anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Dislocation of a hip hemiarthroplasty used to treat a hip fracture is a serious complication. The aim of this study was to identify whether a delay in the time from fracture to surgery causes an increase in the rate of post-operative hip dislocation. From a single center, data from intracapsular neck of femur patients treated with hip hemiarthroplasty was collected between October 1986 to August 2021. The time from both fall to surgery and admission to surgery was recorded. Surviving patients were followed up for one year. The overall dislocation rate was 51 out of 4155 patients (1.2%). The 3019 patients who had surgery within two days of the injury had a lowest dislocation rate (29 dislocations, 0.96%). For the 197 patients with no history of a fall, there were 5 (2.5%) dislocations (p=0.036, 95% confidence interval of difference 0.15 to 0.97 for comparison with surgery within two days). For the 399 patients with a delay of more than four days from injury till surgery, there were nine dislocations (2.3%) (p=0.045, 95% confidence intervals of difference 0.20 to 0.89 for comparison with surgery within two days). This study demonstrates an increase in the risk of dislocation for those patients with no history of a fall and those with a delay of more than four days from injury to surgery.
Women in Group I (Springfusor® arm) will receive a 8 mL loading dose containing 4g magnesium sulfate heptahydrate (MgSO4\*7H2O) 50% solution, which is approximately 2 mmoL magnesium/mL. The loading dose of 8mL with 4 g MgSO4will be administered using the Springfusor® pump. For women in Group I, the administration of the loading dose will be immediately followed by a maintenance infusion. The maintenance dose of 4 g (8 cc, 50% MgSO4) will be administered with the Springfusor® pump continuously over four hours. The pump will be started immediately after the initial bolus and the 4g dose repeated (and syringe replaced) every four hours for upto 24 hours postpartum.
Doxycycline is an antibacterial drug synthetically derived from oxytetracycline, and is available as doxycycline for oral suspension USP (doxycycline monohydrate) for oral administration.

The structural formula of doxycycline monohydrate is

with a molecular formula of C22H24N2O8•H2O and a molecular weight of 462.46. The chemical designation for doxycycline is 4-(Dimethylamino)-1,4,4a,5,5a,6,11,12a-octahydro-3,5,10,12,12a-pentahydroxy-6-methyl-1,11-dioxo-2-naphthacenecarboxamide monohydrate. Doxycycline is a light-yellow crystalline powder. Doxycycline monohydrate is very slightly soluble in water.

Doxycycline has a high degree of lipoid solubility and a low affinity for calcium binding. It is highly stable in normal human serum. Doxycycline will not degrade into an epianhydro form.

Inert ingredients for the oral suspension formulation are: carboxymethylcellulose sodium, FD & C Blue No. 1, methylparaben, microcrystalline cellulose, propylparaben, raspberry flavor, D & C Red 28 and sucrose.
PURPOSE: To obtain an indolizinone derivative useful for curing and preventing a gastrointestinal disease such as peptic ulcer or gastritis and also useful for curing and preventing of a mental disease symptom as exhibiting a curing effect for a neoformation derived from gastrointestine. CONSTITUTION: This derivative is expressed by the formula (R1 , R2 R3 , R4 and R5 are each H, a halogen or an alkyl group which may have a substituted group, etc.; R6 , R7 , R8 , R9 and R10 are each H, a halogen or an alkoxy group which may have a substituted group, etc.), e.g. 1-benzoyl-2,3-dihydro-3,3-bis[N'-(4- methylphenyl) ureide]-indolizin-2-one. The derivative expressed by the formula is obtained from (α-picoline as a starting raw substance by subjecting to deprotonation, a reaction with an arylnitrin, cyclization of a base, a reaction with isocyanate, dehydration, ring opening with hydrolyzing or a re-cyclization reaction, etc. The derivative expressed by the formula has weak side effect derived from a CCK-A receptor antagonism, an antagonism selective to a gastrin receptor and an antagonism selective to a CCK-B receptor.
We report a case of chronic infection with Pasteurella multocida in the lower respiratory tract in a man with a cat. A 77-year-old man presented with recurrent hemoptysis accompanied by bronchiectasis and an opacity in the left lung on chest computed tomography. Although the patient was seropositive for Mycobacterium avium complex, repeated sputum cultures were negative for any specific pathogen. Three years later, he was referred to our hospital for hemoptysis with enhanced opacity in the lower lobe of the left lung. Culture of bronchial lavage fluid obtained via bronchoscopy was positive for P. multocida. The patient was treated with amoxicillin-clavulanic acid for 14 days and was instructed to avoid close contact with his cat. His symptoms and chest imaging findings improved and have not recurred during more than 1 1/2 years of follow up. P. multocida can cause chronic lower respiratory infections.
PURPOSE: To obtain a preparation for systemic administration or delivery, comprising a support composed of lipid ingredient and ganglioside ingredient and a stimulating factor associated with or incorporated in the support, and enabling sustained release of the stimulating factor and/or protection form catabolic enzyme. CONSTITUTION: This preparation comprises a therapeutically effective amount of a stimulating factor for treating neurodegenerated diseases and regenerating or protecting nervous tissue [e.g. nerve growth factor(NGF)] and a support composed of lipid ingredient(s) and ganglioside ingredient (pref. mixed bovine- brain ganglioside). In this case, the support is associated with or contains the stimulating factor. This preparation is obtained by the following process: the lipid ingredient composed of phospholipid and a cholesterol derivative as stabilizing component and the ganglioside ingredient are dissolved in an organic solvent followed by evaporating the solvent at 45 deg.C to form a smooth lipid film, and a phosphate buffer saline solution of NGF is added to the dried lipid film followed by agitation to effect encapsulation of the NGF into liposome.
Postinfarction ventricular free-wall rupture is a rare mechanical complication, accounting for <0.01% to 0.02% of cases. As an often-catastrophic event, death typically ensues within minutes due to sudden massive hemopericardium resulting in cardiac tamponade. Early recognition is pivotal, and may allow for pericardial drainage and open surgical repair as the only emergent life-saving procedure. In cases of contained rupture with pseudo-aneurysm (PSA) formation, hospitalization with subsequent early surgical intervention is warranted. Not uncommonly, PSA may go unrecognized in asymptomatic patients and diagnosed late during subsequent cardiac imaging. In these patients, the unsettling risk of complete rupture demands early surgical repair. Novel developments, in the field of transcatheter-based therapies and multimodality imaging, have enabled percutaneous PSA repair as a feasible alternate strategy for patients at high or prohibitive surgical risk. Contemporary advancements in the diagnosis and treatment of postmyocardial infarction ventricular free-wall rupture and PSA are provided in this review.
PR Interval Prolongation, Atrioventricular Block, and Ventricular Tachyarrhythmia

Dose-dependent prolongations in PR interval with VIMPAT have been observed in clinical studies in adult patients and in healthy volunteers [ see Clinical Pharmacology (12.2)]. In adjunctive clinical trials in adult patients with partial-onset seizures, asymptomatic first-degree atrioventricular (AV) block was observed as an adverse reaction in 0.4% (4/944) of patients randomized to receive VIMPAT and 0% (0/364) of patients randomized to receive placebo. One case of profound bradycardia was observed in a patient during a 15-minute infusion of 150 mg VIMPAT. When VIMPAT is given with other drugs that prolong the PR interval, further PR prolongation is possible. 

In the postmarketing setting, there have been reports of cardiac arrhythmias in patients treated with VIMPAT, including bradycardia, AV block, and ventricular tachyarrhythmia, which have rarely resulted in asystole, cardiac arrest, and death. Most, although not all, cases have occurred in patients with underlying proarrhythmic conditions, or in those taking concomitant medications that affect cardiac conduction or prolong the PR interval. These events have occurred with both oral and intravenous routes of administration and at prescribed doses as well as in the setting of overdose [ see Overdosage (10)]. 

VIMPAT should be used with caution in patients with underlying proarrhythmic conditions such as known cardiac conduction problems (e.g., marked first-degree AV block, second-degree or higher AV block and sick sinus syndrome without pacemaker), severe cardiac disease (such as myocardial ischemia or heart failure, or structural heart disease), and cardiac sodium channelopathies (e.g., Brugada Syndrome). VIMPAT should also be used with caution in patients on concomitant medications that affect cardiac conduction, including sodium channel blockers, beta-blockers, calcium channel blockers, potassium channel blockers, and medications that prolong the PR interval [ see Drug Interactions (7.2)] . In such patients, obtaining an ECG before beginning VIMPAT, and after VIMPAT is titrated to steady-state maintenance dose, is recommended. In addition, these patients should be closely monitored if they are administered VIMPAT through the intravenous route [ see Adverse Reactions (6.1), Drug Interactions (7.2)]. 

Atrial Fibrillation and Atrial Flutter

In the short-term investigational trials of VIMPAT in adult patients with partial-onset seizures there were no cases of atrial fibrillation or flutter. Both atrial fibrillation and atrial flutter have been reported in open label partial-onset seizure trials and in postmarketing experience. In adult patients with diabetic neuropathy, for which VIMPAT is not indicated, 0.5% of patients treated with VIMPAT experienced an adverse reaction of atrial fibrillation or atrial flutter, compared to 0% of placebo-treated patients. VIMPAT administration may predispose to atrial arrhythmias (atrial fibrillation or flutter), especially in patients with diabetic neuropathy and/or cardiovascular disease.
Absorption of azelastine following ocular administration was relatively low. A study in symptomatic patients receiving one drop of azelastine hydrochloride ophthalmic solution in each eye two to four times a day (0.06 to 0.12 mg azelastine hydrochloride) demonstrated plasma concentrations of azelastine hydrochloride to generally be between 0.02 and 0.25 ng/mL after 56 days of treatment. Three of nineteen patients had quantifiable amounts of N-desmethylazelastine that ranged from 0.25 - 0.87 ng/mL at Day 56. 

Based on intravenous and oral administration, the elimination half-life, steady-state volume of distribution and plasma clearance were 22 hours, 14.5 L/kg and 0.5 L/h/kg, respectively. Approximately 75% of an oral dose of radiolabeled azelastine hydrochloride was excreted in the feces with less than 10% as unchanged azelastine. Azelastine hydrochloride is oxidatively metabolized to the principal metabolite, N-desmethylazelastine, by the cytochrome P450 enzyme system. In vitro studies in human plasma indicate that the plasma protein binding of azelastine and N-desmethylazelastine are approximately 88% and 97% respectively.
Cerebellar syndromes are clinically and etiologically heterogeneous and can be classified as hereditary, neurodegenerative non-hereditary, or acquired. Few data are available on the frequency of each form in the clinical setting. Growing interest is emerging regarding the genetic forms caused by triplet repeat expansions. Alleles with repeat expansion lower than the pathological threshold, termed intermediate alleles (IAs), have been found to be associated with disease manifestation. In order to assess the relevance of IAs as a cause of cerebellar syndromes, we enrolled 66 unrelated Italian ataxic patients and described the distribution of the different etiology of their syndromes and the frequency of IAs. Each patient underwent complete clinical, hematological, and neurophysiological assessments, neuroimaging evaluations, and genetic tests for autosomal dominant cerebellar ataxia (SCA) and fragile X-associated tremor/ataxia syndrome (FXTAS). We identified the following diagnostic categories: 28% sporadic adult-onset ataxia, 18% cerebellar variant of multiple system atrophy, 9% acquired forms, 9% genetic forms with full-range expansion, and 12% cases with intermediate-range expansion. The IAs were six in the FMR1 gene, two in the gene responsible for SCA8, and one in the ATXN2 gene. The clinical phenotype of patients carrying the IAs resembles, in most of the cases, the one associated with full-range expansion. Our study provides an exhaustive description of the causes of cerebellar ataxia, estimating for the first time the frequency of IAs in SCAs- and FXTAS-associated genes. The high percentage of cases with IAs supports further screening among patients with cerebellar syndromes.
Participants will spend 30 minutes colouring. They will be provided with bowls of snacks, which will be weighed before and after their session.
Participants in this group will participate in monthly learning collaborative webinars. Feed-forward of patient reported outcomes (PRO) data collected from the main study (NCT04735406) will be used.
Pulmonary hypertension (PH) is an incurable disease characterized by pulmonary vascular remodeling. Endothelial injury and inflammation are the key triggers of disease initiation. Recent findings suggest that STING (stimulator of IFN genes) activation plays a critical role in endothelial dysfunction and IFN signaling. Here, we investigated the involvement of STING in the pathogenesis of PH. Patients with PH and rodent PH model samples, a Sugen 5416/hypoxia PH model, and pulmonary artery endothelial cells (PAECs) were used to evaluate the hypothesis. We found that the cyclic guanosine monophosphate-AMP synthase-STING signaling pathway was activated in lung tissues from rodent PH models and patients with PH and in TNF-α-induced PAECs in vitro. Specifically, STING expression was significantly elevated in the endothelial cells in PH disease settings. In the Sugen 5416/hypoxia mouse model, genetic knockout or pharmacological inhibition of STING prevented the progression of PH. Functionally, knockdown of STING reduced the proliferation and migration of PAECs. Mechanistically, STING transcriptionally regulates its binding partner F2RL3 (F2R-like thrombin or trypsin receptor 3) through the STING-NF-κB axis, which activated IFN signaling and repressed BMPR2 (bone morphogenetic protein receptor 2) signaling both in vitro and in vivo. Further analysis revealed that F2RL3 expression was increased in PH settings and identified negative feedback regulation of F2RL3/BMPR2 signaling. Accordingly, a positive correlation of expression amounts between STING and F2RL3/IFN-stimulated genes was observed in vivo. Our findings suggest that STING activation in PAECs plays a critical role in the pathobiology of PH. Targeting STING may be a promising therapeutic strategy for preventing the development of PH.
We included adult patients who (1) admitted for primary ICH; (2) underwent blood routine test (hemoglobin included) and CT scan as soon as they arrived at hospital; (3) were not treated with neurosurgical procedures. We excluded patients who (1) had ICH secondary to known causes, including trauma, intracranial neoplasm and systemic diseases, as well as anticoagulative agents; or had isolated intraventricular hemorrhage (IVH); (2) mRS \>2 before the current ICH episode (according to past medical records or description from guardians.
The order of application was determined by lottery. HT7, LI4 and EX-HN3 points were applied respectively. Before starting the application, the area around to be pressurized was gently rubbed with the palm of the hand for 20-30 seconds. The surrounding tissue was relieved by rubbing gently. After rubbing, pressure was applied to the point determined based on the pain threshold level of each individual with a depth of 1-1.5 cm with the thumb for 5 seconds, rested for 2 seconds and the application was continued for 2 minutes. Acupressure was applied to each point for 2 minutes and the total application time was 15 minutes on average (for 5 points).
Telmisartan tablets are indicated for reduction of the risk of myocardial infarction, stroke, or death from cardiovascular causes in patients 55 years of age or older at high risk of developing major cardiovascular events who are unable to take ACE inhibitors. 

High risk for cardiovascular events can be evidenced by a history of coronary artery disease, peripheral arterial disease, stroke, transient ischemic attack, or high-risk diabetes (insulin-dependent or non-insulin dependent) with evidence of end-organ damage [see Clinical Studies (14.2)]. Telmisartan tablets can be used in addition to other needed treatment (such as antihypertensive, antiplatelet or lipid-lowering therapy) [see Clinical Studies (14.2)]. 

Studies of telmisartan in this setting do not exclude the possibility that telmisartan may not preserve a meaningful fraction of the effect of the ACE inhibitor to which it was compared. Consider using the ACE inhibitor first, and, if it is stopped for cough only, consider re-trying the ACE inhibitor after the cough resolves. 

Use of telmisartan with an ACE inhibitor is not recommended [see Warnings and precautions (5.6)].
Autoimmune encephalitis is a relatively novel nosological entity characterized by an immune-mediated damage of the central nervous system. While originally described as a paraneoplastic inflammatory phenomenon affecting limbic structures, numerous instances of non-paraneoplastic pathogenesis, as well as extra-limbic involvement, have been characterized. Given the wide spectrum of insidious clinical presentations ranging from cognitive impairment to psychiatric symptoms or seizures, it is crucial to raise awareness about this disease category. In fact, an early diagnosis can be dramatically beneficial for the prognosis both to achieve an early therapeutic intervention and to detect a potential underlying malignancy. In this scenario, the radiologist can be the first to pose the hypothesis of autoimmune encephalitis and refer the patient to a comprehensive diagnostic work-up - including clinical, serological, and neurophysiological assessments.In this article, we illustrate the main radiological characteristics of autoimmune encephalitis and its subtypes, including the typical limbic presentation, the features of extra-limbic involvement, and also peculiar imaging findings. In addition, we review the most relevant alternative diagnoses that should be considered, ranging from other encephalitides to neoplasms, vascular conditions, and post-seizure alterations. Finally, we discuss the most appropriate imaging diagnostic work-up, also proposing a suggested MRI protocol.
The study will include 30 subjects with a diagnosis of alcohol use disorder. The study uses a breathalyzer device with facial recognition to confirm the patient's identity and sends the information to the study staff using cellular technology. A second device is used which is a wireless blood pressure cuff that connects to the patient's smartphone and sends blood pressure and heart rate measurements directly to the study physician for enhanced monitoring during alcohol withdrawal management. The duration of the study is 8 days, starting with an initial appointment to set up the equipment. Throughout the study, surveys are completed by subjects in regards to their experience with the device. Subjects undergo a brief 30-60 minute appointment on the first day of the study, appointments as needed throughout the study, and an appointment on the last day of the study to check in with the physician for ongoing ambulatory management of alcohol withdrawal, including medication adjustments if indicated.
Surgery days randomized to intraoperative microbreaks and exercises will include standardized breaks lasting approximately 1.5-2 minutes. During these breaks, surgeons will perform a set of targeted stretches or exercises while remaining sterile. The exercises will be performed just before surgical time-out, at a surgically safe and convenient time 45-75 mins after the start of the case and at the end of the case. A surgically safe and convenient time means the surgeon feels that it is safe to take an approximately 1.5-2 minute break during the procedure at that time. Surgeons will skip the microbreak if there is no surgically convenient or safe time during the case. Surgeons will stop the microbreak at any point if needed to ensure patient safety.
Study TDE-PH-206 was a multicenter, open-label study designed to investigate the safety, tolerability, and PK of oral treprostinil administered 3 times daily (TID) or 4 times daily (QID), at the discretion of the Investigator, with food in pediatric PAH subjects aged 7 to 17 years of age (1) transitioning from continuous IV/SC Remodulin, (2) transitioning from inhaled prostacyclin, or (3) as add-on to current PAH therapies in de novo prostacyclin subjects. Eligible subjects were assigned to a cohort based upon their background therapy. All subjects received oral treprostinil provided as 0.125, 0.25, 1, or 2.5 mg extended-release tablets. Subjects in Cohort 1 began the transition from IV/SC Remodulin in the hospital with a goal of complete transition to oral treprostinil within 5 days. The initial dose of oral treprostinil for Cohort 1 was calculated from the subject's dose of IV/SC Remodulin and weight. Subjects in Cohorts 2 and 3 were initiated on 0.125 mg TID or QID oral treprostinil with dose escalations possible every 24 hours in increments of 0.125 mg TID or QID at the discretion of the Investigator during the first 4 weeks, and in increments of either 0.125 mg or 0.25 mg every 24 hours thereafter. Cross titration occurred for Cohorts 1 and 2 such that doses of IV/SC Remodulin or inhaled prostacyclin were decreased as subjects were fully transitioned to oral treprostinil.
A common second course of radiation therapy for recurrent glioblastoma uses 35 Gy in 10 fractions to a small area defined by gadolinium enhancement on MRI. This is based in part on a recent cooperative group trial (RTOG 1205, NCT01730950) with concurrent bevacizumab resulting in very low toxicity and borderline progression free survival benefit. We hypothesize that radiation therapy would be more effective for recurrent glioblastoma when delivered to a larger area defined by spectroscopic MRI. The spectroscopic MRI can delineate occult microscopic disease not seen on clinical MRI. Our group was a partner in the multi-institutional spectroscopic MRI guided dose escalation pilot trial in the first line for glioblastoma (NCT03137888) showing safety and efficacy of planning radiation therapy based on spectroscopic MRI Choline to NAA (Cho:NAA) ratio maps. A local Cho:NAA ratio above 2 (Cho:NAA\>2) is known to correlate with high local GBM burden on pathology. In this study, we will use the same technique to target radiation therapy to recurrent glioblastoma in a larger area of the brain harboring microscopic tumor. We will start with the conventional radiation dose of 35 Gy in 10 fractions to the larger area defined by the spectroscopic MRI. If this is safe and feasible, we will perform a dose escalation to 40 Gy in 10 fractions to areas of gadolinium enhancement and sMRI Cho:NAA\>2 since existing data suggests that those areas harbor the highest risk of future progression. Use of proton radiotherapy to limit brain targeted outside of the treated regions and bevacizumab to prevent radiation toxicity are hypothesized to limit the side effects of this approach.