anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
The present invention discloses medicine which is prepared from traditional Chinese medicine and used for treating urinary system stone diseases, and a preparation method thereof. The medicine comprises Chicken's Gizzard-membrane, japanese climbing fern spore, rhubarb, earthworm, talcum, longhairy antenoron herb, plantain seed, folium pyrrosiae, Chinese sage, pangolin scale, cowherb seed, water plantain, radix glycyrrhiza, etc. which have the functions of clearing away heat, promoting diuresis, dissolving and expelling stones, stimulating circulation to end stasis, shattering firmness, removing stasis and clearing away toxic materials. The method comprises the following steps: Chicken's Gizzard-membrane, japanese climbing fern spore and rhubarb are dried and crushed to form fine powder which is uniformly mixed to prepare powder I; earthworm, talcum, longhairy antenoron herb, plantain seed, pyrrosia leaf, Chinese sage, pangolin scale, cowherb seed, water plantain, radix glycyrrhiza, etc. are taken, decocted with water twice, the filter liquor is merged, decompressed and condensed to form thick paste, and vacuum drying at a normal temperature and crushing are carried out to the thick paste to prepare powder II; powder I and powder II are uniformly mixed to prepare watered pills to be orally taken. The present invention has the characteristics of high clinical curative effect, safety and reliability, convenient use, reasonable price, etc.
1,157,741. Preparation of aminomethylenemalononitrile. F. HOFFMANN-LA ROCHE & CO. A.G. 21 Sept., 1966 [24 Sept., 1965], No. 42125/66. Heading C2C. Aminomethylene-malononitrile is obtained by condensing formamidine or a salt thereof with malononitrile. The reaction is suitably effected in the presence of a weak base condensing agent and an inert organic solvent, preferably an alcohol, at 10-30 C., and the formamidine salt employed as starting material may be a salt with a mineral or organic acid. The reaction may also be effected by reacting a formamidine salt with a cation-exchange resin and treating the resulting formamidine resin salt with malononitrile thereby condensing the formamidine with the malononitrile and removing the condensate from the resin; the resinous material employed as the cation-exchange resin suitably contains acidic groups such as sulphonic groups and any insoluble sulphonated polymerizate of a poly-vinyl-aryl compound may be used. The resin employed is preferably of the styrene- (divinyl-benzene) type characterized by the presence of sulphonic acid groups.
Adult granulosa cell tumors (AGCTs) are rare ovarian tumors with generally good prognosis after surgical resection; however, they do have recurrence potential. Therapeutic and management options for recurrences are currently limited, and the need for expanded adjuvant therapies is increasingly recognized. Anti-hormonal therapy is being explored as an option, which relies on the detection and assessment of hormone receptor expression (androgen, estrogen, and progesterone receptors) as a biomarker and therapeutic target. Our study identifies several clinicopathologic characteristics with significant associations for recurrence of AGCT, which were younger age, higher stage, and larger tumor size. Our study also demonstrates that androgen receptor (AR) expression may be utilized as a potential biomarker for hormonal therapy and that detection of AR expression in AGCT by immunohistochemistry (IHC) varies depending on the antibody clone used for testing. AR was detected in 95% of samples tested with antibodies derived from clone AR27. This detection rate is much higher than previously reported.
Abstract

At the Department of Highly Specialized Neurorehabilitation/Traumatic Brain Injury, Rigshospitalet (satellite department at Hvidovre Hospital), approximately 100 patients (pt.) are admitted with severe brain damage every year. From 2015 to 2017, 305 pt. were admitted. Out of the 305 pt., 162pt. (53%) had traumatic brain injury (TBI), 48pt. (16%) had apoplexy, 35pt. (12%) had other diagnoses (infections, tumors and almost drowning, etc.), 20pt. (7%) had spontaneous subarachnoid hemorrhage (SAH) and 24pt. (8%) had brain damage as a result of cardiac arrest.

TBI is a leading cause of injury-related morbidity and mortality worldwide. According to the Global Burden of Disease Study (2016), there were 27,08 million new cases of TBI globally in 2016. In Denmark, there were 17.302 new cases of TBI in 2016. Clinical studies have repeatedly shown major changes in cerebral energy metabolism after TBI. The secondary brain injury leads to metabolic cellular dysfunction, cerebral edema, and a complex injury cascade. The injury spread includes processes such as inflammation, edema, free radical damage, oxidative damage, ischemic injury, cerebral glucose metabolism disorder, and ion-mediated cell damage. Much of the neurological dysfunction that occurs in acute TBI also occurs in apoplexy, SAH and cerebral ischemia.

A very important adaptive metabolic response after brain injury is the utilization of alternative cerebral energy substrates, including lactate, but also ketone bodies (KB) such as β-hydroxybutyrate (BHB) and acetoacetate (AcAc). In addition to having a central role in the regulation of cerebral energy metabolism after brain injury, KB has other important neuroprotective properties, including attenuation of oxidative stress, apoptotic cell death, and microglial activation. Increasing KB metabolism through fasting or diet-induced ketosis promotes brain resistance to stress and injury, and attenuates acute cerebral injury. Therefore, supplementing with KB, e.g. through the use of a ketogenic diet (KD) with added medium chain fatty acids (MCT), has emerged as a potential non-pharmacological neuroprotective therapy.

KD has been used for many years for the treatment of refractory epilepsy in children and studies done on adults show promising results, but experience from several studies shows major compliance issues. KD has been shown to reduce cerebral edema and apoptosis, as well as improve cerebral metabolism and behavioral outcomes in TBI rodent models, but clinical human trials on adults with TBI are lacking. Apoplexy animal models show positive effects on pathological and functional outcomes of KD intervention or exogenous ketone administration. The only human trial of KD and apoplexy shows that KD is safe and tolerated by patients with acute apoplexy. Our hypothesis is that diet-induced ketosis will reduce the extent of secondary brain damage. The purpose of the trial is to investigate whether an intervention with a ketogenic diet supplemented with MCT is feasible for 6 weeks on hospitalized pt. with severe brain damage. This is the pre-study for a controlled study.
Diabetes is on the rise worldwide, with a global prevalence in adults in 2021 being 537 million adults (20-79 years) living with diabetes -one in ten. This number is predicted to rise to 643 million by 2030 and 783 million by 2045. Over 3 in 4 adults with diabetes live in low- and middle-income countries. Although physical activity (PA) is a key element in the prevention and management of type 2 diabetes. Structured interventions combining Physical Activity and modest weight loss have been shown to lower type 2 diabetes risk by up to 58% in high-risk populations. The increase in T2DM prevalence can only partly be attributed to the increasing prevalence of obesity and a sedentary lifestyle. The exercise recommendations for individuals with type 2 diabetes are similar as for the general population, suggesting a minimum of 150 min of moderate-vigorous-intensity aerobic exercise each week. However, the general population doesn't adhere to these guidelines.

The goal of treatment in type 2 diabetes is to achieve and maintain optimal BG, lipid, and blood pressure (BP) levels to prevent or delay chronic complications of diabetes. A fundamental principle in exercise physiology is that a small muscle mass working in isolation can achieve a higher local oxygen consumption (VO2/min per kg) than when recruiting a large muscle mass. The soleus (1% body mass) has a highly pennated architecture favoring greater amounts of muscular work during plantarflexion. It has an exceptionally high physiological cross-sectional area (3-8 times more than most of the 20 other limb muscles studied).
PURPOSE: A self-emulsifying nanemulsion composition containing coenzyme Q10 having high solubility is provided to improve solubility in solution of water-insoluble coenzyme Q10 and bioavailability. CONSTITUTION: A self-emulsifying nanoemulsion of insoluble drug contains hydrogenated cocoglyceride as a solubilizer of insoluble active ingredient. The insoluble active ingredient is coenzyme Q10. The content of the insoluble active ingredient is 0.5-40 weight%. The content of the hydrogenated cocoglyceride is 5-40 weight%. The composition additionally contains emulsifying agent having 9-17 hydrophilic lipophilic balance. The composition additionally contains cosurfactant having 1-8 of hydrophilic lipophilic balance.
Parkinson's disease (PD) is a neurodegenerative disease characterized by the progressive loss of dopaminergic neurons in the substantia nigra, the etiology of which remains unclear. Studies have shown that neuroinflammation and oxidative stress (OS) play an important role in neuronal damage in patients with PD. Disturbances in the gut microbiota influence neuroinflammation and OS through the microbiota-gut-brain axis. Ginkgolide C (GC), a traditional Chinese medicine extracted from the leaves of Ginkgo biloba, has been reported to exhibit anti-inflammatory effects and the ability to modulate intestinal microbial composition. However, the potential of GC to positively impact PD by modulating the gut microbiota remains unexplored. This study aimed to explore the effects of GC on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD in mice and elucidate its underlying mechanisms. Our findings elucidated that GC treatment significantly ameliorates behavioral deficits as well as pathological damage via restoring gut microbial homeostasis to downgrade OS and neuroinflammation in MPTP-induced PD mice. Mechanistically, GC treatment exerts antioxidant effects via activating the AKT/Nrf2/HO-1 pathway in MPP+-exposed SN4741 neuronal cells and significantly downregulates the expression of inflammatory mediators via regulating NF-κB and MAPK signaling in lipopolysaccharide (LPS)-stimulated BV2 microglial cells. Overall, our study demonstrates that GC administration alleviates MPTP-induced neurodegeneration via rebuilding gut microbial homeostasis to inhibit OS and neuroinflammation in mice, indicating that GC might serve as a promising candidate medicine for PD.
Participants in the non-intervention group at another clinic in Soweto, will receive an enhanced form of standard care. This will include, in conjunction with the normal form of care at each clinic,a health awareness brochure that will focus specifically on health information relating to obesity, diabetes, diet, exercise and breastfeeding at each follow-up sessions. These participants will also be asked to fill out the 24 hour dietary recall assessment and short messaging service technology questionnaire (exactly the same as the intervention group) with help from a healthcare worker.
UNLABELLED: Phosphatase of regenerating liver 2 (also known as PTP4A2) has been linked to cancer progression. Still, its exact role in glioblastoma (GBM), the most aggressive type of primary brain tumor, remains elusive. In this study, we report that pharmacologic treatment using JMS-053, a pan-phosphatase of regenerating liver inhibitor, inhibits GBM cell viability and spheroid growth. We also show that PTP4A2 is associated with a poor prognosis in gliomas, and its expression correlates with GBM aggressiveness. Using a GBM orthotopic xenograft model, we show that PTP4A2 overexpression promotes tumor growth and reduces mouse survival. Furthermore, PTP4A2 deletion leads to increased apoptosis and proinflammatory signals. Using a syngeneic GBM model, we show that depletion of PTP4A2 reduces tumor growth and induces a shift in the tumor microenvironment (TME) toward an immunosuppressive state. In vitro assays show that cell proliferation is not affected in PTP4A2-deficient or -overexpressing cells, highlighting the importance of the microenvironment in PTP4A2 functions. Collectively, our results indicate that PTP4A2 promotes GBM growth in response to microenvironmental pressure and support the rationale for targeting PTP4A2 as a therapeutic strategy against GBM.
SIGNIFICANCE: High levels of PTP4A2 are associated with poor outcomes in patients with glioma and in mouse models. PTP4A2 depletion increases apoptosis and proinflammatory signals in GBM xenograft models, significantly impacts tumor growth, and rewires the TME in an immunocompetent host. PTP4A2 effects in GBM are dependent on the presence of the TME.
The children in the control group will be wait just 10 weeks. The second evaluation will be repeated 10 weeks after the first evaluation. In order for the children in the control group to benefit from sensory integration therapy, after a 10-week waiting period, after the result measurements are applied again, Ayres sensory integration therapy will be applied 3 days a week with 60 minutes each session in accordance with the Ayres Sensory Integration Fidelity Measure (ASI-FM).
PURPOSE: To obtain a composition useful for treating the symptom related to growth hormone shortage, enhancing growing speed and growth state of a commercial animal, etc., by compounding a growth stimulating agent and a synthetic peptide having pituitary growth hormonereleasing activity. CONSTITUTION: This is a mixture composed of (A) a growth-stimulating agent, e.g. zeranol, theophyline or an E-type prostaglandin and (B) a peptide having a formula selected from the group consisting of formula I and formula II [X2 is RCO or R (R is H or CH3 ); Al is Tyr, OMeTyr, His, etc.; A3 is Ala, Ser, Gly, Val, etc.; A5 is D-Phe, D-His, D-Tyr, etc.; A6 is Arg, Lys, Glu, Asn, etc.; Y is OH or NH2 ] or its salt. The mixture is useful for increasing milk yield of a commercial animal and also for reducing the number of mucosa ulcers associated with hypoxemia.
The intervention in the present study is a 10 week parent training group session (More and Less Program) followed by a 6-month mobile phone based intervention. Both components aim to develop healthy lifestyle behaviours regarding dietary habits and physical activity in 2-6 year olds. The intervention is delivered towards the parents.
Human milk oligosaccharides (HMO) affect gut microbiota during neonatal development, particularly with respect to the immune system. Bovine milk-based infant formulas have low oligosaccharide contents. Thus, efforts to fortify infant formulas with HMO are being undertaken. Two major HMO, 2'-fucosyllactose (2'-FL) and 6'-sialyllactose (6'-SL), exert anti-inflammatory effects; however, the associations between anti-inflammatory effects induced by 2'-FL and 6'-SL cotreatment and gut microbiota composition and metabolite modulation remain unclear. Therefore, in this study, we evaluated the effects of a mixture of these HMO. To determine the optimal HMO ratio for anti-inflammatory effects and elucidate its mode of action, LPS-induced inflammatory HT-29 epithelial cells and intestinal-inflamed suckling mice were treated with various mixtures of 2'-FL and 6'-SL. A 2'-FL:6'-SL ratio of 5:1 was identified as the most effective pretreatment HMO mixture in vitro; thus, this ratio was selected and used for low-, middle-, and high-dose treatments for subsequent in vivo studies. In vivo, high-dose HMO treatment restored LPS-induced inflammation symptoms, such as BW loss, colon length reduction, histological structural damage, and intestinal gene expression related to inflammatory responses. High-dose HMO was the only treatment that modulated the major phyla Bacteroidetes and Firmicutes and the genera Ihubacter, Mageeibacillus, and Saccharofermentans. These changes in microbial composition were correlated with intestinal inflammation-related gene expression and short-chain fatty acid production. To our knowledge, our study is the first to report the effects of Ihubacter, Mageeibacillus, and Saccharofermentans on short-chain fatty acid levels, which can subsequently affect inflammatory cytokine and tight junction protein levels. Conclusively, the HMO mixture exerted anti-inflammatory effects through changes in microbiota and metabolite production. These findings suggest that supplementation of infant formula with HMO may benefit formula-fed infants by forming unique microbiota contributing to neonatal development.
For children undergoing bone marrow transplantation, respiratory failure carries mortality expectations well above 60%. The researchers have published preliminary evidence that continuous hemofiltration may greatly improve survival, if filtration is begun when the child first fulfills clinical criteria for ARDS. This is a departure from standard practice, as hemofiltration is usually begun later in the course (if at all) when multiple organ failure is entrenched. Hemofiltration, a 'renal replacement therapy' for critically ill patients, is a slow, continuous process in which a semi-permeable membrane removes plasma water and solutes (up to about 35 kiloDaltons). Many cytokine and chemokine molecules are smaller than the molecular weight limit of the filter; hemofiltration might remove a critical amount, attenuating the unregulated inflammatory response responsible for respiratory failure and progression to multiple organ failure and death. The researchers will conduct a multi-center randomized trial assessing the effect of hemofiltration on survival from respiratory after bone marrow (or more precisely, hematopoietic stem cell) transplantation. The researchers will perform sensitive proteomic assays of serum and ultrafiltrate, to detect the presence of cytokines and chemokines known to be active in idiopathic pneumonia syndrome. Resulting profiles will constitute a uniquely complex description of ultrafiltrate and may provide evidence for modulation of immune function by hemofiltration.
Following ischemia/reperfusion, AMPA receptors (AMPARs) mediate pathologic delayed neuronal death through sustained expression of calcium-permeable AMPARs, leading to excitotoxicity. Preventing the surface removal of GluA2-containing AMPARs may yield new therapeutic targets for the treatment of ischemia/reperfusion. This study utilized acute organotypic hippocampal slices from aged male and female Sprague Dawley rats and subjected them to oxygen-glucose deprivation/reperfusion (OGD/R) to examine the mechanisms underlying the internalization and degradation of GluA2-containing AMPARs. We determined the effect of OGD/R on AMPAR subunits at the protein and mRNA transcript levels utilizing Western blot and RT-qPCR, respectively. Hippocampal slices from male and female rats responded to OGD/R in a paradoxical manner with respect to AMPARs. GluA1 and GluA2 AMPAR subunits were degraded following OGD/R in male rats but were increased in female rats. There was a rapid decrease in GRIA1 (GluA1) and GRIA2 (GluA2) mRNA levels in the male hippocampus following ischemic insult, but this was not observed in females. These data indicate a sex-dependent difference in how AMPARs in the hippocampus respond to ischemic insult, and may help explain, in part, why premenopausal women have a lower incidence/severity of ischemic stroke compared with men of the same age.
Disclosed is a technique for allowing an active ingredient as an agent for improving or maintaining the dermal environment to reach a dermis. Specifically disclosed is a vesicle comprising the following components 1) to 3): 1) an α,ε-bis(γ-N-(C)acylglutamyl)lysine and/or a salt thereof; 2) ceramide and/or a derivative thereof; and 3) one or more members selected from a glycerin fatty acid ester, a polyglycerin fatty acid ester and a pyroglutamic acid glycerin fatty acid ester. The acyl group in the α,ε-bis(γ-N-(C)acylglutamyl)lysine is preferably a lauroyl group. The ceramide or the derivative thereof is preferably ceramide type-2 or-3. The vesicle can enclose an active ingredient. The vesicle can be contained in an external preparation for the skin.
PURPOSE: No large-mammal surgical models exist for geographic atrophy (GA), choroidal neovascularization (CNV), and pachychoroidal vascular remodeling. Our goal was to develop a porcine RPE debridement model of advanced macular degeneration to study photoreceptor cell loss and choroidal remodeling.
METHODS: Seven 2-month-old female domestic pigs were used for this study. After 25G vitrectomy, the area centralis was detached via subretinal bleb. A nitinol wire (Finesse Flex Loop) was used to debride RPE cells across a 3- to 5-mm diameter region. Fluid-air exchange was performed, and 20% SF6 gas injected. Animals underwent fundus photography, fluorescein angiography, optical coherence tomography (OCT), and OCT-angiography (OCTA) at 2 weeks, 1 month, 2 months, 3 months, and 6 months postoperatively. Retinal histology was obtained at euthanasia, 2 months (n = 3), 3 months (n = 2), or 6 months (n = 2) after surgery.
RESULTS: RPE debridement resulted in GA with rapid loss of choriocapillaris, progressive loss of photoreceptors, and pachychoroidal changes in Sattler's and Haller's layers in all seven eyes undergoing debridement within 2 months. OCT and histological findings included subretinal disciform scar with overlying outer retinal atrophy; outer retinal tubulations and subretinal hyper-reflective material. OCTA revealed type 2 CNV (n = 4) at the edges of the debridement zone by 2 months, but there was no significant exudation noted at any time point.
CONCLUSIONS: Surgical debridement of the RPE results in GA, CNV, and pachychoroid and reproduced all forms of advanced macular degeneration. This surgical model may be useful in examining the role of RPE and other cell replacement in treating advanced macular disease.
The following generally relates to the field of medical monitoring, medical alarm systems with respect to monitored patients, and the like. In a clinical setting, an alarm is typically triggered when a single-parameter or multi-parameter score exceeds certain thresholds. When a score needs to be determined, if some parameters are not available, it is common practice to use the latest measurements of the parameters for the score calculation. However, the state of the patient may change from moment to moment. The parameter measured a few hours ago may not be a good indicator of the current state of the patient. This uncertainty can place deteriorating patients at great risk. If old measurements must be used for score determination, one embodiment uses statistical methods to estimate the range of scores and the probability of these scores. Instead of giving a single value at a time, a confidence interval may be displayed to emphasize the fact that the score is determined based in part on old measurements. If there is a likelihood that the actual score is higher and may exceed the critical alarm threshold, a notification may be issued to suggest new measurement readings to improve the score confidence.