anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
BoNT/A is a common treatment in patients with NDO. Possible known side effects are urinary retention or increased post void residual. Systemic side effects seems to be rare. However this has not been investigated in detail. Although in very small amounts, BoNT/A can enter the systemic circulation during intradetrusor injections and might cause distant effects on other neuro-muscular systems, i.e. the heart. Aim of this trial is to asses potential systemic adverse effects of BoNT/A on the heart following intradetrusor injections for NDO. Potential effects on the cardiac autonomic function can be detected using HRV analysis. Patients without relevant preexisting disorders of cardiac function and proven NDO are included. During four separate visits, all subjects receive two ECG measurements before (Visit 1 and 2) and two ECG measurements following BoNT/A intradetrusor injections (Visit 3 and 4). We investigate three different groups: 1) patients not receiving BoNT/A intradetrusor injections (= control group), 2) patients receiving intradetrusor injections with 100 units BoNT/A, and 3) patients receiving intradetrusor injections with 300 units BoNT/A.
The purpose of this research study is to compare two different treatments for patients with recurrent Clostridiodies difficile infections: MTC01 vs fecal microbiota transplantation (FMT). FMT is the transfer of bacteria from a healthy donor's colon to a recipient's colon. To do this, stool from a healthy donor is blended with salt water and made into a liquid solution rich in bacteria. This solution is sprayed into the recipient's colon during a colonoscopy. This treatment is now considered standard medical care for recurrent Clostridioides difficile infections.

One FMT dose contains the entire collection of microbes in a healthy donor and is made up of billions of microbes. Each dose of FMT is different from the next and it is unknown exactly what microbes are present in each dose.
Preeclampsia is caused by placental hypoxia and systemic inflammation and is associated with reduced placental growth factor (PlGF) and endothelial nitric oxide synthase (eNOS) levels. The molecular signaling axes involved in this process may play a role in the pathogenesis of preeclampsia. Here, we found that hypoxic exposure increased hypoxia-inducible factor-1α (HIF-1α)/Twist1-mediated miR-214-3p biogenesis in trophoblasts, suppressing PlGF production and trophoblast invasion. TNF-α stimulation increased NF-κB-dependent miR-214-3p expression in endothelial cells, impairing eNOS expression and causing endothelial dysfunction. Synthetic miR-214-3p administration to pregnant mice decreased PlGF and eNOS expression, resulting in preeclampsia-like symptoms, including hypertension, proteinuria, and fetal growth restriction. Conversely, miR-214-3p deletion maintained the PlGF and eNOS levels in hypoxic pregnant mice, alleviating preeclampsia-like symptoms and signs. These findings provide new insights into the role of HIF-1/Twist1- and NF-κB-responsive miR-214-3p-dependent PlGF and eNOS downregulation in the pathogenesis of preeclampsia and establish miR-214-3p as a therapeutic or preventive target for preeclampsia and its complications.
Ofatumumab as a solution for injection in an autoinjector containing 20 mg ofatumumab (50 mg/mL, 0.4 mL content) for subcutaneous administration. A loading dose at Day1, Day 7 and Day 14 and then injections every 4 weeks/ 6 weeks (depending on patient's body weight).
All patients who are enrolled into the NUHS@Home Programme will be recruited into this arm. Patients will be sent home via ambulance, where they will be reviewed by a NUHS@Home nurse. Intravenous therapies, pillboxes for medication, remote monitoring software, and telecommunication tools will be set up as indicated. NUHS@Home doctors will visit at least once daily, and nurses at least twice daily as required. Therapists will conduct home visits as necessary. The NUHS@Home team is available 24/7. When conventional discharge criteria are met, the patient will be discharged. The NUHS@Home clinical team will be under clinical governance of Division of Advanced Internal Medicine at NUH and patients will be considered 'inpatients' throughout the treatment period.
Group 2 will receive 4 vaccinations of the EP-1043 vaccine or placebo. Vaccinations will be given at Months 0, 1, 3, and 6. This group was discontinued as of 12/26/06.
PCT No. PCT/GB95/00008 Sec. 371 Date Nov. 18, 1996 Sec. 102(e) Date Nov. 18, 1996 PCT Filed Jan. 4, 1995 PCT Pub. No. WO95/18638 PCT Pub. Date Jul. 13, 1995The invention is concerned with wound healing and in particular with the use of a collagen-containing membrane in guided tissue regeneration. The invention provides a resorbable collagen membrane for use in guided tissue regeneration wherein one face of the membrane is fibrous thereby allowing cell growth thereon and the opposite face of the membrane is smooth, thereby inhibiting cell adhesion thereon.
BACKGROUND AND OBJECTIVES: In patients with mechanical heart valves and recent intracranial hemorrhage (ICH), clinicians need to balance the risk of thromboembolism during the period off anticoagulation and the risk of hematoma expansion on anticoagulation. The optimal timing of anticoagulation resumption is unknown. We aimed to investigate the relationship between reversal therapy and ischemic stroke, between duration off anticoagulation and risk of ischemic strokes or systemic embolism and between timing of anticoagulation resumption and risk of rebleeding and ICH expansion.
METHODS: We conducted a retrospective cohort observational study in 3 tertiary hospitals. Consecutive adult patients with mechanical heart valves admitted for ICH between January 1, 2000, and July 13, 2022, were included. The primary end points of our study were thromboembolic events (cerebral, retinal, or systemic) while off anticoagulation and ICH expansion after anticoagulation resumption (defined by the following criteria: increase by one-third in intracerebral hematoma volume, increase by one-third in convexity subdural hemorrhage diameter, or visually unequivocal expansion of other ICH locations to the naked eye).
RESULTS: A total of 171 patients with mechanical heart valves who experienced ICH were included in the final analysis. Most of the patients (79.5%) received reversal therapy for anticoagulation. Patients who received anticoagulation reversal therapy did not have increased risk of thromboembolic complications. Time off anticoagulation was not associated with risk of ischemic stroke; only 2 patients had a stroke within 7 days of the ICH, and both had additional major risk factors of thromboembolism. The rate of ischemic stroke/transient ischemic attack while off anticoagulation was lower than the rate of ICH expansion once anticoagulation was resumed (6.4% vs 9.9%). Furthermore, patients who developed ICH expansion had higher mortality compared with patients who had ischemic stroke while being off anticoagulation (41% vs 9%). Use of intravenous heparin bridging upon resumption of warfarin was strongly associated with increased risk of ICH expansion as compared with restarting warfarin without a heparin bridge.
DISCUSSION: Withholding anticoagulation for at least 7 days after ICH may be safe in patients with mechanical heart valves. Heparin bridging during anticoagulation resumption may be associated with increased risk of bleeding.
Start to administer placebo 1 Tab PO QD within 2 weeks after the 1st TACE. Maximum duration of tenofovir treatment: 3 years.
The invention discloses a dihydroartemisinin controlled-release preparation used for treating lupus erythematosus. The controlled-release preparation shows at least one property of the following: (1) according to an in-vitro release curve, when the preparation is placed for 0.5h according to a standard dissolution test, an accumulative release rate of dihydroartemisinin is 10-25%; and (2) according to a healthy adult single-dose oral administration dihydroartemisinin in-vivo absorption curve, an average time for 40% absorption is longer than approximately 2h, and/or an average time for 70% absorption is longer than approximately 6h. With the preparation, dihydroartemisinin in-vivo release speed can be controlled. The preparation can be taken only once every day, and long-time effective blood concentration can be maintained, such that medication is more convenient. The preparation has stable performance, and low toxic and side effect. Because the preparation only needs to be taken once a day, treatment cost is reduced.
VS-6766 will be administered twice weekly in 4 week cycles in patients with solid tumours with a mutation in the RAS-RAF-MEK pathway. Upon occurrence of specified G2 toxicity, dosing intensity will be reduced to 3 weeks followed by a week interruption in a 4 week cycle.
Elevations of ALT or AST (three or more times the upper limit of the normal [ULN]) have been reported in approximately 1% of NSAID-treated patients in clinical trials. In addition, rare, and sometimes fatal, cases of severe hepatic injury, including jaundice and fatal fulminant hepatitis, liver necrosis, and hepatic failure have been reported.

Elevations of ALT or AST (less than three times ULN) may occur in up to 15% of patients treated with NSAIDs including naproxen.

Inform patients of the warning signs and symptoms of hepatotoxicity (e.g., nausea, fatigue, lethargy, diarrhea, pruritus, jaundice, right upper quadrant tenderness, and "flu-like" symptoms). If clinical signs and symptoms consistent with liver disease develop, or if systemic manifestations occur (e.g., eosinophilia, rash, etc.), discontinue VIMOVO immediately, and perform a clinical evaluation of the patient.

VIMOVO should be avoided in patients with severe hepatic impairment [see Dosage and Administration (2), Use in Specific Populations (8.6), and Clinical Pharmacology (12.3)].
Chronic coronary artery stenosis can lead to regional myocardial dysfunction in the absence of myocardial infarction by repetitive stunning, hibernation or both. The molecular mechanisms underlying repetitive stunning-associated myocardial dysfunction are not clear. We used non-targeted metabolomics to elucidate responses to chronically stunned myocardium in a canine model with and without β-adrenergic blockade treatment. After development of left ventricular systolic dysfunction induced by ameroid constrictors on the coronary arteries, animals were randomized to 3 months of placebo, metoprolol or carvedilol. We compared these two β-blockers with their different β-adrenergic selectivities on myocardial function, perfusion and metabolic pathways involved in tissue undergoing chronic stunning. Control animals underwent sham surgery. Dysfunction in stunned myocardium was associated with reduced fatty acid oxidation and enhanced ketogenic amino acid metabolism, together with alterations in mitochondrial membrane phospholipid composition. These changes were consistent with impaired mitochondrial function and were linked to reduced nitric oxide and peroxisome proliferator-activated receptor signalling, resulting in a decline in adenosine monophosphate-activated protein kinase. Mitochondrial changes were ameliorated by carvedilol more than metoprolol, and improvement was linked to nitric oxide and possibly hydrogen sulphide signalling. In summary, repetitive myocardial stunning commonly seen in chronic multivessel coronary artery disease is associated with adverse metabolic remodelling linked to mitochondrial dysfunction and specific signalling pathways. These changes are reversed by β-blockers, with the non-selective inhibitor having a more favourable impact. This is the first investigation to demonstrate that β-blockade-associated improvement of ventricular function in chronic myocardial stunning is associated with restoration of mitochondrial function. KEY POINTS: The mechanisms responsible for the metabolic changes associated with repetitive myocardial stunning seen in chronic multivessel coronary artery disease have not been fully investigated. In a canine model of repetitive myocardial stunning, we showed that carvedilol, a non-selective β-receptor blocker, ameliorated adverse metabolic remodelling compared to metoprolol, a selective β1-receptor blocker, by improving nitric oxide synthase and adenosine monophosphate protein kinase function, enhancing calcium/calmodulin-dependent protein kinase, probably increasing hydrogen sulphide, and suppressing cyclic-adenosine monophosphate signalling. Mitochondrial fatty acid oxidation alterations were ameliorated by carvedilol to a larger extent than metoprolol; this improvement was linked to nitric oxide and possibly hydrogen sulphide signalling. Both β-blockers improved the cardiac energy imbalance by reducing metabolites in ketogenic amino acid and nucleotide metabolism. These results elucidated why metabolic remodelling with carvedilol is preferable to metoprolol when treating chronic ischaemic left ventricular systolic dysfunction caused by repetitive myocardial stunning.
PURPOSE:To obtain an unshakable specific drug for burn embrocation for external use, leaving no scar after healing, useful for early recovery, by blending honey with cinnabar and hen's egg. CONSTITUTION:8.30mg, 33.2% honey, 0.55mg, 2.2% cinnabar and 16.15mg, 64.6% glair are used as components. In blending, powder cinnabar is added to honey and well blended. Further chalaza attached to the glair itself is removed and only the glair is well kneaded with the blend. In blending, materials to be used, including splittable chopsticks, etc., are thermally disinfected and used. The blend is kept at 2-4 deg.C and the effective period is two months. In use, use of other ointment is wholly forbidden.
Tretinoin Cream, USP (Emollient) 0.05% is to be used as described below unless otherwise directed by your physician:

  1. It is for use on the face only.
  2. Avoid contact with the eyes, ears, nostrils, angles of the nose, and mouth. Tretinoin Cream, USP (Emollient) may cause severe redness, itching, burning, stinging, and peeling if used on these areas.
  3. In the evening, gently wash your face with a mild soap. Pat skin dry and wait 20-30 minutes before applying Tretinoin Cream, USP (Emollient). Apply only a pea-sized amount of Tretinoin Cream, USP (Emollient) to your face at one time. This should be enough to cover the entire affected area lightly.
  4. Do not wash your face for at least one hour after applying Tretinoin Cream, USP (Emollient).
  5. For best results, you are advised not to apply another skin care product or cosmetic for at least one hour after applying Tretinoin Cream, USP (Emollient).
  6. In the morning, apply a moisturizing sunscreen, SPF 15 or greater.
  7. Tretinoin Cream, USP (Emollient) is a serious medication. Do not use Tretinoin Cream, USP (Emollient) if you are pregnant or attempting to become pregnant. If you become pregnant while using Tretinoin Cream, USP (Emollient), please contact your physician immediately.
  8. Avoid sunlight and other medicines that may increase your sensitivity to sunlight.
  9. Tretinoin Cream, USP (Emollient) does not remove wrinkles or repair sun-damaged skin.



Please refer to the Patient Package Insert for additional patient information.
Oxaliplatin will be administered by IV infusion once every 21 days at a fixed dose of 130 mg/m2 for up to 6 cycles. Each cycle will last 21 days.
BACKGROUND: Vascular smooth muscle cells (VSMCs) are highly plastic. Vessel injury induces a phenotypic transformation from differentiated to dedifferentiated VSMCs, which involves reduced expression of contractile proteins and increased production of extracellular matrix and inflammatory cytokines. This transition plays an important role in several cardiovascular diseases such as atherosclerosis, hypertension, and aortic aneurysm. TGF-β (transforming growth factor-β) is critical for VSMC differentiation and to counterbalance the effect of dedifferentiating factors. However, the mechanisms controlling TGF-β activity and VSMC phenotypic regulation under in vivo conditions are poorly understood. The extracellular matrix protein TN-X (tenascin-X) has recently been shown to bind TGF-β and to prevent it from activating its receptor.
METHODS: We studied the role of TN-X in VSMCs in various murine disease models using tamoxifen-inducible SMC-specific knockout and adeno-associated virus-mediated knockdown.
RESULTS: In hypertensive and high-fat diet-fed mice, after carotid artery ligation as well as in human aneurysmal aortae, expression of Tnxb, the gene encoding TN-X, was increased in VSMCs. Mice with smooth muscle cell-specific loss of TN-X (SMC-Tnxb-KO) showed increased TGF-β signaling in VSMCs, as well as upregulated expression of VSMC differentiation marker genes during vascular remodeling compared with controls. SMC-specific TN-X deficiency decreased neointima formation after carotid artery ligation and reduced vessel wall thickening during Ang II (angiotensin II)-induced hypertension. SMC-Tnxb-KO mice lacking ApoE showed reduced atherosclerosis and Ang II-induced aneurysm formation under high-fat diet. Adeno-associated virus-mediated SMC-specific expression of short hairpin RNA against Tnxb showed similar beneficial effects. Treatment with an anti-TGF-β antibody or additional SMC-specific loss of the TGF-β receptor reverted the effects of SMC-specific TN-X deficiency.
CONCLUSIONS: In summary, TN-X critically regulates VSMC plasticity during vascular injury by inhibiting TGF-β signaling. Our data indicate that inhibition of vascular smooth muscle TN-X may represent a strategy to prevent and treat pathological vascular remodeling.
The invention discloses a chitosan-based MRI contrast medium and a preparation method. The contrast medium comprises polyethyleneimine-grafted chitosan taken as a main body of the contrast medium and a gadolinium chelate mainly connected to side chains of polyethyleneimine-grafted chitosan. Furthermore, the contrast medium also comprises a targeting group, such as folic acid, connected to side chains of polyethyleneimine-grafted chitosan. The preparation method comprises: firstly, providing polyethyleneimine-grafted chitosan, then coupling a gadolinium chelating ligand, such as diethylene triamine pentaacetic acid to polyethyleneimine-grafted chitosan, enabling the obtained product together with Gd3+ to form the gadolinium chelate, and optionally connecting the targeting group, such as folic acid to the obtained polyethyleneimine-grafted chitosan to produce the contrast medium. The chitosan-based targeting MRI contrast medium is good in biocompatibility, is easy to biologically degrade, and has a high relaxation rate. The preparation method is simple, needs medium reaction temperature, and is easy to control.
Although a number of susceptibility loci for neuroblastoma (NB) have been identified by genome-wide association studies, it is still unclear whether variants in the HLA region contribute to NB susceptibility. In this study, we conducted a comprehensive genetic analysis of variants in the HLA region among 724 NB patients and 2863 matched controls from different cohorts. We exploited whole-exome sequencing data to accurately type HLA alleles with an ensemble approach on the results from three different typing tools, and carried out rigorous sample quality control to ensure a fine-scale ancestry matching. The frequencies of common HLA alleles were compared between cases and controls by logistic regression under additive and non-additive models. Population stratification was taken into account adjusting for ancestry-informative principal components. We detected significant HLA associations with NB. In particular, HLA-DQB1*05:02 (OR = 1.61; padj = 5.4 × 10-3) and HLA-DRB1*16:01 (OR = 1.60; padj = 2.3 × 10-2) alleles were associated to higher risk of developing NB. Conditional analysis highlighted the HLA-DQB1*05:02 allele and its residue Ser57 as key to this association. DQB1*05:02 allele was not associated to clinical features worse outcomes in the NB cohort. Nevertheless, a risk score derived from the allelic combinations of five HLA variants showed a substantial predictive value for patient survival (HR = 1.53; p = 0.032) that was independent from established NB prognostic factors. Our study leveraged powerful computational methods to explore WES data and HLA variants and to reveal complex genetic associations. Further studies are needed to validate the mechanisms of these interactions that contribute to the multifaceted pattern of factors underlying the disease initiation and progression.
Clinical monitoring. MGI (0: no bleeding when a periodontal tube is passed along the mucosal margin adjacent to the implant; 1: visible isolated bleeding points; 2: blood forms a confluent red line at the mucosal margin and 3: profuse bleeding) and the MPI (0: no plaque; 1: plaque recognized only by probing through the smooth marginal surface of the implant; 2: plaque can be seen with the naked eye; 3: abundance of alba matter). PD was determined using a soft plastic periodontal probe for torque-controlled implants at 0.15 N / cm. Three buccal and three lingual reference points for each implant were used to calculate the mean probing depth in millimeters for each implant. PB was dichotomously evaluated: the presence of bleeding was considered positive when it occurred within 20 seconds after insertion of the probe to measure PD. The height of the keratinized mucosa present around each implant was also measured.

All clinical parameters described above were recorded at baseline (pre-intervention period) as well as at 12 and 24 weeks after study initiation.

Treatment of peri-implant mucositis and maintenance care. Prior to the beginning of the intervention, all patients received oral hygiene instruction. Mechanical debridements were performed with titanium curves and polishing using a rubber bowl and polishing paste. In the Test Group the treatment session was completed by a professional topical application around the carboxymethylcellulose gel implants containing 109 colony (CFU) forming units of B. lactis HN019. The gel was applied sub and supragingivally. The patients then received commercial capsules containing the same bacteria and were instructed to dissolve the capsule contents in 20 mL of water and rinse for 30 to 60 seconds, followed by swallowing twice a day for 12 weeks. The control group received the same oral hygiene instructions, mechanical debridement and was treated with gel and placebo tablets. At 3 months postoperatively, the same local mechanical and chemical treatment was repeated for the Test and Control groups.