Career in radiology; the ghanaian clinical medical Student's perception.

Background: The importance of radiology in this era of evidence-based medicine cannot be disputed. This has resulted in the increase in demand for radiologists. Thus, the issue of whether there would be sufficient numbers of medical students to meet this growing demand needs further probing. Purpose: To assess Ghanaian clinical medical students' perceptions about a career in radiology. Materials and methods: This was an online questionnaire-based survey of 575 clinical medical students in five public medical schools in Ghana from September 2020 to February 2021. Student's t-test and one way analysis of variance was used to compare means. For the Likert scale questions, differences in the mean Likert scale responses were assessed among various clinical year groups and across gender using Kruskal-Wallis test and Mann-Whitney U tests. A logistic regression was used to determine the significant predictors of the choice of radiology as a career. Results: Most 340 (59.1%) of the participants were males. The average age of participants was 24.64 ± 3.084 years. Students agreed that, radiology is relevant in this era of evidence-based medicine (mean Likert score = 4.62, SD = 0.819), which yielded significant responses in the third clinical year (p = 0.004). Nearly 30% of respondents stated they did not receive enough didactic lectures or tutorials in radiology, citing insufficient lectures (89.9%), a lack of lecturers (9.5%), and trouble grasping ideas (0.7%) as their main concerns. 133 (23.1%) stated they would choose radiology as a specialty, with flexible working schedule (61.9%) and high income (68.3%) as their topmost reasons. Less patient contact (8.0%) was the least observed reason. A flexible working schedule increased the choice of radiology as a specialty by 2.319 folds (95% CI: 1.413-3.805, P = 0.001). Teleradiology significantly contributed to the choice of radiology as a career (p = 0.001). Conclusion: Generally, the clinical students had varied but positive perceptions on radiology as a specialty.

Review of rigid esophagoscopy in a Tertiary Hospital in Ghana.

Rigid esophagoscopy is a common endoscopic procedure worldwide for both diagnostic and therapeutic purposes. Even though this procedure is performed commonly in our center no published reports exist. We reviewed our experience with rigid esophagoscopy. This was a 9-year review of rigid esophagoscopy, done under general anaesthesia, at ENT and Cardiothoracic Units of Tamale Teaching Hospital. Parameters evaluated were patients´ demographics, indication for rigid esophagoscopy and outcome of the procedure. One hundred and fifteen cases of rigid esophagoscopies were evaluated. The ages ranged from 10 months to 87 years with a peak incidence 69.6% (n = 80) occurring within the first decade of life and a male preponderance of 54.8% (n = 63). Majority of the cases were emergencies 87.8% (n =101) and for therapeutic reasons 87% (n =100). The most common findings during esophagoscopy were: coins 60.9% (n = 70), fish bone 11.3% (n = 13), esophageal tumours 7.8% (n = 9) and dentures 5.2% (n = 6). All the cases were successfully treated with no mortality recorded. Rigid esophagoscopy was more commonly performed in males with peak age incidence occurring during the first decade of life. Emergency patients and esophagoscopy with therapeutic intent constituted the largest two groups in this study. Coins, fish bone, esophageal tumours and dentures were the most common findings. There was no mortality recorded.

Flexible bronchoscopy in Ghana: initial experience in a tertiary hospital.

INTRODUCTION: the use of flexible bronchoscopy in developing countries is limited. We report our initial experience and outcome with the use of flexible bronchoscopy at the Tamale Teaching Hospital in Ghana. This is the first reported case series of flexible bronchoscopy in Ghana. METHODS: a retrospective review of patients who had flexible bronchoscopy from 2017-2019 was analyzed. Patient demographics and outcomes were summarized using frequency distribution and percentages. RESULTS: we performed flexible bronchoscopies in 33 patients with mean age of 43 years. All patients were symptomatic at the time of presentation with the most common symptoms being chest pain (63.6%), dyspnea (57.6%) and cough (48.5%). The indication for bronchoscopy in most of the cases were suspected malignancy in 16 (48.5%) followed by infection 9 (27.3%), trauma 4 (12.1%) and others 4 (12.1%). We observed abnormal bronchoscopic findings in 25 (75.8%) of the cases with most of the pathologies in the right main bronchus. Twelve patients had toilet bronchoscopy, 6 had biopsy, 5 had no intervention and 4 patients had bronchoalveolar lavage (BAL). Culture and sensitivity results were available for 11 patients, of which 7 patients had negative results. Thirteen (13) malignancies and 11 inflammatory/infectious diseases were diagnosed in this case series. The mean procedure time was 32 minutes with mean hospital stay of 7 days. There was no complication or mortality in our series. Conclusion: flexible bronchoscopy is a safe procedure and indispensable in Ghana where there is an increasing incidence of lung diseases.

The Role of KDM2B and EZH2 in Regulating the Stemness in Colorectal Cancer Through the PI3K/AKT Pathway.

Background: The incidence of colorectal cancer (CRC) has been increasing worldwide in recent years. Targeting cancer stem cells (CSCs) in CRC remains a difficult challenge. KDM2B and EZH2 play important role in the maintenance of CSCs' self-renewal capacity and tumorigenic ability; however, the biological functions of those genes in CRC remain unclear. In this study, we aimed to define the contribution of the expression of KDM2B in the features of CRC and establish the relationship between KDM2B and EZH2 in colorectal CSCs. Methods: The expression of KDM2B and EZH2 in the specimens of CRC and CRC cell lines were analyzed by immunohistochemistry, Western blot, and immunofluorescence. The underlying mechanisms of altered expressions of KDM2B and EZH2 and their impact on the biologic features of CRC and stemness in CRC were investigated. Results: The KDM2B gene was highly expressed in CRC tissues, and its overexpression positively correlated with tumor stages and tumor/node/metastasis (TNM) classification. The downregulation of KDM2B retarded cell proliferation, induced DNA damage, reduced spheroid formation, and decreased CRC stem cell markers: CD44, CD133, and ALDH-1. Moreover, the downregulation of KDM2B decreased the expression of EZH2 and both regulated cell migration, invasion, and stemness in the CRC cell line. Additionally, the interaction between KDM2B and EZH2 significantly increased the components of the PI3K/AKT pathway including AKT and PI3K. The high expression of KDM2B positively correlated with EZH2 in CRC tissues. Conclusion: This study shows that the downregulation of KDM2B and EZH2 can regulate CRC cell stemness, and their interaction may serve as a novel prognostic marker and therapeutic target for patients with CRC.

Upregulation of sulfatase-1 decreases metastatic potential of SKOV3 human ovarian cancer cells in vitro and in vivo.

AIM: Sulfatase-1 (SULF-1) is one of the genes associated with the inhibition of several signaling pathways by desulfating HSPG in cancer cells. The aim of this study is to investigate the effect of SULF-1 upregulation on SKOV3 ovarian cancer cell line and its influence on cell proliferation, migration, invasion in vitro, and lymph node metastasis in 615 inbred mice in vivo. MATERIALS AND METHODS: In in vitro study, we upregulated SULF-1 in SKOV3 cells using SULF-1 expression plasmid. Quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) and western blotting were used to measure SULF-1 expression levels after stable upregulation. CCK-8, flow cytometry, Boyden Transwell-chamber, and scratch-wound healing assay were performed to explore the effect of SULF-1 on the proliferation, migration, and invasion. In in vivo study, immunohistochemistry and eosin stain (H and E) were used to evaluate the expression level of SULF-1 gene and to measure the lymph node metastatic rate of mice inoculated with SULF-1-SKOV3-expressed plasmid, SKOV3, and Nc-SKOV3 cells. RESULTS: qRT-PCR and western blot assay confirmed that SULF-1 was upregulated both in mRNA and protein levels. Following SULF-1 stable upregulation, the cell proliferation, migration, and invasion were significantly reduced in the SULF-1 upregulated cells (SULF-1-SKOV3) compared with the nontransfected (SKOV3) and the nonspecific sequence transfected cells (Nc-SKOV3). IHC results showed that SULF-1 was highly expressed after stably upregulation in SKOV3 cells, and H and E stain confirmed that the mice inoculated with SULF-1-SKOV3 cells decreased lymph node metastatic rate compared to the two control groups. CONCLUSIONS: Our findings showed that overexpression of SULF-1 in SKOV3 results in a decrease in ovarian cancer cell proliferation, migration, and invasion in vitro and decreased lymph node metastasis in vivo. This finding could have a potential therapeutic window in the management of ovarian cancer.

IL-8 analogue CXCL8 (3-72) K11R/G31P, modulates LPS-induced inflammation via AKT1-NF-kß and ERK1/2-AP-1 pathways in THP-1 monocytes.

IL-8 is elevated during inflammation, and it initiates cascade of down-stream reactions. Its antagonist, CXCL8 (3-72) K11R/G31P (G31P), represses inflammatory reactions via competitive binding to CXC chemokine family, preferentially G protein-couple receptors (GPCRs) CXCR1/2. This study reports the effect of G31P on the transcription profile of lipopolysaccharide (LPS) induced inflammation in THP-1 monocytes ex-vivo. LPS (1 µg/ml) induced elevation of IL-8 was significantly reduced by G31P (20 µg/ml and 30 µg/ml), with relatively increased inhibition of CXCR2 than CXCR1. Transcription of IL-1ß, IL-6, and TNF-α were significantly inhibited, while IL-10 remained relatively unchanged. G31P treatment also had repressing effect on the inflammatory associated enzymes COX-2, MMP-2, and MMP-9. Significant restriction of c-Fos, and NF-kß mRNA expression was observed, while that of c-Jun was marginally elevated. Conversely, SP-1 mRNA expression was seen to increase appreciably by G31P treatment. While the translation of pAKT, pERK1/2, and p65- NF-kß were down-regulated by the G31P following THP-1 cells stimulation with LPS, reactive oxygen species (ROS) expression was on the positive trajectory. Collectively, the IL-8 analogue, G31P, modulates the inflammatory profile of LPS induced inflammation in THP-1 monocytes via AKT1-NF-kß and ERK1/2-AP-1 pathways.

miR-501 is upregulated in cervical cancer and promotes cell proliferation, migration and invasion by targeting CYLD.

BACKGROUND: Cervical cancer is the common gynecological deadly malignancy worldwide. Here we attempted to evaluate the effects and mechanisms of microRNA-501-5p (miR-501) on the cell proliferation, migration, invasion and the clinical significance in the cervical cancer. METHODS: Cervical cancer HeLa cells were transfected with miR-501 mimic or inhibitor or siRNA against Cylindromatosis (CYLD) using Lipofectamine 2000. miR-501 expression was assessed in HeLa cells and cervical cancer specimens by real-time qRT-PCR. The functional roles of miR-501 were determined by CCK-8, colony formation, scratch wound healing and transwell assays. The apoptosis rate was detected by flow cytometry assay. CYLD, BCL-2, BAX, NF-κB p65 and phosphorylated p65 (p-p65) proteins were examined by Western blotting. CYLD expression was evaluated by immunohistochemistry in cervical cancer tissues. RESULTS: miR-501 was upregulated, whereas CYLD protein was downregulated in cervical cancer tissues compared to normal cervical tissues. miR-501 overexpression and CYLD protein downregulation were positively correlated with poor differentiation, tumor size, International Federation of Gynecology and Obstetrics (FIGO) stage and lymph node metastasis. CYLD was downregulated by miR-501 at both mRNA and protein levels in HeLa cells. miR-501 promoted cell proliferation, migration and invasion in cervical cancer, while inhibited the apoptosis. This is possibly due to the downregulation of CYLD and subsequent activation of NF-κB p65. CONCLUSIONS: miR-501 upregulation and CYLD downregulation are associated with the development and progression of cervical cancer. miR-501 promotes cervical cancer cell proliferation, migration and invasion possibly via downregulating CYLD and subsequently activating NF-κB p65. miR-501 might be a potential therapeutic target for cervical cancer.

Cisatracurium-induced proliferation impairment and death of colorectal cancer cells, HCT116 is mediated by p53 dependent intrinsic apoptotic pathway in vitro.

Activation of oncogenes and suppression of repressor genes are believed to play crucial roles in the pathogenesis of human colorectal carcinoma. Cisatracurium, a nondepolarizing neuromuscular blocking agent, has been reported to inhibit cell proliferation while promoting apoptosis. However, the underlining mechanism, of these growth setbacks are not well understood. We assessed the growth of human colorectal carcinoma (HCT116) and its cell cycle distribution upon cisatracurium exposure. Significant cell growth inhibition and accumulation of cells in G1 phase of the cell cycle was observed in treated cells compared with untreated cells (control). In furtherance to these observations, FITC Annexin V and propidium iodide apoptosis assay demonstrated concentration and time dependent percentage increase in apoptosis of cells treated with cisatracurium compared with untreated cells. qRT-PCR analysis showed concentration-dependent alterations in CD1, E2F, CE1, p53 and p21 mRNA expression. Western blot analysis indicated remarkable concentration dependent alterations in the expression of proliferation and survival proteins CD1, E2F, CE1, p53, p21, BAX, BCL-2, cytochrome C and cleaved PARP in cisatracurium-treated groups as compared with the untreated group. Cisatracurium also significantly promoted caspase-9 and caspase-3 activities in cells treated with cisatracurium compared with untreated cells. Thus, cisatracurium effectively inhibited proliferation and induced apoptosis of HCT116 cells in vitro at least via alteration of p53-dependent apoptotic pathway.

Ezrin expression is altered in mice lymphatic metastatic hepatocellular carcinoma and subcellular fractions upon Annexin 7 modulation in-vitro.

Ezrin and Annexin seven (A7) have been suggested to be involved in several roles in cancers metastasis. However, the role of Ezrin and the effect of A7 on Ezrin expression in lymphatic metastatic hepatocellular carcinoma (LNM-HCC) have not been extensively explored yet. This study reports expression of Ezrin in high lymphatic metastasis (Hca-F >70%) and low metastatic metastasis (Hca-P <30%) HCC cell lines, and the effect of A7 on Ezrin expression. Real-Time PCR, Western blot, Subcellular fractionation, Immunocytochemistry and Immunofluorescence were used to investigate Ezrin expression in addition to migration and invasion behaviors of A7 up-regulated Hca-F cells, A7 down-regulated Hca-P and in their respective negative control (NC) cells. Ezrin expression was higher in high LNM-HCC than low LNM-HCC (p=0.0046). Cell fractionation analysis reveals that Ezrin was highly present in the cytoplasm, nucleus and cytoskeleton of NC-Hca-F cells. However, Ezrin was highly observed in the cell membrane, nucleus and cytoskeleton of NC-Hca-P cells. A7 up-regulation in Hca-F suppressed Ezrin expression (p=0.0248), but increase the migration and invasion, whereas Ezrin was mainly located in the cytoplasm and nucleus fractions. Down-regulation of A7 in Hca-P cells, enhanced Ezrin expression (p<0.0001) in the cytoplasm and nucleus fractions, and suppressed migration and invasion. In conclusion, Ezrin may play a role in LNM-HCC and might be inversely associated with A7 expression. The subcellular localization of Ezrin and A7 was varied according to the metastatic levels. Ezrin may thus be a potential diagnostic and/or prognostic biomarker for HCC.