anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Child will be anesthetized with midazolam 0.05 mg/kg IV bolus and propofol 1mg/kg IV bolus, paracetamol 15mg\\kg IV infusion, and atracurium 0.25mg/kg IV bolus ,then anesthesia will be maintained with propofol infusion according to Mcfarlan protocol, then BIS will be recorded after intubation and every five minutes till end of surgery. Position of the globe will recorded every five minutes till the end of surgery. Angle of deviation will be calculated in same way as group A. Bis should be 40-65. If more than 65 or less than 40, sevoflurane concentration will be adjusted till having the target range. pupillary dilation in surgical eye will be assessed after speculum insertion, 20 minutes after speculum insertion, and before speculum removal by pupil ruler((pupil gauge) and will be observed all over the surgery with the help of surgeon feedback whether it will be maintained or not (considered maintained if pupil size equal or more than 5mm).
The present invention relates to a transcription regulatory region of a myostatin gene. In particular, the invention relates to a 2.5 kb polynucleotide immediately 5' to the myostatin coding sequence, its nucleotide sequence and methods of using this regulatory region, and fragments thereof. The present invention relates to the use of the myostatin promoter of the present invention to direct expression of a target gene in a tissue specific manner, i.e. muscle tissue. The present invention relates to the use of the myostatin promoter of the present invention in high throughput screens to identify test compounds which inhibit myostatin promoter activity or myostatin expression. In accordance with the present invention, inhibitors of the myostatin promoter may be used to inhibit myostatin expression as a method of engineering animals with increased lean meat in order to decrease the time required to bring the animals to slaughter, and of promoting muscle growth for treating disorders related to expression of the myostatin gene, such as muscle wasting associated with aging or disease in humans and companion animals, particularly cats and dogs.
BACKGROUND AND AIMS: An appendectomy for appendiceal inflammation has been suggested to ameliorate the clinical course of patients with ulcerative colitis [UC]. In contrast, for Crohn's disease [CD] an inverse association has been suggested with a higher incidence of CD and worse prognosis after appendectomy. The aim of this study was to analyse the clinical relevance of an inflamed appendix in CD patients undergoing ileocaecal resection [ICR].
METHODS: All consecutive patients undergoing primary ICR between 2007 and 2018 were considered for inclusion. Microscopic data of available appendiceal resection specimens [n = 99] were revised by a dedicated inflammatory bowel disease [IBD] pathologist and scored as inflamed or not inflamed. Eighteen patients had a previous appendectomy. Pathological findings were correlated with disease characteristics and recurrence rates [clinical, endoscopic, and intervention-related].
RESULTS: In total 117 patients were included, 77 [65.8%] females, with a median age of 30 years (interquartile range [IQR] 24-43), and a median follow up of 102 months [IQR 76-114]. Of patients without previous appendectomy [n = 99], 39% had an inflamed appendix. No significant differences in disease characteristics [eg, disease location, behaviour, time to surgery] or prognosis could be demonstrated between the two groups. In contrast, previous appendectomy [n = 18] was associated with penetrating disease and numerically shorter disease duration at the time of resection. Furthermore, a trend was seen towards a stronger association with postoperative recurrence.
CONCLUSION: The current study could not confirm a different prognosis for CD patients with and without an inflamed appendix. In contrast, in patients with a previous appendectomy, a trend was seen towards increased postoperative recurrence, which might be related to the higher incidence of penetrating disease.
BACKGROUND: Entomopathogenic fungal infection-induced dysbiosis of host microbiota offers a window into understanding the complex interactions between pathogenic fungi and host symbionts. Such insights are critical for enhancing the efficacy of mycoinsecticides. However, the utilization of these interactions in pest control remains largely unexplored.
RESULTS: Here, we found that infection by the host-specialist fungus Metarhizium acridum alters the composition of the symbiotic microbiota and increases the dominance of some bacterial symbionts in locusts. Meanwhile, M. acridum also effectively limits the overgrowth of the predominant bacteria. Comparative transcriptomic screening revealed that the fungus upregulates the production of MaCFEM1, an iron-binding protein, in the presence of bacteria. This protein sequesters iron, thereby limiting its availability. Functionally, overexpression of MaCFEM1 in the fungus induces iron deprivation, which significantly suppresses bacterial growth. Conversely, MaCFEM1 knockout relieves the restriction on bacterial iron availability, resulting in iron reallocation. Upon ΔMaCFEM1 infection, some host bacterial symbionts proliferate uncontrollably, turning into opportunistic pathogens and significantly accelerating host death.
CONCLUSIONS: This study elucidates the critical role of pathogenic fungal-dominated iron allocation in mediating the shift of host microbes from symbiosis to pathogenicity. It also highlights a unique biocontrol strategy that jointly exploits pathogenic fungi and bacterial symbionts to increase host mortality. Video Abstract.
Bronchopulmonary dysplasia (BPD) is the most common chronic lung disease among neonates, with increasing morbidity and mortality. This study aims to investigate the effect and mechanism of lysine demethylase 3A (KDM3A) on hyperoxia-induced BPD. Hyperoxia-induced BPD mouse and alveolar epithelial cell models were constructed. The effects of hyperoxia on lung development were evaluated by histological and morphological analysis. The levels of KDM3A, E26 transformation specific-1 (ETS1), H3 lysine 9 dimethylation (H3K9me2), and endoplasmic reticulum (ER) stress-related indexes were quantified by RT-qPCR, Western blot, and IF staining. Cell apoptosis was assessed by flow cytometry and TUNEL staining. Transfection of oe-ETS1, oe-KDM3A, and sh-ETS1 was applied in hyperoxia-induced alveolar epithelial cells to explore the mechanism of the KDM3A/ETS1 axis in hyperoxia-induced apoptosis. KDM3A inhibitor IOX1 was applied to validate the in vivo effect of KDM3A in hyperoxia-induced BPD mice. The results displayed that hyperoxia-induced BPD mice showed reduced body weight, severe destruction of alveolar structure, decreased radial alveolar count (RAC), and increased mean linear intercept (MLI) and mean alveolar diameter (MAD). Further, hyperoxia induction down-regulated ETS1 expression, raised ER stress levels, and increased apoptosis rate in BPD mice and alveolar epithelial cells. However, transfection of oe-ETS1 improved the above changes in hyperoxia-induced alveolar epithelial cells. Moreover, transfection of oe-KDM3A up-regulated ETS1 expression, down-regulated H3K9me2 expression, inhibited ER stress, and reduced apoptosis rate in hyperoxia-induced alveolar epithelial cells. In addition, transfection of sh-ETS1 reversed the inhibitory effect of KDM3A on hyperoxia-induced apoptosis by regulating ER stress. In vivo experiments, KDM3A inhibitor IOX1 intervention further aggravated BPD in newborn mice. In a word, KDM3A alleviated hyperoxia-induced BPD in mice by promoting ETS1 expression.
BACKGROUND: Lack of evaluations of the dietary phosphorus and dialysis phosphorus removal in daily clinical practice are common obstacles to assessing phosphorus balance and controlling phosphorus in hemodialysis patients. We aimed to investigate whether individualized therapy using a phosphorus balance calculator improves phosphorus control.
METHODS: A randomized, open-label, multicenter, 4-week clinical trial was conducted. A total of 119 maintenance hemodialysis patients aged 18-85 years old and with serum phosphorus level >1.45 mmol/L from three university teaching hospitals in Shanghai were enrolled. Patients were randomized in a 1:1 ratio to individualized therapy (n = 60) or conventional therapy (n = 59). The primary outcome was the serum phosphorus concentration after 4-week treatment. Secondary outcomes included the serum calcium and parathyroid hormone (PTH) concentrations, changes in serum phosphorus, calcium and PTH concentrations, and the proportion of patients achieving target ranges of serum phosphorus, calcium and PTH after 4-week treatment.
RESULTS: Among 119 randomized participants [mean age 62 years; 68 male (57%)], 116 completed the trial. Using the phosphorus balance calculator, the individualized group achieved a better phosphorus balance state and significantly reduced serum phosphorus (1.62 ± 0.45 mmol/L versus 1.85 ± 0.45 mmol/L, P = .006), increased the proportions of patients achieving target serum phosphorus range (41% versus 18%, P = .006) and had greater adjusted mean difference in change in serum phosphorus over the 4 weeks (-0.47 versus -0.23 mmol/L, P = .010) when compared with conventional therapy. No significant changes were observed in serum calcium and PTH levels, the proportion of patients achieving target serum calcium or PTH levels, or the adjusted mean difference of serum calcium and PTH levels over the treatment period.
CONCLUSION: Phosphorus balance calculator was proved to improve serum phosphorus control in patients undergoing maintenance hemodialysis, offering a new tool for managing hyperphosphatemia.
BACKGROUND: As a multi-disease model, neuroinflammation, mitochondrial dysfunction, and oxidative stress might be involved in the pathogenic process of perioperative neurocognitive dysfunction (PND). Dynamin-related protein 1 (Drp1) could mediate mitochondrial fission and play important roles in mitochondrial dynamic homeostasis and mitochondria function. The Drp1 may be involved in PND development. The cold-inducible RNA-binding protein (Cirbp) could bind to the 3'-UTR of the thioredoxin 1 (Trx1) mRNA, control oxidative stress, and improve mitochondrial function. In this study, we hypothesized that the Cirbp-Trx1 pathway could ameliorate mitochondrial dysfunction and Drp1 levels in PND mice.
METHODS: Differentially expressed genes were screened using the Gene Expression Omnibus (GEO) database GSE95426 and validated using PCR. Eighteen-month-old C57BL/6 mice were subjected to tibial fracture surgery to generate a PND model. Cirbp was upregulated by hippocampal stereotaxic injections of over-Cirbp plasmid according to the manufacturer's instructions for the in vivo DNA transfection reagent. Cirbp expression was measured using western blot (WB) and immunofluorescence (IF). The Morris water maze (MWM) was used to assess cognitive function. After behavioral testing, the hippocampal tissue was extracted to examine changes in mitochondrial Drp1, mitochondrial function, neuroinflammation, and oxidative stress.
RESULTS: Differential gene screening showed that Cirbp expression was significantly downregulated (fold change >1.5, p = 0.003272) in the PND model. In this study, we also found that Cirbp protein levels were downregulated, accompanied by an impairment of cognition, a decrease in superoxide dismutase (SOD) activity, and an increase in malondialdehyde (MDA) content, mitochondrial Drp1 levels, neuroinflammation, and apoptosis. Cirbp overexpression increased Trx1 protein levels and reversed the damage. However, this protective effect was abolished by PX-12 treatment with a Trx1 inhibitor.
CONCLUSIONS: The Cirbp-Trx1 pathway may regulate mitochondrial dysfunction and mitochondrial Drp1 expression in the hippocampus of PND mice to ameliorate cognitive dysfunction.
Background: This study was designed to investigate the effect of thiopental sodium sedation on the occurrence of maternal hypotension in preoperatively anxious parturients undergoing urgent category-1 Cesarean section (C/S) under spinal anesthesia.

Methods: After institutional ethics committee approval, prospectively collected data of 1824 parturients undergoing C/S at Van Training and Research Hospital between August 2014 and February 2015 were reviewed. Parturients with high preoperative anxiety scores (visual analogue scale for anxiety (VAS-A)≥70) undergoing C/S under spinal anesthesia with thiopental (Group S=49) and without any other type of sedation (Group NS=53) were included in the analysis. All parturients received SA with hyperbaric bupivacaine 0.5% 2.5 mL. Hemodynamic parameters were documented and maximum systolic arterial pressure (SAP) reductions from the baseline after spinal anesthesia were calculated. Incidences of hypotension (SAP≥30% decrease from baseline or \<100 mmHg) and bradycardia (HR\<55 beats/min), and related-ephedrine and -atropine requirements were noted. All data were obtained from the surgical database and patient charts. Primary endpoint of our study was to compare the maximum SAP reductions from the baseline values in Groups S and NS. Secondary endpoints were incidences of hypotension and bradycardia, required ephedrine and atropine doses, newborn Apgar scores at 1st and 5th min.
The invention discloses a paclitaxel compound which is a compound of acryloylated cyclodextrin modified polyacrylic polymer and paclitaxel. Cyclodextrin (CD) in the compound is one or more selected from the group consisting alpha-CD, beta-CD and gamma-CD. The mass ratio of paclitaxel to acryloylated CD modified polyacrylic acid is 2: 1-5. The molecular weight of the acryloylated cyclodextrin modified polyacrylic polymer is 5000 to 50000, wherein a molar ratio of a CD unit to an acrylic acid unit is in a range of 1: 4 to 1: 10. Acryloylated beta-CD (PACD) is synthesized at first by using acylation between beta-CD and acryloyl chloride; and then beta-CD modified polyacrylic acid (CDPAA) is directly prepared in an aqueous solution through radical copolymerization. The compound formed by CDPAA and paclitaxel can exert a solubilizing effect on paclitaxel and enables solubility of paclitaxel to be increased from 0.25 mu g/ml to 3.6 mg/ml, so a novel feasible approach is provided for clinical application of the anti-cancer drug--paclitaxel.
Sacubitril and valsartan lowers blood pressure and may cause symptomatic hypotension [see Adverse Reactions (6.1)]. Patients with an activated renin-angiotensin system, such as volume- and/or salt-depleted patients (e.g., those being treated with high doses of diuretics), are at greater risk. Correct volume or salt depletion prior to administration of sacubitril and valsartan or start at a lower dose. If hypotension occurs, consider dose adjustment of diuretics, concomitant antihypertensive drugs, and treatment of other causes of hypotension (e.g., hypovolemia). If hypotension persists despite such measures, reduce the dosage or temporarily discontinue sacubitril and valsartan. Permanent discontinuation of therapy is usually not required.
For the most up-to-date information on the management of CLOZARIL overdosage, contact a certified Regional Poison Control Center (1-800-222-1222). Telephone numbers of certified Regional Poison Control Centers are listed in the , a registered trademark of Thomson PDR. Establish and maintain an airway; ensure adequate oxygenation and ventilation. Monitor cardiac status and vital signs. Use general symptomatic and supportive measures. There are no specific antidotes for CLOZARIL. **Physicians’ Desk Reference®

In managing overdosage, consider the possibility of multiple-drug involvement.
Patients undergo conventional or intensity-modulated pelvic radiation therapy once daily, 5 days a week, for 5-6 weeks (total of 25-28 fractions) in the absence of disease progression or unacceptable toxicity. Patients with stage II disease or stage I disease with a confirmed diagnosis of clear cell and/or papillary serous histology may also undergo 1 or 2 intravaginal (i.e., vaginal cuff) brachytherapy boost treatments.
Choosing the adequate size of endotracheal tube(ETT) in pediatric patients is important in all anesthesiologists, pediatricians, and critical care specialists. Inadequate ETT size will results in soft tissue injury to trachea by means of the pressure, insufficient ventilation, and aspiration, therefore choosing the adequate ETT size has very important clinical aspect.

Subglottis is the narrowest portion of upper airway. Thus, ETT size should be determined according to the subglottic diameter. Several conventional methods are available to determine ETT size. These methods are based on the demographic data of patient, such as age, weight, height, but could not be customized for each patient. Ultrasonography (US) is one of the most accurate method to measure the subglottic diameter. Also, US is quick, easy to perform, and non-invasive measure. The investigators tried to measure the exact subglottic diameter with US and analyze the correlation of the diameter and demographical data. Furthermore, the investigators will try to develop the equation that could determine the adequate ETT size based on demographical data, instead of actually measuring the subglottic diameter using US.
OBJECTIVE: This study aimed to investigate the influence of familial predisposition on substance-induced psychosis among healthy siblings of patients diagnosed with substance-induced psychotic disorder, who themselves lack any family history of psychotic disorders. Additionally, the study aimed to explore clinical high-risk states for psychosis, schizotypal features, and neurocognitive functions in comparison to a healthy control group.
METHOD: The study compared healthy siblings of 41 patients diagnosed with substance-induced psychotic disorder with 41 healthy volunteers without a family history of psychotic disorders, matching age, gender, and education. Sociodemographic and clinical characteristics of participants were obtained using data collection forms. The Comprehensive Assessment of At-Risk Mental States (CAARMS) and the Structured Interview for Schizotypy-Revised Form (SIS-R) scales were utilized to assess clinical high risk for psychosis. Neurocognitive functions were evaluated with digit span test (DST), trail making test part A-B (TMT), verbal fluency test (VFT), and Stroop test (ST).
RESULTS: Analysis using the CAARMS scale revealed that 39% of siblings and 7.3% of the control group were at clinically high risk for psychosis, indicating a significant difference in rates of psychotic vulnerability. Comparison between siblings and the control group showed significant differences in mean SIS-R subscale scores, including social behavior, hypersensitivity, referential thinking, suspiciousness, illusions, and overall oddness, as well as in mean neurocognitive function scores, including errors in TMT-A, TMT-B, and VFT out-of-category errors, with siblings exhibiting poorer performance.
CONCLUSION: Our study suggests that healthy siblings of patients with substance-induced psychosis exhibit more schizotypal features and have a higher risk of developing psychosis compared to healthy controls. Additionally, siblings demonstrate greater impairment in attention, response inhibition, and executive functions compared to healthy controls, indicating the potential role of genetic predisposition in the development of substance-induced psychotic disorder.
Reagents, kits and methods for preventing and/or treating intestinal inflammation and/or infection caused by anaerobic microorganisms using oxygen supply are provided. In several embodiments, the formulation is provided as a capsule within a capsule to isolate the oxygen prodrug from the catalyst prior to the formulation reaching a target site within the intestinal tract. In several embodiments, a catalyst is provided in excess of the oxygen prodrug. In several embodiments, the prodrug is within an inner capsule or coating, and the biological material (e.g., yeast, spirulina, chlorella, etc.) comprising the catalyst surrounds the encapsulated prodrug, and the biological material is within the capsule or coating. The reagents, kits and methods can be used for preventing and/or treating anaerobic bacterial infections of the intestinal lumen by intestinal aerobic therapy.
OBJECTIVE: To evaluate clinical characteristics and long-term outcomes in patients with guanidinoacetate methyltransferase (GAMT) deficiency with a special emphasis on seizures and electroencephalography (EEG) findings.
METHODS: We retrospectively analyzed the clinical and molecular characteristics, seizure types, EEG findings, neuroimaging features, clinical severity scores, and treatment outcomes in six patients diagnosed with GAMT deficiency.
RESULTS: Median age at presentation and diagnosis were 11.5 months (8-12 months) and 63 months (18 months -11 years), respectively. Median duration of follow-up was 14 years. Global developmental delay (6/6) and seizures (5/6) were the most common symptoms. Four patients presented with febrile seizures. The age at seizure-onset ranged between 8 months and 4 years. Most common seizure types were generalized tonic seizures (n = 4) and motor seizures resulting in drop attacks (n = 3). Slow background activity (n = 5) and generalized irregular sharp and slow waves (n = 3) were the most common EEG findings. Burst-suppression and electrical status epilepticus during slow-wave sleep (ESES) pattern was present in one patient. Three of six patients had drug-resistant epilepsy. Post-treatment clinical severity scores showed improvement regarding movement disorders and epilepsy. All patients were seizure-free in the follow-up.
CONCLUSIONS: Epilepsy is one of the main symptoms in GAMT deficiency with various seizure types and non-specific EEG findings. Early diagnosis and initiation of treatment are crucial for better seizure and cognitive outcomes. This long-term follow up study highlights to include cerebral creatine deficiency syndromes in the differential diagnosis of patients with global developmental delay and epilepsy and describes the course under treatment.
The present application provides novel inhibitors of indoleamine 2,3-dioxygenase-1 and/or indoleamine 2,3-dioxygenase-2 and/or tryptophan 2,3-dioxygenase, metabolites thereof, and pharmaceutically acceptable salts or prodrugs thereof. Also provided are methods for preparing these compounds. A therapeutically effective amount of one or more of the compounds of formula (I) is useful in treating diseases resulting from dysregulation of the kynurenine pathway. Compounds of formula (I) act by inhibiting the enzymatic activity or expression of indoleamine 2,3-dioxygenase-1 and/or indoleamine 2,3-dioxygenase-2 and/or tryptophan 2,3-dioxygenase. By doing so, these compounds are effective in treating diseases associated with the dysregulation of the kynurenine pathway. A variety of diseases can be treated using these compounds and include diseases which are characterized by abnormal immune suppression, abnormal cellular proliferation and/or inflammation. In one embodiment, the disease is cancer. In another embodiment, the disease is a viral infection. In a further embodiment, the disease is depression. In a still further embodiment, the disease is Alzheimer's disease.