anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Corrosive injuries (CI) become medical problems related complications include esophageal, pyloric stricture and squamous cell carcinoma, physical and quality of life. Endoscopic (ED) dilatation is primary therapy. The ultrathin endoscope-assisted method is potentially safe and useful in avoiding technical failure. Describe clinical outcomes of ED ED-related CI including successful, refractory, recurrent, and complications-related procedures. Case series study of esophageal and/or pyloric stricture patients after CI who underwent dilatation at Soetomo General Hospital (July 2018 - July 2022). One - biweekly ED using Through The Scope (TTS) balloon or Savary Bougie dilator. The target diameter is 14mm. Fifteen patients with stricture-related CI. Eleven patients underwent ED with a total of 73 procedures. Mean age 31,45 years, predominantly male patients (6), suicide attempt (7), acid agent (9), located at esophagus (3), pylorus (3), or both (5). Number of esophageal dilatation to achieve the target of 14 mm was 1-2 and 2-15 procedures for simple and complex stricture. Five esophageal strictures were successfully dilated but 2 patients were recurrent and 3 cases were refractory to ED. Pyloric dilatation resulted in a lower success rate. Recurrent and refractory cases were 5 and 3 patients respectively. ED with ultrathin endoscope method is useful for traversing guidewire during ED. Ongoing inflammation and fibrosis were linked to recurrent and refractory stricture.
PURPOSE: To obtain slow-releasable micropheres by dispersing hormone into an org. solvent, dissolving a matrix material therein and executing solvent evaporation. CONSTITUTION: The hormone is dispersed into the org. solvent (e.g.; THF) and the material (e.g.; poly(lactide glycolide) to form a matrix in the solvent is dissolved. The resulted org. phase is suspended in a water phase and the org. solvent is evaporated under a reduced pressure. The formed microphseres are filtered after the solvent evaporation and are washed wit desalted water. The micropsheres are then washed with a nonsolvent (e.g.; trichlorotrifluoroethane) at need, by which the micrpsheres having a grain size below 250 μm are obtd. The micropsheres which are formed by using the small amt. of the solvent, contains the residual solvent to a lesser extent and is capable of capsulating the LHRH hormone and its analog at a high yield are easily obtd.
The mechanism(s) underlying obesity-related postmenopausal (PM) breast cancer (BC) are not clearly understood. We hypothesized that the increased local presence of 'obese' mammary adipocytes within the BC microenvironment promotes the acquisition of an invasive and angiogenic BC cell phenotype and accelerates tumor proliferation and progression. BC cells, treated with primary mammary adipocyte secretome from premenopausal (Pre-M) and PM obese women (ObAdCM; obese adipocyte conditioned-media) upregulated the expression of several pro-tumorigenic factors including VEGF, lipocalin-2 and IL-6. Both Pre-M and PM ObAdCM stimulated endothelial cell recruitment and proliferation and significantly stimulated BC cell proliferation, migration and invasion. IL-6 and LCN2 induced STAT3/Akt signaling in BC cells and STAT3 inhibition abrogated the ObAdCM-stimulated BC cell proliferation and migration. Expression of proangiogenic regulators including VEGF, NRP1, NRP2, IL8RB, TGFβ2, and TSP-1 were found to be differentially regulated in mammary adipocytes from obese PM women. Comparative RNAseq indicated an upregulation of PI3K/Akt signaling, ECM-receptor interactions and lipid/fatty acid metabolism in PM versus Pre-M mammary adipocytes. Our results demonstrate that irrespective of menopausal status, cross-talk between obese mammary adipocytes and BC cells promotes tumor aggressiveness and suggest that targeting the LCN2/IL-6/STAT3 signaling axis may be a useful strategy in obesity-driven breast tumorigenesis.
For patients older than 65 years or who cannot tolerate FCR regimens: Patients in this group will receive zanubrutinib monotherapy for 12 months, then receive 4 cycles of bendamostine and rituximab(BR). Efficacy evaluation and MRD test of peripheral blood and bone marrow were performed at the 17th cycle after 16 cycles to obtain study end point data. Patients with CR/CRi and MRD negative could stop taking zanubrutinib and other patients could stop taking zanubrutinib or continue treatment.
BACKGROUND: Uraemia causes a generalised encephalopathy as its most common neurological complication. Isolated brainstem uraemic encephalopathy is rare. We report a case of fatigable ptosis and complex ophthalmoplegia in brainstem uraemic encephalopathy.
CASE PRESENTATION: A 22-year-old Sri Lankan man with end stage renal failure presented with acute onset diplopia and drooping of eyelids progressively worsening over one week. The patient had not complied with the prescribed renal replacement therapy which was planned to be initiated 5 months previously. On examination, his Glasgow coma scale score was 15/15, He had a fatigable asymmetrical bilateral ptosis. The ice-pack test was negative. There was a complex ophthalmoplegia with bilateral abduction failure and elevation failure of the right eye. The diplopia did not worsen with prolonged stare. The rest of the neurological examination was normal. Serum creatinine on admission was 21.81 mg/dl. The repetitive nerve stimulation did not show a decremental pattern. Magnetic resonance imaging (MRI) of the brain demonstrated diffuse midbrain and pontine oedema with T2 weighted/FLAIR hyperintensities. The patient was haemodialyzed on alternate days and his neurological deficits completely resolved by the end of the second week of dialysis. The follow up brain MRI done two weeks later demonstrated marked improvement of the brainstem oedema with residual T2 weighted/FLAIR hyperintensities in the midbrain.
CONCLUSIONS: Uraemia may rarely cause an isolated brainstem encephalopathy mimicking ocular myasthenia, which resolves with correction of the uraemia.
This study is a phase 1/2 multicenter, open-label study of SL-401 (tagraxofusp-erzs) in combination with standard doses of pomalidomide and dexamethasone in patients with relapsed and refractory multiple myeloma (MM). The study will be conducted in 2 phases: Phase 1 is the dose-escalation phase to determine the maximum tested dose (MTD) of SL-401 in combination with standard doses of pomalidomide and dexamethasone. In Phase 1, each evaluated SL-401 dose level will incorporate an initial "Run-in Cycle" (i.e. cycle 1) of single agent SL-401 in at least 3 patients; following the Run-in Cycle, patients who have not experienced a dose-limiting toxicity (DLT) will receive combination SL-401/pomalidomide and dexamethasone in cycles 2 and beyond. All patients in Phase 2 will receive 1 cycle of SL-401 monotherapy in cycle 1, followed by combination of SL-401/pomalidomide/dexamethasone in cycle 2 and beyond. The dose of SL-401 will be the MTD of SL-401 or MTD given in combination with pomalidomide/dexamethasone determined during Phase 1.
FIELD: medicine. ^ SUBSTANCE: rats' spinal cord is cut completely at the inferior thoracic level Th7. IT is followed with electrical stimulation with electrodes placed on a dorsal surface of the spinal cord on segments L2 and S1, as well as with introduction of quipazine and 8-OHDRAT. Hind limbs of an animal rest against a treadmill. Quipazine is administered intraperitoneally 0.3 mg/kg, 8-OHDRAT is introduced 5 min later subcutaneously 0.1-0.3 mg/kg, and electrical stimulation is started 10 min later. Spinal cord segments L2 and S1 are stimulated simultaneously by rectangular pulses of duration 0.2 ms, frequency 40-50 Hz, intensity 1-4 V. An integrated effect is started from the 7th day following a cutting procedure and carried on daily within a therapeutic course of 7 days. ^ EFFECT: method allows to induce interrelated step motions. ^ 2 dwg, 1 ex
Subjects will receive 6 manipulation treatments within 3 weeks period. The manipulated segments are determined individually in baseline assessment.
This trial is designed single arm. All the subjects enrolled will receive the experimental intervention, ScTIL210(Super circulating tumor infiltrating lymphocytes).
Cognitive deficits in the autosomal dominant disorder Neurofibromatosis type 1 (NF1) typically consist of a lower than average IQ, impaired visual-spatial learning, attention problems and impaired executive functioning. These deficits have a substantial influence on the daily life of pediatric and adolescent individuals with NF1. One of the key underlying mechanisms of these deficits is an increased gamma-aminobutyric acid (GABA)-ergic inhibition and a subsequent decrease in synaptic plasticity. The ENCORE laboratory has recently shown that loss of the NF1-gene is associated with attenuated function of the hyperpolarization-activated cyclic nucleotide-gated channel 1 (HCN1). These channels, enriched in membranes of inhibitory interneurons, play an important role in the pathophysiology underlying the cognitive deficits in NF1. Lamotrigine, an HCN-agonist, restored function of HCN1, together with the electrophysiological and visual-spatial learning deficits in Nf1-mice. Thus, lamotrigine is a novel candidate drug for treating cognitive deficits associated with NF1.
FIELD: medicinal, chemical-pharmaceutical and food industry. SUBSTANCE: method involves wetting brown algae in water, their washing out, milling, treatment with 0.5-1.0% hydrochloric acid solution at hydromodulus = 1:10 for 1.5-2 h at temperature 20-30 C. Extraction is carried out with addition of 10-12% of sodium carbonate (to mass of dry algae) at temperature 75-80 C, hydromodulus = 1 : 40 for 2.5-3.0 h, at stirring and infusion for 6-8 h followed by purification of extract. Alginic acid is precipitated by addition of precipitating agent consisting of the mixture of 20% solutions of hydrochloric acid and calcium chloride taken in the ratio = 3:2, respectively. Alginic acid is mixed with mixture of salts potassium carbonate and magnesium carbonate taken in the amount 25-30% (as measured for dry matter of alginic acid gel) or potassium carbonate and magnesium hydroxide taken in the amount 20- -25% (for dry matter of alginic acid gel) in the ratio of salts = 1 : 2.4 : 1 : 1.64, respectively, (by mass) and infused for 5-24 h at stirring. Invention provides preparing the novel complex salt. EFFECT: improved preparing method. 3 cl, 3 ex
Ahi Evren Chest Cardiovascular Surgery Training Research Hospital In sleep lab, polysomnography will be directed to the physiotherapist by the pulmonologist with severe OSAS patients. Patients will be divided into two groups by block randomization method. The study was planned as double-blind. Patients will not know what treatment they are receiving, the doctor does not know what treatment the patient is receiving, and technicians who take and analyze polysomnography will not know what treatment the patients are receiving.

Severe OSAS patients with MEP 30% (low intensity) to the first group, MEP 60% (high intensity) to the second group with expiratory muscle training device, 7 days / week, 25 breaths per day, 1 minute rest for 5 breaths will be run with the cycle. The training will take a total of 8 weeks. The follow-up of the patients will be done remotely by phone. MEP measurements will be repeated every 2 weeks in the hospital and the new training workload will be calculated.
The recommended initial dose of XEOMIN for cervical dystonia is 120 Units. In a placebo-controlled trial utilizing initial XEOMIN doses of 120 Units and 240 Units, no meaningful difference in effectiveness was demonstrated between the doses [see Clinical Studies (14.3)]. In previously treated patients, their past dose, response to treatment, duration of effect, and adverse event history should be taken into consideration when determining the XEOMIN dose.

In the treatment of cervical dystonia, XEOMIN is usually injected into the sternocleidomastoid, levator scapulae, splenius capitis, scalenus, and/or the trapezius muscle(s) (see Figure 5). This list is not exhaustive, as any of the muscles responsible for controlling head position may require treatment [see Clinical Studies (14.3)]. The dose and number of injection sites in each treated muscle should be individualized based on the number and location of the muscle(s) to be treated, the degree of spasticity/dystonia, muscle mass, body weight, and response to any previous botulinum toxin injections.

The frequency of XEOMIN repeat treatments should be determined by clinical response, but should generally be no more frequent than every 12 weeks [see Clinical Studies (14.3)].

Figure 5: Muscles Involved in Cervical Dsytonia
After the first week of e-cigarette use (JUUL), participants will be given bupropion (150 mg each morning for days 1-3, then 300 mg daily) with zonisamide (100 mg daily). The combination of zonisamide and bupropion use will continue for 7 weeks of treatment, and e-cigarette use will continue until the end of the study (an additional 4 weeks).
EGF receptor (EGFR) tyrosine kinase inhibitors (TKIs) have achieved clinical success in lung adenocarcinoma (LUAD). However, tumors often show profound but transient initial response and then gain resistance. We identify transcription factor ZNF263 as being significantly decreased in osimertinib-resistant or drug-tolerant persister LUAD cells and clinical residual tumors. ZNF263 overexpression improves the initial response of cells and delays the formation of persister cells with osimertinib treatment. We further show that ZNF263 binds and recruits DNMT1 to the EGFR gene promoter, suppressing EGFR transcription with DNA hypermethylation. ZNF263 interacts with nuclear EGFR, impairing the EGFR-STAT5 interaction to enhance AURKA expression. Overexpressing ZNF263 also makes tumor cells with wild-type EGFR expression or refractory EGFR mutations more susceptible to EGFR inhibition. More importantly, lentivirus or adeno-associated virus (AAV)-mediated ZNF263 overexpression synergistically suppresses tumor growth and regrowth with osimertinib treatment in xenograft animal models. These findings suggest that enhancing ZNF263 may achieve complete response in LUAD with EGFR-targeted therapies.
Blood samples for inflammation markers are carried out from patients with сolorectal cancer surgery in a single center on the day of the surgery in the operating room before intravenous fluid application started. Each patient receives systemic antibiotic prophylaxis for gramnegative and anaerobic bacteria on induction of anesthesia and prior to skin incision. A standardized protocol for general and epidural anesthesia is used. Values of WBC count, CRP, PCT, CD64n and HLA-DR monocyte are recorded before surgery and after surgery on POD (postoperative day) 1, 3 and 6 or 7. SIRS criteria on POD 1, 3, 6 or 7 and postoperative infections up to 30 days after surgery are recorded. SSIs (incisional, organ / space), pneumonia, central venous catheter related bloodstream infections (CRBSIs), urinary tract infections (UTIs) and enterocolitis records are taken. Microbial cultures are using as the gold standard. Criteria for SIRS reconsidered in the year 2001 by SCCM / ESICM / ACCP / ATS / SIS International Sepsis Definitions Conference and criteria for Dosage Control and Prevention (CDC) are taken into consideration. After discharge, each patient is being monitored by outpatient clinic examinations. The study will recruit approximately 100 patients during three consecutive years.
Participants are initially given oral capsules with 0.5g tid osalmid daily for two weeks. Thereafter, the dosage will be increased by 0.25g tid every two weeks as tolerated by participants to a maximum daily dosage of 1.0g tid for up to one year. One course of osalmid treatment lasts four weeks. Response will be assessed at the end of each treatment course, and patients who have achieved MR (minor remission) or more than MR at the end of the fourth course will continue to take 1.0g tid osalmid daily for consolidation / maintenance therapy. Otherwise, patients who have not achieved MR at the end of the fourth course and patients who are assessed for PD (progression of disease) at the end of each course will receive salvage treatment, such as a combined treatment of osalmid and dexamethasone or the VCD (bortezomib, cyclophosphamide and dexamethasone) regimen.
BACKGROUND: Malignant catatonia is a potentially lethal neuropsychiatric syndrome characterized by psychomotor abnormalities and autonomic instability. Patients with this syndrome require immediate treatment. Various psychiatric conditions and nonpsychiatric medical problems can trigger malignant catatonia. Use of psychostimulant drugs, including methamphetamine and cocaine, has not been previously reported to precipitate malignant catatonia.
CASE SUMMARY: This case concerns a 35-year-old man hospitalized for psychosis due to methamphetamine and cocaine intoxication. He developed malignant catatonia the day after admission. He was treated with lorazepam for malignant catatonia, and his blood pressure was controlled with clonidine. Over 7 days, his condition resolved, and his mental status and vital signs returned to baseline. He was discharged to the community in stable condition and has returned to his baseline functional status. He remains free of catatonia and has maintained abstinence from methamphetamine and cocaine.
CONCLUSIONS: Acute intoxication with psychostimulant drugs is a possible trigger for malignant catatonia, and administration of high potency first-generation antipsychotics in this setting may increase the risk. Patients hospitalized for stimulant intoxication should be monitored for signs and symptoms of catatonia, and D 2 receptor antagonist medications should be used with caution in this population. Our case supports the potential role of altered dopamine and norepinephrine signaling in the pathogenesis of malignant catatonia. The patient provided written and verbal consent to publish the information in this case report.
Sickle cell disease (SCD) is a hereditary hemoglobinopathy marked by hemolytic anemia and vaso-occlusive events (VOEs). Chronic endothelial activation, inflammation, and coagulation activation contribute to vascular congestion, VOEs, and end-organ damage. Coagulation proteases such as thrombin and activated protein C (APC) modulate inflammation and endothelial dysfunction by activating protease-activated receptor 1 (PAR1), a G-protein-coupled receptor. Thrombin cleaves PAR1 at Arg41, while APC cleaves PAR1 at Arg46, initiating either proinflammatory or cytoprotective signaling, respectively, a signaling conundrum known as biased agonism. Our prior research established the role of thrombin and PAR1 in vascular stasis in an SCD mouse model. However, the role of APC and APC-biased PAR1 signaling in thrombin generation, inflammation, and endothelial activation in SCD remains unexplored. Inhibition of APC in SCD mice increased thrombin generation, inflammation, and endothelial activation during both steady state and tumor necrosis factor α challenge. To dissect the individual contributions of thrombin-PAR1 and APC-PAR1 signaling, we used transgenic mice with point mutations at 2 PAR1 cleavage sites, ArgR41Gln (R41Q) imparting insensitivity to thrombin and Arg46Gln (R46Q) imparting insensitivity to APC. Sickle bone marrow chimeras expressing PAR1-R41Q exhibited reduced thrombo-inflammatory responses compared with wild type PAR1 or PAR1-R46Q mice. These findings highlight the potential benefit of reducing thrombin-dependent PAR1 activation while preserving APC-PAR1 signaling in SCD thromboinflammation. These results also suggest that pharmacological strategies promoting biased PAR1 signaling could effectively mitigate vascular complications associated with SCD.
The proposed study is a prospective, split cohort, randomized controlled trial which seeks to characterize blastocyst formation rates following culture in a benchtop incubator in comparison to a box incubator. Following enrollment, participants will undergo ovarian stimulation and oocyte retrieval per routine as previously consented to at the clinic. IVF stimulation protocol will be at the discretion of the participant's individual provider, per routine. Those participants that develop 4 or more mature oocytes will proceed with randomization. Intracytoplasmic Sperm Injection (ICSI) will be performed, as well as assisted hatching on day 3 and embryos will be cultured to the blastocyst stage per routine. It is important to note that there are no changes to the routine embryology care itself, the only difference within the study is that the participant's cohort of oocytes will be split into two groups and randomized to placement within each type of incubator (benchtop and conventional box incubator). The participant, physician, and the clinical team will all be blinded to the randomization of the oocytes and subsequent embryos until study completion. All embryologists making any assessments or selecting the embryo for transfer will also be blinded.
OBJECTIVE: Breast cancer is a malignant tumor with high invasion and metastasis. TGF-β1-induced epithelial-mesenchymal transition (EMT) is crucially involved in the growth and metastasis of breast cancer. Wedelolactone (Wed) is extracted from herbal medicine Ecliptae Herba, which is reported to have antineoplastic activity. Here, we aimed to elucidate the efficacy and mechanism of Wed against breast cancer.
METHODS: The effects of Wed on migration and invasion of 4T1 were detected. The expression of EMT-related markers was detected by Western blot and qPCR. The 4T1 orthotopic murine breast cancer model was established to evaluate the therapeutic effect of Wed on the growth and metastasis of breast cancer through TGF-β1/Smad pathway.
RESULTS: Wed inhibited the proliferation, migration and invasion of 4T1. It exhibited concentration-dependent inhibition of p-Smad2/3. Wed also reversed the expression of EMT-markers induced by TGF-β1. In addition, Wed suppressed the growth and metastasis of breast cancer in mice. It also affected p-Smad3 expression as well as EMT-related genes, suggesting that its anti-breast cancer effect may be related to the TGF-β1/Smad pathway.
CONCLUSION: Wed reverses EMT by regulating TGF-β1/Smad pathway, potentially serving as a therapeutic agent for breast cancer. Wed is expected to be a potential drug to inhibit TGF-β1/Smad pathway-related diseases.
Two modiﬁed dot-like electrodes delivered the stimulation to the left earlobe. Stimulation parameters: frequency = 20/4 Hz; pulse width = 200 μs; 20 Hz lasting 7 seconds, alternated with 4 Hz lasting 3 seconds，repeat until 30 min. Every PD patient received stimulation twice daily , 30 minutes each time, for 14 consecutive days. The stimulation intensity was set as the maximum value the patient could tolerate without causing pain.
ABSTRACT OF THE DISCLOSURE A new type of plasminogen-activating substance is extracted from the bile of hogs.  That substance is characterized by:  (A) a molecular weight of 80,000 ? 10,000;  (B) an isoelectric point of 7.1;  (C) an ultraviolet absorption spectrum showing a peak (.lambda. max) at a wave length of 278 nm;  (D) a fibrinolysis activity such that a Ca-added standard fibrin plate is lysed but a heated fibrin plate is not lysed;  (E) such a high thermal stability that heating at a temperature of 80°C. for 10 min-utes causes the plasminogen-activating activity to be decreased to an extent corresponding to 50% of the original activity and heating at a temperature of 60°C. for 30 minutes causes the plasminogen-activating activity to be decreased to an extent corresponding to from 30 to 40% of the original activity;  (F) a solubility in a salin solution and an insolu-bility in water-soluble organic solvents;  and (G) a synthetic substrate-lysis activity such that Glutaryl-Gly-Arg-MCA and Pro-Phe-Arg-MCA are only marginally hydrolysed.  Such substance can be used as an essential component of a therapeutic medicine for thrombosis.