anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
PURPOSE: Corticotropin-releasing hormone (CRH) plays an important role in relief of pain by releasing analgesia-associated molecules in several inflammatory states. During inflammation, peripheral CRH acts on cells of the immune system to stimulate the local expression of proopiomelanocortin (POMC) and the production of β-endorphin, which in turn binds to opioid receptors on sensory neurons to produce antinociception. In the present study, we further investigated the role of endogenous CRH in inflammatory pain by determining the effects of Crh-deficiency on this process.
METHODS: For this purpose, we used Crh-deficient (Crh-/-) mice and their wildtype (Crh + / +) littermates in the CFA (Complete Freund's Adjuvant)-induced inflammatory pain model. Pain thresholds were evaluated with the Hargreaves apparatus.
RESULTS: Our experiments showed that Crh deficiency led to increased pain response, which was associated with decreased POMC mRNA levels in locally inflamed paws of these mice. Furthermore, Crh-/- mice had higher paw edema than Crh + / + mice. Histological evaluation of inflamed paw tissues revealed increased inflammatory response in Crh-/- mice. Protein levels of proinflammatory cytokines, such as IL-6, TNF-α, and IL-1β, were higher in inflamed tissue of Crh-/- mice compared to wildtype mice. Corticosterone replacement increased the pain threshold of Crh-/- mice, restored their paw volume to the levels of wildtype mice, and significantly reduced their proinflammatory cytokine levels. Furthermore, glucocorticoid administration significantly increased POMC mRNA expression in the inflamed paw.
CONCLUSION: Our data suggest that genetic deficiency of CRH is associated with increased pain. This effect is likely attributable to the accompanying glucocorticoid insufficiency and is in part mediated by opioids expressed locally.
1324197 Coated pharmaceutical preparations ROHM GmbH 23 June 1971 [27 June 1970] 29433/71 Heading A5B Pharmaceutical compositions for oral administration comprise a solid active ingredient coated with a synthetic resin composition which is insoluble in water but permeable under physiological conditions thereby serving to provide delayed release of the active ingredient upon oral administration, the synthetic resin composition comprising a copolymer containing (A) units of at least one hydroxyalkyl ester of an α,#-unstaurated mono- or di-carboxylic acid and (B) units of at least one copolymerisable monomer capable of forming a water-insoluble homopolymer, with the total amount of such units (A) and (B) present in the copolymer being at least 90% by weight, and the copolymer containing from 3 to 10% by weight of hydroxy groups. The hydroxyalkyl ester may comprise an ester of acrylic, methacrylic, crotonic, itaconic, maleic or fumaric acid with an alcohol containing 2 to 4 carbon atoms, e.g. 2-hydroxyethyl, 2-hydroxypropyl, 2-hydroxybutyl or 4- hydroxybutyl acrylate or methacrylate. The monomer (B) is preferably an ester of acrylic or methacrylic acid containing 1 to 4 carbon atoms in the alcohol moiety, styrene or a homologue thereof, a vinyl ester or vinyl chloride. The copolymer may further contain less than 10% by weight of units of at least one α, #-unsaturated mono- or di-carboxylic acid or a salt thereof. The composition may be in the form of a coated tablet or a coated granulate which may be bonded together to form a pharmaceutical core.
RASopathies encompass a diverse set of disorders affecting genes that encode proteins within the RAS-MAPK pathway. RASA1 mutations are the cause of an autosomal dominant disorder called capillary malformation-arteriovenous malformation type 1 (CM-AVM1). Unlike other RASopathies, facial dysmorphism has not been described in these patients. We phenotypically delineated a large family of individuals with multifocal fast-flow capillary malformations, severe lymphatic anomalies of perinatal onset, and dysmorphic features not previously described. Sequencing studies were performed on probands and related family members, confirming the segregation of dysmorphic features in affected members of a novel heterozygous variant in RASA1 (NM_002890.3:c.2366G>A, p.(Arg789Gln)). In this work, we broaden the phenotypic spectrum of CM-AVM type 1 and propose a new RASA1 variant as likely pathogenic.
Acute megakaryoblastic leukemia (AML-M7) is rarely seen in adult patients and patients usually present with cytopenias. Here we discuss diagnostic challenges and pathologic features in a patient with AML-M7 who presented with thrombocytosis and diarrhea. A 63-year-old male patient presented with persistent diarrhea lasting for 2 months, fatigue, and thrombocytosis. The diagnostic workup included a stool analysis, endoscopy colonoscopy, and imaging studies; however, these studies did not reveal any possible etiology. The hematologic evaluation included peripheral blood smear, bone marrow aspiration and biopsy, flow cytometry, and cytogenetic analysis. Eventually, according to pathologic and flow cytometric findings, a diagnosis of AML-M7 was made. Diagnosis of AML-M7 may be challenging, especially in adult patients with atypical presentation. Patients with megakaryoblastic leukemia respond poorly to standard induction regimens and they should be advised to participate in a clinical trial.
OBJECTIVE: The purpose of this study was to evaluate the surgical complications of patients treated for nonsyndromic sagittal craniosynostosis and the necessity for reoperations due to craniocerebral disproportion.
MATERIALS AND METHODS: The patient cohort of this study consisted of patients (N = 82) who were treated in the Oulu University Hospital using the open vault cranioplasty with a modified H-technique between the years 2008 to 2022. There were 69 males (84.1%) and 13 females (15.9%). The mean age at the primary operation was 6.1 months. Mean follow-up time was 9.0 years.
RESULTS: There were no major complications related to the procedures. Two patients (2.4%) had a minor dural lesion. There were no postoperative wound infections. Of the 82 patients, seven patients with primary craniosynostosis (13.0%) developed symptomatic craniocerebral disproportion requiring reoperation to increase intracranial volume. In all these patients, invasive intracranial pressure (ICP) monitoring was performed prior to decision-making. In the majority of cases, the aesthetical outcome was considered good or excellent.
CONCLUSION: The operative method used was feasible and safe. Thirteen percent of patients who were followed over 5 years required major surgery due to development of craniocerebral disproportion later in life.
Individually titrate Benzhydrocodone and Acetaminophen tablets to a dose that provides adequate analgesia and minimizes adverse reactions. Continually reevaluate patients receiving Benzhydrocodone and Acetaminophen tablets to assess the maintenance of pain control and the relative incidence of adverse reactions, as well as monitoring for the development of addiction, abuse, or misuse [see Warnings and Precautions (5.1)]. Frequent communication is important among the prescriber, other members of the healthcare team, the patient, and the caregiver/family during periods of changing analgesic requirements, including initial titration. 

If the level of pain increases after dosage stabilization, attempt to identify the source of increased pain before increasing the Benzhydrocodone and Acetaminophen tablets dosage. If unacceptable opioid-related adverse reactions are observed, consider reducing the dosage. Adjust the dosage to obtain an appropriate balance between management of pain and opioid-related adverse reactions.

Total dosage of Benzhydrocodone and Acetaminophen tablets and any concomitant acetaminophen-containing products should not exceed 4000 mg of acetaminophen in a 24-hour period.
Exemplary materials exhibiting high emissivity and methods for making them are provided. These materials can include a porous coating of small particles provided on a substrate, where the particles can resist sintering and further densification at high temperatures. These materials may be formed by generating an arc using a one-sided electrode apparatus, where particles produced by the arc and electrode can impinge on the substrate and adhere to it. The coating can include predominantly undensified small particles which can have a size less than about 1 μm. These materials can have an emissivity greater than 0.8 or 0.9. Such materials can be used to form infrared emitters which may provide greater energy efficiency and increased operating lifetime as compared to uncoated emitters. Surfaces coated with small particles may be used in further applications such as catalytic or reactive surfaces, engine components, or acoustical dampening surfaces.
Rectovaginal fistulas (RVF) represent less than 5% of anorectal fistulas. The classification of RVF is based on the localization (low vs. high) and the etiology. The most frequent causes of RVF are birth trauma, Crohn's disease, previous surgery and pelvic irradiation. In most cases a clinical diagnostic assessment is sufficient. Additionally, endosonography is a reliable tool to detect sphincter defects. Computed tomography (CT) and magnetic resonance imaging (MRI) are reserved for special situations (e.g., RVF related to anastomotic leakage, after pelvic irradiation or associated with complex perianal fistulizing Crohn's disease). The surgical treatment is primarily oriented to the localization and etiology. Surgical techniques range from local procedures (e.g., endorectal advancement flap repair, transvaginal or transperineal closure) up to more invasive tissue interposition (e.g., bulbocavernosus muscle fat tissue flap or transposition of the gracilis muscle). In "high" RVF transabdominal approaches such as coloanal anastomosis, pull through procedures or omental interposition are indicated. All surgical procedures show high recurrence rates. Several operations are mostly necessary and a stoma creation is often required.
This group will complete a 16-week standard behavioral weight control intervention. They will not be given any recommendations regarding the timing of their energy consumption, but instead encouraged to follow the same energy goals at the BFL group.
Patients will receive 1, 2 or 3 daily (short-dwell) exchanges with XyloCore of an osmotic strength comparable to their pre-randomization prescription of glucose peritoneal dialysis solution (XyloCore Low, Medium and High Strenght have an osmotic strength comparable to Physioneal, Fixioneal or Dianeal 1.36%, 2.27%, 3.86% glucose, respectively, and Balance, Bicavera, Bicanova or Equibalance with 1.5%, 2.5%, 4.25% glucose, respectively). All patients will receive Extraneal (7.5% Icodextrin) for nocturnal (long-dwell) exchange.
Exercises will be done 2 days a week for 8 weeks and last approximately 30 minutes. In general, if individuals can perform 2 sets of 10 repetitions of movements at a difficulty level with quality, they can move on to a higher difficulty level. It consists of warm-up, balance and strengthening exercises. It was developed to increase balance.
Tetra-substd. benzene derivs. of formula (I) and their pharmaceutically utilisable salts are prepared by reacting the reactive carboxylic acid derivs. of formula (III) with the cpd. of formula (IV), and then removing the protecting group of the rotected hydroxyl radical.  In formulas, X is oxygene; R1 is hydroxy, acyloxy or lower alkoxycarbonyloxy; R2 is lower alkoxy, lower alkenyloxy or lower alkylthio; R3 is lower alkoxy; R4 is lower alkyl or p-lower- alkoxybenzoyl, opt. substd. phenyl or benzyl gp.; R1 is protected hydroxy radical.
INTRODUCTION: Knowledge on prevalence and association of human papillomavirus (HPV) in third trimester placentae and adverse pregnancy outcomes is limited. We investigated the prevalence of placental HPV at delivery, explored urine HPV characteristics associated with placental HPV and whether placental HPV increased the risk adverse pregnancy outcomes.
METHODS: Pregnant women were enrolled in the Scandinavian PreventADALL mother-child cohort study at midgestation. Human papillomavirus genotyping was performed on placental biopsies collected at delivery (n = 587) and first-void urine at midgestation and delivery (n = 556). Maternal characteristics were collected by questionnaires at gestational week 18 and 34. Adverse pregnancy outcomes were registered from chart data including hypertensive disorders of pregnancy, gestational diabetes mellitus and newborns small for gestational age. Uni- and multivariable regression models were used to investigate associations.
RESULTS: Placental HPV was detected in 18/587 (3 %). Twenty-eight genotypes were identified among the 214/556 (38 %) with midgestational urine HPV. Seventeen of the 18 women with placental HPV were midgestational HPV positive with 89 % genotype concordance. Midgestational high-risk-(HR)-HPV and high viral loads of Any- or HR-HPV were associated with placental HPV. Persisting HPV infection from midgestation to delivery was not associated with placental HPV. Adverse pregnancy outcomes were seen in 2/556 (0.4 %) of women with placental HPV.
DISCUSSION: In this general cohort of pregnant women, the prevalence of placental HPV was 3 %, and midgestational urinary HPV 38 %. High HPV viral load increased the risk for placental HPV infections. We observed no increased risk for adverse pregnancy outcomes in women with placental HPV.
Morphine is a phenanthrene-derivative opiate agonist. It is the principal alkaloid of opium and is considered to be the prototype of the opiate agonists.

Morphine sulfate occurs as white, feathery, silky crystals; cubical masses of crystals; or a white, crystalline powder. 

When exposed to air it gradually loses water of hydration, and darkens on prolonged exposure to light. It is soluble in water and ethanol at room temperature. The chemical name of morphine sulfate is 7,8-Didehydro-4,5-epoxy-17-methyl-(5α,6α)-morphinan-3,6-diol sulfate (2:1) (salt), pentahydrate, with the following structural formula:

(C17H19NO3)2 • H2SO4 • 5H2O Molecular Weight is 758.83

Morphine Sulfate Injection, USP is a sterile, nonpyrogenic solution, free of antioxidants and preservatives, intended for intravenous administration. Each milliliter of sterile solution contains 4 mg, 8 mg, or 10 mg morphine sulfate and the following inactive ingredients: 0.2 mg edetate disodium, 0.4 mg citric acid monohydrate, sodium chloride to adjust isotonicity and water for injection. Hydrochloric acid and/or sodium hydroxide may be added to adjust pH. The pH range is 2.5 to 4.0.
The propeller flap is based on a perforator that serves as a pivot joint, allowing the flap to rotate up to 180°. It provides the advantages of greater freedom of movement and versatility in flap design.
One double-blind, active-controlled clinical trial was conducted in pediatric cancer patients. The total population (N = 327) had a mean age of 8.3 years (range 2 months to 16.9 years) and were 53% male; and 96% white. Patients were randomized and received a 20 mcg/kg (maximum 1.5 mg) intravenous infusion of palonosetron hydrochloride injection 30 minutes prior to the start of emetogenic chemotherapy (followed by placebo infusions 4 and 8 hours after the dose of palonosetron injection) or 0.15 mg/kg of intravenous ondansetron 30 minutes prior to the start of emetogenic chemotherapy (followed by ondansetron 0.15 mg/kg infusions 4 and 8 hours after the first dose of ondansetron, with a maximum total dose of 32 mg). Emetogenic chemotherapies administered included doxorubicin, cyclophosphamide (<1500 mg/m2), ifosfamide, cisplatin, dactinomycin, carboplatin, and daunorubicin. Adjuvant corticosteroids, including dexamethasone, were administered with chemotherapy in 55% of patients. 

Complete Response in the acute phase of the first cycle of chemotherapy was defined as no vomiting, no retching, and no rescue medication in the first 24 hours after starting chemotherapy. Efficacy was based on demonstrating non-inferiority of intravenous palonosetron injection compared to intravenous ondansetron. Non-inferiority criteria were met if the lower bound of the 97.5% confidence interval for the difference in Complete Response rates of intravenous palonosetron injection minus intravenous ondansetron was larger than -15%. The non-inferiority margin was 15%. 

Efficacy Results 

As shown in Table 8, intravenous palonosetron hydrochloride 20 mcg/kg (maximum 1.5 mg) demonstrated non-inferiority to the active comparator during the 0 to 24-hour time interval. 

In patients that received palonosetron hydrochloride injection at a lower dose than the recommended dose of 20 mcg/kg, non-inferiority criteria were not met.
When fluocinolone acetonide, hydroquinone, and tretinoin in fixed combinations equivalent to 10%, 50%, 100%, and 150% of the concentrations in the clinical formulation of TRI-LUMA Cream were applied topically to male and female CD-1 mice for up to 24 months at dosages approximating up to 50, 19,000, and 250 µg/kg/day, respectively (corresponding to dosages of 150, 57,000, and 750 μg/m 2/day, respectively), no statistically significant changes in tumor incidence were observed. 

When fluocinolone acetonide, hydroquinone, and tretinoin in fixed combinations equivalent to 10%, 25%, 50%, and 100% of the concentrations in the clinical formulation of TRI-LUMA Cream were applied topically to male and female SD rats for up to 24 months at dosages approximating up to 10, 4000, and 50 µg/kg/day, respectively (corresponding to dosages of 60, 24,000, and 300 μg/m 2/day, respectively), statistically significant increases in the incidences of islet cell adenomas and combined islet cell adenomas and carcinomas of the pancreas in both males and females were observed. The clinical relevance of these findings is unknown. 

Studies of hydroquinone in animals have demonstrated some evidence of carcinogenicity. The carcinogenic potential of hydroquinone in humans is unknown.

Studies in hairless albino mice suggest that concurrent exposure to tretinoin may enhance the tumorigenic potential of carcinogenic doses of UVB and UVA light from a solar simulator. This effect has been confirmed in a later study in pigmented mice, and dark pigmentation did not overcome the enhancement of photocarcinogenesis by 0.05% tretinoin. Although the significance of these studies to humans is not clear, patients should minimize exposure to sunlight or artificial ultraviolet irradiation sources.

Mutagenicity studies were not conducted with this combination of active ingredients. Published studies have demonstrated that hydroquinone is a mutagen and a clastogen. Treatment with hydroquinone has resulted in positive findings for genetic toxicity in the Ames assay in bacterial strains sensitive to oxidizing mutagens, in in vitrostudies in mammalian cells, and in the in vivomouse micronucleus assay. Tretinoin has been shown to be negative for mutagenesis in the Ames assay. Additional information regarding the genetic toxicity potential of tretinoin and of fluocinolone acetonide is not available. 

A dermal reproductive fertility study was conducted in SD rats using a 10-fold dilution of the clinical formulation. No effect was seen on the traditional parameters used to assess fertility, although prolongation of estrus was observed in some females, and there was a trend towards an increase in pre-and post-implantation loss that was not statistically significant. No adequate study of fertility and early embryonic toxicity of the full-strength drug product has been performed. In a six-month study in minipigs, small testes and severe hypospermia were found when males were treated topically with the full strength drug product.
HIV-infected subjects who are at least 18 years of age, with no ART in the previous 3 months, and with plasma HIV-1 RNA \>20,000 copies/mL. CD4+ T cell count \>200 cells/mm3. Group A1 will undergo continuous CSF ( cerebrospinal fluid) sampling via intrathecal catheter.
The most widely used synthetic glucocorticoid, dexamethasone (DEX), causes stunted growth in children when used excessively or for long periods of time; however, there are still plenty of pediatric patients require long-term treatment with DEX. As an alternative, growth hormone is used in combination, but it has side effects, a high cost, and psychological factors, and it is not satisfactory in terms of effectiveness. It is necessary to develop a safe and affordable treatment that can replace it. The Korean Food and Drug Administration approved HT042, a standardized functional food ingredient, with the claim that it can help height growth of children. In this study, it was found that HT042 activated the Indian hedgehog/parathyroid hormone-related protein signaling pathway and enhanced the number of growth hormone receptors and insulin-like growth factor-1 receptors on the growth plate surface, which were reduced by DEX treatment, and restored growth retardation. In metatarsal bone and primary chondrocyte models, it was found that HT042 can promote the length of growth plate and recover DEX-induced growth retardation. It was also found that HT042 promotes cell proliferation using bromodeoxyuridine and terminal deoxynucleotidyl transferase dUTP nick end labeling assays; moreover, we verified increased expression of GHR/IGF-1R and Ihh/PTHrP pathway activity using qRT-PCR, western blotting, and siRNA analyses to verify its direct action on the growth plate. The anti-apoptotic effect of HT042 was identified by regulating the expression of apoptotic factors such as caspase-3, Bcl2, Bclx, and Bax. These results were identified using both ex vivo and in vitro models. Our study verified that co-administration of HT042 could recover the DEX induced growth retardation.
Symptoms and Signs

Symptoms following acute NSAIDs overdoses are usually limited to lethargy, drowsiness, nausea, vomiting, and epigastric pain, which are generally reversible with supportive care. Gastrointestinal bleeding can occur. Hypertension, acute renal failure, respiratory depression and coma may occur, but are rare. Anaphylactoid reactions have been reported with therapeutic ingestion of NSAIDs, and may occur following an overdose.

Treatment

Patients should be managed by symptomatic and supportive care following a NSAIDs overdose. There are no specific antidotes. Emesis and/or activated charcoal (60 g to 100 g in adults, 1 g/kg to 2 g/kg in children) and/or osmotic cathartic may be indicated in patients seen within 4 hours of ingestion with symptoms or following a large oral overdose (5 to 10 times the usual dose). Forced diuresis, alkalization of urine, hemodialysis or hemoperfusion may not be useful due to high protein binding.

Single overdoses of ketorolac tromethamine have been variously associated with abdominal pain, nausea, vomiting, hyperventilation, peptic ulcers, and/or erosive gastritis and renal dysfunction which have resolved after discontinuation of dosing.