anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
OBJECTIVE: Iatrogenic skin injury is a common neonatal skin problem that can have a severe impact on the health and life of newborns. The purpose of this study was to explore the factors influencing iatrogenic skin injury in neonates, identify and correct nursing behaviors that may lead to skin damage, thereby reduce the occurrence of skin damage and protect the health of newborns.
METHODS: The clinical data of 87 neonates with iatrogenic skin injury admitted to the Department of Neonatology of Shangrao People's Hospital, China, between January and June 2022, were retrospectively collected as a research group. The causes of iatrogenic skin injury were statistically analyzed. 50 neonates without iatrogenic skin injury in the same department during the same period were selected as the control group. The general data of the two groups were contracted, and the independent risk factors affecting iatrogenic skin injury in neonates were explored using multivariate Logistic regression. The corresponding nursing strategies were analyzed.
RESULT: (1) Among the 87 neonates with iatrogenic skin injury, the causes included adhesive dressing stripping (41.38%, 36/87), skin scratch during blue light phototherapy (25.29%, 22/87), diaper dermatitis (20.69%, 18/87), and skin pressure redness related to ventilator and continuous positive airway pressure (CPAP) (12.64%, 11/87). (2) The gestational age, birth weight, length of stay, use of noninvasive mechanical ventilation, orotracheal intubation, gastric tube, PICC catheterization, and skin allergy history of the two groups had statistically significant differences (P < .05). (3) The results of multivariate Logistic regression analysis indicated that the length of stay (OR=2.994, 95% CI=1.341~6.686), orotracheal intubation use (OR=0.015, 95% CI=0.004~0.060), and gastric tube use (OR=17.132, 95% CI=5.231~56.108) were independent risk factors of iatrogenic skin injury in neonates (P < .05).
CONCLUSION: Length of stay, orotracheal intubation use, and gastric tube use are independent risk factors for iatrogenic skin injury in neonates. Hospital stays and unnecessary use of orotracheal intubation and gastric tube should be reduced in future clinical management. Attention should be paid to strengthening skin observation and care, keeping skin dry and clean, and preventing iatrogenic skin injury.
There is considerable evidence supporting a causal role for truncal visceral fat depots in glucose dysregulation. Individuals with large visceral fat depots have impaired suppression of free fatty acid release in response to insulin, elevated triglycerides and low concentrations of high density lipoprotein cholesterol. The high free fatty acid concentration may induce insulin resistance in the muscle and liver. There is more recent evidence that truncal subcutaneous fat depots are also problematic, though this literature is mixed. In contrast, gluteo-femoral fat depots have not been implicated in insulin resistance and dysregulation of carbohydrate metabolism. Failure to account for differences in the contributions of these depots will add noise to measurements of dietary interventions to mitigate glucose dysregulation. Previous studies have reported evidence indicating acute and chronic consumption of almonds improves glycemia. Acute effects are important indicators of health benefit, but longer-term trials, ones permitting identification of the effects of a dietary intervention on HbA1c, are more telling and clinically relevant. To more definitively establish the association between almond consumption and improved carbohydrate metabolism, we propose a six-month trial that contrasts the effects of almond consumption at optimal times of the day versus consumption of low nutrient dense snack foods on indices of carbohydrate metabolism, food intake and appetite in adults characterized by three distinct fat depots.

Participants will consume either almonds, or no nuts every day for 6 months. At baseline, participants will be weighed and undergo a DEXA scan to determine body fat composition and will be assigned a group. Blood will also be collected fasted and at stipulated times in response to a meal tolerance test to measure insulin, glucose, C-peptide, HbA1c, lipid panel, gut peptides, and compliance to the diet. Participants will be given links to complete appetite ratings and record food intake. Participants will report to the lab every two weeks to be weighed, and get a resupply of almonds (if in the almond group). At the two-week mark on months 2 and 4, participants will be weighed, blood will be taken to assess compliance to the diet, and links will be given to complete appetite ratings and record food intake. At month 6, all measurements from baseline will be repeated.
Flunisolide has demonstrated potent glucocorticoid and weak mineralocorticoid activity in classical animal test systems. As a glucocorticoid it is several hundred times more potent than the cortisol standard. Clinical studies with flunisolide have shown therapeutic activity on nasal mucous membranes with minimal evidence of systemic activity at the recommended doses.

A study in approximately 100 patients that compared the recommended dose of flunisolide nasal solution with an oral dose providing equivalent systemic amounts of flunisolide has shown that the clinical effectiveness of flunisolide nasal solution, when used topically as recommended, is due to its direct local effect and not to an indirect effect through systemic absorption.

Following administration of flunisolide to man, approximately half of the administered dose is recovered in the urine and half in the stool: 65 to 70% of the dose recovered in urine is the primary metabolite, which has undergone loss of the 6α fluorine and addition of a 6β hydroxy group. Flunisolide is well absorbed but is rapidly converted by the liver to the much less active primary metabolite and to glucuronate and/or sulfate conjugates. Because of first-pass liver metabolism, only 20% of the flunisolide reaches the systemic circulation when it is given orally whereas 50% of the flunisolide administered intranasally reaches the systemic circulation unmetabolized. The plasma half-life of flunisolide is 1 to 2 hours.

The effects of flunisolide on hypothalamic-pituitary-adrenal (HPA) axis function have been studied in adult volunteers. Flunisolide was administered intranasally as a spray in total doses over 7 times the recommended dose (2200 mcg, equivalent to 88 sprays/day) in 2 subjects for 4 days, about 3 times the recommended dose (800 mcg, equivalent to 32 sprays/day) in 4 subjects for 4 days, and over twice the recommended dose (700 mcg, equivalent to 28 sprays/day) in 6 subjects for 10 days. Early morning plasma cortisol concentrations and 24-hour urinary 17-ketogenic steroids were measured daily. There was evidence of decreased endogenous cortisol production at all three doses.

In controlled studies, flunisolide nasal solution was found to be effective in reducing symptoms of stuffy nose, runny nose and sneezing in most patients. These controlled clinical studies have been conducted in 488 adult patients at doses ranging from 8 to 16 sprays (200-400 mcg) per day and 127 pediatric patients at doses ranging from 6 to 8 sprays (150 to 200 mcg) per day for periods as long as 3 months. In 170 patients who had cortisol levels evaluated at baseline and after 3 months or more of flunisolide treatment, there was no unequivocal flunisolide-related depression of plasma cortisol levels.

Clinical studies have shown that improvement is usually apparent within a few days after starting flunisolide nasal solution.

The mechanisms responsible for the anti-inflammatory action of corticosteroids and for the activity of the aerosolized drug on the nasal mucosa are unknown.
Naltrexone hydrochloride is a pure opioid receptor antagonist. Although well absorbed orally, naltrexone is subject to significant first pass metabolism with oral bioavailability estimates ranging from 5 to 40%. The activity of naltrexone is believed to be due to both parent and the 6-β-naltrexol metabolite. Both parent drug and metabolites are excreted primarily by the kidney (53% to 79% of the dose), however, urinary excretion of unchanged naltrexone accounts for less than 2% of an oral dose and fecal excretion is a minor elimination pathway. The mean elimination half-life (T-1/2) values for naltrexone and 6-β-naltrexol are 4 hours and 13 hours, respectively. Naltrexone and 6-β-naltrexol are dose proportional in terms of AUC and Cmax over the range of 50 to 200 mg and do not accumulate after 100 mg daily doses.

###  Absorption

Following oral administration, naltrexone undergoes rapid and nearly complete absorption with approximately 96% of the dose absorbed from the gastrointestinal tract. Peak plasma levels of both naltrexone and 6-β-naltrexol occur within one hour of dosing.

###  Distribution

The volume of distribution for naltrexone following intravenous administration is estimated to be 1350 liters. In vitro tests with human plasma show naltrexone to be 21% bound to plasma proteins over the therapeutic dose range.

###  Metabolism

The systemic clearance (after intravenous administration) of naltrexone is ~3.5 L/min, which exceeds liver blood flow (~1.2 L/min). This suggests both that naltrexone is a highly extracted drug (>98% metabolized) and that extra hepatic sites of drug metabolism exist. The major metabolite of naltrexone is 6-β-naltrexol. Two other minor metabolites are 2-hydroxy-3-methoxy-6-β-naltrexol and 2-hydroxy-3-methyl-naltrexone. Naltrexone and its metabolites are also conjugated to form additional metabolic products.

###  Elimination

The renal clearance for naltrexone ranges from 30 to 127 mL/min and suggests that renal elimination is primarily by glomerular filtration. In comparison, the renal clearance for 6-β-naltrexol ranges from 230 to 369 mL/min, suggesting an additional renal tubular secretory mechanism. The urinary excretion of unchanged naltrexone accounts for less than 2% of an oral dose; urinary excretion of unchanged and conjugated 6-β-naltrexol accounts for 43% of an oral dose. The pharmacokinetic profile of naltrexone suggests that naltrexone and its metabolites may undergo enterohepatic recycling.
Title cpds. contain 1-3 g. atoms of silver per 10 moles of cycloheptaamylose, and are pref. of formula: (where x is 0.10-0.30, R is 2-5C alkylene, esp. C2H4, and Y is the anion of a soluble Ag salt, esp. NO3=. They may be prepd. by dissolving the cycloheptylamine in the alkanolamine, dissolving the Ag salt in this soln., and ppting the inclusion cpd. in crystalline form by cooling, or by addn. of a ppting agent.
Anaphylactic and anaphylactoid reactions have been reported with Gadoterate Meglumine Injection, involving cardiovascular, respiratory, and/or cutaneous manifestations. Some patients experienced circulatory collapse and died. In most cases, initial symptoms occurred within minutes of Gadoterate Meglumine Injection administration and resolved with prompt emergency treatment [see Adverse Reactions ( 6)] . 

  * Before Gadoterate Meglumine Injection administration, assess all patients for any history of a reaction to contrast media, bronchial asthma and/or allergic disorders. These patients may have an increased risk for a hypersensitivity reaction to Gadoterate Meglumine Injection.
  * Administer Gadoterate Meglumine Injection only in situations where trained personnel and therapies are promptly available for the treatment of hypersensitivity reactions, including personnel trained in resuscitation.
  * During and following Gadoterate Meglumine Injection administration, observe patients for signs and symptoms of hypersensitivity reactions.
PURPOSE:To provide a fragrance-emitting material emitting harmonized fragrance by the absorption of moisture at a proper temperature, and composed mainly of granular porous zirconium phosphate silicate impregnated with perfume and powdery organic material attached with perfume. CONSTITUTION:The objective composition is composed mainly of (A) granular porous zirconium phosphate silicate [e.g. zirconium complex ZPS (product of Dai-ichi Rare Element Chemical Industry Co., Ltd.)] impregnated with perfume and (B) powdery organic material (e.g. wood flour, hay powder, starch, etc.) attached with perfume. It is preferable to add one or more kinds of additives selected from diluent, excipient, hydrophilic agent, exothermic agent, foaming agent, colorant, lustering agent or electrically conductive agent. The product slowly emits fragrance by the moisture in air. It can be applied for daily goods, industrial goods, agent for removing ill odor, moth-proofing or insecticidal agent, etc.
Several observational studies have reported an association between obesity and primary liver cancer (PLC), while the causality behind this association and the comparison of the risk effects of different obesity indicators on PLC remain unclear. In this study, we performed two-sample Mendelian randomization (MR) analyses to assess the associations of genetically determined liver fat, visceral adipose tissue (VAT), and body mass index (BMI) with the risk of PLC. The summary statistics of exposures were obtained from two genome-wide association studies (GWASs) based on the UK Biobank (UKB) imaging cohort and the Genetic Epidemiology Research on Adult Health and Aging (GERA) cohort. GWAS summary statistics for PLC were obtained from FinnGen consortium R7 release data, including 304 PLC cases and 218 488 controls. Inverse-variance weighted (IVW) was used as the primary analysis, and a series of sensitivity analyses were performed to further verify the robustness of these findings. IVW analysis highlighted a significant association of genetically determined liver fat (OR per SD increase: 7.14; 95% CI: 5.10-9.99; P = 2.35E-30) and VAT (OR per SD increase: 5.70; 95% CI: 1.32-24.72; P = .020) with PLC but not of BMI with PLC. The findings were further confirmed by a series of MR methods. No evidence of horizontal pleiotropy between these associations existed. Our study suggested that genetically determined liver fat and VAT rather than BMI were associated with an increased risk of PLC, which suggested that visceral fat distribution is more predictive of the clinical risk of PLC than common in vitro measures.
BACKGROUND: Electrolyte imbalances are commonly observed in individuals diagnosed with myocardial infarction (MI). The levels of serum sodium have been linked to unfavorable outcomes in relation to MI. Additionally, there exists a correlation between serum sodium and serum chloride, although the combined influence of these electrolytes on the prognosis of MI patients has not been extensively studied. Consequently, our study aimed to examine whether an autonomous association exists between the sodium-to-chloride (Na/Cl) ratio and mortality rates during hospitalization among patients admitted to intensive care unit (ICU) with MI.
METHODS: A retrospective cohort study analysis was conducted on the Na/Cl ratio within the ICU from 2008 to 2019. Patients diagnosed with MI were divided into two groups based on a predetermined cutoff value for the Na/Cl ratio. Various statistical models, including the Cox proportional hazard model, generalized additive model, and two-piecewise linear regression model, were employed to assess the relationship between the initial Na/Cl ratio upon admission and the likelihood of in-hospital mortality while accounting for other relevant covariates.
RESULTS: After adjusting for all other factors, the study revealed that the Na/Cl ratio exhibited an independent association with in-hospital mortality (HR = 1.28; 95% CI: 1.11-1.47, P < 0.001). Further analysis indicated a nonlinear relationship between the Na/Cl ratio and in-hospital mortality among patients with MI, with a threshold at approximately 1.37. Specifically, if the Na/Cl ratio exceeded 1.37, there was a significant and progressively increasing likelihood of mortality during hospitalization (HR = 1.46; 95% CI: 1.20-1.77).
CONCLUSION: The in-hospital mortality of patients admitted to ICU with MI is predicted independently by the ratio of sodium to chloride (Na/Cl). A curvilinear correlation was observed between the Na/Cl ratio and in-hospital mortality, with a statistically significant threshold identified at 1.37.
Studies have shown that prolonged exposure to nicotine reinforces addiction. The act of smoking delivers nicotine through lungs into the blood stream. As a result, during smoking nicotine levels peak and then when smoking stops levels progressively diminish to a base (trough) level. At the peak level a smoker feels rewarded, but at the trough level a smoker starts to experience negative withdrawal affects and a desire to smoke. Nicotine Gum and Inhalers mimic this smoking behaviour maintaining a peak and trough regime, but nicotine patches do not. Instead, nicotine patches deliver a constant base dose considered to be either above that of the smokers trough level or at a level where negative withdrawal effects are reduced.

The question arises as to if nicotine levels delivered by a patch are constant and potentially above that of the baseline smokers level, does this reinforce the addiction and therefore contribute to the high long term relapse rate? To answer this question the investigators will be looking at metabolites which the body uses to breakdown nicotine and several other enzymes. These metabolites respond to the levels of nicotine in the blood stream by increasing or decreasing over time. By testing blood flow, blood and urine the investigators are able to gain an insight into how the body is dealing with a constant stable dose of nicotine rather than a peak and trough dose. In combination with the questionnaires the investigators will be able to determine the level of affect.
The length of this study, including screening is approximately 24 months. Patients at Bariatric Surgery Clinics will be recruited for this study. Both patients that decide to undergo bariatric surgery, and those that do not undergo surgery will be enrolled. Patients will be randomized to either a high intensity interval training (HIIT) or standard exercise regimen after eligibility is confirmed and the baseline visit is complete. All patients will complete follow-up appointments at 3 month, 12 months and 24 months. Patients that are randomized to the HIIT program will compete 2 supervised and 1 unsupervised training sessions a week for 24 months.
Participants in the Qigong group were given a structured program about Chan-Chung qigong for 3 months which was a modified form of the manual of Chan-Chuang qigong (Yeh et al., 2006), to tailor to patients with cognitive impairment. The Chan-Chuang qigong program included warmup prior to qigong practice, preparation for qigong practice . The movements should be repeated and maintained for 10 minutes per time, 3 time a day .
Fibrosis contributes to tissue repair, but excessive fibrosis disrupts organ function. Alagille syndrome (ALGS, caused by mutations in JAGGED1) results in liver disease and characteristic fibrosis. Here, we show that Jag1Ndr/Ndr mice, a model for ALGS, recapitulate ALGS-like fibrosis. Single-cell RNA-seq and multi-color flow cytometry of the liver revealed immature hepatocytes and paradoxically low intrahepatic T cell infiltration despite cholestasis in Jag1Ndr/Ndr mice. Thymic and splenic regulatory T cells (Tregs) were enriched and Jag1Ndr/Ndr lymphocyte immune and fibrotic capacity was tested with adoptive transfer into Rag1-/- mice, challenged with dextran sulfate sodium (DSS) or bile duct ligation (BDL). Transplanted Jag1Ndr/Ndr lymphocytes were less inflammatory with fewer activated T cells than Jag1+/+ lymphocytes in response to DSS. Cholestasis induced by BDL in Rag1-/- mice with Jag1Ndr/Ndr lymphocytes resulted in periportal Treg accumulation and three-fold less periportal fibrosis than in Rag1-/- mice with Jag1+/+ lymphocytes. Finally, the Jag1Ndr/Ndr hepatocyte expression profile and Treg overrepresentation were corroborated in patients' liver samples. Jag1-dependent hepatic and immune defects thus interact to determine the fibrotic process in ALGS.
First-line fluoropyrimidine-based chemotherapy with bevacizumab initiated within 4 weeks of randomization, followed by salvage therapy upon progression at the discretion of the local investigator. Surgery of primary tumour will be performed only when indicated by local signs or symptoms.
BACKGROUND: There are insufficient in-depth studies on whether percutaneous lumbar nucleoplasty (PLN) is effective and safe for the treatment of uncontained lumbar disc herniation (ULDH). This study aimed to investigate the clinical efficacy of PLN on radiating leg pain caused by ULDH.
METHODS: Patients who underwent PLN for ULDH and met the inclusion criteria between June 2018 and July 2022 were included. Clinical outcomes were evaluated using the numeric rating scale (NRS) for radiating pain preoperatively; at 1 day, 1 week, and 1 month postoperatively; and at the last follow-up. Patient satisfaction was assessed using MacNab criteria.
RESULTS: Forty-one patients were enrolled. The mean age was 50.2 years (range 24-73 years). The mean and standard deviation of the preoperative NRS in 39 patients with radiating pain was 9.0 ± 1.2. The NRS scores at 1 day, 1 week, and 1 month postoperatively and at the last follow-up were 4.6 ± 3.2, 3.6 ± 3.3, 2.9 ± 3.2, and 1.4 ± 2.0, respectively, showing significant improvement (all, p < 0.001). The number of patients (percentage) with excellent or good satisfaction according to the MacNab criteria was 29 (70.7%). Major complications were not observed. Three patients underwent additional surgery after PLN because of persistent radiating pain.
CONCLUSIONS: PLN is a safe and feasible treatment option for ULDH. Treatment outcomes were favorable on average; however, the lack of consistency was a drawback.
The effectiveness of Omegaven was established in two open-label clinical trials of 82 pediatric patients, 3 to 42 weeks of age, including preterm neonates with estimated gestational age of greater than 24 weeks at birth. Patients administered Omegaven attained and maintained growth through at least 108 weeks of treatment [see Clinical Studies (14)].

The safety of Omegaven was established in 189 pediatric patients (19 days to 15 years of age). The most common adverse reactions in Omegaven-treated patients were vomiting, agitation, and bradycardia [(see Adverse Reactions (6.1)].

In the postmarketing setting, clinical decompensation with rapid infusion of intravenous lipid emulsion in neonates and infants, sometimes fatal has been reported [see Warnings and Precautions (5.1)].

Preterm neonates and infants who receive treatment with Omegaven may be at risk of aluminum toxicity and other metabolic abnormalities [see Warnings and Precautions (5.7, 5.8)].