anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Effector secretion by different routes mediates the molecular interplay between host plant and pathogen, but mechanistic details in eukaryotes are sparse. This may limit the discovery of new effectors that could be utilized for improving host plant disease resistance. In fungi and oomycetes, apoplastic effectors are secreted via the conventional endoplasmic reticulum (ER)-Golgi pathway, while cytoplasmic effectors are packaged into vesicles that bypass Golgi in an unconventional protein secretion (UPS) pathway. In Magnaporthe oryzae, the Golgi bypass UPS pathway incorporates components of the exocyst complex and a t-SNARE, presumably to fuse Golgi bypass vesicles to the fungal plasma membrane. Upstream, cytoplasmic effector mRNA translation in M. oryzae requires the efficient decoding of AA-ending codons. This involves the modification of wobble uridines in the anticodon loop of cognate tRNAs and fine-tunes cytoplasmic effector translation and secretion rates to maintain biotrophic interfacial complex integrity and permit host infection. Thus, plant-fungal interface integrity is intimately tied to effector codon usage, which is a surprising constraint on pathogenicity. Here, we discuss these findings within the context of fungal and oomycete effector discovery, delivery, and function in host cells. We show how cracking the codon code for unconventional cytoplasmic effector secretion in M. oryzae has revealed AA-ending codon usage bias in cytoplasmic effector mRNAs across kingdoms, including within the RxLR-dEER motif-encoding sequence of a bona fide Phytophthora infestans cytoplasmic effector, suggesting its subjection to translational speed control. By focusing on recent developments in understanding unconventional effector secretion, we draw attention to this important but understudied area of host-pathogen interactions. [Formula: see text] Copyright © 2024 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.
The invention belongs to the technical field of drugs for treating anaphylactic purpura, aims to solve the problems of bad curative effect, strong side effect, long treatment course, and high cost existing in the conventional drugs for treating anaphylactic purpura caused by deficiency of qi and blood, and provides a traditional Chinese medicine preparation for curing anaphylactic purpura caused by deficiency of qi and blood. The preparation is prepared from radix astragali, radix codonopsis, raw rehmannia root charcoal, tree peony bark, peach seed, fried white peony root, sophora flower charcoal, ginger charcoal, ligusticum wallichii, garden burnet root charcoal, bitter organe, and jujube according to a certain ratio. The traditional Chinese medicine preparation is mainly for treating anaphylactic purpura caused by deficiency of qi and blood. The anaphylactic purpura is usually caused by the reason that the spleen and stomach are weak, the qi in middle-jiao is deficient, the spleen fails to manage blood, then blood escapes from the vessels and channels, and finally the blood flows out and is staggered in the skin so as to cause the disease. Radix codonopsis and radix astragali have the function of tonifying qi, raw rehmannia root charcoal, sophora flower charcoal, and tree peony bark have the functions of cooling blood and promoting blood circulation, peach seed has the functions of activating blood and dispersing blood stasis, garden burnet root charcoal has the functions of cooling blood and stopping bleeding, white peony root has the functions of nourishing blood and constraining yin, ligusticum wallichii has the functions of regulating qi and activating blood, bitter orange has the function of regulating qi, ginger charcoal has the function of freeing the collateral vessels, and jujube has the functions of tonifying spleen and nourishing blood; the medicinal materials mentioned above cooperate with each other to have a synergic effect so as to have functions of freeing the collateral vessels and eliminating speckles. The effective rate of the traditional Chinese medicine on treating anaphylactic purpura caused by deficiency of qi and blood reaches 92% or more.
Myofascial Pain Syndrome is a condition characterized by sensory, motor and autonomic symptoms caused by trigger points (TN), which have a source of pain within the muscle and fascia. Trigger points are hyperirritable points located within taut bands. The aim of the treatment is to inactivate trigger points and relax tense muscle bands. The goal is to eliminate muscle tension and achieve normal muscle length, function and strength. Needling methods are still considered the most effective method in the initial treatment of MAS. Local anesthetic (LA) injection is a frequently used method with proven effectiveness .

Although the etiology of the ethical points accompanying MAS has not been elucidated; It is thought that posture disorders, vitamin-mineral deficiencies, metabolic diseases, genetic factors, stress and overuse disrupt the contraction-relaxation cycle in muscle sarcomeres. An acidic and hypoxic environment occurs in the muscle, inflammatory mediators are released, and this situation is more common in phasic muscles than in tonic muscles. Trigger points are divided into two: active and latent. In active trigger points, the patient's complaint is triggered by palpation and a jump sign is obtained, while in latent trigger points, pain occurs with palpation, but the patient's complaint is not triggered. During the examination, the trigger point is compressed and a local twitch response is obtained. Sometimes trigger points can also cause autonomic symptoms and referred pain .

The study was conducted at the Algology Department of Kanuni Sultan Süleyman Training and Research Hospital, between March 2023 and March 2024, on patients aged 18-65 who had MAS and therefore had serratus posterior superior intercostal plane block or trigger point injection applied to the neck-back region in a single session. It will be done by retrospectively scanning the files of the patients . Within the scope of the research, age, gender, Visual Analog Scale (VAS), Neck disability scores and Algometric measurements before and in the first and third months after the procedure will be scanned from patient files and those that can be accessed will be recorded.
PURPOSE:To obtain a DC-52 derivative having excellent antitumor activity. CONSTITUTION:A DC-52 derivative of formula I (X is hydroxymethyl, alkanoyloxymethyl of formyl; Y is CN or OH) or its pharmaceutically acceptable salt. A compound of formula I wherein X is hydroxymethyl and Y is CN is obtained by esterifying a DC-52 derivative (DX-52-1: Japanese patent publication SHO-59-210,086) of formula II in methanol in the presence of an acid catalyst to give a compound of formula III and treating the compound of formula III with a reducing agent (e.g. lithium aluminum halide). The compound of formula III is reacted with a silylating agent, treated with a reducing agent to give a compound of formula IV, which is reacted with a compound of the formula ROH (R is alkanoyl) and desilylated to give the compound of formula I wherein Y is CN and X is alkanoyloxymethyl. A compound wherein Y is OH is obtained by treating a corresponding compound wherein Y is CN in water or an organic solvent in the presence of a silver salt optionally with water or hydrochloic acid.
Decreases in estrogen levels after oophorectomy or menopause lead to increases in bone resorption and accelerated bone loss. Bone is initially lost rapidly because the compensatory increase in bone formation is inadequate to offset resorptive losses. In addition to loss of estrogen, this imbalance between resorption and formation may be due to age-related impairment of osteoblasts or their precursors. In some women, these changes will eventually lead to decreased bone mass, osteoporosis, and increased risk for fractures, particularly of the spine, hip, and wrist. Vertebral fractures are the most common type of osteoporotic fracture in postmenopausal women. 

In both the osteoporosis treatment and prevention trials, EVISTA therapy resulted in consistent, statistically significant suppression of bone resorption and bone formation, as reflected by changes in serum and urine markers of bone turnover (e.g., bone-specific alkaline phosphatase, osteocalcin, and collagen breakdown products). The suppression of bone turnover markers was evident by 3 months and persisted throughout the 36-month and 24-month observation periods. 

In a 31-week, open-label, radiocalcium kinetics study, 33 early postmenopausal women were randomized to treatment with once-daily EVISTA 60 mg, cyclic estrogen/progestin (0.625 mg conjugated estrogens daily with 5 mg medroxyprogesterone acetate daily for the first 2 weeks of each month [hormone therapy]), or no treatment. Treatment with either EVISTA or hormone therapy was associated with reduced bone resorption and a positive shift in calcium balance (-82 mg Ca/day and +60 mg Ca/day, respectively, for EVISTA and -162 mg Ca/day and +91 mg Ca/day, respectively, for hormone therapy). 

There were small decreases in serum total calcium, inorganic phosphate, total protein, and albumin, which were generally of lesser magnitude than decreases observed during estrogen or hormone therapy. Platelet count was also decreased slightly and was not different from estrogen therapy.
###  Risk Summary

Clinical administration of cyclosporine ophthalmic emulsion 0.05% is not detected systemically following topical ocular administration [see Clinical Pharmacology (12.3)], and maternal use is not expected to result in fetal exposure to the drug. Oral administration of cyclosporine to pregnant rats or rabbits did not produce teratogenicity at clinically relevant doses [see Data].

###  Data

#### Animal Data 

At maternally toxic doses (30 mg/kg/day in rats and 100 mg/kg/day in rabbits), cyclosporine oral solution (USP) was teratogenic as indicated by increased pre- and postnatal mortality, reduced fetal weight and skeletal retardations. These doses (normalized to body surface area) are 5,000 and 32,000 times greater, respectively, than the daily recommended human dose of one drop (approximately 28 mcL) of cyclosporine ophthalmic emulsion 0.05% twice daily into each eye of a 60 kg person (0.001 mg/kg/day), assuming that the entire dose is absorbed. No evidence of embryofetal toxicity was observed in rats or rabbits receiving cyclosporine during organogenesis at oral doses up to 17 mg/kg/day or 30 mg/kg/day, respectively. These doses in rats and rabbits are approximately 3,000 and 10,000 times greater, respectively, than the daily recommended human dose. An oral dose of 45 mg/kg/day cyclosporine administered to rats from Day 15 of pregnancy until Day 21 postpartum produced maternal toxicity and an increase in postnatal mortality in offspring. This dose is 7,000 times greater than the daily recommended human dose. No adverse effects in dams or offspring were observed at oral doses up to 15 mg/kg/day (2,000 times greater than the daily recommended human dose).
The present invention provides a method for treating a subject suffering from a neurodegenerative disease by administering at least one triterpenoid which can be obtained from Hedera helix. Further provided is a method for treating a subject suffering from a 5 neurodegenerative disease by administering an effective amount of a Hedera helix extract which comprises the triterpenoid. The neurodegenerative disease is preferably but not exclusively Parkinson's disease or Huntington's disease. The present invention also provides methods for extracting the triterpenoid from Hedera helix and a method for inducing autophagy in cells by contacting them with the triterpenoid. o The triterpenoid of the present invention proved to allow an exceptional induction of autophagy, in particular a significant reduction of the protein level of mutant huntingtin, a significant reduction of the protein level of A53T a-synuclein, a significant inhibition of the oligomerization of a-synuclein and a significant inhibition of the inclusion formation of huntingtin via the AMPK-mTOR dependent autophagy inducing pathway. The present 5 invention, thus, provides a highly promising treatment option for treating neurodegenerative diseases.
Wandering, or elopement, is a life-threatening behavior that has been reported to occur in a third of all children with autism spectrum disorders (ASD). Wearable electronic tracking devices (ETDs) that are able to pinpoint a child's location have emerged as an appealing intervention for families concerned about wandering risk. However, the impact of ETD use on the families of children who wander has never been studied prospectively. In this pilot study, parents will be provided with a commercially-available ETD to use for their child with ASD for 6 weeks. Preliminary data will be obtained to evaluate the impact of ETD use on the strain experienced by families due to their child's wandering behavior. The feasibility of all study procedures will be assessed in preparation for a larger subsequent trial.
The devastating effect of severe acute respiratory syndrome coronavirus-2 (SARS COV-2) infection is caused by a robust cytokine storm that leads to lung tissue damage. Several studies reported a correlation between disease severity and the release of excessive proinflammatory cytokines, such as tumor necrosis factor-α (TNF-α), IL-6, IL-1, IFN-Υ, IFN-Υ-induced protein 10 (IP10), monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-1a (MIP-1a), and granulocyte-colony stimulating factor (G-CSF). This finding was confirmed by the high level of plasma cytokines found in most severe COVID-19 patients associated with extensive lung damage. Therefore, finding an effective therapeutic option to control the devastating cytokine storm of COVID-19 and regenerate the damaged lung is crucial.

Previous studies reported that the hypoxic condition of MSCs could enhance the release of their active soluble molecules known as Secretome-MSCs (S-MSCs), such as IL-10 and TGF-β that useful in alleviating inflammation. Moreover, they could also increase the expression of growth factors such as VEGF and PDGF that accelerate lung injury improvement. These active molecules could potentially serve as a biological therapeutic agent for treating the severe SARS-CoV-2 infection. According to recent studies, we successfully isolated the S-MSCs from their culture medium using tangential flow filtration (TFF) strategy with several molecular weight cut-off category. This study investigated the clinical outcomes of severe COVID-19 patients with several comorbidities treated with S-MSCs in Indonesia.
pathological pain and Attention-deficit/hyperactivity disorder (ADHD) are two complex multifactorial syndromes. The comorbidity of ADHD and altered pain perception is well documented in children, adolescents, and adults. According to pathophysiological investigations, the dopaminergic system's dysfunction provides a common basis for ADHD and comorbid pain. Growing evidence suggests that oxidative stress may be crucial in both pathologies. Recent studies revealed that a small peptide encompassing the redox-active site of selenoprotein T (PSELT), protects dopaminergic neurons and fibers as well as lesioned nerves in animal models. The current study aims to examine the effects of PSELT treatment on ADHD-like symptoms and pain sensitivity, as well as the role of catecholaminergic systems in these effects. Our results demonstrated that intranasal administration of PSELT reduced the hyperactivity in the open field, decreased the impulsivity displayed by 6-OHDA-lesioned male mice in the 5-choice serial reaction time task test and improved attentional performance. In addition, PSELT treatment significantly increased the nociception threshold in both normal and inflammatory conditions. Furthermore, anti-hyperalgesic activity was antagonized with sulpiride pre-treatment, but not by phentolamine, or propranolol pre-treatments. The present study suggests that PSELT reduces the severity of ADHD symptoms in mice and possesses potent antinociceptive effects which could be related to the involvement of D2/D3 dopaminergic receptors.
The investigators will study women who have sustained an unintentional dural puncture at least one year prior to the start date of the study, and the investigators will study cases occurring during a period of 5 years. These women will be matched by type of procedure (labor epidural), month of delivery and age with women who have received an epidural but did not sustain an unintentional dural puncture. The group of women who sustained dural punctures will be further divided into two groups, whether they have received epidural blood patch or not, to study the influence of the epidural blood patch on the outcomes. Women will have their anesthetic records reviewed to collect data on the anesthetic technique, presence of a dural puncture and treatment if applicable. All patients who qualify will be contacted and invited to take part in this study. Those consenting to the study will be interviewed by phone or answer the survey electronically. During the interview, they will answer questions derived from validated questionnaires for the majority of our outcomes of interest. In the few outcomes where a validated questionnaire does not exist, the investigators will search for our endpoint with dichotomic (yes/no) questions. The investigators will then compare the data gathered in the three different groups to validate or invalidate our hypothesis.
Patients with mutations in Cldn16 suffer from familial hypomagnesaemia with hypercalciuria and nephrocalcinosis (FHHNC) which can lead to renal insufficiency. Mice lacking claudin-16 show hypomagnesemia and hypercalciuria, but no nephrocalcinosis. Calcium oxalate and calcium phosphate are the most common insoluble calcium salts that accumulate in the kidney in the case of nephrocalcinosis, however, the formation of these salts is less favored in acidic conditions. Therefore, urine acidification has been suggested to limit the formation of calcium deposits in the kidney. Assuming that urine acidification is causative for the absence of nephrocalcinosis in the claudin-16-deficient mouse model, we aimed to alkalinize the urine of these mice by the ablation of the subunit B1 of the vesicular ATPase in addition to claudin-16. In spite of an increased urinary pH in mice lacking claudin-16 and the B1 subunit, nephrocalcinosis did not develop. Thus, urinary acidification is not the only factor preventing nephrocalcinosis in claudin-16 deficient mice.
The present invention discloses a medicinal composition containing salvianolic acid B, panax notoginseng saponin and borneol, a preparation method thereof and an application thereof. The medicinal composition is a compound freeze-drying injection containing red sage root, which is prepared from extract of red sage root, notoginseng extract, a hydroxypropyl beta-cyclodextrin inclusion compound of borneol and medicinal auxiliary materials, wherein the extract of red sage root uses salvianolic acid B as main effective components and the notoginseng extract uses panax notoginseng saponin as main effective parts. In the present invention, the extract of red sage root is obtained by combining ultrasonic extraction, ultrafiltration, ethyl acetate extraction, rotation, knifing and concentration, the panax notoginseng saponin as effective components is extracted from the notoginseng by the methods of water extraction, alcohol deposition and macroporous resin, and hydroxypropyl beta-cyclodextrin (HP-beta-CD) is used for covering the borneol in the formula. Thus, the present invention solves the problem that the medicinal composition is difficult to dissolve in the water solution of injection solution and enhances the quality and the clinical curative effect of the medicinal composition. The present invention is used for preventing and treating cardio-cerebrovascular disease. Content measurement and pharmacological experiments indicate that the compound freeze-drying injection containing red sage root of the present invention has the characteristics of high content of effective components and obvious curative effect.
Lesion sterilization and tissue repair; preparation of modified triple antibiotic paste tap: the chemotherapeutic agents used are metronidazole tablets 500 mg (flagyl®, sanofi, egypt), ciprofloxacin tablets 500 mg (ciproxcin®,. Epico, egypt,), and doxycycline capsules 100 mg (doxymycin™ dt, el-nile pharmaceuticals, egypt).
Newborns will receive routine medical treatment and nursing care and will not undergo any procedures. Before the procedure, written and verbal consent will be obtained from the newborn's guardian and brief information about the study will be given. Premature babies will have their 24-hour sleep recorded with actigraphy 1 day in advance. Then, the nursing care that premature babies receive in their daily routine will be given for two days. On the morning of the second day, an actigraphy device will be attached to the left foot of the premature babies and their 24-hour sleep on the second day will be recorded.
A human growth hormone fusion protein has enhanced thermal stability. The human growth hormone fusion protein has the amino acid sequence SEQ ID NO: 3 or SEQ ID NO: 4. A gene encoding the human growth hormone fusion protein has  E. coli  codon-optimized nucleotide sequence of SEQ ID NO: 5 or SEQ ID NO: 6. A recombinant vector includes the aforementioned gene. A host cell is transformed with the aforementioned recombinant vector. A method for producing in a host cell a human growth hormone fusion protein includes transforming a host cell with the aforementioned recombinant vector. The human growth hormone fusion protein may improve skin wrinkle and maintain skin elasticity. As the human growth hormone fusion protein has thermal stability and also has an effect of improving skin wrinkle and increasing the effect of maintaining skin elasticity, it can be advantageously used as a raw material of cosmetics.
The invention belongs to the field of biological pharmacy, and discloses an expression vector, lipid nanoparticles, an antitumor drug, and a preparation method and application thereof. The expression vector comprises a tumor specific promoter and a melittin gene, wherein the melittin gene comprises a sequence shown by SEQID No. 1. The invention also provides a lipid nanoparticle which comprises the expression vector and a lipid layer coated on the surface of the expression vector. The lipid nanoparticle of the invention does not express melittin in non-tumor cells, but can specifically express melittin in tumor cells, and can target tumor cells for delivery, thereby playing an anti-tumor role by destroying the lipid biomembrane structure of the tumor cells, inducing the apoptosis of the tumor cells and the like, and realizing better anti-tumor treatment effect. The lipid nanoparticle has lower toxicity and high-efficiency anti-tumor treatment effect, and can be widely applied to anti-tumor application.
Some patients have experienced serious complications of constipation without warning. 

Serious complications of constipation, including obstruction, ileus, impaction, toxic megacolon, and secondary bowel ischemia, have been reported with use of alosetron hydrochloride during clinical trials. Complications of constipation have been reported with use of 1 mg twice daily and with lower doses. A dose response relationship has not been established for serious complications of constipation. The incidence of serious complications of constipation was approximately 0.1% (1 per 1,000 patients) in women receiving either alosetron hydrochloride or placebo. In addition, rare cases of perforation and death have been reported from postmarketing clinical practice. In some cases, complications of constipation required intestinal surgery, including colectomy. Patients who are elderly, debilitated, or taking additional medications that decrease gastrointestinal motility may be at greater risk for complications of constipation. 

Alosetron hydrochloride should be discontinued immediately in patients who develop constipation [see Boxed Warning].