anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Skeletal muscle aging and sarcopenia result in similar changes in the levels of aging markers. However, few studies have examined cancer sarcopenia from the perspective of aging. Therefore, this study investigated aging in cancer sarcopenia and explored its causes in vitro and in vivo. In mouse aging, in vitro cachexia, and mouse cachexia models, skeletal muscles showed similar changes in aging markers including oxidative stress, fibrosis, reduced muscle differentiation potential, and telomere shortening. Furthermore, examination of mitochondrial DNA from skeletal muscle revealed a 5 kb deletion in the major arc; truncation of complexes I, IV, and V in the electron transport chain; and reduced oxidative phosphorylation (OXPHOS). The mouse cachexia model demonstrated high levels of high-mobility group box-1 (HMGB1) and tumor necrosis factor-α (TNFα) in cancer ascites. Continuous administration of neutralizing antibodies against HMGB1 and TNFα in this model reduced oxidative stress and abrogated mitochondrial DNA deletion. These results suggest that in cancer sarcopenia, mitochondrial oxidative stress caused by inflammatory cytokines leads to mitochondrial DNA damage, which in turn leads to decreased OXPHOS and the promotion of aging.
INTRODUCTION: Optical coherence tomography angiography (OCT-A) is a novel tool that allows the detection of retinal vascular changes. We investigated the association of macular vessel density (VD) in the superficial plexus assessed by OCT-A with measures of cerebrovascular pathology and atrophy quantified by brain magnetic resonance imaging (MRI) in non-demented individuals.
METHODS: Clinical, demographical, OCT-A, and brain MRI data from non-demented research participants were included. We analyzed the association of regional macular VD with brain vascular burden using the Fazekas scale assessed in a logistic regression analysis, and the volume of white matter hyperintensities (WMH) assessed in a multiple linear regression analysis. We also explored the associations of macular VD with hippocampal volume, ventricle volume and Alzheimer disease cortical signature (ADCS) thickness assessed in multiple linear regression analyses. All analyses were adjusted for age, sex, syndromic diagnosis and cardiovascular variables.
RESULTS: The study cohort comprised 188 participants: 89 with subjective cognitive decline and 99 with mild cognitive impairment. No significant association of regional macular VD with the Fazekas categories (all, p > 0.111) and WMH volume (all, p > 0.051) were detected. VD in the nasal quadrant was associated to hippocampal volume (p = 0.007), but no other associations of macular VD with brain atrophy measures were detected (all, p > 0.05).
DISCUSSION: Retinal vascular measures were not a proxy of cerebrovascular damage in non-demented individuals, while VD in the nasal quadrant was associated with hippocampal atrophy independently of the amyloid status.
There is provided on-demand, oxygen generating topical compositions having a built-in indicator specifically to indicate a color change upon the complete mixing of the oxygen precursor and catalyst. The first part of the composition contains a carrier and manganese dioxide (MnO2) nanoparticles. The second part of the composition comprises the oxygen precursor; hydrogen peroxide. When the two parts, one with manganese dioxide nanoparticles and exhibiting a characteristic color, (e.g. yellow brown) and the second part with hydrogen peroxide are mixed together, the color imparted by the manganese dioxide nanoparticles essentially disappears and the final composition (enriched with oxygen) either appears colorless or takes on the original color of the catalyst comprising part prior to addition of manganese dioxide. Thus, the manganese dioxide catalyst nanoparticles themselves serve as the colorimetric indicator of peroxide decomposition to oxygen, precluding the need for an external colorant. Manganese dioxide particles that are not nanoparticles fail to exhibit this color changing phenomenon.
Risk Summary

There are no data on the presence of RAPIVAB in human milk, the effects on the breastfed infant, or the effects on milk production. Peramivir is present in rat milk [see Data]. Limited clinical data during lactation preclude a clear determination of the risk of RAPIVAB to an infant during lactation; therefore, the developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for RAPIVAB and any potential adverse effects on the breastfed child from the drug or from the underlying maternal condition. 

Data

A pharmacokinetic study was performed in lactating rats administered a single intravenous dose of peramivir (10 mg/kg) on Lactation/Postpartum Days 11 to 13. The maximum concentration of peramivir in milk was reached at 0.75 hours post-dose. The milk to plasma AUC ratio of peramivir was approximately 0.5.
How Supplied   
ProHance Multipack is supplied as a sterile, nonpyrogenic, and colorless to slightly yellow solution containing 279.3 mg/mL (0.5 mmol/mL) of gadoteridol in rubber stoppered vials. ProHance Multipack is supplied in boxes of five 50 mL pharmacy bulk packages (NDC 0270-1111-70) and boxes of five 100 mL pharmacy bulk packages (NDC-0270-1111-85). 

Storage and Handling   
Store at 25°C (77° F). Excursions permitted to 15°C to 30°C (59°F to 86°F) [See USP Controlled Room Temperature]. Protect from light. DO NOT FREEZE. Should freezing occur in the vial, ProHance Multipack should be brought to room temperature before use. If allowed to stand at room temperature for a minimum of 60 minutes, ProHance Multipack should return to a clear, colorless to slightly yellow solution. Before use, examine the product to assure that all solids are redissolved and that the container and closure have not been damaged. Should solids persist, discard vial.
An exemplary computer implemented method for prescribing a therapeutic regimen is provided. The computer implemented method includes receiving, by one or more computing devices, prescription information for a patient. The prescription information includes information representing a medical condition diagnosed by a prescriber. An identifier or identifiers may be extracted from the prescription information. At least one identifier indicates a diagnosis associated with the diagnosed medical condition. Thereupon, virtual kit information from a virtual treatment kit having one or more updatable components may be identified from a database using the identifier. Each of the updatable components includes component information representing at least one predetermined medication and a treatment plan for administering the predetermined medication for treating the identified medical condition. At least part of the component information may be provided from the virtual treatment kit for distributing the medications and treatment plan to the patient.
1\. If marked excitement is present, a short acting barbiturate, chloral hydrate of paraldehyde may be used for sedation. Large doses should be avoided if possible and must be carefully controlled so that they will not add to the depressive stages of atropine poisoning.   
2\. Artificial respiration with oxygen is necessary when respiration is depressed.   
3\. Depression may be controlled by use of caffeine, sodium benzoate or picrotoxin together with the inhalation of oxygen.   
4\. As a physiologic antidote, neostigmine methylsulfate may be given by intramuscular injection in doses of 500 mcg to 1 mg and repeated every 2 to 9 hours.   
5\. Remaining therapy is purely symptomatic. Icebags and alcohol sponges help to reduce fever, especially in children. Careful nursing is essential. The room should be darkened, because of the patient’s marked photophobia.
The invention provides a novel application of a DPP-4 inhibitor, which can be used for treating lupus nephritis. The influence of the DPP-4 inhibitor on proliferation and migration of the mesangial cells is examined, and the DPP-4 inhibitor has the capability of inhibiting the mesangial cells and is shown as concentration dependency, and the greater the concentration, the more obvious the inhibition effect. And the DPP-4 inhibitor can inhibit the proliferation and migration promoting function of CXCL12 protein on kidney membranous cells. The DPP-4 inhibitor 3mg/kg/d dose of the mice with the stomach system lupus erythematosus shows that the DPP-4 inhibitor treatment group is lighter than the control group in various aspects of inflammatory infiltration, mesangial cell proliferation, matrix expansion, small ball damage degree and small tube inflammatory infiltration. Measurement results of 24h proteinuria before and after gastric lavage show that most of proteinuria in a control group is aggravated, and the DPP-4 inhibitor treats the reduction of the proteinuria. Suggesting that DPP-4 inhibitors can be used for the treatment of lupus nephritis.
First, the protocol team will finalize the development and manualization of Health 4 Life (H4L) a comparison intervention, which will serve as the basis of comparison for Mobilizing Our Voices for Empowerment (MOVE), the treatment intervention. H4L will be a health promotion and life skills intervention to account for time and attention. Following this the protocol team will then implement Trial 1. In this trial, the intervention specialist and a "peer buddy" (intervention co-facilitator) from one AMTU will conduct one wave of both MOVE and H4L. The team will then conduct an analysis of the process data and revise the two interventions (MOVE and H4L). Upon revising the interventions, the protocol team will implement Trial 2. In this trial, the protocol co-chairs and the interventionist from Trial 1 will train interventionists and peer buddies from four new AMTUs; these interventionists and peer buddies will run the revised MOVE and H4L interventions. Each site will be designated as either a treatment or comparison site, and they will conduct two waves of their assigned intervention. The team at that time will conduct data analyses and then modify and manualize the final version of MOVE and H4L.
During open-heart surgery, an incision is made along the chest and the sternum (breastbone) is divided. The sternum is held open throughout the surgery so that the doctors can reach the heart. Sternal wound infection is an uncommon but serious complication of cardiac surgery that occurs when an infection develops at this site of entry. Sternal wound infections are associated with increased hospital stays, subsequent surgical procedures, and higher mortality rates.

The purpose of this research is to determine if using the antibiotic vancomycin as a preventative topical (on the surface of the skin) treatment during open-heart surgery will reduce the risk of developing a sternal wound infection. The results of this study could provide important information to guide new standards of practice in cardiac surgery. The ultimate goal of this research project is to improve patient care by reducing the number of sternal wound infections at our hospital.
This study is a multi-center, prospective, interventional study, in which subjects who meet the selection criteria are registered at each institution during the study period from the date of research approval. Regardless of the order, paracentesis using KARAHOC and conventional angiocatheter will be performed once in all patients. The criteria for successful paracentesis is set as 3L or more of ascites drainage. During paracentesis, albumin will be infused in all patients. Heart rate and blood pressure will be measured before the procedure and right after the completion of drainage, and 30 minutes later. The incidence of complications will be compared between two methods. In addition, patient and operator satisfaction will be investigated using a visual analogue scale.
The N-demethylation and N,N-demethylation derivatives of the two conformational isomers toluidine blue O (""TBO"") have been isolated, identified and prepared. An in vivo biological stain composition includes the conformational isomers of TBO and these N- and N,N-demethylation derivatives. The ratio of these isomers to these demethylation derivatives is at least 6:1. An improved method for detecting displastic oral tissue includes application of such TBO products, in a liquid carrier, to oral tissue. A process for preparing TBO products includes (1) oxidizing N,N-dimethyl-rho-phenylenediamine to form an intermediate 2-amino-5-dimethylaminophenyl thiosulfonic acid, (2) oxidizing this intermediate and condensing the oxidizate with o-toluidine, forming indamine thiosulfonic acid and (3) further oxidizing the indamine intermediate to form a TBO-containing reaction product, which is precipitated from the reaction mixture as a complex, from which the final TBO product is separated. The complexing agent is added to the reaction mixture at least before the final oxidation stop, preferably before the second oxidation step. An HPLC method for characterizing TBO products containing the conformational isomers of TBO and their N- and N,N-demethylation derivatives. The a mobile phase comprises an aqueous solution of an organic acid compound.
Pain of unknown etiology is frequent in individuals with the tumor predisposition syndrome neurofibromatosis 1 (NF1), even when tumors are absent. Nerve Schwann cells (SCs) were recently shown to play roles in nociceptive processing, and we find that chemogenetic activation of SCs is sufficient to induce afferent and behavioral mechanical hypersensitivity in wild-type mice. In mouse models, animals showed afferent and behavioral hypersensitivity when SCs, but not neurons, lacked Nf1. Importantly, hypersensitivity corresponded with SC-specific upregulation of mRNA encoding glial cell line-derived neurotrophic factor (GDNF), independently of the presence of tumors. Neuropathic pain-like behaviors in the NF1 mice were inhibited by either chemogenetic silencing of SC calcium or by systemic delivery of GDNF-targeting antibodies. Together, these findings suggest that alterations in SCs directly modulate mechanical pain and suggest cell-specific treatment strategies to ameliorate pain in individuals with NF1.
BEVESPI AEROSPHERE should not be initiated in patients with acutely deteriorating COPD, which may be a life-threatening condition. BEVESPI AEROSPHERE has not been studied in patients with acutely deteriorating COPD. The use of BEVESPI AEROSPHERE in this setting is inappropriate.

BEVESPI AEROSPHERE should not be used for the relief of acute symptoms, i.e., as rescue therapy for the treatment of acute episodes of bronchospasm. BEVESPI AEROSPHERE has not been studied in the relief of acute symptoms and extra doses should not be used for that purpose. Acute symptoms should be treated with an inhaled short-acting beta2-agonist.

When beginning BEVESPI AEROSPHERE, patients who have been taking inhaled, short-acting beta2-agonists on a regular basis (e.g., four times a day) should be instructed to discontinue the regular use of these medicines and use them only for symptomatic relief of acute respiratory symptoms. When prescribing BEVESPI AEROSPHERE, the healthcare provider should also prescribe an inhaled, short acting beta2-agonist and instruct the patient on how it should be used. Increasing inhaled beta2-agonist use is a signal of deteriorating disease for which prompt medical attention is indicated.

COPD may deteriorate acutely over a period of hours or chronically over several days or longer. If BEVESPI AEROSPHERE no longer controls the symptoms of bronchoconstriction, or the patient’s inhaled, short-acting beta2-agonist becomes less effective, or the patient needs more inhalations of short-acting beta2-agonist than usual, these may be markers of deterioration of disease. In this setting, a re-evaluation of the patient and the COPD treatment regimen should be undertaken at once. Increasing the daily dosage of BEVESPI AEROSPHERE beyond the recommended dose is not appropriate in this situation.
The initial daily dose consisted of 225 IU of Menopur administered by subcutaneous (SC) injection for 5 days. Dosing adjustments were allowed as of day 6. Dose could vary between 150-450 IU daily and treatment could not continue beyond day 20.
Regulation of host miRNA expression is a contested node that controls the host immune response to mycobacterial infection. The host must counter subversive efforts of pathogenic mycobacteria to launch a protective immune response. Here, we examine the role of miR-126 in the zebrafish-Mycobacterium marinum infection model and identify a protective role for infection-induced miR-126 through multiple effector pathways. We identified a putative link between miR-126 and the tsc1a and cxcl12a/ccl2/ccr2 signalling axes resulting in the suppression of non-tnfa expressing macrophage accumulation at early M. marinum granulomas. Mechanistically, we found a detrimental effect of tsc1a expression that renders zebrafish embryos susceptible to higher bacterial burden and increased cell death via mTOR inhibition. We found that macrophage recruitment driven by the cxcl12a/ccl2/ccr2 signalling axis was at the expense of the recruitment of classically activated tnfa-expressing macrophages and increased cell death around granulomas. Together, our results delineate putative pathways by which infection-induced miR-126 may shape an effective immune response to M. marinum infection in zebrafish embryos.
PCT No. PCT/US93/09582 Sec. 371 Date May 11, 1995 Sec. 102(e) Date May 11, 1995 PCT Filed Oct. 13, 1993 PCT Pub. No. WO94/12152 PCT Pub. Date Jun. 9, 1994An asymmetric membrane, osmotic, delivery device having coated macroparticulate solubility modifiers. The device comprises a beneficial agent, an osmagent, a coated macroparticulate solubility modifier and an asymmetric membrane that surrounds the device components. The device is useful for dispensing a beneficial agent to an aqueous environment of use. The coated macroparticles modify the solubility of the beneficial agent so that it's release can be controlled. The larger size of the solubility modifier macroparticles provides, for example, a longer release duration than would have been possible with a smaller size.
Precocious puberty (PP) in girls is classically defined by the onset of secondary sexual characteristics before eight years of age, but subsequent pubertal maturation can be quite varied. In many girls, PP takes a rapid course of progression (rapidly progressive precocious puberty; RP-PP) with an early menarche and fusion of the epiphyseal growth plates, leading eventually to a reduced final height if not treated. In a subset of girls with PP however, the growth rate slows to normal for age, skeletal maturation progresses in accordance with chronological age and there is little to no risk of impairment of final height (slowly progressive precocious puberty; SP-PP). Other conditions of non-progressive PP include premature thelarche and unsustained PP that is characterized by a regression of sexual precocity. Due to their benign course, slowly progressive (SP) PP and other non-progressive forms of PP do not warrant therapy with GnRH agonists. Differentiating these forms from RP-PP is therefore essential to prevent unnecessary intervention in a population that accounts for at least 50% of girls with PP. A distinction between these forms of PP may be difficult on clinical grounds however, since all these patients may present initially as isolated breast development.

The gold standard for the diagnosis of true (central) PP is the measurement of gonadotropins following GnRH stimulation test , where peak LH and peak LH/FSH ratio are the most valuable diagnostic parameters. There is however an overlap between prepubertal and early pubertal values and between girls with premature thelarche and progressive PP. It was suggested therefore that progressive pubertal development and growth acceleration should be documented over a 3- to 6-months period before GnRHa therapy in initiated.

More than a decade ago, along with the development of high-sensitive immunoassay for gonadotropins that replaced the RIA, Demir and colleagues have shown that urinary gonadotropins are age related and significantly increased during puberty. It has been suggested by others that urinary gonadotropins measurements can be used for differential diagnosis of pubertal disorders. This is based on the assumption that gradual elevation of nocturnal LH secretion prior to and at the onset of puberty can be reflected by first-voided urinary LH (ULH). In this prospective study, the investigators aimed to evaluate the value of first-voided ULH measurements in predicting pubertal course and differentiating SP-PP from RP-PP, by comparison to GnRH-stimulated gonadotropins.
The present study investigated the effect of orally administered Limosilactobacillus fermentum HY7302 (HY7302) on the relationship between ocular tissue and the microbiome in a corneal injury dry eye mouse model. Specifically, 0.1% benzalkonium chloride (BAC) was applied to the ocular surface for 14 days to induce corneal injury in male Balb/c mice. During the BAC treatment period, HY7302 (1 × 108 CFU/kg/day or 1 × 109 CFU/kg/day) or an omega-3 positive control (400 mg/kg/day) were administered orally (n = eight/group). To examine the signaling pathways affected by the HY7302 treatment, the in vitro effects of HY7302 on the tight junctions and the inflammatory response were investigated in the mouse colon epithelial cell line, CMT-93. BAC exposure decreased tear production, induced ocular inflammation and corneal epithelial detachment, and altered the gut microbiota. However, oral administration of HY7302 restored tear secretion and decreased corneal epithelial detachment in BAC-treated corneal injury mice. Further, HY7302 alleviated corneal inflammation via modulation of matrix metalloproteinase-9 (MMP-9) expression and affeted alterations in gut microbiota composition. These findings suggest that the gut-eye axis interaction between gut microbiota and corneal tissue affects disease severity in corneal injury, and that the alteration of the microbiota by HY7302 could improve eye health by regulating the inflammatory response.
An improved controlled release composition for non-parenteral administration of active agents and other therapeutics, particularly for oral or topical administration, has been developed. The composition is made by dispersing a complex formed of an active agent bound to an ion-exchange resin or to another form of resin or carrier, in a non-ionic non-aqueous (“NINA”) vehicle. The complexes are optionally coated with one or more layers of coating material to provide a controlled pattern of release of active agent from the carrier. Replacing the usual aqueous vehicle with a NINA vehicle, such as an oil or an ointment, allows the active agent-carrier complexes, with or without coatings, to be both orally and topically administered. The compositions can be formulated as powders, liquids, liquid suspensions, gels, capsules, soft gelatin capsules, tablets, chewable tablets, topical ointments, lotions, pourable or pumpable fluids, semisolid, crushable tablets, and unit-of-use sachets or capsules for reconstitution or direct application. The combination of multiple active agents is possible with this system, in which one or more active agents are bound to particles and one or more active agents are dissolved or dispersed in the NINA vehicle. This allows the combination of two or more active agents, which are otherwise incompatible, into a single dosage form.