anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Subjects who met the study population conditions were treated with Cadonilimab 10mg/kg + bevacizumab 7.5 mg/kg + carboplatin (AUC 5) + pemetrexed 500mg/m2. Every 3 weeks is a cycle, with a total of 4-6 cycles (the number of chemotherapy cycles is determined by the researchers). Cadonilimab 10mg/kg, bevacizumab 7.5 mg/kg and pemetrexed 500mg/m2 were then maintained until disease progression, intolerable toxicity or other causes specified in the regimen occurred. When the subject first has imaging disease progression, if the researcher judges that it is clinically beneficial and tolerant to the test drug, he will be allowed to continue treatment.
Premature Closure of Fetal Ductus Arteriosus   
Avoid use of NSAIDS, including VIVLODEX, in pregnant women at about 30 weeks of gestation and later. NSAIDs, including VIVLODEX, increase the risk of premature closure of the fetal ductus arteriosus at approximately this gestational age.

Oligohydramnios/Neonatal Renal Impairment   
Use of NSAIDs, including VIVLODEX, at about 20 weeks gestation or later in pregnancy may cause fetal renal dysfunction leading to oligohydramnios and, in some cases, neonatal renal impairment. These adverse outcomes are seen, on average, after days to weeks of treatment, although oligohydramnios has been infrequently reported as soon as 48 hours after NSAID initiation.

Oligohydramnios is often, but not always, reversible with treatment discontinuation. Complications of prolonged oligohydramnios may, for example, include limb contractures and delayed lung maturation. In some postmarketing cases of impaired neonatal renal function, invasive procedures such as exchange transfusion or dialysis were required.

If NSAID treatment is necessary between about 20 weeks and 30 weeks gestation, limit VIVLODEX use to the lowest effective dose and shortest duration possssible. Consider ultrasound monitoring of amniotic fluid if VIVLODEX treatment extends beyond 48 hours. Discontinue VIVLODEX if oligohydramnios occurs and follow up according to clinical practice [see Use in Specific Populations (8.1)].
PROBLEM TO BE SOLVED: To obtain a composition for amelioration and prophylaxis of diseases, having a low possibility of causing adverse effects, and further excellent ameliorating and preventing effects on hypertension, hyperlipemia and obesity, or the like, and to provide a method for producing the composition. SOLUTION: The liquid composition for amelioration and prophylaxis comprises a yeast fermentation product of a vegetable, a fruit, sea grass and/or a grain and saccharides. In the liquid composition, the yeast is preferably a yeast of an accession number FERM P-18540. In the liquid composition, the saccharide content is preferably 50-60%. Furthermore, diseases mentioned in the liquid composition are hypertension, hyperlipemia and obesity. The method for producing the liquid composition comprises the following steps (A) to (C). (A) a step of adding the yeast to the vegetable, fruit, sea grass and/or grain, (B) a step of adding the saccharides and extracting a stock solution and (C) a step of fermenting and aging the resultant stock solution.
For external use only. For Professional and Hospital use only. Do not • use in the eyes • apply over large areas of the body. Consult a doctor in case of deep or puncture wounds, animal bites, or serious burns. Stop use and consult a doctor if the condition persists or gets worse. Do not use longer than 1 week unless directed by a doctor.

Keep out of reach of children. If swallowed, get medical help or contact a Poison Control Center right away.
A container suitable for cosmetics, fragrances and the like wherein the container is formed of a solid material comprising a mixture of sodium bicarbonate and an acid or is formed of a soap. Preferably the acid is citric acid or is in the form of cream of tarter mixed with a surfactant. A solid material comprising a mixture of sodium bicarbonate and citric acid will effervesce strongly when immersed in water and dissolve or disperse quickly. The solid material thus readily provides a product such as bath salts or the like. The purchaser therefore receives two products and when the cosmetic or fragrance product or the like has been used, disposal of the container is easy and at the same time useful. Adverse impact on the environment is thus significantly reduced. Similar advantages are obtained with the other embodiments.
Patients who are randomized to this group will take a low-dose aspirin 81mg pill once per day (standard-of-care) for at least 6 months along with cytoreductive therapy, if applicable. Patients will then be treated and followed up as per standard of care at the discretion of his or her treating physician after the completion of the study.
AIMS: Dopamine transporter (DAT) can regulate DA homeostasis and has been implicated in many nervous system diseases. Whether DAT is involved in the protection against ischemic stroke is unclear.
METHODS: In vivo microdialysis measurements of DA were recorded in the ischemic penumbral area of mice with middle cerebral artery occlusion (MCAO). DAT coding gene, Slc6a3 mutation, and DAT overexpression animals were performed MCAO. Madopar (compound formulation of levodopa) and nomifensine (DA reuptake inhibitor) were administered in MCAO animals. Brain slices were prepared in Slc6a3 mutation or wild-type (WT) animals with MCAO to record miniature excitatory postsynaptic currents (mEPSCs) and miniature inhibitory postsynaptic currents (mIPSCs). The effects of DA and its dopamine-1 receptor (D1R) antagonists (SCH-23390) on mEPSCs, mIPSCs, and neurons protection were recorded.
RESULTS: MCAO caused a prominent increase in DA. Slc6a3 mutation significantly attenuated the ischemic injury, whereas DAT overexpression aggravated this injury. Both nomifensine and madopar protected against brain injury. Slc6a3 mutation and DA restored the disturbance of mEPSCs and mIPSC, and protected against neuron death, which was abolished by SCH-23390.
CONCLUSION: DAT inhibition might be explored as a strategy for ischemic stroke prevention. DA and D1R involve in the restoration of synaptic dysfunction and neuron protection.
A system for determining a probability (or likelihood) of exacerbation of a respiratory disease in a subject is provided. The system comprises an inhaler arrangement for delivering medicament to a subject. The medicament may be, for example, a rescue medicament or a maintenance medicament. The inhaler arrangement has a use detection system configured to determine inhalation by a subject using the inhaler arrangement. The sensor system is configured to measure a parameter related to the airflow during inhalation. The user interface allows the user to input an indication of the respiratory disease condition the subject is experiencing. The processor is configured to determine a probability of respiratory disease deterioration based on the recorded inhalation from the usage detection system, the parameters received from the sensor system, and the indication received from the user interface. A method for determining a probability of exacerbation of a respiratory disease in a subject is also provided.
White matter hyperintensities (WMH) are the most prevalent markers of cerebral small vessel disease (SVD), which is the major vascular risk factor for dementia. Microvascular pathology and neuroinflammation are suggested to drive the transition from normal-appearing white matter (NAWM) to WMH, particularly in individuals with hypertension. However, current imaging techniques cannot capture ongoing NAWM changes. The transition from NAWM into WMH is a continuous process, yet white matter lesions are often examined dichotomously, which may explain their underlying heterogeneity. Therefore, we examined microvascular and neurovascular inflammation pathology in NAWM and severe WMH three-dimensionally, along with gradual magnetic resonance imaging (MRI) fluid-attenuated inversion recovery (FLAIR) signal (sub-)segmentation. In WMH, the vascular network exhibited reduced length and complexity compared to NAWM. Neuroinflammation was more severe in WMH. Vascular inflammation was more pronounced in NAWM, suggesting its potential significance in converting NAWM into WMH. Moreover, the (sub-)segmentation of FLAIR signal displayed varying degrees of vascular pathology, particularly within WMH regions. These findings highlight the intricate interplay between microvascular pathology and neuroinflammation in the transition from NAWM to WMH. Further examination of neurovascular inflammation across MRI-visible alterations could aid deepening our understanding on WMH conversion, and therewith how to improve the prognosis of SVD.
FIELD: pharmacy, cosmetology. SUBSTANCE: invention relates to the solid anhydrous dispersion based on fat substance and polyhydric alcohol. The solid anhydrous dispersion has the following components, wt.-% per total dispersion weight: fat substance 20-95; dispersed polyhydric alcohol 0.5-50 and at least a single fluoroorganic hydrocarbon compound 0.1-50. The developed solid anhydrous dispersion provides to solve the problem of exudation of solid dispersions containing polyhydric alcohol in the fat phase. EFFECT: improved quality of dispersion. 14 cl, 11 ex
Insulin resistance (IR) is the key pathophysiological cause of type 2 diabetes, and inflammation has been implicated in it. The death domain (DD) of the adaptor protein, MyD88 plays a crucial role in the transduction of TLR4-associated inflammatory signal. Herein, we have identified a 10-residue peptide (M10), from the DD of MyD88 which seems to be involved in Myddosome formation. We hypothesized that M10 could inhibit MyD88-dependent TLR4-signaling and might have effects on inflammation-associated IR. Intriguingly, 10-mer M10 showed oligomeric nature and reversible self-assembly property indicating the peptide's ability to recognize its own amino acid sequence. M10 inhibited LPS-induced nuclear translocation of NF-κB in L6 myotubes and also reduced LPS-induced IL-6 and TNF-α production in peritoneal macrophages of BALB/c mice. Remarkably, M10 inhibited IL-6 and TNF-α secretion in diabetic, db/db mice. Notably, M10 abrogated IR in insulin-resistant L6 myotubes, which was associated with an increase in glucose uptake and a decrease in Ser307-phosphorylation of IRS1, TNF-α-induced JNK activation and nuclear translocation of NF-κB in these cells. Alternate day dosing with M10 (10 and 20 mg/kg) for 30 days in db/db mice significantly lowered blood glucose and improved glucose intolerance after loading, 3.0 g/kg glucose orally. Furthermore, M10 increased insulin and adiponectin secretion in db/db mice. M10-induced glucose uptake in L6 myotubes involved the activation of PI3K/AKT/GLUT4 pathways. A scrambled M10-analog was mostly inactive. Overall, the results show the identification of a 10-mer peptide from the DD of MyD88 with anti-inflammatory and anti-diabetic properties, suggesting that targeting of TLR4-inflammatory pathway, could lead to the discovery of molecules against IR and diabetes.
FIELD: biochemistry. SUBSTANCE: erythrocyte waste from human blood are subjected for hemolysis at simultaneous denaturation of hemoglobin by heating at 60-64 C. Then method involves filtration and purification of Cu,Zn-superoxide dismutase (SOD)-containing filtrate by two-step ion-exchange chromatography on anionite DEAE-Spheranite at pH 5.7-6.3 using 0.01M phosphate buffer and elution of SOD with 0.1M phosphate buffer at the same pH values and then on cationite Soloza KG by elution at pH 5.1-5.3. Invention ensures to increase the yield of the end product up to 65-70% at purity 98-99%. Product can be used in medicinal industry and laboratory studies. EFFECT: increased yield and purity. 4 tbl
This method is based on iris and sclera segmentation in both eyes from the acquired images, using state of the art deep learning encoder-decoder neural architectures (DLED). The sequence of the segmented frames is post-processed to calculate the distance between the eyelids of each eye (palpebral fissure) and the corresponding iris diameter. Theses quantities are temporally filtered and their fraction is subject to adaptive thresholding to identify blinks and determine their type, independently for each eye. The two DLEDs were trained with manually segmented images and the post-process was parameterized using a 4-minute video. After DLED training, the proposed system was tested on 8 different subjects, each one with a 4-10-minute video. Several metrics of blink detection and classification accuracy were calculated against the ground truth, which was generated by 3 independent experts, whose conflicts were resolved by a senior expert. Two independent blink identifications are assumed to be in agreement, if and only if there is sufficient temporal overlapping and the type of blink is the same between the DLED system and the ground truth.
BACKGROUND: The objective of this document is to provide recommendations on the formal reliability of major clinical predictors often associated with intracerebral hemorrhage (ICH) neuroprognostication.
METHODS: A narrative systematic review was completed using the Grading of Recommendations Assessment, Development, and Evaluation methodology and the Population, Intervention, Comparator, Outcome, Timing, Setting questions. Predictors, which included both individual clinical variables and prediction models, were selected based on clinical relevance and attention in the literature. Following construction of the evidence profile and summary of findings, recommendations were based on Grading of Recommendations Assessment, Development, and Evaluation criteria. Good practice statements addressed essential principles of neuroprognostication that could not be framed in the Population, Intervention, Comparator, Outcome, Timing, Setting format.
RESULTS: Six candidate clinical variables and two clinical grading scales (the original ICH score and maximally treated ICH score) were selected for recommendation creation. A total of 347 articles out of 10,751 articles screened met our eligibility criteria. Consensus statements of good practice included deferring neuroprognostication-aside from the most clinically devastated patients-for at least the first 48-72 h of intensive care unit admission; understanding what outcomes would have been most valued by the patient; and counseling of patients and surrogates whose ultimate neurological recovery may occur over a variable period of time. Although many clinical variables and grading scales are associated with ICH poor outcome, no clinical variable alone or sole clinical grading scale was suggested by the panel as currently being reliable by itself for use in counseling patients with ICH and their surrogates, regarding functional outcome at 3 months and beyond or 30-day mortality.
CONCLUSIONS: These guidelines provide recommendations on the formal reliability of predictors of poor outcome in the context of counseling patients with ICH and surrogates and suggest broad principles of neuroprognostication. Clinicians formulating their judgments of prognosis for patients with ICH should avoid anchoring bias based solely on any one clinical variable or published clinical grading scale.
OBJECTIVE: The indications for and approaches to extracapsular dissection for parotid gland benign tumours are debated in the literature. This study retrospectively evaluates a single site's short- and long-term results with a standardised extracapsular dissection approach to benign parotid tumours.
METHODS: A retrospective review of a single institution's records identified cases with extracapsular dissection as the primary surgery for non-recurrent benign parotid tumours. A total of 194 eligible patients were identified (124 women and 70 men, age 47.75 ± 15.62 years). Pre-, intra- and post-surgical data were reviewed for complications and recurrences.
RESULTS: Histology reported pleomorphic adenoma in 165 patients, Warthin's tumour in 28 patients and both in one patient. Mean follow up was 36 ± 16 months (range, 12-84 months). The incidences of complications following extracapsular dissection were temporary (n = 13) and permanent (n = 0) facial nerve dysfunction, Frey's syndrome (n = 1)) and recurrences (n = 5). These rates align with prior literature.
CONCLUSION: This case series shows how a standardised approach to extracapsular dissection for benign parotid tumours yields favourable results, supporting a progressive change of strategy towards reduced invasiveness.
PURPOSE:To obtain a carcinostatic active substance free from side effects, comprising precipitate prepared by adding an organic solvent to a water extracted solution of sporophyll of sea mustard as an active ingredient. CONSTITUTION:Sporophyll (blastema) of sea mustard, an edible marine algae is immersed in water for several hours - tens hours to give an extracted solution. The extracted solution is incorporated with about an equivalent amount of an organic solvent such as methanol, ethanol or acetone. Immediately white precipitate is produced. Then the precipitate is subjected to solid-liquid separation by centrifugal separation and separated from the supernatant liquid. The precipitate can be directly used carcinostatic active substance as it is, but preferably dissolved in distilled water, incorporated with the organic solvent again, allowed to stand at a low temperature, subjected to solid-liquid separation to recover precipitate, which is dried to give the objective substance.
The present invention relates to methods for inducing cellular mutation by promoting the reaction of nonenzymatic glycosylation of genetic material, such as DNA and RNA, by incubation of the genetic material with certain protein structure modifying agents. Suitable such agents are reducing sugars, such as glucose, glucose-6-phosphate and a reactive intermediate comprising a complex between glucose 6-phosphate and lysine. The methods include the in vitro reaction of the agent with genetic material, such as a particular gene-bearing plasmid, under conditions promoting mutation followed by the introduction of the plasmid bearing the reacted gene into a host cell, and allowing the reacted gene to be mutated and expressed, after which the mutant protein of interest may be isolated. In a variation on the last-mentioned method, a first genetic material may be incubated with the agent and reacted, and this reacted genetic material may then be introduced into a distinct cellular strain and appropriately incubated whereupon the first reacted genetic material will cause the mutation of the genetic material in the distinct cellular strain. The invention also includes an in vivo embodiment wherein the particular genetic material of interest may be isolated and introduced into a host cell which contains high intracellular concentrations of the protein structure modifying agent(s). In this instance, the mutation is promoted by the host cell, and the mutant material may thereafter be isolated and recovered. Diagnostic methods employing the principles of the invention are also disclosed.
Participants were treated with desipramine, up to 300 mg per day. All patients received weekly individual manual-guided relapse prevention therapy.
Disclosed is a medical apparatus. The medical apparatus comprises a fist sub-component, a second sub-component and an activation device or a reagent to produce an activation signal. The first sub-component is implantable or ingestible in a body. The first sub-component comprises a drug, a medical kit, a micro-disease detection system, or an auto-navigation system. The second sub-component comprises a decomposable material (0201) that is integrated with the first sub-component. The decomposition of the decomposable material (0201) of the second sub-component causes breaking up of the whole apparatus. The second sub-component comprises at least first portions of a first type of material (0201) and second portions of a second type of material (0202, 0203), the first (0201) and second portions (0202, 0203) being arranged in a pattern in an interlaced structure of the first (0201) and second portions (0202, 0203), at least the first type of material being decomposable material (0201). The decomposition of the material of the second sub-component is triggered by application of the activation signal to the second sub-component.
The invention discloses an anti-CTLA4 single domain antibody, wherein the amino acid sequence of a variable region of the anti-CTLA4 single domain antibody is shown as SEQ ID NO. 1; the anti-CTLA4 single domain antibody is a shark source antibody. The invention also discloses a gene for encoding the anti-CTLA4 single domain antibody, and the nucleotide sequence of the gene is shown as SEQ ID NO. 2. The invention also discloses a recombinant plasmid which contains a nucleotide sequence shown as SEQ ID NO. 2. The invention also discloses a recombinant expression bacterium which contains the recombinant plasmid. The anti-CTLA4 single-domain antibody prepared by the invention has good binding activity and anti-tumor activity on CTLA4, so that the single-domain antibody has good application prospect. The recombinant CTLA4 single-domain antibody prepared by the invention also has the advantage of the recombinant single-domain antibody.
The invention relates to a Manganning preparation and a preparation method thereof. The method comprises the following steps of: selecting and cleaning 16 medicinal materials such as rehmannia root, prepared radix polygoni multiflori, coastal glehnia root, Chinese angelica and the like; taking 7 medicinal materials such as rehmannia root and the like, adding ethanol into the medicinal materials for backflow extraction, separating out an extract, adding ethanol into dregs for backflow extraction, merging a secondary extract, filtering, standing filtrate, absorbing supernate, and concentrating the supernate into extractum under the reduced pressure and at the low temperature; taking 7 medicinal materials such as the prepared rehmannia root and the like, adding water to decoct the mixture, separating out a water liquid, adding water into the dregs to decoct the mixture, merging a secondary water extract, filtering, standing filtrate, absorbing supernate, and concentrating the supernate into extractum under the reduced pressure and at the low temperature; taking and mixing remaining radix pseudo-ginseng and turmeric root-tuber, and crushing the mixture to obtain fine powder; drying and crushing the extractum to obtain fine powder; and taking the fine powder and adding pharmaceutic adjuvant to prepare tablets or granules. The preparation method has the advantages of novel design, reasonable design, standard operation, no environmental pollution, easy forming of industrialized production and the like. The product prepared by the method is a Chinese medicinal preparation, can be continuously taken, has the obvious curative effect and is convenient to carry, and is easily accepted by consumers. The Chinese medicinal preparation is suitable for curing chronic hepatitis B, particularly chronic virus hepatitis B, and liver-kidney yin deficiency type and damp-heat blood stasis syndromes. The preparation can improve clinical symptoms.