anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Alzheimer's disease (AD) is a complex neurodegenerative disorder influenced by various genetic factors. In addition to the well-established amyloid precursor protein (APP), Presenilin-1 (PSEN1), Presenilin-2 (PSEN2), and apolipoprotein E (APOE), several other genes such as Sortilin-related receptor 1 (SORL1), Phospholipid-transporting ATPase ABCA7 (ABCA7), Triggering Receptor Expressed on Myeloid Cells 2 (TREM2), Phosphatidylinositol-binding clathrin assembly protein (PICALM), and clusterin (CLU) were implicated. These genes contribute to neurodegeneration through both gain-of-function and loss-of-function mechanisms. While it was traditionally thought that heterozygosity in autosomal recessive mutations does not lead to disease, haploinsufficiency was linked to several conditions, including cancer, autism, and intellectual disabilities, indicating that a single functional gene copy may be insufficient for normal cellular functions. In AD, the haploinsufficiency of genes such as ABCA7 and SORL1 may play significant yet under-explored roles. Paradoxically, heterozygous knockouts of PSEN1 or PSEN2 can impair synaptic plasticity and alter the expression of genes involved in oxidative phosphorylation and cell adhesion. Animal studies examining haploinsufficient AD risk genes, such as vacuolar protein sorting-associated protein 35 (VPS35), sirtuin-3 (SIRT3), and PICALM, have shown that their knockout can exacerbate neurodegenerative processes by promoting amyloid production, accumulation, and inflammation. Conversely, haploinsufficiency in APOE, beta-secretase 1 (BACE1), and transmembrane protein 59 (TMEM59) was reported to confer neuroprotection by potentially slowing amyloid deposition and reducing microglial activation. Given its implications for other neurodegenerative diseases, the role of haploinsufficiency in AD requires further exploration. Modeling the mechanisms of gene knockout and monitoring their expression patterns is a promising approach to uncover AD-related pathways. However, challenges such as identifying susceptible genes, gene-environment interactions, phenotypic variability, and biomarker analysis must be addressed. Enhancing model systems through humanized animal or cell models, utilizing advanced research technologies, and integrating multi-omics data will be crucial for understanding disease pathways and developing new therapeutic strategies.
NEW MATERIAL:A compound shown by the formula I (R<1> is 15-20C aliphatic hydrocarbon residue; R<2> is lower alkyl; R<3> is H or lower alkyl) and its salt. EXAMPLE:3-Octadecyloxy-2-methoxypropyl 2-dimethylaminoethyl phosphate. USE:An antitumor agent. Having low toxicity. PREPARATION:For example, sodium salt of 2-O-methylglycerol is dissolved or suspended in an inert solvent under anhydrous conditions, and treated with a compound shown by the formula R<1>Q (Q is halogen, sulfate, or sulfonate) to give a compound shown by the formula II. This compound is reacted with a compound shown by the formula III (X and Y are halogen), and treated with water to give a compound shown by the formula IV. This compound is reacted with a compound shown by the formula V to give a compound shown by the formula I .
The invention discloses a capsule containing Pradaxa or its salt. The capsule is composed of drug-containing particles and organic acid particles. The drug-containing particles include active material particles of active ingredient Pradaxa or its pharmaceutically acceptable salt or hydrate and a filler and/or adhesive or optional disintegrating agent; and an isolation layer covering the surfaces of the active material particles. Organic acid particles contain organic acid and/or the filler and/or adhesive and/or disintegrating agent, and the surfaces can be optionally covered with an isolation layer. The organic acid is selected from tartaric acid, succinic acid, citric acid, glutamic acid, fumaric acid, malic acid, aspartic acid or other available organic acid or its hydrate or acid salt. Through screening, the inventor prepares Pradaxa active substance into particles, the surfaces of which are coated with an isolation layer; and the organic acid is made into granules to fill the capsule together with the isolated drug-containing particles. The prepared Pradaxa oral capsule has good solubility, dissolution rate and stability, and can meet the clinical use requirements of Pradaxa.
PURPOSE: A method for manufacturing a cosmetic film and a cosmetic film composition containing vitamin C is provided to obtain the cosmetic film composition and the cosmetic film with persistent stability, and to apply the cosmetic film and cosmetic film composition without stickiness. CONSTITUTION: A cosmetic film composition contains vitamin C, a film forming polymer, a gelling agent, and a plasticizer. The composition additionally contains an antioxidant containing natural product extracts. The cosmetic film composition contains 10-50 wt% of vitamin C, 5-18 wt% of the antioxidant, 15-25 wt% of the film forming polymer, 0.1-7 wt% of the gelling agent, 8-18 wt% of the plasticizer, and 1-50 wt% of water. A method for manufacturing a cosmetic film comprises: a step of dissolving vitamin C, the film forming polymer, the gelling agent, and the plasticizer in water and preparing the cosmetic film composition; a step of coating a support with the mixture and preparing a film; and a step of drying the film at 40-120 deg. C. [Reference numerals] (AA) Detection area(uV x sec) x 10000; (BB) Days; (CC) Comparative example 1; (DD) Example 1
The invention discloses medicinal liquor for treating cough. The medicinal liquor has the advantages of high recovery rate and no side effect. The medicinal liquor is preferably prepared from the following medicaments in parts by weight: 35 parts of szechuan lovage rhizome, 35 parts of pericarpium zanthoxyli, 30 parts of white paeony root, 35 parts of cassia seed, 30 parts of apricot kernel, 22 parts of pinellia tuber, 20 parts of honeysuckle flower, 20 parts of indigowoad root, 20 parts of liquoric root, 20 parts of dried ginger and 25 parts of rock candy. A preparation method comprises the following steps: weighing the medicaments in proportion, mixing, crushing into coarse ground particles, tightly packaging to form a medicament bag by using gauze, putting into a container, adding 2000ml of 70-degree distilled spirit, soaking, sealing the container, and then storing. The medicinal liquor can be drunk after one month, and the dose is 15-20 ml each time. The medicinal liquor for treating cough disclosed by the invention is low in medicament price, easily-available in raw material, simple in manufacturing method and good in taking effect; and the medicaments adopted in a medicament formula totally adopt natural herbal medicines, and do not have side effects to the body.
PROBLEM TO BE SOLVED: To obtain a solid teprenone agent stably preservable over a long period. SOLUTION: Teprenone is used singly or in combination with >=1.0wt.% of L-ascorbic acid or erythorbic acid or their salt, supported on a powdery carrier (e.g. light silica) and prepared in the form of a drug. The amount of teprenone to be supported on the powdery carrier is about 0.05-2 pts.wt. based on 1 pt.wt. of the carrier. The product is optionally compounded with arbitrary other components and prepared in the form of powder, fine particle, granule, etc. The decomposition of teprenone can be prevented and a stable solid agent can be prepared even by using water-soluble L-ascorbic acid, erythorbic acid, etc., as an antioxidant by supporting the acid on a powdery carrier at the aforementioned ratio.
The invention provides a compound traditional Chinese medicine according to characteristics and rules of stubborn diseases. The compound traditional Chinese medicine can be prepared into instant granules, powder, capsules, tablets and nano medicaments, and comprises the following components: 10g of high-quality cinnabar, 15g of dried ginger, 10g of prepared liquorice, 10g of Chinese honeylocust fruit and 15g of glabrous greenbrier rhizome. The compound traditional Chinese medicine can regulate imbalanced vital organs of a human body, promote weak internal organs and inhibit excitation. The compound traditional Chinese medicine has the greatest advantage of bidirectionally regulating physical energy of the human body. After a patient takes the medicine, pathological products are rapidly expelled from the human body through defecation, and the internal organs are quickly balanced relatively so as to make the body recovered. The compound traditional Chinese medicine has the advantages of high curative effect, short cure time and low cost.
PAEONIFLORIN PREPARATIONS AND USES THEREOF FOR FAT Abstract Disclosed are methods and preparations useful for reducing fat at a targeted area(s) on a human. The preparations comprise as an active ingredient an adipolysis enhancing (i.e., fat melting) amount of an active ingredient, paeoniflorin (PF). The preparations may be provided as an injectable preparation or as a topically applied preparation, such as in the form of a creme or lotion. In topical preparations, the active ingredient paeoniflorin may be contained within nanospheres, such as albumin nanospheres. The PF-containing preparations may also include a permeant, such as azone. The method may be accompanied by the application of ultrasound to the area being treated prior to, during or after, or prior to, during, and after application of the paeoniflorin preparation to an area of the body in which fat reduction is desired. By way of example, the methods and preparations are effective for reducing targeted fat deposits at various anatomical sites of the body, such as the midsection ("love handles"), jowls, hips, arms, thighs and buttocks area.
Ages 18-35. Performed 4 weeks of an at-home, hand grip resistance training intervention.
This is a multi-center, international, open-label, safety study of ND0612, a solution of LD/CD delivered via a pump system as a continuous SC infusion in subjects with advanced PD. Two cohorts of subjects are candidates for this study: subjects who completed treatment in study ND0612H-006 within one month prior to enrollment (Cohort 1) and ND0612 naïve subjects or subjects who completed treatment in a ND0612 clinical study more than one month before screening (Cohort 2). After screening procedures and confirmation of the inclusion/exclusion criteria, subjects and their study partners will be trained and assisted at their homes during the first week of treatment on the proper operation of the pump system. One mandatory home visit will be performed during the first week and then on a monthly basis during 12-months of treatment. Subjects will return for in-clinic visits at Week 1 and at Months 1, 2, 3, 4, 6, 9, and 12 for assessment of safety and efficacy variables. Subjects will be allowed to continue with study treatment for an optional treatment extension period of up to Month 102 and the clinic visits will be performed every 3 months to assess subject long-term safety. Safety follow-up visits will occur 1, 2, and 3 months after the last SC infusion of ND0612 or after early termination.
In a process for producting mixtures of amphoteric surface-activeimidazoline derivatives, containing principally compounds of formula (I), in which R1? is a C5-21? alkyl residue, B a C2-4? aminoalkyl or hydroxyalkyl residue and D an -R2?-COOM residue, where R2? stands for a C1-4? alkylene residue or a C2-4? alkenyl residue and M for H, NH4? or an alkali metal: A) an imidazoline offormula (II) is hydrolysed with water in a molar ratio of 1:8 to 1:20 at 50 to 130C under atmospheric pressure or slightly above in 1 to 24 hours to a mixture of amidoamines; B) the amidoamine mixture so obtained is alkylized with an alkylation agent of formula X-D, in which X stands for a halogen or hydrogen atom and D has the meaning given above, in a molar ratio of alkylation agent to amidoamines of 1:1 to 4:1 in the presence of a base at 40 to 70C and pH 10 to 11.5 measured in a 10 wt.% aqueous solution of the reaction mixture; and C) the excess alkylation agent is hydrolysed at 80 to 95C and pH 10 to 11.5 measured in a 10 wt.% aqueous solution of the reaction mixture.
Williams syndrome (WS) is a rare genetic disorder caused by a microdeletion of chromosome 7q11.23. Although the mortality rate of patients with WS is not very high, sudden cardiac death can occur, particularly in cases complicated by coronary artery stenosis. A 3-month-old female infant with supravalvular aortic stenosis and peripheral pulmonary stenosis was discovered unconscious in bed by her mother. She was immediately transferred to an emergency hospital but succumbed despite multiple attempts as resuscitation. DNA microarray analysis revealed microdeletions of 7q11.23 and 16p11.2, confirming WS and unexpectedly identifying 16p11.2 deletion syndrome which is known to be associated with neurodevelopmental disorders. Postmortem computed tomography revealed a severely enlarged heart, indicative of cardiac dysfunction. External examination revealed moderate-to-severe developmental delays in height and body weight. The heart, on internal examination, revealed whitish-discolored lesions; histologically severe fibrotic changes and thickening of the intima in the coronary arteries and aorta. In the brain, the dentate gyrus of the hippocampus appeared malformed. Taken together, these findings suggest that the cause of death was cardiac dysfunction due to WS. In addition, it could be possible that 16p11.2 deletion syndrome and dentate gyrus malformation contributed to her death. Future autopsy studies are warranted to clarify the precise role of microdeletion disorders in sudden death to reduce future preventable deaths in children.
Chronic kidney disease (CKD) represents a significant global health concern, with renal fibrosis emerging as a prevalent and ultimate manifestation of this condition. The absence of targeted therapies presents an ongoing and substantial challenge. Accumulating evidence suggests that the integrity and functionality of mitochondria within renal tubular epithelial cells (RTECs) often become compromised during CKD development, playing a pivotal role in the progression of renal fibrosis. Mitophagy, a specific form of autophagy, assumes responsibility for eliminating damaged mitochondria to uphold mitochondrial equilibrium. Dysregulated mitophagy not only correlates with disrupted mitochondrial dynamics but also contributes to the advancement of renal fibrosis in CKD. While numerous studies have examined mitochondrial metabolism, ROS (reactive oxygen species) production, inflammation, and apoptosis in kidney diseases, the precise pathogenic mechanisms underlying mitophagy in CKD remain elusive. The exact mechanisms through which modulating mitophagy mitigates renal fibrosis, as well as its influence on CKD progression and prognosis, have not undergone systematic investigation. The role of mitophagy in AKI has been relatively clear, but the role of mitophagy in CKD is still rare. This article presents a comprehensive review of the current state of research on regulating mitophagy as a potential treatment for CKD. The objective is to provide fresh perspectives, viable strategies, and practical insights into CKD therapy, thereby contributing to the enhancement of human living conditions and patient well-being.
The ventrolateral periaqueductal gray (vlPAG) serves as a central hub for descending pain modulation. It receives upstream projections from the medial prefrontal cortex (mPFC) and the ventrolateral orbitofrontal cortex (vlOFC), and projects downstream to the locus coeruleus (LC) and the rostroventral medulla (RVM). While much research has focused on upstream circuits and the LC-RVM connection, less is known about the PAG-LC circuit and its involvement in neuropathic pain. Here we examined the intrinsic electrophysiological properties of vlPAG-LC projecting neurons in Sham and spared nerve injury (SNI) operated mice. Injection of the retrotracer Cholera Toxin Subunit B (CTB-488) into the LC allowed the identification of LC-projecting neurons in the vlPAG. Electrophysiological recordings from CTB-488 positive cells revealed that both GABAergic and glutamatergic cells that project to the LC exhibited reduced intrinsic excitability after peripheral nerve injury. By contrast, CTB-488 negative cells did not exhibit alterations in firing properties after SNI surgery. An SNI-induced reduction of LC projecting cells was confirmed with c-fos labeling. Hence, SNI induces plasticity changes in the vlPAG that are consistent with a reduction in the descending modulation of pain signals.
1) Abstract of the study A positive energy balance (greater intake than expenditure) can explain weight gain and, when protracted, leads to overweight and obesity. The major question addressed in this proposal is if the timing of activation of specific regions of the brain is predictive of excessive food intake. Functional near infra-red spectroscopy (fNIR), seldom used in human eating studies, provides data similar to functional magnetic resonance imaging (fMRI) but allows for measurement of brain activation during food consumption. The investigator's pilot fNIR data reveal that varying patterns of regional PFC activation are associated with "loss of control" over eating, and that only 60% of individuals respond to acute protein intake with a reduction in food intake. Using fNIR and an acute protein challenge, the investigator will assess the effect of family history of obesity in humans on the satiation response to protein and concomitant activation of the prefrontal cortex (PFC). It is hypothesized that activation of the human medial PFC before the lateral PFC will result in greater intake of palatable food in those subjects with a proneness to obesity, and that these subjects will be less sensitive to the satiety-inducing effects of a protein preload. These results should provide an innovative and useful method for assessing risk for developing obesity and usefulness of preventative interventions.
Live vaccines are provided and methods for preparing the live vaccines for protection of a host from a pathogenic microorganism. The vaccines are prepared by introducing at least one modification in a gene involved in at least one, normally at least two, biosynthetic pathways, involving the production of products which are unlikely to be found in the disease susceptible host. The modification results in a gene change which cannot be repaired by a single step e.g. polynucleotide deletions and inversions. Where the aro gene suffers such a change, the resultant auxotrophic mutants require aromatic amino acids, p-aminobenzoic acid and 2, 3-dihydroxybenzoic acid or a highly concentrated source of absorbable iron. The auxotrophic mutations have substantially reduced or nonexistent virulence, while retaining the desired immunogenicity to initiate the immunogenic response. Various techniques can be employed for providing the desired change. Salmonella typhimurium strain SL1479 was deposited at the ATCC on September 7, 1982 and given ATGG Accession No. 39183; Salmonella dublin strain SL1438 was deposited on September 7, 1982 at the ATCC and given ATCC Accession No. 39184. Salmonella typhi strain 531Ty was deposited at the ATCC on November 21, 1984, and granted ATCC Accession No. 39926. This application is a continuation-in-part of U.S. Serial No. 675,381, filed November 27, 1984 which is a continuation-in-part of U.S. Serial No. 415,291, filed September 7, 1982 now U.S. Patent No. 4,550,081, issued October 29, 1985, which is a continuation-in-part of U.S. Serial No. 151,002, filed May 19, 1980, now abandoned, which disclosures are incorporated herein by reference.
A late adolescent patient was admitted after a collapse and was found to have an intracranial haemorrhage due to an underlying midline arteriovenous malformation (AVM). The patient underwent trans-arterial squid embolisation of the AVM with good radiological resolution. 18 months later, the patient presented with new onset headaches. Cranial imaging demonstrated an enhancing lesion at the site of the previously thrombosed AVM in the corpus callosum. This was deemed to be a foreign body granuloma, a rare complication of intravascular embolisation of AVMs. The patient continued to have periodic imaging with subsequent scans demonstrating progressive changes in the granuloma and this was then resected surgically. We describe the natural history of the granuloma formation, outline the cranial imaging features associated with this rare condition and review the literature of similar cases.
Subjects : Patients with non-ischemic cardiomyopathy who need medical treatment Procedures : This is a prospective, randomized trial to compare cardiopulmonary motor tests, cardiac MRI including myocardial fibrosis parameters (ECV, etc.), and incidence of various heart failure-related cardiovascular events during the follow-up period between patients with ertugliflozin drug therapy and placebo drug. Patients meeting inclusion criteria without any exclusion criteria will be randomized 1:1 to ertugliflozin (5mg) or placebo therapy. Randomization will be stratified according to presence of diabetes mellitus, and the upper limit of randomized non-DM patients will be set as 36 patients (70%). The estimated enrollment period is 18 months (n=52) and all patients will be followed for 12 months after randomization. Random assignment is performed at random assignment visit (V1) through eCASE web system and following study procedures will be conducted according to the randomization. CMR, Cardiopulmonary exercise test, serum biomarkers, and clinical endpoints will be measured at 3,6,12 months.
50 subjects (25 subjects with Crohn's Disease and 25 subjects with Ulcerative Colitis) who are 2 to 22 years of age will be enrolled in the trial over 3 years. The fecal donors, preferably a parent or sibling, will be extensively screened for infectious diseases prior to providing stool for the transplant. Patients who are failing primary therapy, are in a flare, and require restaging of their IBD by an endoscopy and colonoscopy will be approached for the study. Standard of care endoscopy and colonoscopy will be performed on each subject and 2 additional biopsies will be taken for analysis. Microbiota analysis will also be performed on both the donor and recipient stool sample prior to transplantation, and on the recipient sample at 1 week, 1 month, and 6 months post transplantation. The primary objective will be to study the safety of FMT in all enrolled subjects. The study will also correlate efficacy and patient outcomes with the fecal microbiome prior to, and after FMT. The secondary objectives are to examine the efficacy of FMT in the treatment of children with IBD using the Pediatric Ulcerative Colitis Activity Index (PUCAI) and the Pediatric Crohn Disease Activity Index (PCDAI) analysis. Correlate the patient outcomes with the fecal microbiome prior to, and after FMT.
Beverage containing a blend of sweeteners based on mogroside V and stevia rebaudioside M. Same aspect and flavour than the control beverage. About 1/4 of participants will start with this beverage first.