anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Preeclampsia (PE) is characterized by hypertension, proteinuria, and fetal growth restriction during pregnancy, suggesting that the preeclamptic intrauterine environment may affect the growth and health of the offspring. This study aimed to how maternal hypertension affects male offspring growth, focusing on lipid metabolism and blood pressure in mice. Female mice were infused with angiotensin II (Ang II) on gestational day 12. Dysregulation and accumulation of lipid were observed in the placenta of Ang II-induced maternal hypertensive dams, associating with fetal growth restriction. Ang II-offspring showed lower birth weight than in the control-offspring. Isolated and differentiated adipocyte from neonatal mice of Ang II-dams showed higher Pparγ mRNA expression compared with the control group. Lower body weight tendency had continued in Ang II-offspring during long period, body weight of Ang II-offspring caught up the control-offspring at 16 weeks of age. The adipose tissue of Ang II-offspring in adult also showed higher Pparγ mRNA expression with the accumulation of neutrophils and inflammatory monocytes than in those control. In addition, Ang II-offspring had higher basal blood pressure and higher sensitivity to hypertensive stimuli than in the control-offspring. Taken together, maternal hypertension induced by Ang II changes placental function, causing a lower birth weight. These changes in the intrauterine environment may affect adipocyte function and blood pressure of offspring after growth.
Atherosclerosis is a primary cause of cardiovascular and cerebrovascular diseases, with the unpredictable rupture of vulnerable atherosclerotic plaques enriched with lipid-laden macrophages being able to lead to heart attacks and strokes. Activating macrophage autophagy presents itself as a promising strategy for preventing vulnerable plaque formation and reducing the risk of rupture. In this study, we have developed a novel metal-free nanozyme (HCN@DS) that integrates the functions of multimodal imaging-guided therapy for atherosclerosis. HCN@DS has demonstrated high macrophage-targeting abilities due to its affinity toward scavenger receptor A (SR-A), along with excellent photoacoustic and photothermal imaging capabilities for guiding the precise treatment. It combines mild photothermal effects with moderate reactive oxygen species (ROS) generation to treat atherosclerosis. This controlled approach activates autophagy in atherosclerotic macrophages, inhibiting foam cell formation by reducing the uptake of oxidized low-density lipoproteins (oxLDL) and promoting efferocytosis and cholesterol efflux in macrophages. Additionally, it prevents plaque rupture by inhibiting apoptosis and inflammation within the plaque. Therefore, this metal-free nanozyme holds great potential for reducing the risk of atherosclerosis due to its high biosafety, excellent targeting ability, dual-modality imaging capability, and appropriate modulation of autophagy.
PCT No. PCT/EP80/00136 Sec. 371 Date Jul. 2, 1981 Sec. 102(e) Date Jul. 2, 1981 PCT Filed Nov. 21, 1980 PCT Pub. No. WO81/01367 PCT Pub. Date May 28, 1981.Water soluble biologically active fraction obtainable from the physiologically inter-cellular medium bone-marrow and process for preparing said fraction and the pharmaceutical compositions containing said fraction. The characteristics are notably the following: it is substantially free of the inhibitors having molecular weights lower than 30,000; it is lyophilizable without loss of biological properties; it exhibits the biological activities in the form of a solution having a pH of at least 7; it stimulates H-thymidin incorporation by bone-marrow cells in vitro and in vivo; the water soluble fraction is capable of controlling the immune reactions of a host against allogenic cells or tissue.
Chloramphenicol administered orally is absorbed rapidly from the intestinal tract. In controlled studies in adult volunteers using the recommended dosage of 50 mg/kg/day, a dosage of 1 g every 6 hours for 8 doses was given. Using the microbiological assay method, the average peak serum level was 11.2 mcg/mL one hour after the first dose. A cumulative effect gave a peak rise to 18.4 mcg/mL after the fifth dose of 1 g. Mean serum levels ranged from 8 to 14 mcg/mL over the 48-hour period. Total urinary excretion of chloramphenicol in these studies ranged from a low of 68% to a high of 99% over a three-day period. From 8% to 12% of the antibiotic excreted is in the form of free chloramphenicol; the remainder consists of microbiologically inactive metabolites, principally the conjugate with glucuronic acid. Since the glucuronide is excreted rapidly, most chloramphenicol detected in the blood is in the microbiologically active free form. Despite the small proportion of unchanged drug excreted in the urine, the concentration of free chloramphenicol is relatively high, amounting to several hundred mcg/mL in patients receiving divided doses of 50 mg/kg/day. Small amounts of active drug are found in bile and feces. Chloramphenicol diffuses rapidly, but its distribution is not uniform. Highest concentrations are found in liver and kidney, and lowest concentrations are found in brain and cerebrospinal fluid. Chloramphenicol enters cerebrospinal fluid even in the absence of meningeal inflammation, appearing in concentrations about half of those found in the blood. Measurable levels are also detected in pleural and in ascitic fluids, saliva, milk, and in the aqueous and vitreous humors. Transport across the placental barrier occurs with somewhat lower concentration in cord blood of neonates than in maternal blood.
Arginine methylation is catalyzed by protein arginine methyltransferases (PRMTs) and is involved in various cellular processes, including cancer development. PRMT2 expression is increased in several cancer types although its role in acute myeloid leukemia (AML) remains unknown. Here, we investigate the role of PRMT2 in a cohort of patients with AML, PRMT2 knockout AML cell lines as well as a Prmt2 knockout mouse model. In patients, low PRMT2 expressors are enriched for inflammatory signatures, including the NF-κB pathway, and show inferior survival. In keeping with a role for PRMT2 in control of inflammatory signaling, bone marrow-derived macrophages from Prmt2 KO mice display increased pro-inflammatory cytokine signaling upon LPS treatment. In PRMT2-depleted AML cell lines, aberrant inflammatory signaling has been linked to overproduction of IL6, resulting from a deregulation of the NF-κB signaling pathway, therefore leading to hyperactivation of STAT3. Together, these findings identify PRMT2 as a key regulator of inflammation in AML.
High risk classification if the change in rising hCG levels ≤ 63 % or the change in declining hCG ≤ 50 %. If these cut-offs are exceeded the PUL is classified as low risk and predicted to be either an IUP or failed PUL depending on rising or declining hCG levels.
The aim of this study is to assess alterations in heart function and structure in patients diagnosed with non-ST segment elevation acute myocardial infarction (NSTEAMI), unstable angina (UA), and stable angina (SA) 1 year after undergoing off-pump coronary artery bypass grafting (OPCABG) performed without extracorporeal circulation. A total of 182 patients who underwent OPCABG were included and classified into 3 groups based on their preoperative diagnosis: the NSTEAMI group (n = 68), the UA group (n = 64), and the SA group (n = 50). Cardiac ultrasonography data were collected for all groups both preoperatively and 1 year postoperatively. Clinical data were subjected to statistical analysis. In the NSTEAMI group, postoperative observations revealed increases in left ventricular stroke volume and left ventricular end-systolic diameter, along with reductions in left ventricular end-diastolic volume (LVEDV) and left ventricular end-diastolic diameter (LVEDD) 1-year post-surgery. The UA group demonstrated decreases in LVEDV and LVEDD 1-year post-surgery. Similarly, the SA group exhibited an increase in left ventricular ejection fraction (LVEF) and reductions in LVEDV and LVEDD 1-year post-surgery. Comparative analysis of cardiac ultrasonography data revealed that the NSTEAMI group displayed significantly lower left ventricular stroke volume and notably higher left ventricular end-systolic diameter and volume compared to the UA and SA groups 1-year post-surgery. Furthermore, the SA group exhibited significantly elevated LVEF compared to the UA and NSTEAMI groups 1-year post-surgery. Cardiac ultrasonography findings indicate that all 3 groups exhibited improvements in cardiac function and left ventricular structure 1-year post-surgery. However, the NSTEAMI group demonstrated more substantial improvements in comparison to the UA and SA groups.
Liu, Bo, Minlan Yuan, Mei Yang, Hongru Zhu, and Wei Zhang. The effect of high-altitude hypoxia on neuropsychiatric functions. High Alt Med Biol. 25:26-41, 2024. Background: In recent years, there has been a growing popularity in engaging in activities at high altitudes, such as hiking and work. However, these high-altitude environments pose risks of hypoxia, which can lead to various acute or chronic cerebral diseases. These conditions include common neurological diseases such as acute mountain sickness (AMS), high-altitude cerebral edema, and altitude-related cerebrovascular diseases, as well as psychiatric disorders such as anxiety, depression, and psychosis. However, reviews of altitude-related neuropsychiatric conditions and their potential mechanisms are rare. Methods: We conducted searches on PubMed and Google Scholar, exploring existing literature encompassing preclinical and clinical studies. Our aim was to summarize the prevalent neuropsychiatric diseases induced by altitude hypoxia, the potential pathophysiological mechanisms, as well as the available pharmacological and nonpharmacological strategies for prevention and intervention. Results: The development of altitude-related cerebral diseases may arise from various pathogenic processes, including neurovascular alterations associated with hypoxia, cytotoxic responses, activation of reactive oxygen species, and dysregulation of the expression of hypoxia inducible factor-1 and nuclear factor erythroid 2-related factor 2. Furthermore, the interplay between hypoxia-induced neurological and psychiatric changes is believed to play a role in the progression of brain damage. Conclusions: While there is some evidence pointing to pathophysiological changes in hypoxia-induced brain damage, the precise mechanisms responsible for neuropsychiatric alterations remain elusive. Currently, the range of prevention and intervention strategies available is primarily focused on addressing AMS, with a preference for prevention rather than treatment.
Methods of forming clear fragrances and formulations are described herein. The method includes providing a commercial fragrance formulation including a first concentration of a fragrance component and a second concentration of a nonessential component. The method further includes identifying the nonessential component, wherein the nonessential component includes an alcohol, an ester, a hydrocarbon, an aldehyde, a resin, other crystalline aroma chemicals, a first essential oil or combinations thereof, determining the second concentration and removing at least a portion of the nonessential component from the commercial fragrance formulation to form a first formulation, wherein the portion of the nonessential component is from about 5 wt. % to about 95 wt. % of the commercial fragrance formulation. The method further includes adding an essential component to the first formulation to form a second formulation, wherein the essential component is added to the first formulation in an amount substantially equal to the portion of the nonessential component removed from the commercial fragrance formulation. The method can further include preparing a second composition from the second formulation and processing the second composition to form the clear fragrance, wherein the processing comprises mixing, heating to a temperature of from about 20° C. to about 68° C. or combinations thereof, and wherein the clear fragrance is adapted to enhance solubility, enhance functional compatibility, enhance performance, reduce sweating or combination thereof, of the clear fragrance when added to an article.
BACKGROUND & AIMS: Desmoid tumors (DT) are an important cause of morbidity and mortality in patients with familial adenomatous polyposis (FAP). DT development might be related to the type and approach of colectomy. We aimed to compare DT development after colectomy with ileorectal anastomosis (IRA) and proctocolectomy with ileal pouch-anal anastomosis (IPAA).
METHODS: We performed an international historical cohort study in patients with FAP who underwent IRA or IPAA between 1961 and 2020. The primary outcome was the incidence of abdominal DT (either mesenteric, retroperitoneal, or abdominal wall). Patients with a DT diagnosis before or at colectomy were excluded. Time to DT was considered censored at an eventual secondary proctectomy after IRA. We used multivariable Cox regression modelling to adjust for potential confounders.
RESULTS: We analyzed data from 852 patients: 514 after IRA and 338 after IPAA (median follow-up, 21 and 16 years, respectively). DTs were diagnosed in 64 IRA patients (12%) and 66 IPAA patients (20%). The cumulative DT incidence at 5 and 10 years was 7.5% and 9.3% after open IRA and 4.7% and 10.9% after laparoscopic IRA. These estimates were 13.6% and 15.4% after open IPAA and 8.4% and 10.0% after laparoscopic IPAA. The postoperative risk was significantly higher after IPAA (P < .01) in multivariable analysis, whereas approach did not significantly influence the risk.
CONCLUSIONS: The risk of developing an abdominal DT was found to be significantly higher after IPAA than after IRA. Postoperative DT risk should be taken into account when choosing between IRA and IPAA in FAP.
BACKGROUND: Intracranial aneurysms are more commonly associated with inflammation as a cause of their development, progression, and rupture. Macrophages and other cells can express the CD68 antigen. The aim of this study was to assess the CD68 antigen levels in cerebral aneurysm (CA) patients compared to a control group at a referral center in Iran.
METHODS: A case-control investigation was undertaken on 88 individuals (44 of whom were cases and 44 were controls). Individuals with CA as the case group consisted of 28 ruptured and 16 unruptured subgroups. Clinical, radiographic, and CD68 levels were evaluated and registered.
RESULTS: The average age of the participants was 49 years. Males comprised 43.2% of the patients, while 56.8% were females (p = 0.002). There was a statistically significant difference in the CD68 levels between the two groups. There was no significant difference (p = 0.42) between the ruptured and unruptured subgroups (23.66 and 20.47, respectively) in this comparison. No significant correlation was seen between the patients' CD68 and Glasgow Coma Scale (GCS) levels and their aneurysm diameter (p = 0.74 and 0.45, respectively). A link between CD68 levels and age was found, but it was not statistically significant (r = 0.44 and p = 0.002).
CONCLUSIONS: A possible involvement of CD68 as an inflammatory agent in the development of CAs but not in aneurysm rupture has been suggested. Inflammation and CD68 were positively associated with age. The CD68 antigen should be studied further in population-based cohort studies.
Forensic pathologists often encounter cases of acute subdural hematoma (SDH) due to trauma, whereas those attributable to endogenous causes are rare. Here, we report a case of the latter type in a 42-year-old man who was found dead at home after several months of fever and malaise. Postmortem computed tomography (PMCT) and autopsy were undertaken to clarify the cause of death. PMCT images revealed a fatal SDH and a localized hyper-density area in the right parietal lobe; macroscopic and microscopic examinations revealed SDH due to rupture of a mycotic aneurysm (MA) associated with meningitis. The PMCT images also indicated thickening and calcification of the mitral valve, while autopsy demonstrated infective endocarditis (IE). In addition, PMCT demonstrated a low-density area in the spleen, which was shown to be a splenic abscess at autopsy. PMCT also demonstrated tooth cavities. Based on the findings of autopsy, the cause of death was considered to be SDH due to rupture of the MA resulting from meningitis with IE and splenic abscess. Although PMCT was unable to clarify the significance of any individual feature, a retrospective review of the PMCT images might have suggested IE, bacteremia, or ruptured MA leading to SDH. This case suggests that, instead of interpreting individual features demonstrated on PMCT images, integrated interpretation of overall PMCT findings might provide clues for identifying causes of death, despite the fact that PMCT lacks diagnostic accuracy for infectious diseases such as IE and meningitis.
The invention discloses a medicament for promoting the repair of peripheral nerve injury. The invention provides application of a nerve growth factor specifically bound with a collagen and/or a coding gene of the nerve growth factor specifically bound with the collagen in preparing a medicament for repairing the peripheral nerve injury. An active ingredient of the medicament for repairing the peripheral nerve injury is the nerve growth factor specifically bound with the collagen and/or the coding gene of the nerve growth factor specifically bound with the collagen. The CBD-NGF is applied in vivo, and is specifically bound to a nerve-injured part by utilizing an intrinsic nerve extracellular matrix collagen to form higher concentration around a neuron so as to reduce the effective consumption of beta-NGF and improve the efficiency of repairing the peripheral nerve injury. The CBD-NGF has better effect of repairing sciatic nerve injury. The medicament has good clinical application prospect.
All patients undergone surgery for the removal of a pituitary adenoma. Tissue samples of these cases were sent to biochemical essay to measure the expression and localisation of KLHL14.
In embodiments, a pre-analyzing computer receives a data record that is created by a wearable medical system (“WMS”) which may implement a wearable cardioverter defibrillator (“WCD”). The WMS has created such data records from patient data captured when the WMS has detected that the patient was having episodes of potential interest for review by clinicians. Before this review, however, the pre-analyzing computer may parse the contents of a received data record and accordingly give it a score. The score may reflect the clinician's expected preference to review this data record before or after the others. For instance, a low score may be given to data records whose contents are likely not interpretable reliably due to noise or likely of low interest after all. The pre-analyzing computer may then perform a characterizing action with reference to the data record, for facilitating the clinician to find it by its score.
FIELD: pharmaceutical chemistry. SUBSTANCE: invention relates to improved method for preparing amlodipin benzolsulfonate, which is also known as amlodipin bezilate and is really 2-[(2-aminoethoxy)methyl]-4-(2-chlorophenyl)-1,4-dihydro-6-methyl- 3,5-pyridinedicarboxylic acid 3-ethyl-5-methyl ester benzolsulfonate salt, which is worthy antiischemic and antihypertensive compound. Preparation consists in adding aqueous benzenesulfonic acid solution to above named ester preliminarily suspended in water, keeping resulting mixture for 8-10 h at 30-50 C, preferably at 35 C, separating thus obtained amlodipin benzolsulfonate, drying and purifying product by dissolving it in methanol, heating resulting suspension to 45-50 C, adding charcoal followed by stirring, vacuum filtration, and removing methanol, after which is added ethyl acetate, reaction mixture is heated to 55-60 C, kept at this temperature for 1.5, cooled to 18-20 C, and aged for 1 h before vacuum filtration giving product, which is washed with ethyl acetate and dried. Purity of product is 99.5-99.8%. EFFECT: minimized level of polar solvents in product so that it cannot be used for preparing drugs without further purification. 1 tbl
PURPOSE:To obtain a paper pressure-sensitive tape for medical use with good adhesiveness with a skin and low skin irritation by incorporating a crosslinked product of a copolymer of an alkyl acrylate, a mixture of the alkyl acrylate and an alkoxyalkyl acrylate and a carboxyl or hydroxyl group-contg. monomer in a crosslinkable pressure-sensitive adhesive layer. CONSTITUTION:99.5 pts. isononyl acrylate and 0.5 pt. acrylic acid are copolymerized in ethyl acetate in an inert gas atmosphere to prepare a copolymer soln. 90 pts. solid content of this soln. and 10 pts. metoprolol are mixed and in addition, 0.3 pt. ethyl acetoacetate aluminum diisopropylate is made into a 10% acetylacetone soln., which is then incorporated therein. one face of a polyethylene terephthalate film with a thickness of 12mum is coated with the obtd. soln. and is dried so as to obtain the thickness of 80mum after drying. It is possible thereby to satisfy stability of a drug, adhesiveness with a skin and releaseness of the drug and to decrease skin irritation.
FIELD: medicine; nourishment hygiene. SUBSTANCE: method includes introduction of pantocrine production waste into fodder of rats. Every day in the morning rats are placed in climate chamber whish sets up constant mode of cooling at minus 15 C. Rats are exposed to cold in the course of 28 days for 3 h daily. Use of pantocrine production waste at continuous effect of cold on rats results in normalization of structural homeostasis in mucous coat of air-carrying tracts and stimulates adaptation of worm-blooded organism to effect of cold. EFFECT: improved adaptation. 1 tbl
Post-burn hypertrophic scars often exhibit abnormal pigmentation. Exosomes play important roles in maintaining normal physiological homeostasis and in the pathological development of diseases. This study investigated the effects of the exosomes derived from hypertrophic scar fibroblasts (HTSFs) on melanocytes, which are pigment-producing cells. Normal fibroblasts (NFs) and HTSFs were isolated and cultured from normal skin and hypertrophic scar (HTS) tissue. Both the NF- and HTSF-exosomes were isolated from a cell culture medium and purified using a column-based technique. The normal human epidermal melanocytes were treated with both exosomes at a concentration of 100 μg/mL at different times. The cell proliferation, melanin content in the medium, apoptotic factors, transcription factors, melanin synthesis enzymes, signaling, signal transduction pathways, and activators of transcription factors (STAT) 1, 3, 5, and 6 were investigated. Compared with the Dulbecco's phosphate-buffered saline (DPBS)-treated controls and NF-exosomes, the HTSF-exosomes decreased the melanocyte proliferation and melanin secretion. The molecular patterns of apoptosis, proliferation, melanin synthesis, Smad and non-Smad signaling, and STATs were altered by the treatment with the HTSF-exosomes. No significant differences were observed between the DPBS-treated control and NF-exosome-treated cells. HTSF-derived exosomes may play a role in the pathological epidermal hypopigmentation observed in patients with HTS.