Biomedicine (Journal)
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Benzyl isothiocyanate (BITC) triggers mitochondria-mediated apoptotic machinery in human cisplatin-resistant oral cancer CAR cells
No full textComparison of two methods of laparoscopic trocar insertion (Hasson and Visiport) in terms of speed and complication in urologic surgery
No full textCan multidetector CT scan replace MRI for evaluation of mesorectal fasca in rectal cancer?
No full textAbstract
Background
Colorectal cancer is the 4th leading cause of cancer mortality.
Aim
This study aimed to can multidetector CT scan (MDCT) replace Magnetic resonance imaging (MRI) for mesorectal fasca in rectal cancer?
Methods
This cross-sectional was conducted on patients with rectal cancer in Alzahra and Seyed-Shohada hospitals. MRI, mesorectal fascia (MPR), and axial MDCT were provided from patients to assess the involvement of mesorectal fascia. Sensitivity, specificity, positive and negative predictive values were assessed in these patients. Kappa coefficient agreement was used for analysis. Patients were also divided into different subgroups based on gender, tumoral location, nodal involvement, and tumoral description as mass or wall thickening to evaluate the accuracy of MDCT for assessing mesorectal fascia involvement.
Results
The current study was conducted on 60 patients with rectal cancer. Regarding MRF involvement, the frequency of patients who were correctly diagnosed by MPR and axial MDCT was 45 (75%) and 35 (58.3%), respectively. There was no agreement between axial MDCT and MRI regarding MRF involvement (P\u3e0.05), however, an agreement was seen between Multiplanar reconstruction CT (MPRCT) and MRI method regarding MRF involvement (Pkappa=0.44). Moreover MPRCT scan has a more acceptable agreement with MRI in patients with wall thickening (comparing with patients described as having mass lesion) (Kappa= 0.699, P=0.001) and negative nodal involvement. Also, there was more agreement between MPRCT scan and MRI in tumors located in the middle or upper rectum compared with the lower rectum.
Conclusion
According to these findings, there was good agreement between MRI and MPRCT regarding MRF involvement at patients with wall thickening and negative nodal involvement in the upper and middle rectum; it seems that MPRCT method which is now used for routine staging can be comparable with MRI for some subgroups of patients for evaluating MRF and can replace it in these patients
The Impact of Procalcitonin in Assessing Outcomes in Pediatrics Severe Trauma Cases: A Three-Year Experience from a Tertiary Hospital
No full textBackground Although procalcitonin levels are raised in patients with systemic inflammation, its usage in pediatric patients, particularly those in the intensive care unit who are most susceptible to sepsis. Methods It is a retrospective research study that included pediatric patients aged more than two weeks who were brought to the King Fahd Hospital of the University\u27s PICU owing to serious trauma or post-acute postoperative occurrences from January 2017 to December 2019. At 24 hours after admission, data such as age, gender, comorbidities, trauma severity as measured by the Injury Severity Score, and PRISM III score were collected. Results Following a surgery abscess, there were a total of 39 (15.9%) deaths. Patients who died during their hospital stay had significantly higher mean levels of biomarkers such as PRISM III, PCT at 24 hours, PCT 48-72 hours, and PCT at day 5 (p = 0.001). The area under the ROC curve for PCT level 48/72 hours was 0.89 (% CI: 0.85-0.93), p=0.001, indicating that PCT had highly significant predictive validity in predicting inhospital mortality at the best cutoff point of \u3e 1.35 with a high level of accuracy and precision of 82.1% and 82.0%, respectively. Conclusion The serum procalcitonin level (PTCL) can help predict the in-hospital prognosis of pediatrics that has had surgery. A combined control system is designed based on PTC expression for the examination of a patient receiving medication over a longer length of time
New-onset diabetes in COVID-19: The molecular pathogenesis
No full textDiabetes mellitus (DM) is still a challenging metabolic disease worldwide. In the current situation, the world is facing a COVID-19 pandemic due to SARS-CoV-2 infection. DM is one of comorbid that can worsen the severity of the COVID-19 condition. Surprisingly, SARS-CoV-2 infection can induce new-onset diabetes, a condition in which acute hyperglycemia occurs and may potentially develop into a complication in non-diabetic patients. Angiotensin-converting enzyme 2 (ACE2) is a crucial entry factor of SARS-CoV-2 infection. ACE2 will bind to the spike protein of SARS-CoV-2, making its entrance to the potentially damaging process of many tissues in the human body, including that of metabolic tissues. This mechanism suggests a potential role of ACE2 in the pathogenesis of diabetes since ACE2 has been proven to localize in essential metabolic tissues, one of which is the acini and islets part of the pancreas. This interrelated ACE2 in COVID-19 and DM is thought as the mechanism that induces new-onset diabetes in COVID-19 patients. This review will thoroughly describe the current findings and theories regarding the molecular mechanism of SARS-CoV-2induced new-onset diabetes and the possible therapeutic intervention
High levels of Histone H3 K27 acetylation and tri-methylation are associated with shorter survival in Oral Squamous Cell Carcinoma patients
No full textBackground: Acetylation and trimethylation of histone H3 lysine 27 (H3K27ac and H3K27me3) generally activate and repress transcription, respectively. Concurrent activation of H3K27ac and H3K27me3 has been reported to correlate with poor prognosis in hepatocellular carcinoma. A high level of H3K27me3 has been shown to be associated with advanced oral squamous cell carcinoma (OSCC) tumour stage, but prognostic impact of H3K27ac level alone/or in combination with H3K27me3 in OSCC patients had not yet been reported. Material and Methods: In this study, immunohistochemistry using specific antibodies against H3K27ac and H3K27me3 was performed on a series of 72 OSCC samples to investigate the association between H3K27ac and H3K27me3 levels and OSCC patient’s survival. For each mark, the proportion of labelled cells (percentage) and the intensity of the labelling were measured, and a score of percentage x intensity was calculated. Results: A high percentage of H3K27me3 positive cells was significantly associated with survival in univariate and multivariate analyses (logrank p-valu
Precision Medicine Advancements in Glioblastoma: A Systematic Review
No full textBackground. Glioblastoma multiforme, commonly known as GBM or glioblastoma is a grade IV astrocytoma. Brain tumors are difficult to treat and lead to poor prognosis and survival in patients. Gliomas are categorized into four different grades among which GBM is the worst grade primary brain tumor with a survival of less than a year. The genomic heterogeneity of the brain tumor results in different profiles for patients diagnosed with glioblastoma. Precision medicine focuses on this specific tumor type and suggests specialized treatment for better prognosis and overall survival (OS). Purpose. With the recent advancements in Genome-Wide Studies (GWS) and various characterizations of brain tumors based on genetic, transcriptomic, proteomic, epigenetic, and metabolomics, this review discusses the advancements and opportunities of precision medicine therapeutics, drugs, and diagnosis methods based on the different profiles of glioblastoma. Methods. This review has exhaustively surveyed several pieces of works from various literature databases. Conclusion. It is evident that most primary brain tumors including glioblastoma require specific and precision therapeutics for better prognosis and OS. In present and future, molecular understanding and discovering specific therapies are essential for treatment in the field of neurooncology
Metformin induces autophagy of cisplatin-resistant human gastric cancer cells in addition to apoptosis
No full textMetformin has been used to treat cases of type 2 diabetes mellitus, and mounting studies have shown that metformin can act alone or in synergy with other anticancer agents to achieve anti-cancer efficacies on various types of tumors. However, the role of metformin in either inducing autophagy and cisplatin-resistance of human gastric cancer (GC) cells has never been examined. The study has established a cisplatin-resistant GC cell line and investigated the effects of metformin on inducing autophagy on it. The results demonstrated that treatment with metformin can concentration-dependently suppress the cell viability and cell confluence of cisplatin-resistant GC cells, while having no effects on human primary stomach epithelial cells (HPSEC). For the first time, we found that metformin can significantly increase the acidic vesicular organelles (AVO) level and decrease the acridine orange (AO) level spontaneously in the cisplatin-resistant GC cells. Thus, we further checked the other markers, Atg5, Atg12 and LC3-II, which showed that metformin indeed induced autophagy in the cisplatin-resistant GC cells. In addition, treatment of 3-Methyladenine (3-MA) can significantly rescue the metformin-induced autophagy. At the same time, metformin can induce the alterations of apoptosis-associated signal molecules, such as caspase-3 and caspase-7 activities. Overall, the pilot study provided evidence for metformin induced autophagy in addition to apoptosis, making it as an effective anticancer drug for the therapy of cisplatin-resistant GC. Killing the cisplatin-resistant GC cells with non-toxic metformin via both autophagy and apoptosis might extend its usefulness in our fighting with chemo-resistance of gastric cancer cells
Mutation Patterns of Integrase Gene Affect Antiretroviral Resistance in Various non-B Subtypes of Human Immunodeficiency Virus Type-1 and Their Implications for Patients’ Therapy
No full textAlthough primary integrase strand transfer inhibitor resistance mutations are currently uncommon, the increasing use of integrase strand transfer inhibitor as a key component of the first, second and third-line antiretroviral regimens suggests that the prevalence of integrase drug resistance mutations will likely increase. The rise of several polymorphic mutations and natural polymorphisms also affects the level of susceptibility of human immunodeficiency virus (HIV) type-1 to integrase strand transfer inhibitor. The considerable variability among the various subtypes of human immunodeficiency virus type-1 may contribute to differences in integrase mutations associated with integrase strand transfer inhibitors. Notably, non-B subtypes of HIV type-1 (HIV-1) are the predominant cause of human immunodeficiency virus infection worldwide. The presence of diverse integrase drug resistance mutations can have significant implications on the administration of integrase strand transfer inhibitorbased antiretroviral therapy to patients with human immunodeficiency virus infection
A1 adenosine receptor antagonist induces cell apoptosis in KYSE-30 and YM-1 esophageal cancer cell lines
No full textBackground and Aim: Adenosine A1 receptor (AA1R) has been shown to have an inhibitory effect on cell growth in several cancers; however, its function in esophageal cancer is still unclear. In this study, we examined the effect of AA1R on cell growth and apoptosis in esophageal cancer cells. Materials and methods: In this study, YM-1 and KYSE-30 esophageal cancer cell lines were cultured. AA1R gene expression was determined by quantitative Real-time Polymerase Chain Reaction (qRT-PCR). As well, the AA1R antagonist (DPCPX) effect on cell viability was evaluated by the MTT assay. Moreover, apoptosis was assessed by annexin-V and propidium iodide staining, and the caspase-3/7 activity assay kit. Result: qRT-PCR results indicated that the AA1R was expressed in YM-1 and KYSE30 cells. In addition, DPCPX significantly decreased cell proliferation in both cell lines. Furthermore, the A1AR antagonist induced apoptosis in KYSE-30 and YM-1 cells. After treatment of both cell lines with DPCPX, the caspase 3/7 activity was increased. Conclusion: Our finding indicates the AA1R antagonist induces apoptosis through caspase 3/7 activation and can be considered a potential target in esophageal cancer therapy