anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
The neuroprotective effects of choline chloride, an essential nutrient, a precursor for the acetylcholine and synthesis of membrane phospholipids, have been associated with neurological and neurodegenerative diseases. Its contribution to autism spectrum disorder, a neurodevelopmental disorder, remains unknown. Thus, we aimed to evaluate the effects of choline chloride on social behaviours, and histopathological and biochemical changes in a rat autism model. The autism model was induced by administration of 100 μg/kg lipopolysaccharide (LPS) on the 10th day of gestation. Choline chloride treatment (100 mg/kg/day) was commenced on PN5 and maintained until PN50. Social deficits were assessed by three-chamber sociability, open field, and passive avoidance learning tests. Tumour necrosis factor alpha (TNF-α), interleukin-2 (IL) and IL-17, nerve growth factor (NGF), and glutamate decarboxylase 67 (GAD67) levels were measured to assess neuroinflammatory responses. In addition, the number of hippocampal and cerebellar neurons and glial fibrillary acidic protein (GFAP) expression were evaluated. Social novelty and passive avoidance learning tests revealed significant differences in choline chloride-treated male rats compared with saline-treated groups. TNF-α, IL-2, and IL-17 were significantly decreased after choline chloride treatment in both males and females. NGF and GAD67 levels were unchanged in females, while there were significant differences in males. Histologically, significant changes in terms of gliosis were detected in hippocampal CA1 and CA3 regions and cerebellum in choline chloride-treated groups. The presence of ameliorative effects of choline chloride treatment on social behaviour and neuroinflammation through neuroinflammatory, neurotrophic, and neurotransmission pathways in a sex-dependent rat model of LPS-induced autism was demonstrated.
Patients were treated with intrathecal pemetrexed at dose escalation. The regimen of intrathecal pemetrexed is 10/15/20 mg, plus dexamethasone 5 mg, twice per week for 2 weeks, followed by once per week for 2-4 weeks. Pemetrexed is administrated by intrathecal injection via lumbar puncture. Folic acid 200-400 μg is administered orally once daily, prior to the first intrathecal pemetrexed, until 21 days after the last intrathecal pemetrexed. A single dose of vitamin B12 1000 μg is administered by intramuscular injection before the first intrathecal pemetrexed，once per 3 weeks. To detect the pharmacokinetics of intrathecal pemetrexed, the serum and cerebrospinal fluid samples are collected. These samples would be analyzed by spectrometer for drug concentration.
PROBLEM TO BE SOLVED: To obtain the subject composition having little irritating smell with causing little damage to the hair and having a high hair coloring or bleaching effect by bringing the composition to comprise a first agent containing monoisopropanol amine and a protein hydrolyzate and a second agent containing an oxidant. SOLUTION: This hair dye composition comprises (A) a first agent containing (i) monoisopropanol amine and (ii) at least one species selected from a group comprising a protein hydrolyzate (e.g. a hydrolyzed collagen solution, a hydrolyzed elastin solution, a hydrolyzed keratin solution, a powdery hydrolyzed keratin, etc.), or its derivative and (B) a second agent containing an oxidizing agent (e.g. hydrogen peroxide, a peroxide, etc.). The first agent preferably contains 0.5-10 wt.% of the ingredient (i) and 0.01-5 wt.% of the ingredient (ii) based on the whole weight of the first agent. In the second agent, about 0.01-70 wt.% of the oxidizing agent is preferably added based on the whole weight of the second agent.
A medical device for delivering a drug compound through a stratum corneum includes a support having an aperture, an array of microneedles extending outwardly from the support, a plurality of nanostructures associated with each microneedle, and a reservoir wherein the drug compound is retained. At least one microneedle contains a shaft extending from the support. The shaft includes a tip configured to penetrate the stratum corneum. The shaft defines a channel extending from the support to the tip. The channel is in at least partial alignment with the aperture. At least some of the microneedles of the array of microneedles each have a cross-sectional dimension of from about 1 micrometer to about 1 millimeter. At least some of the nanostructures have a cross-sectional dimension less than about 500 nanometers and greater than about 5 nanometers and an aspect ratio of from about 0.2 to about 5.
BACKGROUND: Placental mesenchymal dysplasia (PMD) is a rare, benign, placental disorder characterised macroscopically by an enlarged multi-cystic placenta. It is a condition associated with a range of reported clinical outcomes and can be misdiagnosed as a molar or partial molar pregnancy given the similarities in clinical presentation. We present an unusual case of PMD complicated by fetal growth restriction and oligohydramnios in the second trimester.
CASE PRESENTATION: A 33 year old female was referred to our fetal medicine unit with a multi-cystic placenta at dating scan suspected initially to be a partial molar pregnancy. She opted for conservative management and declined invasive testing. At 16 weeks severe fetal growth restriction was present with an estimated fetal weight < 3rd centile and associated with oligohydramnios. Whilst live births in cases of PMD have been reported in the literature, to our knowledge there are no reported successful outcomes in cases of early onset growth restriction at this gestation. The patient opted to proceed with termination of pregnancy given the suspected poor prognosis. Post mortem results confirmed a diagnosis of PMD and fetal growth restriction with normal genetic testing.
CONCLUSIONS: Placental mesenchymal dysplasia can be a difficult condition to manage, particularly when counselling about prognosis and deciding whether to continue the pregnancy. More evidence is needed about prognostic factors in PMD associated with a successful outcome. Early onset fetal growth restriction and/or oligohydramnios prior to 20 weeks are likely poor prognostic factors which should be considered in the antenatal counselling.
Mindfulness-based Stress Reduction (MBSR) is a 9-week class that meets 2.5 hours/week and involves training in mindfulness (being present in the moment), meditation, and yoga. The MBSR course is taught by a certified MBSR instructor.
PHARC, polyneuropathy, hearing loss, cerebellar ataxia, retinitis pigmentosa and cataracts, or PHARC is a very rare progressive neurodegenerative autosomal recessive disease caused by biallelic mutations in the ABHD12 (a/b-hydrolase domain containing 12) gene, which encodes a lyso-phosphatidylserine (lyso-PS) lipase. The Orpha number for PHARC is ORPHA171848. The clinical picture of PHARC syndrome is very heterogeneous with a wide range of age at onset for each symptom, making a clinical diagnosis very challenging. Differential diagnoses of the disease include Refsum disease, Charcot-Marie-Tooth disease, and Usher syndrome. Many aspects of the disease, such as the biochemistry and pathophysiology, are still not fully understood. We generated a clinical overview of all PHARC patients, including their mutations, described in literature so far. Furthermore, we give an outline of the most recent developments in research on the pathophysiology of PHARC syndrome in an attempt to gain more insight into and increase awareness of the heterogeneity of the disease. We included 58 patients with PHARC from 37 different families with 27 known ABHD12 mutations. The age at onset (from early childhood to late thirties) and the severity of each feature of PHARC varied widely among patients. Demyelinating polyneuropathy was reported in 91% of the patients. In 86% of patients, hearing loss was present and 74% had cerebellar ataxia, the most variable symptom of PHARC. Retinitis pigmentosa and cataracts occurred in 82% and 86% of patients, respectively. Due to the rareness of the disease and the variable clinical phenotype, a diagnosis of PHARC is often delayed and mostly only made after an extensive genetic work-up. Therefore, we recommend adding the ABHD12 gene to diagnostic gene panels for polyneuropathy, cerebellar ataxia, hearing loss, retinal dystrophy, and cataracts. In addition, a full clinical work-up, neurological (with EMG and neuroimaging of the brain) and ophthalmological (with ERG) examination and audiological tests are indispensable to obtain a comprehensive overview of the clinical phenotype as some symptoms in PHARC may be very subtle and easily overlooked if not tested for. In conclusion, we strongly recommend that patients with (suspected) PHARC should be evaluated in a multidisciplinary setting involving ophthalmologists, audiologists, neurologists, and geneticists to ensure the best possible care. Furthermore, we discuss whether PHARC is a spectrum with various incomplete phenotypes even later in life, or whether it is a syndrome in which the clinical symptoms are variable in severity and age of onset.
BACKGROUND: Bronchopleural fistula (BPF) is a rare but fatal complication after pneumonectomy. When a BPF occurs late (weeks to years postoperatively), direct resealing of the bronchial stump through the primary thoracic approach is challenging due to the risks of fibrothorax and injury to the pulmonary artery stump, and the surgical outcome is generally poor. Here, we report a case of late left BPF following left pneumonectomy successfully treated using a right thoracic approach assisted by extracorporeal membrane oxygenation (ECMO).
CASE PRESENTATION: We report the case of a 57-year-old male patient who underwent left lower and left upper lobectomy, respectively, for heterochronic double primary lung cancer. A left BPF was diagnosed at the 22nd month postoperatively, and conservative treatment was ineffective. Finally, the left BPF was cured by minimally invasive BPF closure surgery via the right thoracic approach with the support of veno-venous extracorporeal membrane oxygenation (VV-ECMO).
CONCLUSIONS: Advanced BPF following left pneumonectomy can be achieved with an individualized treatment plan, and the right thoracic approach assisted by ECMO is a relatively simple and effective method, which could be considered as an additional treatment option for similar patients.
<P>PROBLEM TO BE SOLVED: To provide a novel knowledge sharing system in medical work.  <P>SOLUTION: The knowledge sharing system 10 includes a server 12, and the server is coupled with a medical doctor terminal 15, a nurse terminal 16, and a station terminal 18 via a network 14. The server stores data of an electronic chart, and nursing records, and a medical doctor can access to the electronic chart of the server from the medical doctor terminal. A printer 20 prints and issues a worksheet on electronic paper in accordance with an order of the doctor. When a nurse writes in the worksheet by an electronic pen 22, the written contents are transferred to the server through the station terminal and the network, and the nurse records are updated. When the doctor tries to refer to the nurse records of the server, the up-to-date nurse records can be seen, and since the worksheet of the nurse can carry out nursing work in accordance with the up-to-date order from the doctor also, accidents or mistakes caused by information transmission insufficiency between the two can be reduced.  <P>COPYRIGHT: (C)2007,JPO&INPIT
The vibration group will stand on a platform that emits a mild vibration 10 minutes per day for 6 months. There will also be a 6 month no-treatment period.
The present invention is an inhibitory peptide capable of inhibiting β pleated sheet formation in amyloid β-peptide. The inhibitory peptide is a βsheet breaker peptide analog designed by chemical modification of β sheet breaker peptide capable of inhibiting β pleated sheet formation in amyloid β-peptide. The present invention also includes an inhibitory peptide capable of inhibiting conformational changes in prion PrP protein associated with amyloidosis. The inhibitory peptide being a βsheet breaker peptide analog designed by chemical modification of a βsheet breaker peptide capable of inhibiting the conformational changes in prior PrP protein associated with amyloidosis. In addition, the present invention includes a peptide mimetic with the structure PMiAβ5. In another embodiment, the peptide mimetic has the structure PMiPrP13. In yet another embodiment, the peptide mimetic has the structure PMiPrP5.
BACKGROUND: To comprehend the influences of fenofibrate on hepatic lipid accumulation and mitochondrial function-related signaling pathways in mice with non-alcoholic fatty liver disease (NAFLD) secondary to high-fat diets together with free fatty acids-influenced HepG2 cells model.
MATERIALS AND METHODS: A random allocation of male 6-week C57BL/6J mice into three groups was done, including controls, model (14 weeks of a high-fat diet), and fenofibrate [similar to the model one with administered 0.04 g/(kg.d) fenofibrate by gavage at 11 weeks for 4 weeks] groups, which contained 10 mice each. This study verified NAFLD pathogenesis via mitochondrial functions in hepatic pathological abnormalities, liver index and weight, body weight, serum biochemical indexes, oxidative stress indicators, mitochondrial function indexes, and related signaling pathways. The effect of fenofibrate intervention was investigated in NAFLD model mice. In vitro, four groups based on HepG2 cells were generated, including controls, the FFA model (1.5 mmol/L FFA incubation for 24 h), LV-PGC-1α intervention (similar to the FFA model one after PPARGC1A lentivirus transfection), and LV control intervention (similar to the FFA model one after negative control lentivirus transfection) groups. The study investigated the mechanism of PGC-1α related to lipid decomposition and mitochondrial biosynthesis by Oil red O staining, colorimetry and western blot.
RESULTS: In vivo experiments, a high-fat diet achieved remarkable changes regarding liver weight, liver index, serum biochemical indicators, oxidative stress indicators, liver pathological changes, mitochondrial function indicators, and body weight of the NAFLD model mice while fenofibrate improved the objective indicators. In the HepG2 cells model, the lipid accumulation increased significantly within the FFA model group, together with aggravated hepatocytic damage and boosted oxidative stress levels. Moreover, FFA induced excessive mitosis into fragmented in mitochondrial morphology, ATP content in cells decreased, mtDNA replication fold decreased, the expression of lipid decomposition protein PPARα reduced, mitochondrial biosynthesis related protein PGC-1α, NRF-1 and TFAM decreased. PGC-1α overexpression inhibited lipid deposition by improving mitochondrial biosynthesis and lipid decomposition.
CONCLUSION: Fenofibrate up-regulated PPARα/PGC-1α signaling pathway, promoted mitochondrial β-oxidation, reduced oxidative stress damage and lipid accumulation of liver. PGC-1α overexpression enhanced mitochondrial biosynthesis and ATP production, and reduced HepG2 intracellular accumulation of lipids and oxidative stress.
Bronchiectasis is an important chronic pulmonary disease that endangers the health of children. It is characterized by recurrent respiratory tract infection, cough, massive pus sputum, hemoptysis, etc. The chronic progression of bronchiectasis may affect the lung function of children. It affects the quality of life, growth and development, and even leads to the death of children, and brings great harm to children and their families. A New Zealand study of non-cystic fibrotic bronchiectasis found that overall forced expiratory volume at one second (FEV1) declined at an average annual rate of 1.6%. Other studies have shown a significant decline in lung function in children with bronchiectasis even after treatment. Some reports on the prognosis of children with bronchiectasis in China show that most of the children have remission in clinical symptoms, but there are still some cases of chronic recurrence and death. A non-controlled study showed that adult bronchiectasis patients who received long-term azithromycin had fewer acute exacerbations and improved symptoms, which might be associated with the antimicrobial activity and anti-inflammatory of macrolide antibiotics. In children, the effect of macrolide antibiotics on cystic fibrosis is positive. Studies have shown that macrolides can effectively improve pulmonary function and reduce the incidence of acute exacerbation of pulmonary lesions. The course of treatment is at least 6 months. For non-cystic fibrosis bronchiectasis, recent studies have shown that long-term azithromycin treatment can reduce the exacerbation of pulmonary lesions. However, the treatment of bronchiectasis children in China is still lack of standard. The aim of this study was to explore the effect of macrolides on the long term prognosis of children with bronchiectasis in China, in order to standardize the treatment and improve the prognosis of the children with bronchiectasis.
Sign-tracking is a Pavlovian conditioned approach behavior thought to be important in understanding cue-driven relapse to drug use, and strategies for reducing sign-tracking may have some benefit in preventing relapse. A previous study successfully employed the NMDA receptor antagonist MK-801 in preventing the development of sign-tracking (but not goal-tracking) in a conditioned approach task. In this study, we focused on whether MK-801 would have similar effects on previously established sign-tracking behavior. MK-801 was administered after training in a standard sign-/goal-tracking task using a retractable lever as a conditioned stimulus and a sucrose pellet as unconditioned stimulus. It was found that MK-801 increased measures of both sign- and goal-tracking in subjects who had previously learned the task. The NMDA receptor appears to play a complex role in governing behavior related to sign-tracking.
Target organ damage is more closely associated with ambulatory (ABPM) than with clinic blood pressure (BP). In particular, the reduction of the normal 10 to 20% sleep-time BP decline (non-dipper pattern) is associated with elevated risk of end-organ injury, particularly to the heart, brain and kidney. These results suggest that cardiovascular risk could be influenced not by BP elevation alone, but also by the magnitude of the circadian BP variability. Moreover, at least two independent prospective studies have suggested that nighttime BP is a better predictor of risk than daytime BP. Common to all previous trials is that prognostic significance of ABPM has relied on a single baseline profile from each participant, without accounting for possible changes in the BP pattern, mainly associated to antihypertensive therapy and aging during follow-up. The MAPEC study investigates, first, the comparative prognostic value of several BP parameters (including, among many others, BP variability, the diurnal/nocturnal ratio, diurnal and nocturnal means, slope of morning rise, etc) in the prediction of cardiovascular morbidity and mortality; and, second, whether potential changes in the circadian BP pattern after Chronotherapy with antihypertensive drugs are associated to changes in cardiovascular risk.
It was recently reported that IL-10 is protective in Acetaminophen (APAP) toxicity and it down-regulates iNOS production. In an ongoing Pediatric Pharmacology Research Unit (PPRU) Network study, plasma IL-10 levels were higher in patients that developed significant toxicity, as compared to those with minimal hepatic transaminase elevations. In these patients IL-10 elevation is likely a compensatory response to hepatic injury. To further examine the relationship of IL-10 and iNOS in the APAP overdose patients, we will examine genetic variability in the promotor regions of iNOS and IL-10 in patients with APAP overdose. Data from the literature indicate the polymorphisms in the promotor regions of iNOS and IL-10 influence the severity and expression of various diseases. In addition to genotyping for iNOS and IL10 promotor region polymorphisms, plasma levels of nitrotyrosine and IL-10 will be measured in overdose patients.

Blood samples will be obtained from study patients for the analysis of inflammatory cytokines and nitrotyrosine. Blood samples will be obtained at the time of blood sampling for the routine clinical management of the APAP overdose patient. Patients who are hospitalized will have study blood samples drawn at the time daily blood samples are obtained. The sampling will continue daily until the patient is discharged. In addition to blood sampling the following data will be collected: age, gender, race, circumstances of the ingestion, dose of the ingestion, treatment for the ingestion, concomitant therapy, medical history and cigarette use.
Pulmonary embolism (PE) is the third-leading cause of cardiovascular mortality and the second-leading cause of death in cancer patients. The clinical efficacy of thrombolysis for acute PE has been proven, yet the therapeutic window seems narrow, and the optimal dosing for pharmaceutical reperfusion therapy has not been established. Higher doses of systemic thrombolysis inevitably associated with an incremental increase in major bleeding risk. To date, there is no high-quality evidence regarding dosing and infusion rates of thrombolytic agents to treat acute PE. Most clinical trials have focused on thrombolysis compared with anticoagulation alone, but dose-finding studies are lacking. Evidence is now emerging that lower-dose thrombolytic administered through a peripheral vein is efficacious in accelerating thrombolysis in the central pulmonary artery and preventing acute right heart failure, with reduced risk for major bleeding. The present review will systematically summarize the current evidence of low-dose thrombolysis in acute PE.
Yangzheng mixture has been used as an adjuvant tumor therapy as a traditional Chinese medicine in clinical. However, less is known about the activity of Yangzheng mixture. In our study, we explored the anti-tumor activity of Yangzheng mixture for HCC in vitro and in vivo. The effects of Yangzheng mixture on HCC biological behaviors were assessed using colony formation assay, EdU staining, cell cycle assay, Annexin V/PI staining, and wound healing assay. Migration and invasion of HCC cells were further evaluated via transwell assays, while molecular mechanisms were investigated through western blotting and immunofluorescence staining. Additionally, the anticancer effect of Yangzheng mixture in vivo were examined using H22 xenograft and H22 metastatic hepatocellular carcinoma models. Our results revealed that Yangzheng mixture inhibited colony formation, EdU incorporation, cell migration, and invasion, while arresting cell cycle at the G2-M phase in Bel-7402 and SMMC-7721 cells. Mechanistic studies demonstrated that Yangzheng mixture showed a markedly inhibition on Bel-7402 and SMMC-7721 cells with higher NLRP3 expression. We further confirmed that Yangzheng mixture could activate NLRP3 inflammasome through NF-κB by western blotting and immunofluorescence staining. Additionally, Yangzheng mixture inhibited β-catenin nucleus translocation and reversed EMT process. In vivo, the H22 xenograft model depicted that Yangzheng mixture significantly reduced tumor size and weight compared with control. Moreover, H22 lung metastasis model showed that Yangzheng mixture significantly inhibited liver cancer cell spreading to lungs in mice. Overall, our finding revealed that Yangzheng mixture inhibited HCC proliferation and migration in vitro and in vivo by reversing EMT via NF-κB/NLRP3/β-catenin pathway. These results may serve new therapeutic evidences for Yangzheng mixture application in clinical.
This phase will give patients \< 18 years old two infusions (on Day 0 and Day 14) of multi-TAA specific T cells at a fixed dose of 1x10\^7 cells/m2. This phase will test the safety and efficacy of multiTAA-specific T cells in pediatric patients with active HL/NHL.