Evaluating knowledge, attitude, and physical activity levels related to cardiovascular disease in Egyptian adults with and without cardiovascular disease: a community-based cross-sectional study.

BACKGROUND: Cardiovascular disease (CVD) represents a significant health challenge in Egypt, yet there exists limited understanding regarding the knowledge, attitudes, and physical activity levels associated with CVD. These factors play a pivotal role in developing effective prevention and management strategies. Hence, this cross-sectional study aimed to evaluate Egyptian adults' knowledge, attitudes, and physical activity (KAP) levels. METHODS: Data were collected using a previously validated questionnaire encompassing demographic characteristics, CVD knowledge (including risk factors and symptoms), attitudes toward CVD, and self-reported physical activity levels. The survey was distributed among social media channels, and trained researchers administered the questionnaire via face-to-face interviews with adult patients with and without CVD admitted to Cairo University Hospital clinics. RESULTS: The study involved 591 participants, of whom 21.7% had CVD. Overall, participants exhibited poor knowledge regarding CVD, with a mean score of 21 ± 7 out of 40, equivalent to 52.5%. Attitudes toward CVD were moderate, with a mean score of 66.38 ± 8.7 out of 85, approximately 78%. Physical activity levels per week were also moderate, averaging 1188 MET-min with a range of 1121-18,761. Subgroup analysis revealed that individuals with CVD had lower average knowledge, attitude, and physical activity levels than those without CVD. Working in the healthcare field was a predictor of higher knowledge score (standard error (SE) 5.89, 95% confidence interval (CI) 4.61 to 7.17, P < 0.001), while those with CVD and smokers were predictors of lower attitude score (SE -4.08, 95% CI -6.43 to -1.73, P < 0.001) and (SE -2.54, 95% CI -4.69 to -0.40, P = 0.02), respectively. CONCLUSION: The study findings highlight a significant disparity in knowledge, attitudes, and physical activity levels related to CVD in Egypt. Targeted interventions aimed at improving awareness, fostering positive attitudes, and promoting physical activity among individuals at risk for CVD are crucial for effective prevention and management.

Sel1-like proteins and peptides are the major Oxalobacter formigenes-derived factors stimulating oxalate transport by human intestinal epithelial cells.

Kidney stones (KSs) are very common, excruciating, and associated with tremendous healthcare cost, chronic kidney disease (CKD), and kidney failure (KF). Most KSs are composed of calcium oxalate and small increases in urinary oxalate concentration significantly enhance the stone risk. Oxalate also potentially contributes to CKD progression, kidney disease-associated cardiovascular diseases, and poor renal allograft survival. This emphasizes the urgent need for plasma and urinary oxalate lowering therapies, which can be achieved by enhancing enteric oxalate secretion. We previously identified Oxalobacter formigenes (O. formigenes)-derived factors secreted in its culture-conditioned medium (CM), which stimulate oxalate transport by human intestinal Caco2-BBE (C2) cells and reduce urinary oxalate excretion in hyperoxaluric mice by enhancing colonic oxalate secretion. Given their remarkable therapeutic potential, we now identified Sel1-like proteins as the major O. formigenes-derived secreted factors using mass spectrometry and functional assays. Crystal structures for six proteins were determined to confirm structures and better understand functions. OxBSel1-14-derived small peptides P8 and P9 were identified as the major factors, with P8 + 9 closely recapitulating the CM's effects, acting through the oxalate transporters SLC26A2 and SLC26A6 and PKA activation. Besides C2 cells, P8 + 9 also stimulate oxalate transport by human ileal and colonic organoids, confirming that they work in human tissues. In conclusion, P8 and P9 peptides are identified as the major O. formigenes-derived secreted factors and they have significant therapeutic potential for hyperoxalemia, hyperoxaluria, and related disorders, impacting the outcomes of patients suffering from KSs, enteric hyperoxaluria, primary hyperoxaluria, CKD, KF, and renal transplant recipients.NEW & NOTEWORTHY We previously identified Oxalobacter formigenes-derived secreted factors stimulating oxalate transport by human intestinal epithelial cells in vitro and reducing urinary oxalate excretion in hyperoxaluric mice by enhancing colonic oxalate secretion. We now identified Sel1-like proteins and small peptides as the major secreted factors and they have significant therapeutic potential for hyperoxalemia and hyperoxaluria, impacting the outcomes of patients suffering from kidney stones, primary and secondary hyperoxaluria, chronic kidney disease, kidney failure, and renal transplant recipients.

Activation of the PKA signaling pathway stimulates oxalate transport by human intestinal Caco2-BBE cells.

Most kidney stones are composed of calcium oxalate, and small increases in urine oxalate enhance the stone risk. The mammalian intestine plays a crucial role in oxalate homeostasis, and we had recently reported that Oxalobacter-derived factors stimulate oxalate transport by human intestinal Caco2-BBE (C2) cells through PKA activation. We therefore evaluated whether intestinal oxalate transport is directly regulated by activation of the PKA signaling pathway. To this end, PKA was activated with forskolin and IBMX (F/I). F/I significantly stimulated (3.7-fold) [14C]oxalate transport by C2 cells [≥49% of which is mediated by the oxalate transporter SLC26A6 (A6)], an effect completely blocked by the PKA inhibitor H89, indicating that it is PKA dependent. PKA stimulation of intestinal oxalate transport is not cell line specific, since F/I similarly stimulated oxalate transport by the human intestinal T84 cells. F/I significantly increased (2.5-fold) A6 surface protein expression by use of immunocytochemistry. Assessing [14C]oxalate transport as a function of increasing [14C]oxalate concentration in the flux medium showed that the observed stimulation is due to a F/I-induced increase (1.8-fold) in Vmax and reduction (2-fold) in Km. siRNA knockdown studies showed that significant components of the observed stimulation are mediated by A6 and SLC26A2 (A2). Besides enhancing A6 surface protein expression, it is also possible that the observed stimulation is due to PKA-induced enhanced A6 and/or A2 transport activity in view of the reduced Km. We conclude that PKA activation positively regulates oxalate transport by intestinal epithelial cells and that PKA agonists might therapeutically impact hyperoxalemia, hyperoxaluria, and related kidney stones.

Patterns of Mycobacterium avium-intracellulare complex infection in duodenal endoscopic biopsies in HIV/AIDS patients.

Mycobacterium avium-intracellulare complex (MAIC) is a nontuberculous opportunistic infection in immunocompromised patients. Involvement of the gastrointestinal tract (GIT) is usually part of a disseminated disease in AIDS patients with a low CD4 count, however with standard antiretroviral therapy (ART), a localized presentation is more likely. It can affect any part of the GIT, mostly the duodenum and typically as patches. Incomplete or refractory ART for HIV-strains, therapy-related side effects, noncompliant or incomplete treatment to previous MAIC infections, superimposed complications and comorbid opportunistic infections may result in atypical clinical, endoscopic and histopathologic manifestations. We performed a retrospective review study retrieving cases of MAIC in duodenal endoscopic biopsy. We found five cases of MAIC in HIV/AIDS patients. They were males with an average age of 40-years. They showed different histopathologic features, variable patterns of MAIC-histiocytic infiltrates, and varying intensity of intracellular acid-fast positive bacilli. Enterocytes vacuolization and transepithelial elimination were also observed. Three cases were associated with cytomegalovirus and cryptococcal infections. A case was complicated by lymphangiectasia-associated protein-losing enteropathy. Initially, three cases were morphologically missed. Ziehl-Neelsen stain helped reach the correct diagnosis. Pathologists have an important role in patients' management by guiding clinicians to the correct diagnosis. Pathologists should be aware of these different histopathologic manifestations, their potential pitfalls, look for certain helpful clues complemented with multiple levels and special stains. In particular, AFB stains are mandatory in all mucosal biopsy specimens from HIV/AIDS patients regardless of their appearances.

Enhanced gastrointestinal passive paracellular permeability contributes to the obesity-associated hyperoxaluria.

Most kidney stones (KS) are composed of calcium oxalate and small increases in urine oxalate enhance the stone risk. Obesity is a risk factor for KS, and urinary oxalate excretion increases with increased body size. We previously established the obese ob/ob ( ob) mice as a model (3.3-fold higher urine oxalate) to define the pathogenesis of obesity-associated hyperoxaluria (OAH). The purpose of this study was to test the hypothesis that the obesity-associated enhanced small intestinal paracellular permeability contributes to OAH by increasing passive paracellular intestinal oxalate absorption. ob Mice have significantly higher jejunal (1.6-fold) and ileal (1.4-fold) paracellular oxalate absorption ex vivo and significantly higher (5-fold) urine [13C]oxalate following oral gavage with [13C]oxalate, indicating increased intestinal oxalate absorption in vivo. The observation of higher oxalate absorption in vivo compared with ex vivo suggests the possibility of increased paracellular permeability along the entire gut. Indeed, ob mice have significantly higher fractions of the administered sucrose (1.7-fold), lactulose (4.4-fold), and sucralose (3.1-fold) excreted in the urine, reflecting increased gastric, small intestinal, and colonic paracellular permeability, respectively. The ob mice have significantly reduced gastrointestinal occludin, zonula occludens-1, and claudins-1 and -3 mRNA and total protein expression. Proinflammatory cytokines and oxidative stress, which are elevated in obesity, significantly enhanced paracellular intestinal oxalate absorption in vitro and ex vivo. We conclude that obese mice have significantly higher intestinal oxalate absorption and enhanced gastrointestinal paracellular permeability in vivo, which would likely contribute to the pathogenesis of OAH, since there is a transepithelial oxalate concentration gradient to drive paracellular intestinal oxalate absorption. NEW & NOTEWORTHY This study shows that the obese ob/ob mice have significantly increased gastrointestinal paracellular oxalate absorption and remarkably enhanced paracellular permeability along the entire gut in vivo, which are likely mediated by the obesity-associated increased systemic and intestinal inflammation and oxidative stress. A transepithelial oxalate concentration gradient driving gastrointestinal paracellular oxalate absorption exists, and therefore, our novel findings likely contribute to the hyperoxaluria observed in the ob/ob mice and hence to the pathogenesis of obesity-associated hyperoxaluria.

Trefoil factors peptide-3 is associated with residual invasive breast carcinoma following neoadjuvant chemotherapy.

BACKGROUND: Breast carcinoma is the commonest cancer among UAE population and the most common cancer among females. Examination of the 5' promoter regions of trefoil factor 3 (TFF3) gene has identified putative estrogen and progesterone receptor-DNA binding domains as direct response elements to estrogen and progesterone that are linked to breast functions or steroid regulation. The study was designed to determine the role of TFF3 in breast cancer chemoresistance with the aim of establishing TFF3 expression as a biomarker for drug resistance. METHODS: In total, 133 cases of breast carcinoma treated with neo-adjuvant therapy were collected. Tissue samples from pre-neoadjuvant therapy as well as tissues from post-neo-adjuvant therapy of those cases were collected and stained with immunohistochemistry for TFF3, Bcl2, BAX, cleaved caspase-3, AKT-1, NF kappa B and Ki-67. RESULTS: There was increased expression of TFF3 in residual invasive carcinoma cells. There was a significant correlation between the expression of TFF3 in breast carcinoma cells and response to neoadjuvant chemotherapy (p = 0.0165). There was significant co-expression of TFF3 with AKT1 (p = 0.0365), BCl2 (p = 0.0152), and NF Kappa-B (p = 0.0243) in breast carcinoma cases with residual carcinoma following neoadjuvant therapy which support the role of TFF3 in chemoresistance. CONCLUSION: The expression of TFF3 is significantly associated with residual breast carcinoma following neoadjuvant chemotherapy suggesting its expression is associated with increased resistance to chemotherapy. This is supported by its co-expression with antiapoptotic proteins; BCl2, AKT1 and NF Kappa-B in residual breast carcinoma cells and very low proliferating index and apoptotic bodies in residual tumors.

Adenosinergic signaling inhibits oxalate transport by human intestinal Caco2-BBE cells through the A2B adenosine receptor.

Most kidney stones (KS) are composed of calcium oxalate, and small increases in urine oxalate affect the stone risk. Intestinal oxalate secretion mediated by anion exchanger SLC26A6 (PAT1) plays a crucial role in limiting net absorption of ingested oxalate, thereby preventing hyperoxaluria and related KS, reflecting the importance of understanding regulation of intestinal oxalate transport. We previously showed that ATP and UTP inhibit oxalate transport by human intestinal Caco2-BBE cells (C2). Since ATP is rapidly degraded to adenosine (ADO), we examined whether intestinal oxalate transport is regulated by ADO. We measured [14C]oxalate uptake in the presence of an outward Cl gradient as an assay of Cl-oxalate exchange activity, ≥49% of which is PAT1-mediated in C2 cells. We found that ADO significantly inhibited oxalate transport by C2 cells, an effect completely blocked by the nonselective ADO receptor antagonist 8- p-sulfophenyltheophylline. ADO also significantly inhibited oxalate efflux by C2 cells, which is important since PAT1 mediates oxalate efflux in vivo. Using pharmacological antagonists and A2B adenosine receptor (A2B AR) siRNA knockdown studies, we observed that ADO inhibits oxalate transport through the A2B AR, phospholipase C, and PKC. ADO inhibits oxalate transport by reducing PAT1 surface expression as shown by biotinylation studies. We conclude that ADO inhibits oxalate transport by lowering PAT1 surface expression in C2 cells through signaling pathways including the A2B AR, PKC, and phospholipase C. Given higher ADO levels and overexpression of the A2B AR in inflammatory bowel disease (IBD), our findings have potential relevance to pathophysiology of IBD-associated hyperoxaluria and related KS.

Reduced active transcellular intestinal oxalate secretion contributes to the pathogenesis of obesity-associated hyperoxaluria.

Most kidney stones are composed of calcium oxalate, and minor changes in urine oxalate affect the stone risk. Obesity is a risk factor for kidney stones and a positive correlation of unknown etiology between increased body size, and elevated urinary oxalate excretion has been reported. Here, we used obese ob/ob (ob) mice to elucidate the pathogenesis of obesity-associated hyperoxaluria. These ob mice have significant hyperoxaluria (3.3-fold) compared with control mice, which is not due to overeating as shown by pair-feeding studies. Dietary oxalate removal greatly ameliorated this hyperoxaluria, confirming that it is largely enteric in origin. Transporter SLC26A6 (A6) plays an essential role in active transcellular intestinal oxalate secretion, and ob mice have significantly reduced jejunal A6 mRNA (- 80%) and total protein (- 62%) expression. While net oxalate secretion was observed in control jejunal tissues mounted in Ussing chambers, net absorption was seen in ob tissues, due to significantly reduced secretion. We hypothesized that the obesity-associated increase in intestinal and systemic inflammation, as reflected by elevated proinflammatory cytokines, suppresses A6-mediated intestinal oxalate secretion and contributes to obesity-associated hyperoxaluria. Indeed, proinflammatory cytokines (elevated in ob mice) significantly decreased intestinal oxalate transport in vitro by reducing A6 mRNA and total protein expression. Proinflammatory cytokines also significantly reduced active mouse jejunal oxalate secretion, converting oxalate transport from net secretion in vehicle-treated tissues to net absorption in proinflammatory cytokines-treated tissues. Thus, reduced active intestinal oxalate secretion, likely secondary to local and systemic inflammation, contributes to the pathogenesis of obesity-associated hyperoxaluria. Hence, proinflammatory cytokines represent potential therapeutic targets.

Oxalobacter formigenes-Derived Bioactive Factors Stimulate Oxalate Transport by Intestinal Epithelial Cells.

Hyperoxaluria is a major risk factor for kidney stones and has no specific therapy, although Oxalobacter formigenes colonization is associated with reduced stone risk. O. formigenes interacts with colonic epithelium and induces colonic oxalate secretion, thereby reducing urinary oxalate excretion, via an unknown secretagogue. The difficulties in sustaining O. formigenes colonization underscore the need to identify the derived factors inducing colonic oxalate secretion. We therefore evaluated the effects of O. formigenes culture conditioned medium (CM) on apical 14C-oxalate uptake by human intestinal Caco-2-BBE cells. Compared with control medium, O. formigenes CM significantly stimulated oxalate uptake (>2.4-fold), whereas CM from Lactobacillus acidophilus did not. Treating the O. formigenes CM with heat or pepsin completely abolished this bioactivity, and selective ultrafiltration of the CM revealed that the O. formigenes-derived factors have molecular masses of 10-30 kDa. Treatment with the protein kinase A inhibitor H89 or the anion exchange inhibitor 4,4'-diisothiocyano-2,2'-stilbenedisulfonic acid completely blocked the CM-induced oxalate transport. Knockdown of the oxalate transporter SLC26A6 also significantly restricted the induction of oxalate transport by CM. In a mouse model of primary hyperoxaluria type 1, rectal administration of O. formigenes CM significantly reduced (>32.5%) urinary oxalate excretion and stimulated (>42%) distal colonic oxalate secretion. We conclude that O. formigenes-derived bioactive factors stimulate oxalate transport in intestinal cells through mechanisms including PKA activation. The reduction in urinary oxalate excretion in hyperoxaluric mice treated with O. formigenes CM reflects the in vivo retention of biologic activity and the therapeutic potential of these factors.

In vitro assessment of antitumor activities of the PI3K/mTOR inhibitor GSK2126458.

BACKGROUND: Up-regulation of the PI3K/mTOR (phosphatidylinositol-3' kinase/mammalian target of rapamycin) signaling is common in carcinoma. Consistently, targeting these molecules has been shown to halt the growth of many tumors. The main purpose of this study was to develop surrogate biomarkers of the antitumor activity of PI3K/mTOR inhibitors. METHODS: Fragments from eight tumors were collected immediately after resection in ice-cold RPMI gassed with 95% O2 :5% CO2. Viability was determined by measuring tumor cellular respiration (mitochondrial O2 consumption). The specimens were incubated at 37°C with and without 50 nM GSK2126458 (a highly potent and selective inhibitor of PI3K/mTOR) for 90 min. The tissue was then processed for histology, measurement of intracellular caspase-3 activity (using the caspase-3 substrate N-acetyl-asp-glu-val-asp-7-amino-4-methylcoumarin), and immunohistochemical detection of the apoptotic biomarkers caspase-3, cytochrome C, and annexin A2. RESULTS: GSK2126458 induced morphologic changes in four tumors (two invasive ductal carcinomas, one invasive lobular carcinoma, and one ovarian dysgerminoma), intracellular caspase-3 activity in three tumors (two invasive ductal carcinomas and one poorly differentiated signet ring adenocarcinoma of gastric origin), and immunohistochemical evidence of apoptosis in at least four tumors (three invasive ductal carcinomas and one adenocarcinoma of gastric origin). Two tumors (ovarian serous carcinoma and moderately differentiated adenocarcinoma of colorectal origin) demonstrated no treatment effect. CONCLUSION: These preliminary results demonstrate the feasibility of using in vitro biomarkers for detecting antitumor activities of the rapidly emerging PI3K/mTOR inhibitors.

Fabrication and Enhanced Performance Evaluation of TiO2@Zn/Al-LDH for DSSC Application: The Influence of Post-Processing Temperature.

A sequence of dye-sensitized solar cells is proposed, utilizing TiO2@Zn/Al-layered double hydroxide (LDH) as their starting materials, in which Ruthenizer N719 was used as a photon absorber. The anticipated system was turned into sheet-like TiO2@mixed metal oxide (MMO) via post-processing treatment. The crystal quality indicated a relation to power conversion efficiency (PCE); this was combined with a comparable morphology profile. In detail, the optimum DSSC device exhibited average sheet-like thickness and a dye loading amount of 43.11 nm and 4.28 ×10-3 mM/cm-2, respectively. Concurrently, a considerable PCE enhancement of the optimum DSSC device (TiO2@MMO-550°) was attained compared to pristine MMO (0.91%), which could be due to boosted electron transfer efficiency. Of the fabricated devices, DSSC fabricated at 550° exhibited the highest PCE (1.91%), with a 35.6% enhancement compared to that obtained at 450°, as a result of its increased open-circuit voltage (3.29 mA/cm2) and short-circuit current (0.81 V). The proposed work delivers an enhanced efficiency as compared to similar geometries.

Pulmonary sclerosing pneumocytoma - rare diagnosis in a Caucasian woman: case report and review of the literature.

Pulmonary sclerosing pneumocytoma (PSP) is a rare benign pulmonary tumour, most reported cases of PSP are from Eastern Asia, with a female to male ratio of 5:1, and average age at diagnosis in the 5th decade. We present the case of a 63-year-old Caucasian woman diagnosed with PSP who underwent a left lower lobe basal segmentectomy with systematic nodal dissection, performed via video assisted thoracic surgery (VATS).

Low dose insulin infusion versus the standard dose in children with diabetic ketoacidosis: a meta-analysis.

Aim: This systematic review aims to consolidate findings from current clinical trials that compare the effectiveness of insulin infusion at 0.05 IU/kg/h versus 0.1 IU/kg/h in managing pediatric diabetic ketoacidosis. Methods: We searched several databases, including PubMed, Embase, Scopus, Cochrane Central and Web of Science. Our primary outcomes were time to reach blood glucose ≤250 mg/dl and time to resolution of acidosis. Secondary outcomes included rate of blood glucose decrease per hour, incidence of hypoglycemia, hypokalemia, treatment failure, and cerebral edema. Results & conclusion: The present study establishes that a low insulin dose exhibits comparable efficacy to the standard dosage for managing pediatric patients suffering from diabetic ketoacidosis, with a lower incidence of complications.

When kids with type 1 Diabetes (T1DM) face a serious complication called Diabetic Ketoacidosis (DKA), it becomes a life-threatening situation. This condition, responsible for significant mortality, involves high blood sugar, ketone buildup and acidity. Our study delves into a critical aspect of DKA treatment-finding the right insulin dose. By pooling the studies on this point, we discovered that using a lower insulin dose is just as effective as the standard dose in managing DKA in children, with fewer complications. This insight is crucial for improving the care and outcomes for young patients dealing with this challenging condition.

Time to Move Beyond a Binary Criterion for Gestational Diabetes?

Over the years, several international guidelines have been developed by specialist organizations for the diagnosis of gestational diabetes mellitus (GDM). However, these guidelines vary and lack consensus on what level of glycemia defines GDM and worryingly, there is now evidence of over- or- under-diagnosis of women with GDM by current criteria. Towards this end, the National Priorities Research Program (NPRP) funded a program of research aimed at elucidating the problem with GDM diagnosis. It was determined, on completion of the project, that the solution required diagnosis of graded levels of dysglycemia in pregnancy and not just a diagnosis of presence or absence of GDM. A new diagnostic criterion (called the NPRP criterion) was created based on a single numerical summary of the three readings from the oral glucose tolerance test (GTT) that diagnosed women in pregnancy into four levels: normal, impaired, GDM and high risk GDM. This paper now examines existing GDM criteria vis-à-vis the NPRP criterion. It is noted that no significant change has happened over the years for existing criteria except for a gradual reduction in the threshold values of individual time-points or the number of time points, bringing us towards over-diagnosis of GDM in pregnancy. The new criterion unifies all readings from the GTT into one numerical value and, because it results in four levels of glycemia, represents a new way forwards for GDM diagnosis and can potentially reduce the rates of under diagnosis and over diagnosis of GDM.

Immune Checkpoints Receptors Expression of Macrophage/Monocytes in Response to Acute Viral Respiratory Infection.

Background: We aimed to monitor the phenotypic changes in macrophages and their polarization in patients with acute viral respiratory diseases, including coronavirus disease diagnosis, focusing on the variations in the percentages of macrophages and monocytes and their sub-populations in those patients compared to healthy control. Moreover, we defined the correlation between macrophage subtypes and some inflammatory indices. Methods: Twenty-seven patients with clinical and radiologic diagnosis of acute viral respiratory infection admitted in Al-Azhar and Assiut University hospitals were recruited. Fresh peripheral blood samples were collected from all patients and healthy controls for flow cytometric analysis using BD FACSCanto II analyzer equipped with three lasers. Results: Compared to healthy controls, accumulation of cluster of differentiation (CD)11B+CD68+ macrophages (M) (P = 0.018), CD274+ M1 (P = 0.01), CD274+ M2 (P < 0.001), and CD80-CD206+ M2 (P = 0.001) was more evident in patients. Moreover, CD273+ M2 (P = 0.03), CD80+CD206- M1 (P = 0.002), and CD80+CD86+ M1 (P = 0.002) were highly expressed in controls compared with patients. Conclusion: The examination of clinical specimens obtained from patients with signs of acute respiratory viral infection showed the role of the macrophage in the immune response. Dysfunction in macrophages results in heightened immune activity and inflammation, which plays a role in the progression of viral diseases and the emergence of accompanying health issues. This malfunction in macrophages is a common characteristic seen in various viruses, making it a promising focus for antiviral therapies with broad applicability. The immune checkpoint could be a target for immune modulation in patients with severe symptoms.

A Complex Interplay of Tumor Microenvironment Could Enhance Cholangiocarcinoma Progression Even After Surgery: A Prospective Study.

Background: The current study was conducted to explore the impact of macrophages and programmed cell death protein 1 (PD-1) expression on tumor-infiltrating lymphocytes (TILs) on treatment outcomes and to define the interaction between these factors and the clinicopathologic features of advanced cholangiocarcinoma (CCA) patients. Methods: Twenty-five patients with metastatic CCA were recruited for the current study from El-Rajhi Hospital and the Clinical Oncology Department of Assiut University. Additionally, 19 healthy controls were included. Before the flow cytometric detection of immune cells, the diagnosis and staging of CCA were performed based on surgical intervention, imaging, carbohydrate antigen 19-9 (CA19-9), and carcinoembryonic antigen (CEA) determinations. This was followed by flow cytometric detection of CD4+, CD8+, CD4+PD-1+, CD8+PD-1+, and CD11b+CD68+ macrophages in the peripheral blood of both patients and controls. Results: The current results revealed higher levels of CD4+, CD8+, and CD11b+CD68+ macrophages in controls compared to patients. At the same time, PD-1 expression was significantly higher in patients compared to controls. CD4+ was correlated with improved progression-free survival (PFS), while CD8+PD-1 was associated with shorter PFS. In general, CD4+ and CD8+ levels progressively increased with improved response to treatments, differentiation, single organ site metastasis, and surgical interventions. On the contrary, PD-1 expression and macrophages progressively increased with worsening response, dedifferentiation, multiple organ sites, and surgical interventions. The median PFS was 12 months, and the mean ± standard error (SE) was 13.1 ± 1.3. Conclusions: CCA has a desmoplastic microenvironment with complex immunologic topography and tumor-reactive stroma. The immune landscape of the peripheral blood mononuclear cells (PBMCs) in CCA patients before treatment could reflect the state of systemic immune function and response to treatments. Our results revealed that T-lymphocytes correlated with better prognosis while macrophages and PD-1+ expression were associated with poor outcomes.

Discovering medical knowledge using association rule mining in young adults with acute myocardial infarction.

The knowledge discovery has been widely applied to mine significant knowledge from medical data. Nevertheless, previous studies have produced large numbers of imprecise patterns. To reduce the number of imprecise patterns, we need an approach that can discover interesting patterns that connote causality between antecedent and consequence in a pattern. In this paper, we propose association rule mining method that can discover interesting patterns that include medical knowledge in Korean acute myocardial infarction registry that consists of 1,247 young adults collected by 51 participating hospitals since 2005. Proposed method can remove imprecise patterns and discover target patterns that include associations between blood factors and disease history. The association that blood factors affect to disease history is defined as target pattern. In our experiments, the interestingness of a target pattern is evaluated in terms of statistical measures such as lift, leverage, and conviction. We discover medical knowledge that glucose, smoking, triglyceride total cholesterol, and creatinine are associated with diabetes and hypertension in Korean young adults with acute myocardial infarction.

Preparation and Photovoltaic Evaluation of CuO@Zn(Al)O-Mixed Metal Oxides for Dye Sensitized Solar Cell.

In this manuscript, a series of dye-sensitized solar cells (DSSCs) were fabricated as a function of post-processing temperature based on mesoporous CuO@Zn(Al)O-mixed metal oxides (MMO) in conjunction with dye N719 as the main light absorber; the proposed CuO@Zn(Al)O geometry was, in turn, attained using Zn/Al-layered double hydroxide (LDH) as a precursor via combination of co-precipitation and hydrothermal techniques. In particular, the dye loading amount onto the deposited mesoporous materials was anticipated via regression equation-based UV-Vis technique analysis, which evidently demonstrated a robust correlation along with the fabricated DSSCs power conversion efficiency. In detail, of the DSSCs assembled, CuO@MMO-550 exhibited short-circuit current (JSC) and open-circuit voltage (VOC) of 3.42 (mA/cm2) and 0.67 (V) which result in significant fill factor and power conversion efficiency of 0.55% and 1.24%, respectively. This could mainly be due to the relatively high surface area of 51.27 (m2/g) which in turn validates considerable dye loading amount of 0.246 (mM/cm-2).

Looking Beyond What You See: A Rare Cause of Dysphagia.

Hypothyroidism is a common endocrine condition with typical symptoms such as cold intolerance, weight gain, fatigue, constipation, and coarse skin, as well as less common symptoms such as depression, difficulty in concentration, and hair thinning. It is usually diagnosed by combining clinical features and applying clinical judgment; however, the wide spectrum of presenting symptoms can sometimes lead to a diagnostic dilemma. Dysphagia secondary to hypothyroidism is a rarely reported symptom in the literature and is believed to be associated with a hormonal effect on esophageal and gastric motility with neuromuscular incoordination; however, the underlying mechanism remains unknown. The most common cause of hypothyroidism is Hashimoto's disease, which can rarely manifest as heartburn, possibly due to esophageal dysmotility. Herein, we describe an unusual presentation of severe hypothyroidism with dysphagia, for which we could not identify any obstructive cause despite extensive investigations This condition was resolved successfully with levothyroxine treatment. Through this report, we aimed to communicate to the audience the important learning message that hypothyroidism may cause symptoms of dysphagia and to inform practitioners regarding this possibility, which should be considered after ruling out any obstructive pathology.