anand-s/m_qalm huggingface dataset:
Question: What links muscle cellular pathways to ALS?
Answer: Changes to muscle cellular pathways may occur downstream of motor neuron pathology in ALS. Genetic changes to pathways that are important to muscle function may also be causal of the disease. In addition, changes to the muscle may be responsible for motor neuron death. Pathological changes occur in muscle before disease onset and independent from MN degeneration, and the muscle may release toxic elements, such as via extracellular vesicle secretion. Muscle metabolism and mitochondrial activity, RNA processing, tissue-resident stem cell function responsible for muscle regeneration, and proteostasis that regulates muscle mass in adulthood, are all deregulated in ALS. There may also be a link between motor neuron death, the immune system, and muscle cells, as muscle-resident glial cells have been shown to activate upon nerve injury. Muscle-restricted expression of a localized insulin-like growth factor Igf-1 isoform maintained muscle integrity and enhanced satellite cell activity in SOD1(G93A) transgenic mice.
Question: What links lipid metabolism pathways to ALS?
Answer: Dysregulation of lipid metabolism is observed early in the spinal cord of the SOD1 ALS mouse model, and abnormal levels of cholesterol and other lipids are observed in the blood and CNS of ALS patients. In addition, higher blood high density lipoprotein and apolipoprotein A1 levels are associated with reduced risk of developing ALS.
Question: What is the multisystem inflammatory syndrome in children (MIS-C) associated with COVID-19?
Answer: Multisystem inflammatory syndrome in children (MIS-C) is a rare but life-threatening condition that develops in children a few weeks after infection with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). It shares clinical features with Kawasaki disease (KD) and KD shock syndrome. Clinical features include persistent fever, severe illness with involvement of multiple organ systems, and elevated inflammatory markers. Therapy is primarily with immunomodulators, suggesting that the disease is driven by post-infectious immune dysregulation. Most children with MIS-C, even those with severe cardiovascular involvement, recover without sequelae. A very similar syndrome has also been reported in adults in association with COVID-19 infection or exposure and is termed multisystem inflammatory syndrome in adults (MIS-A).
Multisystem inflammatory syndrome in children (MIS-C) is a novel, life-threatening hyperinflammatory condition that develops in children a few weeks after infection with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). This disease has created a diagnostic challenge due to overlap with Kawasaki disease (KD) and KD shock syndrome. The majority of patients with MIS-C present with the involvement of at least four organ systems, and all have evidence of a marked inflammatory state. Therapy is primarily with immunomodulators, suggesting that the disease is driven by post-infectious immune dysregulation. Most patients, even those with severe cardiovascular involvement, recover without sequela
Multisystem inflammatory syndrome in children (MIS-C) is a well described and documented condition that is associated with the active or recent COVID-19 infection. A similar presentation in adults is termed as Multisystem inflammatory syndrome in Adults (MIS-A). Multisystem inflammatory syndrome in children (MIS-C) is a novel, life-threatening hyperinflammatory condition that develops in children a few weeks after infection with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). This disease has created a diagnostic challenge due to overlap with Kawasaki disease (KD) and KD shock syndrome. The majority of patients with MIS-C present with the involvement of at least four organ systems, and all have evidence of a marked inflammatory state. Most patients show an increase in the level of at least four inflammatory markers (C-reactive protein, neutrophil count, ferritin, procalcitonin, fibrinogen, interleukin-6, and triglycerides). Therapy is primarily with immunomodulators, suggesting that the disease is driven by post-infectious immune dysregulation. Most patients, even those with severe cardiovascular involvement, recover without sequelae. Since coronary aneurysms have been reported, echocardiographic follow-up is needed.
Question: What links immune response pathways to ALS?
Answer: Microglia, which are the primary immune cells of the central nervous system, are strongly implicated in ALS, their activation being correlated with various clinical features, and inflammatory microglial responses being correlated withe disease progression. The immune response may be implicated in other ways with ALS molecular pathology. such as through inflammatory regulation and circulating interleukins. It is possible the T cell receptor signalling and activation is involved. It is also possible that the innate / non-specific immune system is involved - i.e. immune protection against foreign substances, viruses, and bacteria.
Question: Which are the uses of deep learning models in Duchenne Muscular Dystrophy?
Answer: Deep learning models enable the evaluation of DMD patients using ultrasound images.
The results show that each deep learning model endows muscle ultrasound imaging with the ability to enable DMD evaluations.
Deep Learning of Ultrasound Imaging for Evaluating Ambulatory Function of Individuals with Duchenne Muscular Dystrophy. The results show that each deep learning model endows muscle ultrasound imaging with the ability to enable DMD evaluations.
URL_0   > Deep learning of Ultrasound imaging for evaluation of Ambulatory Function of Individuals with Duchenne Muscular Dystrophy.
Deep Learning of Ultrasound Imaging for Evaluating Ambulatory Function of Individuals with Duchenne Muscular Dystrophy. The results show that each deep learning model endows muscle ultrasound imaging with the ability to enable DMD evaluations. Deep learning models are used to predict muscle function in DMD patients.
Deep Learning of Ultrasound Imaging for Evaluating Ambulatory Function of Individuals with Duchenne Muscular Dystrophy.
Question: What is "long-COVID"?
Answer: "Long-COVID" is a complex condition where the affected individuals do not recover for several weeks or months following the onset of symptoms suggestive of COVID-19, and the symptoms are not explained by an alternative diagnosis.

Persistent physical symptoms following acute COVID-19 are common and typically include fatigue, dyspnea, chest pain, and cough. Headache, joint pain, myalgias, and loss of smell have also been reported. Common psychological and cognitive symptoms include poor concentration, cognitive impairment/confusion, insomnia, and overall reduced quality of life.
"Long COVID" is the condition whereby affected individuals do not recover for several weeks or months following the onset of symptoms suggestive of COVID-19, whether tested or not. Emerging aspects of the Covid-19 clinical presentation are its long-term effects, which are characteristic of the so-called "long COVID". The main symptoms associated with "long COVID" were headache, fatigue, muscle aches/myalgia, articular pains, cognitive impairment, loss of concentration, and loss of smell. Additionally, the subjects showed significant levels of insomnia (p < 0.05) and an overall reduced quality of life (p < 0.05). Long COVID is a complex condition with prolonged heterogeneous symptoms. The nature of studies precludes a precise case definition or risk evaluation. There is an urgent need for prospective, robust, standardised, controlled studies into aetiology, risk factors and biomarkers to characterise long COVID in different at-risk populations and settings.
Question: Define pseudotumor cerebri. How is it treated?
Answer: Pseudotumor cerebri is a condition characterized by an elevation of the intracranial pressure not associated with an intracranial process or hydrocephaly, and with normal cerebrospinal fluid (CSF) contents. It most often occurs in obese women of childbearing age. The management of patients with pseudotumor cerebri mainly depends on the presence and severity of ocular symptoms and signs on which the prognostic of the disease is based. Repeated lumbar punctures associated with acetazolamide and weight loss are usually efficient enough. However a surgical treatment (optic nerve sheath fenestration or lumboperitoneal shunt) is required when appropriate medical management does not prevent progressive alteration of vision (visual loss or visual field defect), or when the patients complains of severe, refractory headaches. Careful follow-up with repeated formal visual field testing may help preventing a devastating visual loss in these patients.
Benign intracranial hypertension (BIH) is characterized by an elevation of the intracranial pressure not associated with an intracranial process or hydrocephaly, and with normal cerebrospinal fluid (CSF) contents. The elevation of the intracranial pressure is isolated; therefore, diseases such as cerebral venous thrombosis or dural fistulas should not be considered as etiologies of BIH. The exact definition of BIH remains debated, and other terms such as "pseudotumor cerebri" or "idiopathic intracranial hypertension" are often used in the literature. The management of patients with BIH depends mainly on the presence and severity of ocular symptoms and signs on which the prognostic of the disease is based. Repeated lumbar punctures associated with acetazolamide and weight loss are usually efficient enough. However a surgical treatment (optic nerve sheath fenestration or lumboperitoneal shunt) is required when appropriate medical management does not prevent progressive alteration of vision (visual loss or visual field defect), or when the patients complains of severe, refractory headaches. Careful follow-up with repeated formal visual field testing may help preventing a devastating visual loss in these patients.
Question: What is pseudodementia?
Answer: Depression can cause some clinical symptoms and signs of dementia, classically in older adults. This type of "dementia" is called pseudodementia and is typically reversible with treatment.
Pseudodementia is defined as an intellectual impairment in patients with a primary psychiatric disorder, in which the features of intellectual abnormality resemble, at least in part, those of a neuropathologically induced cognitive deficit. This neuropsychological impairment is reversible, and there is no apparent primary neuropathological process that leads to the genesis of this disturbance.
Question: What is Guillain-Barre syndrome (GBS)?
Answer: Guillain-Barré syndrome (GBS) is an acute immune mediated neuropathy, polyradiculoneuritis, characterized by rapid onset of symmetric extremity muscle paralysis, areflexia and albuminocytological dissociation in the cerebrospinal fluid (CSF). Recently, the heterogeneity of GBS has been noticed with definition of several GBS variants. The diagnosis of GBS includes clinical, electrophysiological and laboratory (CSF) criteria.
Guillain-Barr syndrome (GBS) is an acute immune mediated neuropathy, polyradiculoneuritis, characterized by rapid onset of symmetric extremity muscle paralysis, areflexia and albuminocytological dissociation in the cerebrospinal fluid (CSF).
Guillain-Barré syndrome (GBS) is an acute immune mediated neuropathy, polyradiculoneuritis, characterized by rapid onset of symmetric extremity muscle paralysis, areflexia and albuminocytological dissociation in the cerebrospinal fluid (CSF).
Guillain-Barre syndrome (GBS) is an acute immune mediated neuropathy, polyradiculoneuritis, characterized by rapid onset of symmetric extremity muscle paralysis, areflexia and albuminocytological dissociation in the cerebrospinal fluid (CSF).
Question: Are there any tools that could predict protein structure considering amino acid sequence?
Answer: AlphaFold, PredictProtein, PSIPRED, Jpred and Porter do all predict protein stucture from amino acid sequence.
Yes. Tools such as Jpred, Jnet, Porter 4.0 and PSIPRED Workbench have been developed that predict protein structure based solely on its amino acid sequence, whereas the recently updated Jnet algorithm provides a three-state (alpha-helix, beta-strand and coil) prediction of secondary structure at an accuracy of 81.5%.
Question: Which proteins does p110α interact with?
Answer: p110α interacts with p85α and RAS proteins.
RAS interaction with PI3K p110α
Question: Which are the types of cancer that c-Myc is associated with?
Answer: The types of cancer that c-Myc is associates with are breast cancer, non-small-cell lung cancer and pancreatic ductal adenocarcinoma.
c-Myc is known to be deregulated in a variety of tumors, including breast cancer, prostate cancer, non-small cell lung cancer (NSCLC), papillary thyroid cancer (PDA), ovarian cancer, cervical intraepithelial neoplasia, and gastric cancer.
Question: Which pathways are involved in cellular senescence?
Answer: Cellular senescence requires signal transduction, and the two most important signaling pathways are the P16Ink4a/Rb (retinoblastoma protein) pathway and the P19Arf/P53/P21Cip1 pathway, which interact but independently regulate the process of the cells cycle.
Question: Which are the components that evaluate druglikeness?
Answer: Lipinski's rule states that, in general, an orally active drug has no more than one violation of the following criteria:
No more than 5 hydrogen bond donors (the total number of nitrogen–hydrogen and oxygen–hydrogen bonds)
No more than 10 hydrogen bond acceptors (all nitrogen or oxygen atoms)
A molecular mass less than 500 daltons
An octanol-water partition coefficient (log P) that does not exceed 5
In the discovery setting 'the rule of 5' predicts that poor absorption or permeation is more likely when there are more than 5 H-bond donors, 10 H-bond acceptors, the molecular weight (MWT) is greater than 500 and the calculated Log P (CLogP) is greater than 5 (or MlogP > 4.15)
Question: Which small molecules inhibit the c-Myc/Max dimerization?
Answer: The small molecules that inhibit c-Myc/Max dimerization are Mycro1, Mycro2, Mycro3, IIA6B17, celastrol, 10058-F4, 10074-G5, JY-3-094, KJ-Pyr-9, MYCi361 and MYCi975
Mycros are the first inhibitors of c-Myc/Max dimerization, which have been demonstrated to inhibit DNA binding of c-Myc with preference over other dimeric transcription factors in vitroMost Myc inhibitors prevent the association between Myc and its obligate heterodimerization partner Max via their respective bHLH-ZIP domainsPreviously we showed that two c-Myc-Max inhibitors, 10058-F4 and 10074-G5, bound to distinct ID regions of the monomeric c-Myc bHLHZip domainWe tested the efficacy of Mycro3, a small-molecule inhibitor of Myc-Max dimerizationIn a fluorescence polarization screen for the MYC-MAX interaction, we have identified a novel small-molecule inhibitor of MYC, KJ-Pyr-9, from a Kröhnke pyridine libraryWe have previously demonstrated that the small molecule 10058-F4, known to bind to the c-MYC bHLHZip dimerization domain and inhibiting the c-MYC/MAX interaction, also interferes with the MYCN/MAX dimerization in vitro and imparts anti-tumorigenic effects in neuroblastoma tumor models with MYCN overexpressionWe developed a series of small-molecule MYC inhibitors that engage MYC inside cells, disrupt MYC/MAX dimers, and impair MYC-driven gene expression.Inhibition of MYC/MAX dimerization by a small-molecule antagonist (IIA6B17) has been shown to interfere with MYC-induced transformation of chick embryo fibroblasts, suggesting that the functional inhibitors of the MYC family of oncoproteins have potential as therapeutic agents.
Question: Which models are used for predicting disease progression in Duchenne Muscular Dystrophy?
Answer: Models used to predict disease progression of Duchenne Muscular Dyystrophy are: cumulative distribution function using a non-linear mixed effects approach, ...
Longitudinal changes in biomarkers were modeled with a cumulative distribution function using a nonlinear mixed-effects approach.
Modeling disease trajectory in Duchenne muscular dystrophy Longitudinal changes in biomarkers were modeled with a cumulative distribution function using a nonlinear mixed-effects approach.
Longitudinal changes in biomarkers were modeled with a cumulative distribution function using a nonlinear mixed-effects approach. Longitudinal progression of Duchenne Muscular Dystrophy was also modeled using a weighted average probability method. Duchenne muscular dystrophy disease progression was modeled using the following models: linear progression function, logarithmological, multisubunit, linear multiple-parametry, and linear multiple sum
Question: For what known mutations is KRAS gene considered to be oncogenic?
Answer: G12C, G12V, G12D and G12A are all observed mutations of the KRAS oncogene.
Question: Which proteins does the p85α interact with?
Answer: p85α interacts with itself, with p110α and with p110d
Question: Computational tools for predicting allosteric pathways in proteins
Answer: Computational tools for predicting allosteric pathways in proteins include MCPath, MutInf, pySCA, CorrSite, and CARDS.
CorrSite identifies potential allosteric ligand-binding sites based on motion correlation analyses between cavities.
Here, a Monte Carlo (MC) path generation approach is proposed and implemented to define likely allosteric pathways through generating an ensemble of maximum probability paths. Overall, it is demonstrated that the communication pathways could be multiple and intrinsically disposed, and the MC path generation approach provides an effective tool for the prediction of key residues that mediate the allosteric communication in an ensemble of pathways and functionally plausible residues We utilized a data set of 24 known allosteric sites from 23 monomer proteins to calculate the correlations between potential ligand-binding sites and corresponding orthosteric sites using a Gaussian network model (GNM)
We find that CARDS captures allosteric communication between the two cAMP-Binding Domains (CBDs)Overall, it is demonstrated that the communication pathways could be multiple and intrinsically disposed, and the MC path generation approach provides an effective tool for the prediction of key residues that mediate the allosteric communication in an ensemble of pathways and functionally plausible residuesWe utilized a data set of 24 known allosteric sites from 23 monomer proteins to calculate the correlations between potential ligand-binding sites and corresponding orthosteric sites using a Gaussian network model (GNM)Here, we introduce the Correlation of All Rotameric and Dynamical States (CARDS) framework for quantifying correlations between both the structure and disorder of different regions of a proteinWe present a novel method, "MutInf", to identify statistically significant correlated motions from equilibrium molecular dynamics simulationsCorrSite identifies potential allosteric ligand-binding sites based on motion correlation analyses between cavities.Here, a Monte Carlo (MC) path generation approach is proposed and implemented to define likely allosteric pathways through generating an ensemble of maximum probability paths.
A Monte Carlo (MC) path generation approach is proposed and implemented to define likely allosteric pathways through generating an ensemble of maximum probability paths. A novel method, "MutInf", to identify statistically significant correlated motions from equilibrium molecular dynamics simulations. CorrSite identifies potential alloster-binding sites based on motion correlation analyses between cavities. The Correlation of All Rotameric and Dynamical States (CARDS) framework for quantifying correlations between both the structure and disorder of different regions of a protein
Question: What are the classic signs of a basilar skull fracture?
Answer: Basilar skull fractures are fractures of the lower part of the skull. The four classic signs are:
1. Periorbital ecchymosis (“raccoon eyes”).
2. Postauricular ecchymosis (Battle sign).
3. CSF otorrhea or rhinorrhea (leakage of CSF, which is clear in appearance, from the ears or nose).
4. Hemotympanum (blood behind the eardrum).
Possible clinical signs are the presence of cerebrospinal fluid rhinorrhea or otorrhea, periorbital ecchymosis (raccoon eyes), retroauricular ecchymosis (battle sign) and cranial nerve injuries
Question: Which biomarkers are currently used for Duchenne Muscular Dystrophy?
Answer: MRI, fat fraction MRI, MRI mean T2, malate dehydrogenase 2 are some biomarkers that are used for DMD.
MRI measurements can be used as biomarkers of disease severity in ambulant patients with DMD. malate dehydrogenase 2 as candidate prognostic biomarker for Duchenne muscular dystrophy
malate dehydrogenase 2 as candidate prognostic biomarker for Duchenne muscular dystrophyMRI measurements can be used as biomarkers of disease severity in ambulant patients with DMD.
MRI measurements can be used as biomarkers of disease severity in ambulant patients with DMD.
Question: What datasets are available related to Duchenne Muscular Dystrophy?
Answer: MD STARnet, ImagingDMD and PRO-DMD-01 are some of the available DMD datasets.
Using data from the Muscular Dystrophy Surveillance, Tracking, and Research Network (MD STARnet)
Using data from the Muscular Dystrophy Surveillance, Tracking, and Research Network (MD STARnet) Five sources of RWD/NHD were contributed by Universitaire Ziekenhuizen Leuven, DMD Italian Group, The Cooperative International Neuromuscular Research Group, ImagingDMD, and the PRO-DMD-01 study (n = 430 patients, in total).
Using data from the Muscular Dystrophy Surveillance, Tracking, and Research Network (MD STARnet)Five sources of RWD/NHD were contributed by Universitaire Ziekenhuizen Leuven, DMD Italian Group, The Cooperative International Neuromuscular Research Group, ImagingDMD, and the PRO-DMD-01 study (n = 430 patients, in total).
Using data from the Muscular Dystrophy Surveillance, Tracking, and Research Network (MD STARnet). Five sources of RWD/NHD were contributed by Universitaire Ziekenhuizen Leuven, DMD Italian Group, The Cooperative International Neuromuscular Research Group, ImagingDMD, and the PRO-DMD-01 study.
Five sources of RWD/NHD were contributed by Universitaire Ziekenhuizen Leuven, DMD Italian Group, The Cooperative International Neuromuscular Research Group, ImagingDMD, and the PRO-DMD-01 study (n = 430 patients, in total).
Question: Which vitamin deficiencies may present with neurologic signs or symptoms?
Answer: Many vitamin deficiencies have been described as a cause of neurologic signs and symptoms. For instance, vitamin B12 deficiency can cause several types of neurological manifestations, such as subacute combined degeneration of the spinal cord, ataxia, peripheral polyneuropathy, optic nerve neuropathy, and cognitive disorders. In addition, vitamin B1 (Thiamine) and B6 (Pyridoxine) deficiency can both cause peripheral neuropathy. Specifically, vitamin B1 deficiency can also cause confusion, ophthalmoplegia, nystagmus, and ataxia in the context of beriberi and Wernicke's encephalopathy. Finally, vitamin A deficiency has been described to cause retinal change-related visual defects and subsequent vision loss.
Question: What laboratory abnormalities are commonly seen in patients with COVID-19?
Answer: Common laboratory abnormalities among patients with COVID-19 include:

1. Elevated inflammatory markers (e.g., ferritin, C-reactive protein, and erythrocyte sedimentation rate).
2. Elevated aminotransaminase levels (i.e., AST, ALT).
3. Elevated lactate dehydrogenase (LDH) levels.
4. Lymphopenia, leucocytosis.

Abnormalities in coagulation testing (e.g., increased D-Dimers, decreased platelets), elevated procalcitonin levels, and elevated troponin levels have also been reported. The degree of these abnormalities tends to correlate with disease severity.
Question: Which factor is inhibited by Milvexian?
Answer: Milvexian is a small molecule, active-site inhibitor of factor XIa (FXIa) being developed to prevent and treat thrombotic events.
Question: What is Granzyme B?
Answer: Granzyme B is a serine protease that is secreted by Natural Killer (NK) cells and cytotoxic T lymphocytes during a cellular immune response and can induce apoptosis.