Cardiothoracic surgery posits an arrangement of large, significant hemodynamic, and physiologic alterations upon the human body, which predisposes a patient to develop pathology. The care of these ...patients in the postoperative realm requires an astute physician with deep understanding of the cardiopulmonary system, who is able to address subtle developing problems promptly, before the patient suffers further sequelae. In this review, we describe the presentation and management of an assortment of important complications which occur in the pulmonary system. In addition, we aim to shed better light upon how the physiology of a patient responds to the condition of cardiothoracic surgery.
MALAT-1 is extremely elevated in human malignancies thus functions as a prognostic biomarker. Nevertheless, limited data has been discovered concerning MALAT's contribution in stomach cancer. MALAT-1 ...expression appeared considerably greater in gastric cancer (GC) rats with remote miR-122-IGF-1R impact. MALAT-1 depletion inhibited cell cycle development, cell division and invasion, thus boosting death of GC cells. Likewise, miR-122-IGF-1R expression was linked to MALAT-1 deregulations in GC. Biological markers discovery based on biochemical data alongside detailed genome study might enhance prognosis, diagnosis and therapeutic compliance. This article summed up the most recent developments and techniques in GC biomarkers and may have applications for early detection, precise estimation of treatment strategies, and future perspectives according to molecular classification and profiling. In rats, GC was induced by 20-MCA, followed by DOX, Liposomal DOX, and PEGylated-Dox treatment. In addition to histopathological examinations, GC tumor biomarkers such as CEA, CA12–5, KRAS, AKT, PTEN, TP53, JAK-2, lnc- MALAT-1 and miR-122-IGF-1R were tracked. These findings reveal that MALAT-1 may be oncogenic in GC. Prominent MALAT-1 levels may assist as an indicator of metastasis in GC, and that miR-122-IGF-1R expression is associated via reduced MALAT-1 signaling. Finally, PEG-DOX may be an excellent option for GC therapy.
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•Induction of gastric cancer in rats via 20-MCA.•Treatment with DOX, Liposomal DOX and PEG-DOX.•Monitoring miR-122-IGF and MALAT.•Monitoring P53, KRAS, PTEN, JAK2, AKT, CEA and CA12–5.•PEG-DOX could be a prospective DDS.
This paper introduces a planar antipodal meander line antenna fabricated using RO3003 substrate. The proposed antenna is designed to radiate in the end-fire direction, achieving a maximum measured ...gain of 10.43 dBi within its working bandwidth, which ranges from 2.24 GHz to 2.7 GHz, covering long-range WLAN/WiMAX applications. A systematic procedure is adopted in the design process to prove its tunability to cover other application requirements in terms of gain and bandwidth. The proposed design steps show that the bandwidth and the gain can independently be controlled by adjusting specific design parameters such as the number of radiators and the scaling factor. The antenna is fine-tuned using sensitivity analysis and parametric study to guarantee optimum operation at the desired bandwidth. Experimental measurements of the fabricated design demonstrate a high degree of correlation with simulations conducted using CST and HFSS. In comparison to other end-fire antennas presented in the literature, the proposed design manifests its capability to provide high gain for WLAN/WiMAX nodes connectivity. The measurements show that the proposed traveling wave antenna exhibits a high radiation efficiency with maximum value of 99.8% at 2.35 GHz. The measured side lobe level is found to be below
dB and
dB at 2.45 GHz along the
- and
-planes, respectively. Apart from its excellent radiation performance, the antenna is characterized by its low profile and fabrication simplicity.
CRISPR/Cas9 is a recently discovered genomic editing technique that altered scientist's sight in studying genes function. Cas9 is controlled via guide (g) RNAs, which match the DNA targeted in ...cleavage to modify the respective gene. The development in prostate cancer (PC) modeling directed not only to novel resources for recognizing the signaling pathways overriding prostate cell carcinoma, but it has also created a vast reservoir for complementary tools to examine therapies counteracting this type of cancer. Various cultured somatic rat models for prostate cancer have been developed that nearly mimic human prostate cancer. Nano-medicine can passively target cancer cells via increasing bioavailability and conjugation via specific legend, contributing to reduced systemic side-effects and increased efficacy. This article highlights liposomal loaded Nano-medicine as a potential treatment for prostate cancer and clarifies the CRISPR/Cas9 variation accompanied with prostate cancer. PC is induced experimentally in western rat model via ethinyl estradiol for 4 weeks and SC. dose of 3, 2'- dimethyl-4-aminobiphenyl estradiol (DAE) (50mg/kg) followed by treatment via targeted liposomal-coated compounds such as liposomal dexamethasone (DXM), liposomal doxorubicin (DOX) and liposomal Turmeric (TUR) (3mg/kg IP) for four weeks in a comparative study to their non-targeted analogue dexamethasone, doxorubicin and Turmeric. 3, 2'- dimethyl-4-aminobiphenylestradiol elicit prostate cancer in western rats within 5 months. Simultaneous supplementations with these liposomal compounds influence on prostate cancer; tumor markers were investigated via prostate-specific antigen (PSA), Nitric oxide (NOX) and CRISPR/Cas9 gene editing. Several long non-coding RNAs were reported to be deregulated in prostate cell carcinoma, including MALAT1. On the other hand, gene expression of apoptotic biomarkers focal adhesion kinase (AKT-1), phosphatidylinistol kinase (PI3K) and glycogen synthase kinase-3 (GSK-3) was also investigated and further confirming these results via histopathological examination. Liposomal loaded dexamethasone; doxorubicin and Turmeric can be considered as promising therapeutic agents for prostate cancer via modulating CRISPR/Cas9 gene editing and long non coding gene MALAT1.
Aluminum chloride (AlCl
3
) is commonly used in daily life; meanwhile, it is the potential etiology of various neurodegenerative as well as hepatorenal diseases. Therefore, the present study was ...carried out to investigate the correlation between AlCl
3
-induced biochemical alterations and the toxicity induced in various organs such as the brain, liver, and kidney. Male mice received AlCl
3
in an oral dose of 50 mg kg
−1
in addition to (50 mg) in drinking water for 2 weeks. Two weeks post-AlCl
3
intoxication, the brain, liver, and kidney biochemical indices were assessed via molecular and western blot analysis. The results are as follows: AlCl
3
intoxication induced a significant elevation in serum malondialdehyde in addition to a significant reduction in serum glutathione (GSH) and superoxide dismutase (SOD) levels. Brain β-secretase (tubulin-binding protein) and tau proteins which are responsible for the synthesis of β-amyloid protein that may interfere with neuronal communication in Alzheimer’s disease (AD) were also upregulated; regarding hepatic function, AlCl
3
elevated serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities. Moreover, it upregulated hepatic mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK) protein expressions as well as renal kidney-inducible molecule-1 (KIM-1) which indicated the deleterious effect of AlCl
3
on these organs. These results were confirmed by histopathological investigations. So, we hypothesize that acute AlCl
3
administration is responsible for oxidative cell damage that interferes with brain function inducing β-amyloid accumulation, Alzheimer’s disease, and neurodegenerative damage as well as hepatorenal injuries.
A new easily separable core–shell Fe3O4/PVP/ZIF-8 nanostructure adsorbent was synthesized and then examined for removal of Fosfomycin antibiotic from synthetic pharmaceutical wastewater. The removal ...process of Fosfomycin was expressed through testing the total phosphorus (TP). A response surface model (RSM) for Fosfomycin adsorption (as mg-P L−1) was used by carrying out the experiments using a central composite design. The adsorption model showed that Fosfomycin adsorption is directly proportional to core–shell Fe3O4/PVP/ZIF-8 nanostructure adsorbent dosage and time, and indirectly to initial Fosfomycin concentration. The removal increased by decreasing the pH to 2. The Fosfomycin removal was done at room temperature under an orbital agitation speed of 250 rpm. The adsorption capacity of core–shell Fe3O4/PVP/ZIF-8 nanostructure adsorbent reached around 1200 mg-P g−1, which is significantly higher than other MOF adsorbents reported in the literature. The maximum Langmuir adsorption capacity of the adsorbent for Fosfomycin was 126.58 mg g−1 and Fosfomycin adsorption behavior followed the Freundlich isotherm (R2 = 0.9505) in the present study. The kinetics was best fitted by the pseudo-second-order model (R2 = 0.9764). The RSM model was used for the adsorption process in different target modes.
The neuropeptide oxytocin is produced in the paraventricular hypothalamic nucleus and the supraoptic nucleus of the hypothalamus. In addition to its extensively studied influence on social behavior ...and reproductive function, central oxytocin signaling potently reduces food intake in both humans and animal models and has potential therapeutic use for obesity treatment. In this review, we highlight rodent model research that illuminates various neural, behavioral, and signaling mechanisms through which oxytocin’s anorexigenic effects occur. The research supports a framework through which oxytocin reduces food intake via amplification of within-meal physiological satiation signals rather than by altering between-meal interoceptive hunger and satiety states. We also emphasize the distributed neural sites of action for oxytocin’s effects on food intake and review evidence supporting the notion that central oxytocin is communicated throughout the brain, at least in part, through humoral-like volume transmission. Finally, we highlight mechanisms through which oxytocin interacts with various energy balance-associated neuropeptide and endocrine systems (e.g., agouti-related peptide, melanin-concentrating hormone, leptin), as well as the behavioral mechanisms through which oxytocin inhibits food intake, including effects on nutrient-specific ingestion, meal size control, food reward-motivated responses, and competing motivations.
Mate wareware (dementia) is a complex disease of the brain that progressively inhibits memory and cognitive ability, affecting many Māori (the Indigenous people of Aotearoa New Zealand) kaumātua ...(elderly persons) in Aotearoa (New Zealand). Mate wareware care aims to protect and sustain wellbeing, yet Māori perspectives of wellbeing that consider wairuatanga (Māori spirituality) are often neglected within current treatment planning. This study investigates the presence of wairuatanga within kaumātua lives, drawing upon 61 interviews with kaumātua to glean a Māori understanding of mate wareware and to develop a diagnostic screening tool for mate wareware. Recorded responses were thematically analysed using reflexive qualitative analysis, informing four key themes that influence wairuatanga:
he hononga tangata
(social connection),
tūrangawaewae
(places of connection),
tuakiritanga
(identity) and
mahi mauritau
(mindful practices). These themes consider the value of creating rich and gratifying lifestyles for kaumātua that cultivate their spiritual wellbeing. This study validates diverse understandings and experiences of wairuatanga as essential to Māori wellbeing, affirming the relevance of wairuatanga to improve outcomes for Māori living with mate wareware.
The fundamental pathophysiology of ischemic-hypoxia is oxygen depletion. Fischer's ratio is essential for monitoring hypoxia intensity.
the current study highlighted the prophylactic role of ...sophoretin (QRC) and/or melatonin (MLN) versus sodium nitrite (SN) brain hypoxia.
Prophylactic treatment with sophoretin and MLN, was preceded with hypoxia-induction via sodium nitrite (60 mg/kg, S.C.). SN decreased hemoglobin (Hb), elevated
, HSP-70, IL-6 and TNF-α. Sophoretin and/or MLN restored the ameliorated inflammatory biomarkers, modulated norepinephrine, dopamine, serotonin and gamma-aminobutyric acid (GABA). Similarly, single-cell gel electrophoresis (SCGE or COMET) DNA damage assay confirmed this finding.
Treatment via sophoretin and MLN was the most effective therapy for improving sodium nitrite-induced brain injury.
Sodium nitrite is utilized as a preservative, food colorant and in medicine. However, misusage can affect human health, leading to brain injury, cyanosis, hypotension and hypoxia. Therefore, its toxic effect on the brain was investigated in addition to the potential protective impact of sophoretin and/or melatonin was also monitored.
Sophoretin and melatonin revealed a positive impact on certain factors. They regulated hemoglobin level, hypoxia biomarker hypoxia inducible factor (HIF-α), inflammatory biomarkers such as TNF-α and IL-6 and heat shock protein-70 (HSP-70) and DNA damage. When these antioxidants were combined, they had a superior protective impact against brain injury and mutations.
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