabetes patients. Neutrophil dysregulation, characterized by effector dysfunction and inadequate cell death processes, can serve as a biomarker for assessing sepsis severity, particularly in diabetic patients. This review provides information on the relationship between effector function, neutrophil cell death, and the severity of sepsis in individuals with diabetes mellitus, aiming to shed light on the mechanisms underlying sepsis progression. Topics covered in the review include an overview of effector function of neutrophil cells, mechanisms of neutrophil cell death, and dysregulation of effectors and neutrophil cell death processes in sepsis severity with diabetes mellitus.
Objective: To investigate the potential association between anxiety and depression and surgical outcomes in patients undergoing LSS. By analyzing data from the Nationwide Inpatient Sample (NIS) database, we aim to identify whether anxiety and depression serve as predictors for postoperative complications and pain-related symptoms. Methods: A retrospective analysis was conducted via the NIS database. Those undergoing LSS from 2010 to 2019 were divided into four groups: those with a diagnosis of anxiety, depression, both depression and anxiety, and neither depression nor anxiety. The chi-squared test, rank sum test, the Student-Newman-Keuls, least significant difference, and Bonferroni tests were used to identify differences between these groups. Logistic regression analysis was utilized to determine if anxiety and depression were predictors for postoperative complications and pain-related symptoms. Results: From 2010 to 2019, 832,099 patients undergoing LSS were identified. Patients with either anxiety or depression were associated with heavier economic burdens ($85,375, $76,840, $88,542 in the anxiety, depression, and comorbid group, respectively, p < 0.001) and prolonged hospital stay (p < 0.001). They were identified to experience higher risks of various complications especially thrombophilia (OR = 1.82, and 1.55 in the anxiety and the depression group, respectively, p < 0.01). Multiple pain-related symptoms, but face reduced risks of inpatient mortality (OR = 0.71, 0.75, and 0.63 in the anxiety, depression, and comorbid group, respectively, p < 0.01). Conclusions: The overall morbidities of depression and anxiety were relatively high. Psychiatric comorbidities were closely correlated with the negative outcomes after LSS. The psychological health of patients receiving LSS requires necessary attention to ensure pain control and prevent complications postoperatively.
Umbilical cord blood (UCB) is increasingly used as a source of stem cells for patients with blood cancers who need an allogeneic stem cell transplant (a transplant with stem cells from another person) but who have no suitably matched donors. The advantages of UCB are that (1) it is associated with less risk of transmitting an infection from a donor, (2) it can be more safely given even if not completely matched compared to bone marrow or blood stem cells, and (3) it is much more quickly available than unrelated donor bone marrow or blood stem cells. While more commonly used for transplantation in children, UCB is increasingly being used in adults. However, because they are larger than children, the relatively smaller stem cell dose in UCB is major limitation for transplantation in adults, and engraftment can be delayed. This study is investigating whether the drug sitagliptin can be used to increase and speed up engraftment in adults receiving UCB transplantation, overcoming the limitation of small stem cell doses associated with umbilical cord blood.

Sitagliptin is a drug given in tablet form that has been recently approved by the Food and Drug Administration (FDA) for the treatment of certain patients with diabetes mellitus (a disease that results in high blood sugar). Sitagliptin has been given to both normal healthy volunteers and diabetic patients and has been found to be safe and well-tolerated. The drug improves control of blood sugar in diabetics by inhibiting an enzyme called "CD26/DPP-IV." Recent studies at Indiana University (and other centers) have shown that this same enzyme plays an important role in the way transplanted stem cells find their way to the bone marrow and engraft. Transplant studies in mice have found that inhibiting CD26/DPP-IV significantly increases the engraftment of stem cells. Based on these studies, it is believed that drugs that inhibit CD26/DPP-IV, such as sitagliptin, may also increase engraftment in patients who receive clinical stem cell transplants.
Despite substantial progress, causal variants are identified only for a minority of familial Parkinson's disease (PD) cases, leaving high-risk pathogenic variants unidentified1,2. To identify such variants, we uniformly processed exome sequencing data of 2,184 index familial PD cases and 69,775 controls. Exome-wide analyses converged on RAB32 as a novel PD gene identifying c.213C > G/p.S71R as a high-risk variant presenting in ~0.7% of familial PD cases while observed in only 0.004% of controls (odds ratio of 65.5). This variant was confirmed in all cases via Sanger sequencing and segregated with PD in three families. RAB32 encodes a small GTPase known to interact with LRRK2 (refs. 3,4). Functional analyses showed that RAB32 S71R increases LRRK2 kinase activity, as indicated by increased autophosphorylation of LRRK2 S1292. Here our results implicate mutant RAB32 in a key pathological mechanism in PD-LRRK2 kinase activity5-7-and thus provide novel insights into the mechanistic connections between RAB family biology, LRRK2 and PD risk.
The CORTEX group will attend 10, 2-hour sessions for a period of four weeks prior to the initial exercise program start. One hour will be devoted to computerized training (stationary dual-task \& cognitive control training, self-priming, certainty training) whereas the other hour will be devoted to exergaming involving non-stationary, dual-task training.
Patients with nonvalvular atrial fibrillation (NVAF) taking daily oral dose of Prazaxa® Capsules (Dabigatran etexilate). Dosage of Dabigatran etexilate approved in Japan: 300 milligram (mg) daily (150 mg \[as 2 capsules of 75 mg\] twice a day (b.i.d)) or 220 mg (110 mg \[as 1 capsule of 110 mg\] b.i.d) for a treatment duration of 52 weeks.
BACKGROUND: In the current era of effective adjuvant therapies and de-escalation of surgery, distinguishing which patients with high-risk stage II melanoma are at increased risk of recurrence after excision of the primary lesion is essential to determining appropriate treatment and surveillance plans.
METHODS: A single-center retrospective study analyzed patients with stage IIB or IIC melanoma. Demographic and tumor data were collected, and genomic analysis of formalin-fixed, paraffin-embedded tissue samples was performed via an internal next-generation sequencing (NGS) platform (SNaPshot). The end points examined were relapse-free survival (RFS), distant metastasis-free survival (DMFS), overall survival (OS), and melanoma-specific survival (MSS). Uni- and multivariable Cox regressions were performed to calculate the hazard ratios.
RESULTS: The study included 92 patients with a median age of 69 years and a male/female ratio of 2:1. A Breslow depth greater than 4 mm, a higher mitotic rate, an advanced T stage, and a KIT mutation had a negative impact on RFS. A primary lesion in the head and neck, a mitotic rate exceeding 10 mitoses per mm2, a CDH1 mutation, or a KIT mutation was significantly associated with a shorter DMFS. Overall survival was significantly lower with older age at diagnosis and a higher mitotic rate. An older age at diagnosis also had a negative impact on MSS.
CONCLUSION: Traditional histopathologic factors and specific tumor mutations displayed a significant correlation with disease recurrence and survival for patients with high-risk stage II melanoma. This study supported the use of genomic testing of high-risk stage II melanomas for prognostic prediction and risk stratification.
The study aimed to examine matrix metalloproteinase-2 (MMP-2) expression in a rat ligamentum flavum (LF) hypertrophy model in vivo, and the effect of elastin-derived peptides (EDPs) on MMP-2 and tissue inhibitors of metalloproteinases (TIMPs) in rat LF cells in vitro. Surgical destabilization was performed at the rat spinal L3/4 level to induce increased mechanical stress. Rats were killed at 6- and 12-weeks postsurgery for histological staining, immunohistochemical staining, RT-qPCR and western blot. 100 µg/mL EDPs were applied to isolated normal rat LF cells, with or without pretreatment of elastin receptor complex (ERC) inhibitors, to assess the expression of MMP-2, TIMP-1, and TIMP-2. Spinal destabilization led to LF hypertrophy, observed through increased LF thickness and area, along with histological changes of chondrometaplasia and elastic fiber degradation. LF was also stained positively for Col I and Col II, where elastic fiber has broken down. MMP-2 expression was notably elevated in the hypertrophied LF, accompanied by increased TIMP-2 and TIMP-3 levels. EDPs were found to suppress MMP-2 expression and reduce TIMP-1 and TIMP-2 levels in rat LF cells. Interestingly, exposure to EDPs led to a significant rise in MMP-2/TIMP-1 and MMP-2/TIMP-2 ratios, dependent on the ERC. Collectively, the study suggests that increased MMP-2 activity contributes to elastic fiber degradation in hypertrophied LF, generating EDPs that further enhance the MMP-2/TIMPs ratio in LF cells in an ERC-dependent manner. Further research is essential to delve into the mechanisms of EDPs in LF hypertrophy.
FIELD: pharmaceutical technology. SUBSTANCE: method involves milling a drug in the presence of solid milling medium. A solid milling medium is polymeric resin (density is 0.8-3.0 g/cm 3 ) as particles of an average size 0.1-3 mm. Polystyrene cross-linked with divinylbenzene or polycarbonate are used as polymeric resin. Diagnostic contrast image agent, for example, ethyl-3,5-bis-acetamido-2,4,6-triiodobenzoate is used as a drug. EFFECT: decreased content of polluting impurities in medicinal particles. 11 cl, 6 ex
A method performed in a computing device. The method includes receiving, at a computing device, a plurality of spectra acquired from a respective plurality of aliquots containing a biophysiological carrier protein. At least one of the concentration of the spin probe and the concentration of the polar agent varies between aliquots. The computing device then determines a biophysical parameter based on the received spectrum and applies at least a portion of the received spectrum and the biophysical parameter as inputs to a trained logistic regression model. The logistic regression model is trained to determine probabilities of applied input parameters relating to one or more of a plurality of predetermined diseases and/or disease locations. The trained model is used to determine probabilities of input parameters relating to one or more of said predetermined diseases and/or disease localisation and to output the results of the determination.
Participants will receive LEM5 (one lemborexant \[LEM\] 5 milligram \[mg\] tablet and one zolpidem \[ZOL\]-matched placebo \[PBO\] tablet) in Treatment Period 1. In Treatment Period 2, participants will receive LEM10 (one LEM 10 mg tablet and one ZOL-matched PBO tablet). In Treatment Period 3, participants will receive PBO (one LEM-matched PBO tablet and one ZOL-matched PBO tablet). In Treatment Period 4, participants will receive ZOL (one LEM-matched PBO tablet and one ZOL 6.25 mg tablet).
Disclosed are compositions of matter, which are extracts of the microalga  Aphanizomenon flos Aquae Aquae  Rafts ex Born. Rah. Var.  flos aquae  (AFA-Klamath), and purified components thereof. These compositions are useful for the treatment of neurological and neurodegenerative diseases, and of mood conditions. These diseases and conditions include conditions and disorders such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, hyperactivity and attention deficit disorders, autism, depression, memory deficit, and mood disturbances.
Triplet combination of COM902 + COM701 + Pembrolizumab evaluated in subjects with MSS-CRC. All study drugs will be administered IV every 3 weeks.
PURPOSE: An antibody for n-terminus protein of PRDM 10 and a manufacturing method thereof are provided to be usefully used in the PRDM 10 protein function research. CONSTITUTION: An antibody for n-terminus protein of PRDM 10 is described in the sequence number 1(SEQ ID NO:1). The gene which codes the N- terminus protein has the base sequence described in the sequence number 2. The N- terminus protein of the PRDM 10 includes the zinc finger motif. A composition for detecting the PRDM 10 protein includes the antibody which unites with the N- terminus protein of the PRDM 10. The PRDM 10 related disease is inflammatory arthritis or cancer. A manufacturing method of the antibody for N terminus protein of the PRDM 10 comprises the following steps: processing PCR by using a primer in order to amplify the N terminous part of the PRDM 10 by using the PRDM 10 as a mold; ligating the amplified N terminous gene of the PRDM 10 and transforming into a host cell to over express the N-terminous protein of the RPDM 10; and obtaining the antibody for N-terminous protein of the RPDM 10 bt injecting the over expressed N terminus protein of the PRDM 10 into animals. [Reference numerals] (AA) Cloning expression using His tagging system; (BB) Antigen protein purification (IMAC); (CC) Immunization reaction induction inside rabbit body
The invention discloses a miracle drug for curing otitis media. It is made up through marinating serissa serissoides by distilled spirit. The proportion is: serissa serissoides 1-3 shares, distilled spirit 1-6 shares; the distilled spirit can be replaced by medical alcohol. The invention realizes quick-acting, good effect, low cost, hasn't any toxin side effect, so it is very safe and reliable. The medicine has functions of clearing away heat and detoxicating, diminishing inflammation, sterilization, making sensile. It can be used to cure acute and chronic otitis media, deafness, tinnitus, and the amygdalitis, head or throat tumefaction, deglutition handicap.
Xp Endo Finisher file was used with VDW Silver (VDW) endomotor at 800 rpm speed and 1 Ncm torque according to the manufacturer's instructions. The Xp Endo Finisher file was placed in the canal, 2 mm shorter than the working length, and was used with slow movements of 7-8 mm amplitude in the canal during activation. 5 mL of 2.5% NaOCl was applied for 1 minute for each channel. Each canal was then washed with 2 mL of 17% EDTA for 1 minute.