anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
One of the most common bacteria that cause nosocomial infections is Klebsiella pneumonia (K. pneumoniae), especially in patients who are very sick and admitted to the intensive care unit (ICU). The frequency of multi-drug-resistant Klebsiella pneumoniae (MDRKP) has dramatically increased worldwide in recent decades, posing an urgent threat to public health. The Western world's bacteriophage (phage) studies have been revitalized due to the increasing reports of antimicrobial resistance and the restricted development and discovery of new antibiotics. These factors have also spurred innovation in other scientific domains. The primary agent in phage treatment is an obligately lytic organism (called bacteriophage) that kills the corresponding bacterial host while sparing human cells and lessening the broader effects of antibiotic usage on commensal bacteria. Phage treatment is developing quickly, leading to many clinical studies and instances of life-saving medicinal use. In addition, phage treatment has a few immunological adverse effects and consequences in addition to its usefulness. Since K. pneumoniae antibiotic resistance has made treating multidrug-resistant (MDR) infections challenging, phage therapy (PT) has emerged as a novel therapeutic strategy. The effectiveness of phages has also been investigated in K. pneumoniae biofilms and animal infection models. Compared with antibiotics, PT exhibits numerous advantages, including a particular lysis spectrum, co-evolution with bacteria to avoid the emergence of phage resistance, and a higher abundance and diversity of phage resources than found in antibiotics. Moreover, phages are eliminated in the absence of a host bacterium, which makes them the only therapeutic agent that self-regulates at the sites of infection. Therefore, it is essential to pay attention to the role of PT in treating these infections. This study summarizes the state of knowledge on Klebsiella spp. phages and provides an outlook on the development of phage-based treatments that target K. pneumoniae in clinical trials.
BACKGROUND: The need to improve spinal motor behaviour in chronic low back pain (CLBP) rehabilitation remains unclear. The objective of this study was to test if changes in spinal motor behaviour were associated with changes in disability after an interdisciplinary rehabilitation program (IRP) in patients with CLBP.
METHODS: Seventy-one patients with CLBP participating in an IRP were included. Spinal motor behaviour was assessed with biomechanical (lumbar angular amplitude and velocity, erector spinae muscle activity and duration of the task), cognitive-emotional (task-specific fear [PRF]) and pain-related (movement-evoked pain [MEP]) measures during a lifting task before and after the IRP. Disability was measured before and after the IRP, and at 3-month and 1-year follow-ups.
RESULTS: After adjusting for confounders, changes in disability were significantly associated with MEP changes (β adj. = 0.49, p < 0.001) and PRF changes (β adj. = 0.36, p = 0.008), but not with changes in any of the biomechanical measures. MEP at the end of IRP was also associated with disability at 3 months (β adj. = 0.37, p = 0.001) and 1 year (β adj. = 0.42, p = 0.01). Biomechanical measures at the end of the IRP were not associated with disability, except for the duration of the task that was significantly associated with reduction of disability at 3 months (β non-adj = 0.5, p < 0.001).
CONCLUSIONS: Pain-related and cognitive-emotional measures of spinal motor behaviour were associated with reduction in disability following an IRP. Future research is needed to further investigate causal relationships between spinal motor behaviour and disability.
SIGNIFICANCE STATEMENT: This study supports a multidimensional understanding and analysis of spinal motor behaviour, integrating the cognitive-emotional, pain-related and biomechanical domains. It also supports the consideration of spinal motor behaviour as a potentially important treatment target in chronic low back pain management. Moreover, it suggests that reducing movement-evoked pain and task-specific fear may have more influence on disability than changing lumbar amplitude, lumbar angular velocity or erector muscle activity, which may have important implications for rehabilitation.
BACKGROUND: Children with prune belly syndrome (PBS) are at higher risk of developing kidney dysfunction and requiring kidney replacement therapy (KRT). While studies have described surgical and survival outcomes in these populations, there has yet to be a focused synthesis of evidence regarding kidney outcomes in this population. Here, the focus of this scoping review was to highlight knowledge gaps and report standards on kidney outcomes in PBS of all ages.
METHODS: Following scoping review methodology, EMBASE, MEDLINE, and Scopus were searched for peer-reviewed literature that describe kidney outcomes in PBS. All studies with a broad set of kidney outcomes (such as kidney function measures, chronic kidney disease (CKD), KRT and associated outcomes) were included. Findings were summarized and qualitatively synthesized.
RESULTS: Of the 436 unique records identified, 25 were included for synthesis. A total of 17 studies (441 patients) reported on kidney insufficiency outcomes, with an estimated prevalence of CKD ranging from 8 to 66%. A total of 15 studies (314 patients) described KRT, primary kidney transplant, and outcomes. Of these, the age for KRT ranged from 4 to 21 years, and graft survival ranged from 22 to 87% by last follow-up (range 1.3-27 years).
CONCLUSIONS: There is significant variability in studies reporting kidney outcomes in PBS which limits meaningful synthesis. There is a need for future studies with comprehensive reporting of confounders and drivers for kidney insufficiency in PBS.
BACKGROUND: Muscle atrophy is a common consequence of the loss of innervation and is accompanied by mitochondrial dysfunction. Mitophagy is the adaptive process through which damaged mitochondria are removed via the lysosomes, which are regulated in part by the transcription factor TFE3. The role of lysosomes and TFE3 are poorly understood in muscle atrophy, and the effect of biological sex is widely underreported.
METHODS: Wild-type (WT) mice, along with mice lacking TFE3 (KO), a transcriptional regulator of lysosomal and autophagy-related genes, were subjected to unilateral sciatic nerve denervation for up to 7 days, while the contralateral limb was sham-operated and served as an internal control. A subset of animals was treated with colchicine to capture mitophagy flux.
RESULTS: WT females exhibited elevated oxygen consumption rates during active respiratory states compared to males, however this was blunted in the absence of TFE3. Females exhibited higher mitophagy flux rates and greater lysosomal content basally compared to males that was independent of TFE3 expression. Following denervation, female mice exhibited less muscle atrophy compared to male counterparts. Intriguingly, this sex-dependent muscle sparing was lost in the absence of TFE3. Denervation resulted in 45% and 27% losses of mitochondrial content in WT and KO males respectively, however females were completely protected against this decline. Decreases in mitochondrial function were more severe in WT females compared to males following denervation, as ROS emission was 2.4-fold higher. In response to denervation, LC3-II mitophagy flux was reduced by 44% in females, likely contributing to the maintenance of mitochondrial content and elevated ROS emission, however this response was dysregulated in the absence of TFE3. While both males and females exhibited increased lysosomal content following denervation, this response was augmented in females in a TFE3-dependent manner.
CONCLUSIONS: Females have higher lysosomal content and mitophagy flux basally compared to males, likely contributing to the improved mitochondrial phenotype. Denervation-induced mitochondrial adaptations were sexually dimorphic, as females preferentially preserve content at the expense of function, while males display a tendency to maintain mitochondrial function. Our data illustrate that TFE3 is vital for the sex-dependent differences in mitochondrial function, and in determining the denervation-induced atrophy phenotype.
PROBLEM TO BE SOLVED: To provide a mineral absorption-stimulating composition effective as an ingredient for stimulating the absorption of calcium in intestinal tracts, and to provide a mineral absorption stimulating additive, especially a calcium absorption-stimulating additive, which can be used for foods, feeds, medicines, and so on. SOLUTION: This mineral absorption-stimulating composition contains high mol.wt. chitin, especially chitin having an average mol.wt. of >= 200,000, and/or high mol.wt. chitosan, preferably chitosan having an average mol.wt. of >=10,000, as active ingredients, and, if necessary, further contains a calcium salt as an active ingredient. The mineral is preferably calcium.
FENTORA is supplied in individually sealed, child-resistant blister packages. Each carton contains 7 blister cards with 4 white tablets in each card. The blisters are child-resistant, encased in peelable foil, and provide protection from moisture. Each tablet is debossed on one side with , and the other side of each dosage strength is uniquely identified by the debossing on the tablet as described in the table below. In addition, the dosage strength is indicated on the blister package and the carton. See blister package and carton for product information.

Note: Carton/blister package colors are a secondary aid in product identification. Please be sure to confirm the printed dosage before dispensing.

Storage and Handling

Store at 20°C to 25°C (68°F to 77°F) with excursions permitted between 15°C and 30°C (59°F to 86°F) until ready to use. (See USP Controlled Room Temperature.)

Protect FENTORA from freezing and moisture. Do not use if the blister package has been tampered with.

Store FENTORA securely and dispose of properly.
The present disclosure provides a class of compounds comprising a ligand moiety that specifically binds to the cell surface mannose-6-phosphate receptor (M6 PR). The M6PR binding compound may trigger the receptor to internalize the bound compound into the cell. The ligand moieties of the present disclosure can be linked to a variety of moieties of interest without affecting specific binding to the M6PR and the function of the M6 PR. Also provided are compounds that are conjugates of ligand moieties linked to biomolecules, such as antibodies, that can utilize cellular pathways to remove specific target proteins from the cell surface or from the extracellular environment. For example, conjugates described herein can sequester and/or degrade target molecules of interest in a lysosome of a cell. Methods of using the conjugates to target proteins for isolation and/or lysosomal degradation are also provided.
The most commonly used treatment for acute exacerbations of chronic obstructive pulmonary disease (AECOPD) is a 5-day treatment with corticosteroids in moderate-high dose. Some patients receive repeated treatments, although it has been shown that corticosteroids only have temporary beneficial effects and no effect in relation to serious incidents or mortality. It has been found that the higher accumulated prednisolone dose disables patients due to serious side effects, including pneumonia, dysregulated diabetes, bone fracture in the context of osteoporosis, mental disorder and adrenal insufficiency etc. However, the extent of the side effects is unknown. Recent research has shown that it is presumably only a small subset of COPD patients who benefit from corticosteroid therapy. This group can be identified by the biomarker "blood-eosinophils" as already measured on most AECOPD patients during hospitalization.

This is a randomized, controlled, multi-center, non-Inferiority trial evaluating the effect of eosinophil guided corticosteroid therapy to patients with AECOPD. The aim of the study is to investigate whether the accumulated dose corticosteroid treatment during admissions for AECOPD can be reduced, including the presumed side effects, while (still) remaining the optimal treatment effect.
Opioid pain medications, such as morphine, remain the mainstay for treating severe and chronic pain. Prolonged morphine use, however, triggers analgesic tolerance and hyperalgesia (OIH), which can last for a long period after morphine withdrawal. How morphine induces these detrimental side effects remains unclear. Here, we show that morphine tolerance and OIH are mediated by Tiam1-coordinated synaptic structural and functional plasticity in the spinal nociceptive network. Tiam1 is a Rac1 GTPase guanine nucleotide exchange factor that promotes excitatory synaptogenesis by modulating actin cytoskeletal dynamics. We found that prolonged morphine treatment activated Tiam1 in the spinal dorsal horn and Tiam1 ablation from spinal neurons eliminated morphine antinociceptive tolerance and OIH. At the same time, the pharmacological blockade of Tiam1-Rac1 signalling prevented the development and reserved the established tolerance and OIH. Prolonged morphine treatment increased dendritic spine density and synaptic NMDA receptor activity in spinal dorsal horn neurons, both of which required Tiam1. Furthermore, co-administration of the Tiam1 signalling inhibitor NSC23766 was sufficient to abrogate morphine tolerance in chronic pain management. These findings identify Tiam1-mediated maladaptive plasticity in the spinal nociceptive network as an underlying cause for the development and maintenance of morphine tolerance and OIH and provide a promising therapeutic target to reduce tolerance and prolong morphine use in chronic pain management.
Prostaglandins (PGs) play a crucial role in sleep regulation, yet the broader physiological context that leads to the activation of the prostaglandin-mediated sleep-promoting system remains elusive. In this study, we explored sleep-inducing mechanisms potentially involving PGs, including microbial, immune and thermal stimuli as well as homeostatic sleep responses induced by short-term sleep deprivation using cyclooxygenase-2 knockout (COX-2 KO) mice and their wild-type littermates (WT). Systemic administration of 0.4 µg lipopolysaccharide (LPS) induced increased non-rapid-eye movement sleep (NREMS) and fever in WT animals, these effects were completely absent in COX-2 KO mice. This finding underscores the essential role of COX-2-dependent prostaglandins in mediating sleep and febrile responses to LPS. In contrast, the sleep and fever responses induced by tumor necrosis factor α, a proinflammatory cytokine which activates COX-2, were preserved in COX-2 KO animals, indicating that these effects are independent of COX-2-related signaling. Additionally, we examined the impact of ambient temperature on sleep. The sleep-promoting effects of moderate warm ambient temperature were suppressed in COX-2 KO animals, resulting in significantly reduced NREMS at ambient temperatures of 30 °C and 35 °C compared to WT mice. However, rapid-eye-movement sleep responses to moderately cold or warm temperatures did not differ between the two genotypes. Furthermore, 6 h of sleep deprivation induced rebound increases in sleep with no significant differences observed between COX-2 KO and WT mice. This suggests that while COX-2-derived prostaglandins are crucial for the somnogenic effects of increased ambient temperature, the homeostatic responses to sleep loss are COX-2-independent. Overall, the results highlight the critical role of COX-2-derived prostaglandins as mediators of the sleep-wake and thermoregulatory responses to various physiological challenges, including microbial, immune, and thermal stimuli. These findings emphasize the interconnected regulation of body temperature and sleep, with peripheral mechanisms emerging as key players in these integrative processes.
The study will include the patients undergoing hemodialysis. The patients with surgery at upper extremity in last 3 months, the presence of conditions such as cancer, chronic hearing loss and neurologic diseases affect the interview will be excluded. Sociodemographic properties which include age, gender, duration of dialysis, educational level, comorbid diseases, vascular access area, hand dominancy will be asked. The Beck Depression Inventory (BDI), the Nottingham Health Profile (NHP), the Disabilities of the Arm, Shoulder and Hand Score (Q-DASH) and Visual Analogue Scale (VAS) will applied to all patients.

All the demographic results and vascular access area for hemodialysis will be detected. All data for normality will be tested by using Kolmogorov-Smirnov test. To compare the differences between groups, Mann Whitney U test will be used
Cigarette smoke (CS) facilitates adverse effects on the airway inflammation and treatment of asthma. Here, we investigated the mechanisms by which CS exacerbates asthma. The roles of IL-33 and IL-35 in asthma development were examined by treatment with IL-33 knockout (IL-33 KO) or transfection of adenovirus encoding IL-35 (Ad-IL-35) in a murine model of cigarette smoke-exposure asthma. Furthermore, the involvement of IL-33 and IL-35 in regulating DCs and Th2/Th17 cells was examined in a coculture system of DCs with CD4+ T cells. Additionally, we observed the effect of CpG-ODNs on the balance of IL-33 and IL-35. We show that CS and house dust mite (HDM) exposure induced IL-33 and suppressed IL-35 levels in cigarette smoke-exposure asthma in vivo and in vitro. Treatment with IL-33 KO or Ad-IL-35 significantly attenuated airway hyperreactivity, goblet hyperplasia, airway remodelling, and eosinophil and neutrophil infiltration in the lung tissues from asthmatic mice. Furthermore, we demonstrated reciprocal regulation between CS and HDM-modulated IL-33 and IL-35. Mechanistically, IL-33 KO (or anti-ST2) and Ad-IL-35 attenuated Th2- and Th17-associated inflammation by downregulating TSLP-DC signalling. Finally, administration of CpG-ODNs suppressed the expression of IL-33/ST2 and elevated the levels of IL-35, which is mainly derived from CD4+Foxp+ Tregs, to alleviate Th2- and Th17-associated inflammation by inhibiting the activation of BMDCs. Taken together, the IL-33/ST2 pathway drives the DC-Th2 and Th17 responses of cigarette smoke-exposure asthma, while IL-35 has the opposite effect. CpG-ODNs represent a potential therapeutic strategy for modulating the balance of IL-33 and IL-35 to suppress allergic airway inflammation.
This study aimed to evaluate the protective action of oregano (Origanum vulgare) essential oil and its monoterpene constituents (thymol and carvacrol) in L-arginine-induced kidney damage by studying inflammatory and tissue damage parameters. The determination of biochemical markers that reflect kidney function, i.e., serum levels of urea and creatinine, tissue levels of neutrophil-gelatinase-associated lipocalin (NGAL), and kidney injury molecule-1 (KIM-1), as well as a panel of oxidative-stress-related and inflammatory biomarkers, was performed. Furthermore, histopathological and immunohistochemical analyses of kidneys obtained from different experimental groups were conducted. Pre-treatment with the investigated compounds prevented an L-arginine-induced increase in serum and tissue kidney damage markers and, additionally, decreased the levels of inflammation-related parameters (TNF-α and nitric oxide concentrations and myeloperoxidase activity). Micromorphological kidney tissue changes correlate with the alterations observed in the biochemical parameters, as well as the expression of CD95 in tubule cells and CD68 in inflammatory infiltrate cells. The present results revealed that oregano essential oil, thymol, and carvacrol exert nephroprotective activity, which could be, to a great extent, associated with their anti-inflammatory, antiradical scavenging, and antiapoptotic action and, above all, due to their ability to lessen the disturbances arising from acute pancreatic damage. Further in-depth studies are needed in order to provide more detailed explanations of the observed activities.
In order to prevent dehydration of the premature infant during the first days of life, enteral nutrition with milk must be complemented by an additional fluid supply, commonly administered intravenously. We propose to perform a prospective randomised multi-centric study comparing administration of a hypo-osmolar oral hydration solution with the classical hydration via IV (intravenous) infusion in premature infants of more than 30 weeks GA (gestational age).

We define success as a weight loss inferior to 15 % of birth weight and a weight at day 15 superior to birth weight. Failure was defined hence as a weight loss superior to 15% of birth weight or a weight at day 15 inferior to birth weight or a severe complication or death. Major violations of the protocol in the study group will be counted as failures. The other objectives were to determine whether oral hydration demonstrates practical advantages: less complications in initial management, more comfort for the baby and less technical challenges for the nurses/doctors in charge. Furthermore to evaluate the clinical tolerance of oral hydration from a nutritional point of view and to examine it's effects on intestinal function (defecation, gastric residues), signs of intestinal inflammation and GI flora.
Similarities in striatocortical pathway dysfunction have been noted for alcoholism and obesity. In prior studies we have demonstrated an inverse relationship between body mass index and response in the dorsal striatum (DS) during consumption of a palatable milkshake\[1\]. We have also shown that the magnitude of the reduced response predicts weight gain, especially in individuals who carry a copy of the A1 allele of the taq1A polymorphism\[1\]. Since the A1 allele is associated with reduced striatal D2 receptors \[2-7\], this finding implicates the dopamine system in the reduced blood oxygen level dependent (BOLD) response. Our results also indicate that this reduced response is a consequence, rather than a cause of obesity, since gaining weight \[8\], but not risk for obesity \[9\] (by virtue of parental obesity), is associated with reduced DS response to palatable food. Taken together the results indicate that increased adiposity is associated with blunted DS response to palatable food that may reflect altered dopamine signaling. More recently we determined that reduced DS responses in overweight and obese subjects are associated with increased impulsivity measured with the BIS-11 and a go no/no-go task \[10\]. Heavy drinkers are also more likely to be impulsive \[11\]. In preliminary analyses of data on over 300 individuals assessed with the clinical core battery in the Center for the Translational Neuroscience of Alcoholism (CTNA), we found that higher scores on the BIS-11 and other measures of impulsivity were associated with greater alcohol consumption.

Related to these findings in humans, preliminary work in rodents shows that exogenous administration of N-Acylethanolamines, such as oleoylethanolamine (OEA) can normalize high-fat diet induced dopamine decreases in DS. Human testing of OEA supplementation is possible based on the availability of a dietary supplement containing the OEA precursor NOPE-EGCG ((PhosphoLEANtm, 85mg NOPE+50mg EGCG per capsule). PhosphoLEAN has been shown to enhance adherence to dietary advice in overweight healthy subjects \[12-14\]. We therefore propose a pilot study to test whether PhosphoLEAN will improve performance on impulsivity, go/no-go tasks and negative outcome learning. Specifically, we will recruit heavy drinkers because they are more likely to be impulsive \[11\]. Phospholean may improve negative reinforcement learning in this population. This may lead to reductions in drinking as well. We will also explore whether the supplement leads to reductions in alcohol consumption and preference for high fat foods.