anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Genetic variants in relevant genes coexisting with MRI lesions in children with drug-resistant epilepsy (DRE) can negatively influence epilepsy surgery outcomes. Still, presurgical evaluation does not include genetic diagnostics routinely. Here, we report our presurgical evaluation algorithm that includes routine genetic testing. We analyzed retrospectively the data of 68 children with DRE operated at a mean age of 7.8 years (IQR: 8.1 years) at our center. In 49 children, genetic test results were available. We identified 21 gene variants (ACMG III: n = 7, ACMG IV: n = 2, ACMG V: n = 12) in 19 patients (45.2%) in the genes TSC1, TSC2, MECP2, DEPDC5, HUWE1, GRIN1, ASH1I, TRIO, KIF5C, CDON, ANKD11, TGFBR2, ATN1, COL4A1, JAK2, KCNQ2, ATP1A2, and GLI3 by whole-exome sequencing as well as deletions and duplications by array CGH in six patients. While the results did not change the surgery indication, they supported counseling with respect to postoperative chance of seizure freedom and weaning of antiseizure medication (ASM). The presence of genetic findings leads to the postoperative retention of at least one ASM. In our cohort, the International League against Epilepsy (ILAE) seizure outcome did not differ between patients with and without abnormal genetic findings. However, in the 7/68 patients with an unsatisfactory ILAE seizure outcome IV or V 12 months postsurgery, 2 had an abnormal or suspicious genetic finding as a putative explanation for persisting seizures postsurgery, and 3 had received palliative surgery including one TSC patient. This study highlights the importance of genetic testing in children with DRE to address putative underlying germline variants as genetic epilepsy causes or predisposing factors that guide patient and/or parent counseling on a case-by-case with respect to their individual chance of postoperative seizure freedom and ASM weaning. PLAIN LANGUAGE SUMMARY: Genetic variants in children with drug-resistant epilepsy (DRE) can negatively influence epilepsy surgery outcomes. However, presurgical evaluation does not include genetic diagnostics routinely. This retrospective study analyzed the genetic testing results of the 68 pediatric patients who received epilepsy surgery in our center. We identified 21 gene variants by whole-exome sequencing as well as deletions and duplications by array CGH in 6 patients. These results highlight the importance of genetic testing in children with DRE to guide patient and/or parent counseling on a case-by-case with respect to their individual chance of postoperative seizure freedom and ASM weaning.
A wrapper includes a patch and a packaging film. The patch includes a support and a sealing layer including chlorite ions. The support is permeable to chlorine dioxide. The packaging film has an inner surface defining at least a portion of an interior space of a package for positioning the articles. The packaging film is substantially impermeable to chlorine dioxide and is transparent to ultraviolet light. The patch is secured to the interior surface of the packaging film by the sealing layer. Chlorine dioxide can be generated by the following process: the wrapper is subjected to Ultraviolet (UV) light such that the UV light reaches the sealing layer of the patch to convert the chlorite ion to chlorine dioxide.
Beginning in February 2003, there was an outbreak with a novel coronavirus causing an atypical pneumonia, subsequently referred to as Severe Acute Respiratory Syndrome (SARS). This syndrome is associated with a high mortality rate and has no proven treatment. There is, however, some evidence that treatment with convalescent plasma was beneficial.

The primary purpose of this protocol is to collect plasma by apheresis from patients that recovered from SARS, and process this plasma into a high titer anti-SARS intravenous immune globulin (IVIG). This will be a collaboration between the National Institute of Allergy and Infectious Diseases and the Chinese University of Hong Kong. Cangene Corporation has been contracted to manufacture the collected plasma in the United States (U.S.) into an IVIG product, which can then be used for pre-clinical efficacy studies under an IND in a clinical trial if SARS recurs. It is intended that the treatment trial would be conducted in Hong Kong and/or the U.S., as well as any other place the disease recurs.
FIELD: medicine. SUBSTANCE: the suggested medicinal form includes a nucleus containing one or more active substances and surrounded by a membrane. The release of active substance out of a nucleus is caused by membrane rupture after a certain lag period. The nucleus includes one or more carriers at immediate release and has no tendencies for considerable swelling at the impact of gastrointestinal liquids. The suggested medicinal form could be used to deliver active substances if a certain lag period is necessary before release, for example, in case of antiasthmatic, cardiotonic, vasodilative, antiulcerous preparations. It is, also, possible to use the suggested medicinal form to deliver biologically active compounds, such as proteins, peptides, enzymes, vaccines and oligonucleotides. This product provides complete release of active substance at no considerable leakage during the lag period. The latter is reliably reproduced. EFFECT: more simplified and cheaper method. 19 cl, 19 dwg, 20 ex, 38 tbl
FIELD: hygiene.SUBSTANCE: group of inventions relates to oral care. Oral care composition contains an effective amount of the basic amino acid in the free or salt form - arginine in amount of 3 wt. % to 10 wt. %, basic amino acid weight is calculated on free base form; effective amount of mixture containing 1 wt. % zinc oxide and 0.5 wt. % of zinc citrate in terms of weight of composition for oral care; benzyl alcohol in amount of 0.6 wt. % to 0.9 wt. % in terms of weight of the oral care composition; tetrasodium pyrophosphate in amount of 0.5 wt. % and sodium carboxymethyl cellulose in amount of 0.6 wt. % in terms of weight of the composition for oral care. Also disclosed is a method for improving the health of the oral cavity.EFFECT: group of inventions provides the antibacterial effectiveness of the oral care composition.9 cl, 2 tbl, 3 ex
Valsartan – Hydrochlorothiazide: In the controlled trials of various doses of valsartan and hydrochlorothiazide tablets the incidence of hypertensive patients who developed hypokalemia (serum potassium <3.5 mEq/L) was 3.0%; the incidence of hyperkalemia (serum potassium >5.7 mEq/L) was 0.4%.  
Hydrochlorothiazide can cause hypokalemia and hyponatremia. Hypomagnesemia can result in hypokalemia which appears difficult to treat despite potassium repletion. Drugs that inhibit the renin-angiotensin system can cause hyperkalemia. Monitor serum electrolytes periodically.   
  
If hypokalemia is accompanied by clinical signs (e.g. muscular weakness, paresis, or ECG alterations), valsartan and hydrochlorothiazide tablets should be discontinued. Correction of hypokalemia and any coexisting hypomagnesemia is recommended prior to the initiation of thiazides. 

Some patients with heart failure have developed increases in potassium with valsartan therapy. These effects are usually minor and transient, and they are more likely to occur in patients with pre-existing renal impairment. Dosage reduction and/or discontinuation of the diuretic and/or valsartan may be required [see Adverse Reactions (6.1)].
Hair grooming gel compositions comprise (1) a major proportion of water or a mixture of at least one C1-C4 alkanol and water (2) a minor proportion of a hydrolysed and at least partially neutralized copolymer of a C2-C4 olefin and maleic anhydride and (3) a minor proportion of at least one compound selected from esters of C1-C6 monhydric alcohols and C12-C18 fatty acids, aliphatic polyoxyalkylene compounds of the formula R(OCn H2n)x OR1 wherein R and R1 are hydrogen or aliphatic hydrocarbon radicals of up to 6 carbon atoms, n is an average number of from 2 to 6 and x, the total number of axyalkylene groups, is such as to give a product of average molecular weight of at least 300, and poly-oxyalkylene adducts of C3-C6 alkane triols having a molecular weight in the range of 300 to 5,000 and an average hydroxyl number of 30 to 400. The copolymer component (2) is preferably cross-linked, e.g. by incorporating a compound such as vinyl crotonate into the copolymer or after treating the copolymer with a difunctional compound such as a glycol or diamine; neutralization of the hydrolysed copolymer can be effected with alkalis or organic amines, the preferred compounds being 2-amino-2-methyl-1-propanol, diisopropanol-amine and triethanolamine. Optional ingredients include plasticizers, e.g. glycerine, hexylene glycol, propylene glycol, ethylhexane diols, dimethyl and diethyl phthalates and ethoxycarbonyl methyl, methyl phthalate, perfumes, colourants, and germicidal compounds, e.g. hexachlorophene and stearyl dimethyl benzyl ammonium chloride.
This study clarifies the effects of head elevation on cerebral oxygenation in patients with acute cerebral infarction. We included 76 patients with anterior circulation cerebral infarction admitted to the stroke care unit within 7 days of symptom onset. Using near-infrared spectroscopy (NIRS), we measured regional saturation oxygen (rSO2), oxygenated haemoglobin (O2Hb), deoxygenated haemoglobin (HHb), and total haemoglobin (THb) in both the affected hemisphere (AH) and unaffected hemisphere (UH) after raising the head to 0°, 30°, and 60° for 1 minute each. The mean arterial pressure (MAP) was measured non-invasively at each position. Our result demonstrated a significant decrease in O2Hb as the head elevation angle (HEA) increased, with no observable interaction between the AH and UH. A significant decrease in rSO2 interaction was observed. In contrast, the HHb and THb levels changed significantly as the HEA increased, although no interactions were identified. No significant correlations existed between the observed changes in O2Hb, HHb, THb, or rSO2 and changes in MAP at each HEA.
No dosage adjustment of VEMLIDY is required in patients with mild, moderate, or severe renal impairment, or in patients with ESRD (estimated creatinine clearance below 15 mL per minute) who are receiving chronic hemodialysis. On days of hemodialysis, administer VEMLIDY after completion of hemodialysis treatment [see Dosage and Administration (2.3)]. 

The safety and efficacy of VEMLIDY in HBV-infected adult subjects with moderate to severe renal impairment (estimated creatinine clearance between 15 and 59 mL per minute by Cockcroft-Gault method) and ESRD (estimated creatinine clearance of less than 15 mL per minute by Cockcroft-Gault method) receiving chronic hemodialysis were evaluated in 78 and 15 subjects, respectively, in an open-label trial (Trial 4035, Part A). Overall, 98% of subjects achieved HBV DNA <20 IU/mL at Week 24 (Cohort 1, 97%; Cohort 2, 100%) and the safety of VEMLIDY was similar to that observed in clinical trials of VEMLIDY in subjects with compensated liver disease but without renal impairment [see Adverse Reactions (6.1) and Clinical Studies (14.4)].

The safety and efficacy of elvitegravir/cobicistat/emtricitabine/tenofovir alafenamide 150/150/200/10 mg was previously evaluated in 55 virologically suppressed HIV-1 infected subjects with ESRD receiving chronic hemodialysis in an open-label trial (Trial 1825). Tenofovir alafenamide exposures are similar when comparing tenofovir alafenamide 25 mg and tenofovir alafenamide 10 mg as part of elvitegravir/cobicistat/emtricitabine/tenofovir alafenamide.

Among subjects with ESRD receiving chronic hemodialysis and administered tenofovir alafenamide, higher exposures of tenofovir were observed in HBV-infected subjects (Trial 4035 Part A) compared to HIV-infected subjects (Trial 1825). The clinical significance of these higher exposures is not established [see Clinical Pharmacology (12.3)].

VEMLIDY is not recommended in patients with ESRD (estimated creatinine clearance below 15 mL per minute by Cockcroft-Gault method) who are not receiving chronic hemodialysis as the safety of VEMLIDY has not been established in this population [see Dosage and Administration (2.3) and Clinical Pharmacology (12.3)].
A composition comprising a novel flavonoid compound is provided to show cytotoxic effect on cancer cells, thereby being used for treating cancer. And a method for synthesizing the flavonoid compound is provided to shorten a manufacturing time through a total synthesis or a semi-synthesis. A pharmaceutical composition comprises a flavonoid compound represented by a formula(1), (2) or (3). In the formulae, B is 4-oxo-cyclohexa-2,5-dienyl group; and each R1 to R12 is independently H, OH, C1-20 alkyl, C1-20 ether, C1-20 ester, carboxy, halogen or sugar. A method for synthesizing the flavonoid compound comprises the steps of: (a) mixing acetophenone including a first protecting group with benzaldehyde including a second protecting group to generate a first compound through Claisen-Schmidt condensation reaction; (b) reacting the first compound with a first catalyst to generate a second compound; (c) removing the second protecting group from the second compound to generate a third compound; (d) reacting the third compound, a second catalyst and an iodobenzene compound to generate a fourth compound; and (e) adding an acid to the fourth compound to remove the first protecting group therefrom, thereby generating the flavonoid compound. Further, the flavonoid compound is produced by one of total synthesis method or semi-synthesis method.
### Preparation of Solution

Reconstitute Cathflo Activase to a final concentration of 1 mg/mL:

  1. Aseptically withdraw 2.2 mL of Sterile Water for Injection, USP (diluent is not provided). Do not use Bacteriostatic Water for Injection.
  2. Inject the 2.2 mL of Sterile Water for Injection, USP, into the Cathflo Activase vial, directing the diluent stream into the powder. Slight foaming is not unusual; let the vial stand undisturbed to allow large bubbles to dissipate.
  3. Mix by gently swirling until the contents are completely dissolved. Complete dissolution should occur within 3 minutes. DO NOT SHAKE. The reconstituted preparation results in a colorless to pale yellow transparent solution containing 1 mg/mL Cathflo Activase at a pH of approximately 7.3.
  4. Cathflo Activase contains no antibacterial preservatives and should be reconstituted immediately before use. The solution may be used for intracatheter instillation within 8 hours following reconstitution when stored at 2–30°C (36–86°F).



No other medication should be added to solutions containing Cathflo Activase.

### Instillation of Solution into the Catheter

  1. Inspect the product prior to administration for foreign matter and discoloration.
  2. Withdraw 2 mL (2 mg) of solution from the reconstituted vial.
  3. Instill the appropriate dose of Cathflo Activase (see DOSAGE AND ADMINISTRATION) into the occluded catheter.
  4. After 30 minutes of dwell time, assess catheter function by attempting to aspirate blood. If the catheter is functional, go to Step 7. If the catheter is not functional, go to Step 5.
  5. After 120 minutes of dwell time, assess catheter function by attempting to aspirate blood and catheter contents. If the catheter is functional, go to Step 7. If the catheter is not functional, go to Step 6.
  6. If catheter function is not restored after one dose of Cathflo Activase, a second dose of equal amount may be instilled. Repeat the procedure beginning with Step 1 under Preparation of Solution.
  7. If catheter function has been restored, aspirate 4–5 mL of blood in patients ≥10 kg or 3 mL in patients <10 kg to remove Cathflo Activase and residual clot, and gently irrigate the catheter with 0.9% Sodium Chloride Injection, USP.



Any unused solution should be discarded.
Anifrolumab will be administered via controlled IV infusion pump into a peripheral vein over a minimum of 30 minutes Q4W from Week 0 to Week 48. Each dose must be at least 14 days apart.
The present application is directed to a method of inhibiting HDAC in the brain of a mammal. The method comprises administering to a mammal a HDAC  inhibiting amount of a histone deacetylase inhibitor compound. The present application is further directed to a method of treating diseases of the central nervous system (CNS) comprising administering to a individual in need of treatment a therapeutically effective amount of an inhibitor of HDAC. In particular embodiments, the CNS disease is a neurodegenerative disease. In further embodiments, the neurogenerative disease is an inherited neurodegenerative disease, such as those inherited neurodegenerative diseases which are polyglutamine expansion diseases. In other embodiments, the disorder is cancer of the brain. The individual is a mammal, such as a primate or human.
The microcapsules of the invention are comprised of crystallizable polymers which are preferably side-chain crystallizable polymers or cross-linked, side-chain crystallizable polymers having a specific first order transition point or "melt" temperature. The polymers are caused to form microcapsules and thereby encapsulate one or more compounds generally referred to herein as an active ingredient such as a herbicide, insecticide, fungicide, or fertilizer. The polymer of the microcapsule surrounds the active ingredient separating it from the outside environment. Crystallizable polymers used herein have temperature-dependent permeabilities with respect to a given component such that this component is kept out of contact with the active ingredient at a temperature below a given first order transition point and (due to increased permeability) is allowed to contact the active ingredient at a temperature at or above the transition point. The permeability of the polymer is not only temperature-dependent but reversible. The microcapsules are less than 200 microns in median diameter, more generally less than 100 microns in median diameter and preferably less than 50 microns in median diameter. By varying the polymer and reactants used in the formation of the microcapsules, the release rate and timing of the release of active ingredient from the microcapsule can be temperature controlled to obtain the various objects, advantages and features of the present invention.
PURPOSE:The titled enhancer containing cysteine and/or proline as an essential component. CONSTITUTION:An enhancer for poor appetite action containing cysteine and/or proline, preferably obtained by blending both the components in a ratio of 1:1. The enhancer increases poor appetite action of leukocyte and is especially effective for treating bronchial asthma of adult. The cysteine and proline may be purified cysteine and proline obtained by hydrolysis, amino acid fermentation or synthesis of various proteins or crude cysteine and protein containing these amino. Further a purified substance of aloe essence by dialysis is usable because other aloe active ingredients exist. Aloe perryi Baker, A. arbolescens Mill. var natalensis Berger, A. barbadensis Miller, etc., may be used as the aloe. An internal medicine such as tablet, pill, troche, buccal, etc., injection, enema agent, suppository, percutaneous absorption agent, etc., may be cited as the dosage form.
Fluoride, a global environmental pollutant, is ubiquitous in aquatic environments and coexists with selenium, which can cause complex effects on exposed organisms. However, data on the interaction of fluoride and selenium remain scarce. In this study, female zebrafish (Danio rerio) were exposed to fluoride (80 mg/L sodium fluoride) and/or dietary selenomethionine (Se-Met) for 30, 60 and 90 days, the effects on the liver of zebrafish were investigated. The results indicated that an increase in fluoride burden, inhibited growth and impaired liver morphology were recorded after fluoride exposure. Furthermore, fluoride alone caused oxidative stress and inflammation in the liver, as reflected by the increase in ROS and MDA contents, the reduction of anti-oxidative enzymes, the altered immune related enzymes (ACP, AKP, LZM and MPO) and the expression of IL-6, IL-1β, TNF-α, IL-10 and TGF-β. In contrast, co-exposure to fluoride and Se-Met decreased fluoride burden and restored growth. Furthermore, dietary Se-Met alleviated oxidative stress, inflammation and impaired morphology in liver trigger by fluoride. However, dietary Se-Met alone increased the activities of SOD and CAT. These results demonstrate that the protective effect of dietary Se-Met against chronic fluoride toxicity at a certain level.
The invention discloses a preparation method of temperature-sensitive controlled-release Fe3O4/PD-L1 monoclonal antibody-modified nanoparticles, belonging to the technical field of targeted nanomaterials. Thermosensitive phospholipid is used as the skeleton, coated with Fe3O4, and chemically coupled with MnO2, folic acid, glucose oxidase and PD-L1 monoclonal antibody. The nanoparticles prepared by the invention improve the stability and coupling rate of materials, reduce the toxic and side effects of nano-drugs on the body, and reduce the consumption of PD-L1. Temperature-sensitive materials are used to realize the slow-release effect of tumor, and the active targeting characteristics of folic acid improve the tumor aggregation of nano-materials. Glucose oxidase consumes glucose and produces H2O2 at the same time, the raw material of Fenton reaction. H2O2 serves as a raw material for synergistic induction of tumor ferroptosis reaction by Fe3O4 and MnO2, improving the anti-tumor effect. PD-L1 relieves the inhibitory effect on T lymphocytes through competitive inhibition.
Melanoma, the most perilous form of skin cancer, is known for its inherent resistance to chemotherapy. Even with advances in tumor immunotherapy, the survival of patients with advanced or recurrent melanomas remains poor. Over time, melanoma tumor cells may produce excessive angiogenic factors, necessitating the use of combinations of angiogenesis inhibitors, including broad-spectrum options, to combat melanoma. Among these inhibitors, Endostatin is one of the most broad-spectrum and least toxic angiogenesis inhibitors. We found Endostatin significantly increased the infiltration of CD8+ T cells and reduced the infiltration of M2 tumor-associated macrophages (TAMs) in the melanoma tumor microenvironment (TME). Interestingly, we also observed high expression levels of programmed death 1 (PD-1), an essential immune checkpoint molecule associated with tumor immune evasion, within the melanoma tumor microenvironment despite the use of Endostatin. To address this issue, we investigated the effects of a plasmid expressing Endostatin and PD-1 siRNA, wherein Endostatin was overexpressed while RNA interference (RNAi) targeted PD-1. These therapeutic agents were delivered using attenuated Salmonella in melanoma-bearing mice. Our results demonstrate that pEndostatin-siRNA-PD-1 therapy exhibits optimal therapeutic efficacy against melanoma. We found that pEndostatin-siRNA-PD-1 therapy promotes the infiltration of CD8+ T cells and the expression of granzyme B in melanoma tumors. Importantly, combined inhibition of angiogenesis and PD-1 significantly suppresses melanoma tumor progression compared with the inhibition of angiogenesis or PD-1 alone. Based on these findings, our study suggests that combining PD-1 inhibition with angiogenesis inhibitors holds promise as a clinical strategy for the treatment of melanoma.
Experimental group (n=30 surgeries) - the participants will receive the FBM, 1 hour before the surgical procedure, plus a placebo tablet, with the same physical and organoleptic characteristics, composed of corn starch, without harmful effects on health and simulating Dexamethasone (Celsius Laboratory, Montevideo, Uruguay).).