anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Rationale: Patients undergoing percutaneous coronary intervention (PCI) for chronic coronary syndrome (CCS) or acute coronary syndrome (ACS) have a residual risk of ischemic events after PCI due to the progression of atherosclerosis in and outside the stented segments. The residual risk is affected by thrombotic, lipid, inflammation and diabetic risk factors. Secondary prevention after PCI is therefore of major importance to reduce complications and improve the patients' prognosis. Antithrombotic treatment plays a major role in the reduction of thromboembolic events and is therefore key in secondary prevention. However, this treatment increases the risk of bleeding complications. Therefore, a personalized antiplatelet strategy is recommended by the guidelines. Together with the antithrombotic treatment, lipid management is the cornerstone of secondary prevention. As low density lipoproteins cholesterol (LDL-C) increases the risk for atherosclerotic cardiovascular disease, the current ESC guidelines recommend a LDL-C value \<1.4mmol/L in patients undergoing PCI. Personalized medicine in which the treatment and lifestyle advice after PCI is adjusted on the patients' risk factors such as high bleeding- or thromboembolic risk, high LDL cholesterol levels, hypertension or the presence of diabetes mellitus (DM) is of major importance to lower the residual risk of complications and revascularisation. However, due to the large amount of risk factors that should be considered, personalized medicine is challenging which can lead to under treatment.

Objective: To maintain and improve quality of care throughout the Netherlands, all interventional centres deliver data regarding patient- and procedural characteristics and follow-up after PCI to the Netherland Heart Registry (NHR). The NHR processes the data and provides these centres with feedback. (16) However, the registration of baseline-, procedural- and follow-up parameters by the NHR is concise and mainly focuses on mortality and (ischemia driven) revascularisation. To enhance the potency of this PCI registry, a consortium in the South East region of the Netherlands has created an extended version: The "Zuid Oost Nederland Hart Registratie" (ZON-HR). With this comprehensive registry, the ZON-HR provides a more extensive overview on the quality of secondary prevention and personalized medicine. Furthermore, the ZON-HR consortium aims to improve secondary prevention post-PCI by stimulating a personalized approach. Also, it will provide a platform for research regarding secondary prevention.
BACKGROUND: Delayed-onset seizures after deep brain stimulation (DBS) surgery were seldom reported. This study summarized the clinical characteristics of delayed-onset seizures after subthalamic nucleus (STN) DBS surgery for Parkinson's disease (PD) and analyzed risk factors.
METHODS: A single-center retrospective study containing consecutive STN-DBS PD patients from 2006 to 2021 was performed. Seizures occurred during the DBS surgery or within one month after DBS surgery were identified based on routine clinical records. Patients with postoperative magnetic resonance imaging (MRI) were included to further analyze the risk factors for postoperative seizures with univariate and multivariate statistical methods.
RESULTS: 341 consecutive PD patients treated with bilateral STN-DBS surgery wereidentified, and five patients experienced seizures after DBS surgery with an incidence of 1.47 %. All seizures of the five cases were characterized as delayed onset with average 12 days post-operatively. All seizures presented as generalized tonic-clonic seizures and didn't recur after the first onset. In those seizures cases, peri-electrode edema was found in both hemispheres without hemorrhage and infarction. The average diameter of peri-electrode edema of patients with seizures was larger than those without seizures (3.15 ± 1.00 cm vs 1.57 ± 1.02 cm, p = 0.005). Multivariate risk factor analysis indicated that seizures were only associated with the diameter of peri-electrode edema (OR 4.144, 95 % CI 1.269-13.530, p = 0.019).
CONCLUSIONS: Delayed-onset seizures after STN-DBS surgery in PD patients were uncommon with an incidence of 1.47 % in this study. The seizures were transient and self-limiting, with no developing into chronic epilepsy. Peri-electrode edema was a risk factor for delayed-onset seizures after DBS surgery. Patients with an average peri-electrode edema diameter > 2.70 cm had a higher risk to develop seizures.
After cesarean section, mothers face more problems than mothers who give birth normally. Post-cesarean pain, breastfeeding problems, anesthesia-related side effects, and postpartum complications are important reasons affecting maternal comfort. After a cesarean section, mothers may experience hypothermia due to the low temperature in the operating room, the incision, and the effects of spinal/general anesthesia. In mothers who develop hypothermia after cesarean section, undesirable results may occur in physiological parameters such as fever, pulse, blood pressure, pain, and intestinal motility. Therefore, body temperature, blood pressure, pulse, saturation, pain, time to first flatus and defecation are the main factors that determine patient comfort after surgery. In the postoperative period, both pharmacological and non-pharmacological treatment methods are used to reduce pain, increase the amount of milk, and increase intestinal motility. It is stated in the literature that non-pharmacological methods such as early mobilization, chewing gum, early oral hydration (consumption of water, warm water, tea, coffee), and hot application are effective in increasing intestinal motility. Using active and passive heating methods to prevent hypothermia after cesarean section are practices that affect postpartum comfort. With this study, it is expected that heating with an electric blanket will prevent hypothermia, increase postpartum comfort, reduce pain, and increase breastfeeding success by affecting the amount of milk.
In an integrated swine farm with 135 sows in Nagasaki Prefecture, premature births and stillbirths were observed in six sows in June and July 2023, and their etiology was investigated. Leptospiral flaB gene was detected in the kidney of one stillborn fetus and the placenta of its sow by nested PCR. Multilocus sequence typing revealed that the infecting strain was Leptospira interrogans ST118. In addition, leptospiral antigens were detected in lesions of the above tissues by immunohistochemical staining. The examined sow and several other sows in the farm had antibodies against serogroup Hebdomadis. These results suggested that L. interrogans serogroup Hebdomadis ST118 was the causative agent of premature births and stillbirths that occurred in this farm.
Pregnancy Category B. RAPAFLO is not indicated for use in women.

An embryo/fetal study in rabbits showed decreased maternal body weight at 200 mg/kg/day (approximately 13-25 times the maximum recommended human exposure or MRHE of silodosin via AUC). No statistically significant teratogenicity was observed at this dose.

Silodosin was not teratogenic when administered to pregnant rats during organogenesis at 1000 mg/kg/day (estimated to be approximately 20 times the MRHE). No maternal or fetal effects were observed at this dose. Rats and rabbits do not produce glucuronidated silodosin, which is present in human serum at approximately 4 times the level of circulating silodosin and which has similar pharmacological activity to silodosin.

No effects on physical or behavioral development of offspring were observed when rats were treated during pregnancy and lactation at up to 300 mg/kg/day.
ACE2016 recommended dose, in combination with pembrolizumab. Lymphodepleting regimen followed by recommended dose of ACE2016, giving in combination with pembrolizumab.
Magnesium Sulfate Injection, USP 50% is a sterile, nonpyrogenic, concentrated solution of magnesium sulfate heptahydrate in Water for Injection. It is administered by the intravenous (IV) or intramuscular (IM) routes as an electrolyte replenisher or anticonvulsant. Must be diluted before IV use. 

Each mL contains: Magnesium sulfate heptahydrate 500 mg; water for injection, q.s. Sulfuric acid and/or sodium hydroxide may have been added for pH adjustment. The pH of a 5% solution is between 5.5 and 7.0. (Osmolarity: 4,060 mOsmol/L (calc.); 2.03 mM/mL magnesium sulfate anhydrous; 4.06 mEq/mL magnesium sulfate anhydrous). 

The solution contains no bacteriostat, antimicrobial agent or added buffer (except for pH adjustment) and is intended only for use as a single dose injection. When smaller doses are required the unused portion should be discarded with the entire unit.

Magnesium sulfate heptahydrate is chemically designated MgSO4•7H2O, with a molecular weight of 246.47 and occurs as colorless crystals or white powder freely soluble in water.
The gastrointestinal tract is densely colonized by a polymicrobial community known as the microbiota which serves as primary line of defence against pathogen invasion. The microbiota can limit gut-luminal pathogen growth at different stages of infection. This can be traced to specific commensal strains exhibiting direct or indirect protective functions. Although these mechanisms hold the potential to develop new approaches to combat enteric pathogens, they remain far from being completely described. In this study, we investigated how a mouse commensal Escherichia coli can outcompete Salmonella enterica serovar Typhimurium (S. Tm). Using a salmonellosis mouse model, we found that the commensal E. coli 8178 strain relies on a trojan horse trap strategy to limit S. Tm expansion in the inflamed gut. Combining mutants and reporter tools, we demonstrated that inflammation triggers the expression of the E. coli 8178 antimicrobial microcin H47 toxin which, when fused to salmochelin siderophores, can specifically alter S. Tm growth. This protective function was compromised upon disruption of the E. coli 8178 tonB-dependent catecholate siderophore uptake system, highlighting a previously unappreciated crosstalk between iron intake and microcin H47 activity. By identifying the genetic determinants mediating S. Tm competition, our work not only provides a better mechanistic understanding of the protective function displayed by members of the gut microbiota but also further expands the general contribution of microcins in bacterial antagonistic relationships. Ultimately, such insights can open new avenues for developing microbiota-based approaches to better control intestinal infections.
Gestational diabetes mellitus (GDM) is associated with cardiovascular disease in postnatal life. The current study tested the hypothesis that GDM caused the cardiac hypertrophy in fetal (ED18.5), postnatal day 7 (PD7), postnatal day 21 (PD21) and postnatal day 90 (PD90) offspring by upregulation of BRD4 and mitochondrial dysfunction. Pregnant mice were divided into control and GDM groups. Hearts were isolated from ED18.5, PD7, PD21 and PD90. GDM increased the body weight (BW) and heart weight (HW) in ED18.5 and PD7, but not PD21 and PD90 offspring. However, HW/BW ratio was increased in all ages of GDM offspring compared to control group. Electron microscopy showed disorganized myofibrils, mitochondrial swelling, vacuolization, and cristae disorder in GDM offspring. GDM resulted in myocardial hypertrophy in offspring, which persisted from fetus to adult in a sex-independent manner. Echocardiography analysis revealed that GDM caused diastolic dysfunction, but had no effect on systolic function. Meanwhile, myocardial BRD4 was significantly upregulated in GDM offspring and BRD4 inhibition by JQ1 alleviated GDM-induced myocardial hypertrophy in offspring. Co-immunoprecipitation showed that BRD4 interacted with DRP1 and there was an increase of BRD4 and DRP1 interaction in GDM offspring. Furthermore, GDM caused the accumulation of damaged mitochondria in hearts from all ages of offspring, including mitochondrial fusion fission imbalance (upregulation of DRP1, and downregulation of MFN1, MFN2 and OPA1) and myocardial mitochondrial ROS accumulation, which was reversed by JQ1. These results suggested that the upregulation of BRD4 is involved in GDM-induced myocardial hypertrophy in the offspring through promoting mitochondrial damage in a gender-independent manner.
The Autoimmune Lymphoproliferative Syndrome (ALPS) is an inherited disease associated with a defect of lymphocyte apoptosis that leads to lymphoproliferation and autoimmunity. Although, there are immunosuppressive treatments for many of its complications, there currently is no safe and effective therapy for this syndrome itself.

Valproic acid has been recently used as a histone deacetylase (HDAC) inhibitor for inducing apoptosis in malignancies and is being incorporated as part of hematology/oncology clinical trials. A pilot study will be conducted on the safety and efficacy of the drug valproic acid (Depakote \[R\]) for the treatment of ALPS. Twelve subjects with ALPS, will be treated initially for 4 months with twice-daily administration of valproic acid at escalating doses adjusted by weight, with close monitoring of toxicity and side effects including laboratory parameters related to the drug. The effects of valproic acid treatment on lymph node and/or spleen size will be assessed by computerized tomography scan, ultrasound and physical examination. If valproic acid is effective in reducing the size of lymph nodes and/or spleen size as defined in the study design, subjects may be offered the option to continue further therapy with valproic acid for up to 1 year. The effect of treatment on other laboratory features specific to ALPS will also be assessed. Evaluating the effects of valproic acid on these clinical and laboratory parameters will help to determine if this drug demonstrates sufficient activity to warrant study in a larger randomized controlled trial.
Another somatropin lyophilized powder was compared with placebo in six randomized clinical trials involving a total of 172 adult GHD patients. These trials included a 6-month double-blind treatment period, during which 85 patients received this other somatropin and 87 patients received placebo, followed by an open-label treatment period in which participating patients received this other somatropin for up to a total of 24 months. This other somatropin product was administered as a daily SC injection at a dose of 0.04 mg/kg/week for the first month of treatment and 0.08 mg/kg/week for subsequent months.

Beneficial changes in body composition were observed at the end of the 6-month treatment period for the patients receiving this other somatropin product as compared with the placebo patients. Lean body mass, total body water, and lean/fat ratio increased while total body fat mass and waist circumference decreased. These effects on body composition were maintained when treatment was continued beyond 6 months. Bone mineral density declined after 6 months of treatment but returned to baseline values after 12 months of treatment.
Treatment should consist of those general measures employed in the management of overdosage with any SSRI. Consult with a certified poison control center for up-to-date guidance and advice on treatment of overdosage.

Ensure an adequate airway, oxygenation, and ventilation. Monitor cardiac rhythm and vital signs. General supportive and symptomatic measures are also recommended. Induction of emesis is not recommended. In managing overdosage, consider the possibility of multiple drug involvement.
BACKGROUND: Endometriosis is well known as a chronic inflammatory disease. The development of endometriosis is heavily influenced by the estrogen receptor β (ERβ), while NOD-like receptors (NLRs) family CARD domain-containing 5 (NLRC5) exhibits anti-inflammatory properties during endometriosis. However, whether NLRC5-mediated anti-inflammation is involved in the ERβ-mediated endometriosis is still uncertain. This study aimed to assess that relation.
METHODS: Nine cases of eutopic endometrial tissue and ten cases of ectopic endometrial tissue were collected from patients with endometriosis, and endometrial samples from ten healthy fertile women were analyzed, and the expression levels of ERβ were quantified using immunohistochemistry (IHC). Subsequently, we constructed mouse model of endometriosis by intraperitoneal injection. We detected the expression of ERβ, NLRC5, tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, and IL-10 and measured the volume of ectopic lesions in mice with endometriosis. In vitro, human endometrial stromal cells (hESCs) were transfected respectively with ERβ-overexpressing and NLRC5-overexpressing plasmids. We then assessed the expression of ERβ and NLRC5 using quantitative real-time PCR (qRT-PCR) and western blot analysis. Furthermore, we measured the concentrations of TNF-α, IL-6, and IL-10 in the cell culture supernatant through enzyme-linked immunosorbent assay (ELISA). Additionally, we evaluated the migration and invasion ability of hESCs using transwell and wound healing assays.
RESULTS: Inhibition of NLRC5 expression promotes the development of ectopic lesions in mice with endometriosis, upregulates the expression of pro-inflammatory factors TNF-α and IL-6, and downregulates the expression of anti-inflammatory factor IL-10. The high expression of NLRC5 in endometriosis depended on the ERβ overexpression. And ERβ promoted the migration of hESCs partially depend on inflammatory microenvironment. Lastly, NLRC5 overexpression inhibited ERβ-mediated development and inflammatory response of endometriosis.
CONCLUSIONS: Our results suggest that the innate immune molecule NLRC5-mediated anti-inflammation participates in ERβ-mediated endometriosis development, and partly clarifies the pathological mechanism of endometriosis, expanding our knowledge of the specific molecules related to the inflammatory response involved in endometriosis and potentially providing a new therapeutic target for endometriosis.
A method of in vitro screening for compounds for treating strokes at delayed timepoints of administration following the onset of stroke. In a first aspect the method includes the step of contacting neurons with azide/deoxyglucose to induce ischemia, contacting with a compound of interest at a later timepoint and assessing neuronal death. A reduction in neuronal death at the later timepoint relative to one or more controls indicates the compound of interest is a candidate for stroke treatment in vivo at delayed timepoints. In another aspect the method includes the step of contacting neurons with an inflammatory agent, such as a lipopolysaccharide, contacting with a compound of interest and assessing the inflammatory response. The methods allow for screening of compounds at higher throughput and lower cost than in vivo methods currently used. Compounds exhibiting promise in the in vitro system can be further characterized by traditional in vivo screening.
The present disclosure provides methods and systems for providing personalized food and health management recommendations. The method may comprise mapping foods by abstracting information from data relating to foods to develop a food ontology. The method may comprise collecting and aggregating a plurality of data sets related to food, health, or nutritional information of a user. The plurality of data sets may be provided from a plurality of sources in a two or more data formats. The method may comprise converting the plurality of data sets into a standardized format that may be individualized for the user. The method may comprise applying a predictive model to the food ontology and the plurality of data sets of the user in the standardized format to determine effects of food consumption of the user's body.
Paroxetine hydrochloride extended-release tablets are an orally administered psychotropic drug with a chemical structure unrelated to other selective serotonin reuptake inhibitors or to tricyclic, tetracyclic or other available antidepressant or antipanic agents. It is the hydrochloride salt of a phenylpiperidine compound identified chemically as (3S-trans)-3-[(1,3-benzodioxol-5-yloxy)methyl)]4-(4-fluorophenyl)-piperidine hydrochloride hemihydrate and has the molecular formula of C19H20FNO3 • HCl • ½ H2O. The molecular weight is 374.8 (329.4 as free base). The structural formula of paroxetine hydrochloride is: 

Paroxetine hydrochloride (hemihydrate), USP is an odorless, white to almost white crystalline powder, having a melting point range of 120° to 138°C and a solubility of 5.4 mg/mL in water. 

Each enteric film-coated, extended-release tablet contains paroxetine hydrochloride hemihydrate equivalent to 12.5 mg, 25 mg or 37.5 mg paroxetine. Inactive ingredients consist of colloidal silicon dioxide, hydroxypropyl cellulose, hypromellose, lactose monohydrate, magnesium stearate, methacrylic acid copolymer type C, microcrystalline cellulose, polydextrose, polyethylene glycol, polysorbate 80, sodium hydroxide, talc, titanium dioxide, triacetin and triethyl citrate. In addition, the 25 mg product contains the following coloring agents: D&C Red No. 30 Aluminum Lake, FD&C Blue No. 2 Aluminum Lake, FD&C Yellow No. 6 Aluminum Lake and the 37.5 mg product contains D&C Red No. 30 Aluminum Lake, FD&C Yellow No. 6 Aluminum Lake, lecithin and sodium alginate.

In addition, paroxetine hydrochloride extended-release tablets may also contain imprinting ink consisting of either black pigment and natural resin or black iron oxide and propylene glycol.

Paroxetine hydrochloride complies with USP Chromatographic Purity Test 1.
Patients will undergo a radiotherapy planning scan, and an upto date MRI brain with contrast. Patients will receive 5 fractions of DE-iPTV radiotherapy over 1 week.