anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
For continued reduction of the heart rate (up to 24 hours) in patients with atrial fibrillation or atrial flutter, an intravenous infusion of diltiazem hydrochloride injection or diltiazem hydrochloride for injection may be administered. (For reconstitution of diltiazem hydrochloride for injection, see instructions contained within packaging.) Immediately following bolus administration of 20 mg (0.25 mg/kg) or 25 mg (0.35 mg/kg) diltiazem hydrochloride injection and reduction of heart rate, begin an intravenous infusion of diltiazem hydrochloride injection or diltiazem hydrochloride for injection. The recommended initial infusion rate of diltiazem hydrochloride injection or diltiazem hydrochloride for injection is 10 mg/h. Some patients may maintain response to an initial rate of 5 mg/h. The infusion rate may be increased in 5 mg/h increments up to 15 mg/h as needed, if further reduction in heart rate is required. The infusion may be maintained for up to 24 hours.

Diltiazem shows dose-dependent, non-linear pharmacokinetics. Duration of infusion longer than 24 hours and infusion rates greater than 15 mg/h have not been studied. Therefore, infusion duration exceeding 24 hours and infusion rates exceeding 15 mg/h are not recommended.

###  Dilution

To prepare diltiazem hydrochloride injection for continuous intravenous infusion, aseptically transfer the appropriate quantity (see chart) of diltiazem hydrochloride to the desired volume of either Normal Saline, D5W, or D5W/0.45% NaCl. Mix thoroughly. Keep diluted diltiazem hydrochloride injection refrigerated until use. Use within 24 hours.

To prepare diltiazem hydrochloride for injection for continuous intravenous infusion, assemble the ADD-Vantage vial as directed for use with either 0.9% Sodium Chloride or Dextrose (5%) injection. Mix thoroughly. Keep diluted diltiazem hydrochloride for injection at controlled room temperature 15° to 30°C (59° to 86°F) [See USP] or refrigerated 2° to 8°C (36° to 46°F) until use. Use within 24 hours.
Recent exercise interventions have demonstrated statistically significant short-term improvements in muscle strength, fitness, and physical activity in people under the age of 70. This study seeks to determine if those same benefits can be achieved in an older population (mean age 84) with osteoarthritis of the hip or knee. The study will examine the long-term effects of a structured exercise program that seeks to promote adherence to continued exercise.

We will randomly assign people who meet the study criteria to the exercise intervention or control group. We will conduct measures at baseline, at 8 weeks, and at 3-month intervals for 2 years following the intervention. The exercise component of the intervention will include lower extremity muscle strengthening, range-of-motion exercises, and fitness walking. An educational component will focus on arthritis self-efficacy and perceived self-reported exercise efficacy. We hypothesize that treatment group participants will exhibit higher rates of adherence to exercise and higher functional status outcomes over time compared to controls.
* Patients should be instructed to take Ropinirole Extended-release Tablets only as prescribed. If a dose is missed, patients should be advised not to double their next dose. 
  * Ropinirole Extended-release Tablets can be taken with or without food. Taking Ropinirole Extended-release Tablets with food may reduce the occurrence of nausea [see Dosage and Administration (2.1)]. 
  * Ropinirole Extended-release Tablets should be swallowed whole. They should not be chewed, crushed, or divided [see Dosage and Administration (2.1)]. 
  * Ropinirole is the active ingredient that is in both Ropinirole Extended-release Tablets and ropinirole tablets (the immediate-release formulation). Ask your patient if they are taking another medication containing ropinirole.
For manufacturing a solid administration form (2) comprising at least one active pharmaceutical ingredient, wherein a flowable but setting composite material comprising the at least one active pharmaceutical ingredient is added together and set to generate the solid administration form (2), the flowable composite material is liquefied and delivered to a discharge unit (3). Small portions (12) of the liquefied composite material are intermittently discharged through an outlet of the discharge unit (3) into a setting unit(13) where the setting of the small portions (12) occurs. The flowable composite material comprises a polymer and at least one active pharmaceutical ingredient that is dispersed or dissolved within the polymer. The flowable composite material is fabricated during delivery to the discharge unit (3). The small portions(12) of the liquefied composite material are droplets and that the solid administration form (2) is generated by adding droplets that stick together before or during the setting of the liquefiedcomposite material. An average diameter of the droplets can be less than 350 µm, preferably less than 200 µm. There can be a void space between at least some small portions (12) that are placed adjacent to each other, resulting in a porous structure of the solid administration form (2).
A method and composition are presented for enhancing the dissolution and bioavailable properties of CoQ10 nutritional supplements and/or therapeutic agents for a human being and other mammals. The method includes preparing an anhydrous self~microemulsifying base composition by combining: CoQ10, a water-immiscible, and a non-ionic surfactant, containing polyethylene glycol. For an orally administered CoQ10 nutritional supplement in a capsule formulation, a unit dosage from the composition is added to a dissolvable capsule, preferably a soft gelatin capsule, in order to form the nutritional supplement. When a capsule containing the self-microemulsifying composition enters the digestive tract, the temperature of the body's digestive juices warms the composition, causing any of the CoQ10 that may have re-crystallized out of the composition to become re-dissolved into the composition before the capsule dissolves. The re-dissolution of CoQ10 is bioavailable when the capsule dissolves. Upon dissolution of the capsule, the self-microemulsifying composition comes into contact with the digestive juices and naturally forms micellar-type bioavaible microemulsions, consisting of micelles containing CoQ10. In addition to the capsule formulation, the invention includes parenteral, liquid, topical and ophthalmic formulations.
PURPOSE: A Lactobacillus plantarum DSR J1-8(deposit number: KCCM11141P) for preventing and treating metabolic syndrome is provided to suppress alpha-glucosidase activity and to enhance acid and salt tolerance, thermal resistance, and antibiotics resistance. CONSTITUTION: A Lactobacillus plantarum DSR J1-8(deposit number: KCCM11141P) has an activity of suppressing alpha-glucosidase and alpha-amylase. A pharmaceutical composition for preventing and treating metabolic syndrome contains the strain or culture thereof. A probiotic composition contains the strain or culture thereof. A feed composition contains the strain or culture thereof. A food additive composition contains the strain or culture thereof.
<P>PROBLEM TO BE SOLVED: To provide a method for early detection regardless of primary or secondary nephritis and a method to get diagnostic information of renal functions.  <P>SOLUTION: An antibody is consists of an anti-NC1 monoclonal antibody performing an immune reaction with NC1 in human and/or animal renal glomeruli, can immunostain a renal biopsy specimen of a patient by dilution of anti-NC1 monoclonal antibody with a suitable buffer and can detect the NC1 existing in serum and urine as specimens by an antigen-antibody reaction. Furthermore, the method purifies the serum of patients with retinitis by a method removing the anti-NC1 antibody in the serum using NC1 in the serum with the anti-NC1 antibody and/or purified NC1 with the anti-NC1 antibody. In addition, a kidney derived type IV collagen is purified using the anti-NC1 antibody and a specific anti-kidney derived type IV collagen antibody is prepared using this as an antigen. This anti-kidney derived type IV collagen antibody can detect the kidney derived type IV collagen by the antigen-antibody reaction in urine and serum.  <P>COPYRIGHT: (C)2010,JPO&INPIT
OBJECTIVE: To identify and characterize groups of pregnant women with type 2 diabetes with distinct hemoglobin A1c (HbA1c) trajectories across gestation and to examine the association with adverse obstetric and perinatal outcomes.
RESEARCH DESIGN AND METHODS: This was a retrospective Danish national cohort study including all singleton pregnancies in women with type 2 diabetes, giving birth to a liveborn infant, between 2004 and 2019. HbA1c trajectories were identified using latent class linear mixed-model analysis. Associations with adverse outcomes were examined with logistic regression models.
RESULTS: A total of 1,129 pregnancies were included. Three HbA1c trajectory groups were identified and named according to the glycemic control in early pregnancy (good, 59%; moderate, 32%; and poor, 9%). According to the model, all groups attained an estimated HbA1c <6.5% (48 mmol/mol) during pregnancy, with no differences between groups in the 3rd trimester. Women with poor glycemic control in early pregnancy had lower odds of having an infant with large-for-gestational-age (LGA) birth weight (adjusted odds ratio [aOR] 0.57, 95% CI 0.40-0.83), and higher odds of having an infant with small-for-gestational age (SGA) birth weight (aOR 2.49, 95% CI 2.00-3.10) and congenital malformation (CM) (aOR 4.60 95% CI 3.39-6.26) compared with women with good glycemic control. There was no evidence of a difference in odds of preeclampsia, preterm birth, and caesarean section between groups.
CONCLUSIONS: Women with poor glycemic control in early pregnancy have lower odds of having an infant with LGA birth weight, but higher odds of having an infant with SGA birth weight and CM.
An antiperspirant composition which is essentially free from aluminium-, zirconium- and zinc-based astringents, comprises (i) a film forming polymer; (ii) a plant-derived astringent; and (iii) a cosmetically acceptable carrier for the film forming polymer and plant-derived astringent. Preferably the film forming polymer is comprised of methylvinyl ether and maleic acid residues and is preferably cross-linked where the cross-links are provided by 1,9-decadiene residues. The astringent is derived from plants, preferably selected from at least one of the species Equisetum arvense, Hamamelis Virginia, Quercus infectoria and Salvia officinalis. The astringent is preferably present at a level of 0.001 to 20.00 wt% based on the total weight of the composition and the film forming polymer is preferably present at a level of 0.01 to 5 wt% based on the total weight of the composition. The antiperspirant composition may further comprise a particulate absorbent material preferably formed of a naturally occurring plant material selected from at least one of the species Oryza sativa and Bambusa arundinacease. The composition may also include a deodourant such as triethyl citrate.
Patients will undergo Reduced Intensity Conditioning (RIC) consisting of rabbit antithymocyte globulin (rATG), Fludarabine, Melphalan, and Thiotepa. All agents are administered intravenously. rATG is administered from days -9 to -7. Fludarabine is administered from day -8 to day -5, followed by Thiotepa on day -4 and Melphalan on days -3 and -2. On Day 0, patients will undergo infusion of the ex vivo TCRαβ/CD19+ depleted haploidentical HPC graft. On Day +7, patients will undergo infusion of the memory-like NK (ML NK) cells, followed by IL-2 subcutaneously starting 4 hours after the ML NK infusion. IL-2 will continue every other day through Day +19 for a maximum of 7 doses.
During the Run-in Placebo Period, each participant received 1 placebo capsule orally BID for 1 week. Then during the Double-blind Treatment Period, each participant received one 0.1-milligrams (mg) ADL5945 capsule orally BID for 4 weeks. Then during the Run-out Placebo Period, each participant received 1 placebo capsule orally BID for 1 week.
The cognitive strategy training intervention consists of 6 weekly \~1 hour sessions. It is delivered in an individual, face-to-face format in the client's home. It is a behavioral intervention that teaches people metacognitive, problem-solving and other compensatory strategies to address self-identified cognitive performance problems, and it uses practice and homework to promote strategy learning, retention and transfer.
The clinical value of magnetic resonance angiography (MRA), transcranial Doppler ultrasound (TCD) and electroencephalogram (EEG) in the diagnosis of intracranial artery stenosis in ischemic cerebrovascular disease (ICVD) was explored. The clinical data of TCD, MRA and EEG in 98 patients with ICVD were retrospectively analyzed. The clinical value of TCD, MRA combined with EEG in the diagnosis of intracranial artery stenosis in ICVD was analyzed based on the results of digital subtraction angiography (DSA) as the gold standard. A total of 98 patients were diagnosed with 27 cases of normal intracranial artery, 32 cases of mild stenosis, 25 cases of moderate stenosis, and 14 cases of severe stenosis DSA examination. TCD was detected in 23 cases of normal, 25 cases of mild stenosis, 23 cases of moderate stenosis and 13 cases of severe stenosis. MRA showed 24 cases of normal, 28 cases of mild stenosis, 21 cases of moderate stenosis and 12 cases of severe stenosis. EEG examination detected that there were 25 cases of normal, 24 cases of mild stenosis, 22 cases of moderate stenosis, and 14 cases of severe stenosis. Sensitivity, accuracy and negative predictive value had significant differences between combined diagnosis and single diagnosis. The combined detection of TCD, MRA and EEG is consistent with DSA detection in the diagnosis of ICVD intracranial artery stenosis.
Patients in the intervention group will do high intensity interval training (HIIT) in water. In this study, HIIT training will be short intervals (30 seconds) of movements and 15 seconds of rest.Exercises will be done in a floating position in the deep part. The intervention will be done 3 sessions weekly. The length will be 8 weeks.
The small bowel makes a hormone called glucose-dependent insulinotropic peptide (GIP). It is released into the blood stream and goes to the pancreas. It works there with nutrients, especially glucose, in the digested food so that insulin is released in sufficient amounts from the pancreas. The insulin causes the nutrients from the food to be stored in the liver, fat and muscle until they are needed to provide energy. GIP also slows emptying of food from the stomach, which decreases the rate with which fats in food are broken down and stored. Once it is released into the blood, GIP is quickly broken down and becomes inactive. Individuals with type 2 diabetes do not make enough GIP and pharmacological doses of naturally occurring GIP do not increase insulin secretion in patients with type 2 diabetes. This study is testing a modified GIP (it had one amino acid difference from naturally occurring human GIP) that is not broken down as quickly in individuals with type 2 diabetes, to determine if it will improve insulin secretion, after eating, in patients with type 2 diabetes. The study will also compare its effects to that of naturally occurring, human GIP. Both human GIP and the modified GIP (GIP analog) are manufactured by peptide synthesis techniques (not extracted from human gut and not recombinant technology).

A screening visit will be performed including blood work, EKG and physical exam. If eligible, patients would be scheduled for three infusion visits 2 months apart, where they will receive a normal saline infusion on the first visit and GIP or GIP analog on the remaining visits. The infusion visits will begin approximately 6:45 a.m. and patients will have frequent blood sampling through an intravenous line over a period of 7 hours. An additional intravenous line will be placed for the infusion of either the normal saline, GIP or GIP analog over a period of 3 hours. Patients will be given a breakfast meal consisting of 550 calories (one egg, piece of toast with margarine, corn flakes 2% milk and a banana). They will be given 2 Extra-Strength Tylenol to determine time frame that food is emptied from stomach by measuring Tylenol levels in the blood. At the end of each study visit, patients will be given lunch, intravenous lines will be discontinued and they will be discharged to home.
Isoproterenol (ISO) administration is a well-established model for inducing myocardial injury, replicating key features of human myocardial infarction (MI). The ensuing inflammatory response plays a pivotal role in the progression of adverse cardiac remodeling, characterized by myocardial dysfunction, fibrosis, and hypertrophy. The Mst1/Hippo signaling pathway, a critical regulator of cellular processes, has emerged as a potential therapeutic target in cardiovascular diseases. This study investigates the role of Mst1 in ISO-induced myocardial injury and explores its underlying mechanisms. Our findings demonstrate that Mst1 ablation in cardiomyocytes attenuates ISO-induced cardiac dysfunction, preserving cardiomyocyte viability and function. Mechanistically, Mst1 deletion inhibits cardiomyocyte apoptosis, oxidative stress, and calcium overload, key contributors to myocardial injury. Furthermore, Mst1 ablation mitigates endoplasmic reticulum (ER) stress and mitochondrial fission, both of which are implicated in ISO-mediated cardiac damage. Additionally, Mst1 plays a crucial role in modulating the inflammatory response following ISO treatment, as its deletion suppresses pro-inflammatory cytokine expression and neutrophil infiltration. To further investigate the molecular mechanisms underlying ISO-induced myocardial injury, we conducted a bioinformatics analysis using the GSE207581 dataset. GO and KEGG pathway enrichment analyses revealed significant enrichment of genes associated with DNA damage response, DNA repair, protein ubiquitination, chromatin organization, autophagy, cell cycle, mTOR signaling, FoxO signaling, ubiquitin-mediated proteolysis, and nucleocytoplasmic transport. These findings underscore the significance of Mst1 in ISO-induced myocardial injury and highlight its potential as a therapeutic target for mitigating adverse cardiac remodeling. Further investigation into the intricate mechanisms of Mst1 signaling may pave the way for novel therapeutic interventions for myocardial infarction and heart failure.
BACKGROUND Hepatic portal venous gas (HPVG) is a rare radiologic finding mostly associated with life-threatening diseases like bowel necrosis, but can also be benign; its overall mortality rate is 39-75%. In rare cases HPVG is associated with endoscopic procedures such as percutaneous endoscopic gastrostomy (PEG) placement. However, due to the rarity of this condition, there is no recommendation about its management. The aim of this case report was to describe a successful conservative management of HPVG without antibiotic administration based on the clinical presentation. CASE REPORT A 78-year-old male patient known for a history of esophageal cancer treated with radio- and chemotherapy, complicated by a post-radiation esophageal stenosis requiring a PEG tube placement 1 month prior was admitted to our Emergency Department for vomiting and abdominal pain. A contrast-enhanced abdominal CT scan showed small-bowel dilatation without obstruction, as well as gastric wall pneumatosis and HPVG. We opted for a conservative approach. The PEG was put to suction for 2 days. The clinical evolution was favorable, with resolution of abdominal pain and a restored transit on day 2. A follow-up CT scan at day 5 showed resolution of HPVG. Nutrition through the PEG was restored at day 6 without complication. CONCLUSIONS HPVG can be a benign finding after a PEG tube placement. Conservative management without antibiotics can be used in oligosymptomatic and hemodynamically stable patients after life-threatening associated diseases like bowel necrosis have been ruled out.
A phosphazene polymer carrier is prepared that has functional groups capable of binding a biologically active substance such as an enzyme or antibody and groups which are non-reactive and hydrophilic. A bifunctional aldehyde is reacted with primary amino groups of a shaped phosphazene polymer to form side chains having aldehyde groups, an amino group-containing compound is reacted with a portion of the aldehyde groups to produce the groups that are non-reactive and hydrophilic, and aldehyde groups not reacted are capable of binding a biologically active substance. The phosphazene polymer may be crosslinked prior to reacting with the bifunctional aldehyde. In another embodiment, a protecting agent is reacted with a portion of the aldehyde groups to block the aldehyde groups, imino bonds are reduced, a compound having an amino group is reacted with aldehyde groups not blocked to form the groups which are non-reactive and hydrophilic, and the protecting agent is removed to provide aldehyde groups capable of binding a biologically active substance. The non-reactive and hydrophilic groups may also be formed by reacting primary amino groups with formaldehyde or by diazotizing primary amino groups of the polymer followed by hydrolysis to form hydroxyl groups. A biologically active substance immobilized on the polymer can be used to separate a substance that has affinity for the immobilized biologically active substance.
Participants received AG-348 tablets, administered orally, at a starting dose of 5 milligrams (mg), twice daily (BID), followed by two sequential dose level increases to 20 mg and 50 mg BID, for a period of 16 weeks in Part 1. This was followed by optimized dose BID, as determined by the investigator in Part 1, for a period of 24 weeks in Part 2.
Our previous intervention study enrolled 62 term children who were born or admitted at the National Taiwan University Hospital, the Mackay Memorial Hospital and Taipei City Hospital, Branch for Women and Children in Taipei, Taiwan, during the time period of 2006 to 2008. No any intervention was conducted, just the observation.
PURPOSE:To use cell wall component of beer yeast as a diabetes-controlling agent containing a large amount of food fiber. CONSTITUTION:It has ben found that the cell wall of beer yeast is rich in vitamins and minerals, contains 25% crude protein and 50.4% food fiber such as glucan, mannan, etc., and is effective as a fiber diet for controlling diabetes. The beeryeast cell wall is obtained by contacting fresh beer yeast produced by Asahi Beer Co, with a sodium hydroxide solution of 10pH for 50sec to remove the bitter taste, washing with water, letting stand at 50-70 deg.C for >=2hr to effect the autodigestion, and extracting and removing the solubilized component with water. The obtained powder is tableted to a tablet of 243.75mg weight. Daily administration of 30 tablets of the beer yeast corresponds to about 3.5g of food fiber. Improvement in GTT, in renal function such as lowering of HbA value, and hyperlipemia accompanied by diabetes has been confirmed.