Open AccessFeature PaperReview
Implications of PI3K/AKT/PTEN Signaling on Superoxide Dismutases Expression and in the Pathogenesis of Alzheimer’s Disease
Diseases 2018, 6(2), 28; doi:10.3390/diseases6020028 (registering DOI) -
Abstract
Alzheimer’s disease is a neurodegenerative sickness, where the speed of personal disease progression differs prominently due to genetic and environmental factors such as life style. Alzheimer’s disease is described by the construction of neuronal plaques and neurofibrillary tangles composed of phosphorylated tau protein.
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Alzheimer’s disease is a neurodegenerative sickness, where the speed of personal disease progression differs prominently due to genetic and environmental factors such as life style. Alzheimer’s disease is described by the construction of neuronal plaques and neurofibrillary tangles composed of phosphorylated tau protein. Mitochondrial dysfunction may be a noticeable feature of Alzheimer’s disease and increased production of reactive oxygen species has long been described. Superoxide dismutases (SODs) protect from excess reactive oxygen species to form less reactive hydrogen peroxide. It is suggested that SODs can play a protective role in neurodegeneration. In addition, PI3K/AKT pathway has been shown to play a critical role on the neuroprotection and inhibiting apoptosis via the enhancing expression of the SODs. This pathway appears to be crucial in Alzheimer’s disease because it is related to the tau protein hyper-phosphorylation. Dietary supplementation of several ordinary compounds may provide a novel therapeutic approach to brain disorders by modulating the function of the PI3K/AKT pathway. Understanding these systems may offer a better efficacy of new therapeutic approaches. In this review, we summarize recent progresses on the involvement of the SODs and PI3K/AKT pathway in neuroprotective signaling against Alzheimer’s disease. Full article
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Open AccessFeature PaperReview
Update Treatment for HBV Infection and Persistent Risk for Hepatocellular Carcinoma: Prospect for an HBV Cure
Diseases 2018, 6(2), 27; doi:10.3390/diseases6020027 (registering DOI) -
Abstract
Since the discovery of the hepatitis B virus (HBV) by Blumberg et al. in 1965, its genome, sequence, epidemiology, and hepatocarcinogenesis have been elucidated. Globally, hepatitis B virus (HBV) is still responsible for the majority of hepatocellular carcinoma (HCC). HCC is the sixth-most
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Since the discovery of the hepatitis B virus (HBV) by Blumberg et al. in 1965, its genome, sequence, epidemiology, and hepatocarcinogenesis have been elucidated. Globally, hepatitis B virus (HBV) is still responsible for the majority of hepatocellular carcinoma (HCC). HCC is the sixth-most common cancer in the world and the second-most common cancer death. The ultimate goal of treating HBV infection is the prevention of HCC. Fortunately, anti-HBV treatment with nucleos(t)ide analogues (NAs), which began with lamivudine in 1998, has resulted in remarkable improvements in the survival of patients with chronic hepatitis B and a reduced incidence of HCC. These results were documented with lamivudine, entecavir, and tenofovir. Nonetheless, as the duration of antiviral treatment increases, the risk for HCC still remains despite undetectable HBV DNA in serum, as reported by different investigators with observation up to 4–5 years. In our own experience, we are witnessing the development of HCC in patients who have received antiviral treatment. Some have enjoyed negative serum HBV DNA for over 12 years before developing HCC. Current treatment with NAs can effectively suppress the replication of the virus but cannot eradicate the covalently closed circular DNA (cccDNA) that is within the nucleus of hepatocytes. There still remains a great need for a cure for HBV. Fortunately, several compounds have been identified that have the potential to eradicate HBV, and there are ongoing clinical trials in progress in their early stages. Full article
Open AccessArticle
The Voice of the Heart: Vowel-Like Sound in Pulmonary Artery Hypertension
Diseases 2018, 6(2), 26; doi:10.3390/diseases6020026 -
Abstract
Increased blood pressure in the pulmonary artery is referred to as pulmonary hypertension and often is linked to loud pulmonic valve closures. For the purpose of this paper, it was hypothesized that pulmonary circulation vibrations will create sounds similar to sounds created by
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Increased blood pressure in the pulmonary artery is referred to as pulmonary hypertension and often is linked to loud pulmonic valve closures. For the purpose of this paper, it was hypothesized that pulmonary circulation vibrations will create sounds similar to sounds created by vocal cords during speech and that subjects with pulmonary artery hypertension (PAH) could have unique sound signatures across four auscultatory sites. Using a digital stethoscope, heart sounds were recorded at the cardiac apex, 2nd left intercostal space (2LICS), 2nd right intercostal space (2RICS), and 4th left intercostal space (4LICS) undergoing simultaneous cardiac catheterization. From the collected heart sounds, relative power of the frequency band, energy of the sinusoid formants, and entropy were extracted. PAH subjects were differentiated by applying the linear discriminant analysis with leave-one-out cross-validation. The entropy of the first sinusoid formant decreased significantly in subjects with a mean pulmonary artery pressure (mPAp) ≥ 25 mmHg versus subjects with a mPAp < 25 mmHg with a sensitivity of 84% and specificity of 88.57%, within a 10-s optimized window length for heart sounds recorded at the 2LICS. First sinusoid formant entropy reduction of heart sounds in PAH subjects suggests the existence of a vowel-like pattern. Pattern analysis revealed a unique sound signature, which could be used in non-invasive screening tools. Full article
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Open AccessCase Report
ERBB1- and ERBB2-Positive Medullary Thyroid Carcinoma: A Case Report
Diseases 2018, 6(2), 25; doi:10.3390/diseases6020025 -
Abstract
Medullary thyroid carcinomas (MTCs) are rare thyroid tumors occurring in both sporadic and hereditary forms, whose pathogenesis is related to RET proto-oncogene alterations. MTCs originate from parafollicular cells, which produce calcitonin that represents the biochemical activity of MTC. Total thyroidectomy is the main
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Medullary thyroid carcinomas (MTCs) are rare thyroid tumors occurring in both sporadic and hereditary forms, whose pathogenesis is related to RET proto-oncogene alterations. MTCs originate from parafollicular cells, which produce calcitonin that represents the biochemical activity of MTC. Total thyroidectomy is the main treatment for MTC and often cures patients with confined diseases. In the presence of metastasis, the therapeutic approach depends on the rate of disease progression. We report a case of a 54-year-old female with a single, incidentally discovered, thyroid nodule of 1 cm, classified as suspicious MTC after a stimulation test with intravenous (iv) calcium. After surgery, we examined the nodule using immunohistochemistry, immunofluorescence, and electron microscopy. In addition to calcitonin, we found that it expressed intracellular positivity for the tyrosine kinase RTK receptors ERBB1 and ERBB2. Consistently with MTC features, the ultrastructural examination of the tumor displayed heterogeneous spindle-shaped cells containing two groups of secretory granules. Because of the significant correlation found between high ERBB1/ERBB2 levels in MTCs and extrathyroidal growth, the detection of ERBB1 and ERBB2 expression suggests that the two oncoproteins may be involved in the tumor proliferative responses and/or in the differentiation of parafollicular C-cells. The biological, prognostic, and therapeutic significance of these patterns would merit further investigations. Full article
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Open AccessArticle
Genomic Influence in the Prevention of Cardiovascular Diseases with a Sterol-Based Treatment
Diseases 2018, 6(2), 24; doi:10.3390/diseases6020024 -
Abstract
Raised serum cholesterol concentration is a well-established risk factor in cardiovascular disease. In addition, genetic load may have an indirect influence on cardiovascular risk. Plant-based sterol-supplemented foods are recommended to help reduce the serum low-density lipoprotein cholesterol level. The objective was to analyse
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Raised serum cholesterol concentration is a well-established risk factor in cardiovascular disease. In addition, genetic load may have an indirect influence on cardiovascular risk. Plant-based sterol-supplemented foods are recommended to help reduce the serum low-density lipoprotein cholesterol level. The objective was to analyse the influence of different polymorphisms in hypercholesterolemia patients following a dietary treatment with plant sterols. A randomised double-blind cross-over controlled clinical trial was carried out in 45 people (25 women). Commercial milk, containing 2.24 g of sterols, was ingested daily during a 3-week period, and then the same amount of skim milk, without sterols, was consumed daily during the 3-week placebo phase. Both phases were separated by a washout period of 2 weeks. At the beginning and end of each phase, blood draws were performed. Genes LIPC C-514T and APOA5 C56G are Ser19Trp carriers and greatly benefit from sterol intake in the diet. LIPC C-514T TT homozygous carriers had lower low-density lipoprotein cholesterol (LDL-c) levels than CC homozygote and CT heterozygote carriers after the ingestion of plant sterols (p = 0.001). These two genes also showed statistically significant changes in total cholesterol levels (p = 0.025; p = 0.005), and no significant changes in high-density lipoprotein (HDL) cholesterol levels (p = 0.032; p = 0.003), respectively. No statistically significant differences were observed for other genes. Further studies are needed to establish which genotype combinations would be the most protective against hypercholesterolemia. Full article
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Open AccessCommentary
The Brain–Intestinal Mucosa–Appendix– Microbiome–Brain Loop
Diseases 2018, 6(2), 23; doi:10.3390/diseases6020023 -
Abstract
The brain and the gut are connected from early fetal life. The mother’s exposure to microbial molecules is thought to exert in utero developmental effects on the fetus. These effects could importantly underpin the groundwork for subsequent pathophysiological mechanisms for achieving immunological tolerance
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The brain and the gut are connected from early fetal life. The mother’s exposure to microbial molecules is thought to exert in utero developmental effects on the fetus. These effects could importantly underpin the groundwork for subsequent pathophysiological mechanisms for achieving immunological tolerance and metabolic equilibrium post birth, events that continue through to 3–4 years of age. Furthermore, it is understood that the microbiome promotes cues that instruct the neonate’s mucosal tissues and skin in the language of molecular and cellular biology. Post birth mucosal lymphoid tissue formation and maturation (most probably including the vermiform appendix) is microbiota-encouraged co-establishing the intestinal microbiome with a developing immune system. Intestinal mucosal tissue maturation loops the brain-gut-brain and is postulated to influence mood dispositions via shifts in the intestinal microbiome phyla. A plausible appreciation is that dysregulated pro-inflammatory signals from intestinal resident macrophages could breach the loop by providing adverse mood signals via vagus nerve afferents to the brain. In this commentary, we further suggest that the intestinal resident macrophages act as an upstream traffic controller of translocated microbes and metabolites in order to maintain local neuro-endocrine-immunological equilibrium. When macrophages are overwhelmed through intestinal microbiome and intestinal epithelial cell dysbiosis, pro-inflammatory signals are sustained, which may then lead to mood disorders. The administration of probiotics as an adjunctive medicine co-administered with antidepressant medications in improving depressed mood may have biological and clinical standing. Full article
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Open AccessReview
Lipid Target in Very High-Risk Cardiovascular Patients: Lesson from PCSK9 Monoclonal Antibodies
Diseases 2018, 6(1), 22; doi:10.3390/diseases6010022 -
Abstract
The role of low-density lipoproteins (LDLs) as a major risk factor for cardiovascular disease has been demonstrated by several epidemiological studies. The molecular basis for LDLs in atherosclerotic plaque formation and progression is not completely unraveled yet. Pharmacological modulation of plasma LDL-C concentrations
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The role of low-density lipoproteins (LDLs) as a major risk factor for cardiovascular disease has been demonstrated by several epidemiological studies. The molecular basis for LDLs in atherosclerotic plaque formation and progression is not completely unraveled yet. Pharmacological modulation of plasma LDL-C concentrations and randomized clinical trials addressing the impact of lipid-lowering interventions on cardiovascular outcome have clearly shown that reducing plasma LDL-C concentrations results in a significant decrease in major cardiovascular events. For many years, statins have represented the most powerful pharmacological agents available to lower plasma LDL-C concentrations. In clinical trials, it has been shown that the greater the reduction in plasma LDL-C concentrations, the lower the rate of major cardiovascular events, especially in high-risk patients, because of multiple risk factors and recurrent events. However, in a substantial number of patients, the recommended LDL target is difficult to achieve because of different factors: genetic background (familial hypercholesterolemia), side effects (statin intolerance), or high baseline plasma LDL-C concentrations. In the last decade, our understanding of the molecular mechanisms involved in LDL metabolism has progressed significantly and the key role of proprotein convertase subtilisin/kexin type 9 (PCSK9) has emerged. This protein is an enzyme able to bind the LDL receptors (LDL-R) on hepatocytes, favoring their degradation. Blocking PCSK9 represents an intriguing new therapeutic approach to decrease plasma LDL-C concentrations, which in recent studies has been demonstrated to also result in a significant reduction in major cardiovascular events. Full article
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Open AccessArticle
Elevated Gene Expression of Interleukin-32 Isoforms Alpha, Beta, Gamma, and Delta in the Peripheral Blood of Chronic Psoriatic Patients
Diseases 2018, 6(1), 21; doi:10.3390/diseases6010021 -
Abstract
Inflammatory-mediated reactions have been implicated as contributors in a number of dermatological disorders, including psoriasis. However, the potential of interleukin (IL)-32 and its isoforms to contribute to the pathogenesis of psoriasis remains unexplored. This study was undertaken to investigate the role of IL-32
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Inflammatory-mediated reactions have been implicated as contributors in a number of dermatological disorders, including psoriasis. However, the potential of interleukin (IL)-32 and its isoforms to contribute to the pathogenesis of psoriasis remains unexplored. This study was undertaken to investigate the role of IL-32 and its isoforms IL-32α, IL-32β, IL-32γ, and IL-32δ in the peripheral blood of psoriatic patients. The majority of chronic plaque psoriatic patients showed elevated IL-32 mRNA levels in the peripheral blood mononuclear cells (PBMCs) as compared with the levels of IL-32 mRNA in PBMCs of healthy controls (p = 0.001). To further investigate the role of elevated levels of IL-32 in psoriatic patients, IL-32 isoforms mRNAs were determined. All tested isoforms IL-32α, IL-32β, IL-32γ, and IL-32δ were overexpressed in psoriatic patients PBMCs as compared with healthy controls’ PBMCs (p < 0.05). IL-32α mRNA expression was also significantly higher as compared with all other isoforms of IL-32 in PBMCs of psoriatic patients (p < 0.001). In short, this is the first study that shows the role of IL-32 and its isoforms in the peripheral blood of psoriatic patients. Our novel findings support an association between elevated levels of IL-32 and psoriasis. The data also suggest that a major proinflammatory response of IL-32 may derive from IL-32α isoform in psoriasis. Full article
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Open AccessFeature PaperArticle
Toward Generating More Diagnostic Features from Photoplethysmogram Waveforms
Diseases 2018, 6(1), 20; doi:10.3390/diseases6010020 -
Abstract
Photoplethysmogram (PPG) signals collected using a pulse oximeter are increasingly being used for screening and diagnosis purposes. Because of the non-invasive, cost-effective, and easy-to-use nature of the pulse oximeter, clinicians and biomedical engineers are investigating how PPG signals can help in the management
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Photoplethysmogram (PPG) signals collected using a pulse oximeter are increasingly being used for screening and diagnosis purposes. Because of the non-invasive, cost-effective, and easy-to-use nature of the pulse oximeter, clinicians and biomedical engineers are investigating how PPG signals can help in the management of many medical conditions, especially for global health application. The study of PPG signal analysis is relatively new compared to research in electrocardiogram signals, for instance; however, we anticipate that in the near future blood pressure, cardiac output, and other clinical parameters will be measured from wearable devices that collect PPG signals, based on the signal’s vast potential. This article attempts to organize and standardize the names of PPG waveforms to ensure consistent terminologies, thereby helping the rapid developments in this research area, decreasing the disconnect within and among different disciplines, and increasing the number of features generated from PPG waveforms. Full article
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Open AccessArticle
Hyper-Uricemia and Gouty Access in the Adult Population of the Southeast of Gabon: Biochemical Aspects
Diseases 2018, 6(1), 19; doi:10.3390/diseases6010019 -
Abstract
Gout is caused by a chronic hyperuricemia whose complications are not currently well evaluated in Africa. The aim of this study was to determine the prevalence and risk factors of hyperuricemia and gout in 85 patients recruited. A total of 26 cases of
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Gout is caused by a chronic hyperuricemia whose complications are not currently well evaluated in Africa. The aim of this study was to determine the prevalence and risk factors of hyperuricemia and gout in 85 patients recruited. A total of 26 cases of hyperuricemia, i.e., 30.6% of the study population, with 12 cases of gout and seven cases of gouty access. In this population, hyperuricemia was proportional to age (p-value < 10−4, OR = 2.6), but it was more prevalent in men, 23.5% versus 7.1% for women (p-value = 0.0047). In addition, none of these women showed signs of a gouty affection. Consumption of alcohol (OR = 13) and nucleoprotein-rich foods, obesity (BMI 30 kg/m2; OR = 6), family history of gout (OR = 6.8), as well as diseases such as high blood pressure (associated with taking diuretics; OR = 1.7), renal insufficiency (OR = 4.4) and diabetes (p < 0.049) were the main factors of the diseases associated with gout and hyperuricemia in this population. The biochemical role of these factors may increase and/or decrease the processes of synthesis and/or elimination of uric acid by acting on metabolites involved in the regulation of urate production. Full article
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Open AccessFeature PaperShort Note
Less Is More in Biosignal Analysis: Compressed Data Could Open the Door to Faster and Better Diagnosis
Diseases 2018, 6(1), 18; doi:10.3390/diseases6010018 -
Abstract
In the digital medicine field, biosignals, such as those of an electrocardiogram (ECG), are collected regularly for screening and diagnosis, and there continues to be an increasingly substantial shift towards collecting long-term ECG signals for remote monitoring, e.g., in smart homes. ECG signal
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In the digital medicine field, biosignals, such as those of an electrocardiogram (ECG), are collected regularly for screening and diagnosis, and there continues to be an increasingly substantial shift towards collecting long-term ECG signals for remote monitoring, e.g., in smart homes. ECG signal collection is quite simple and only requires the use of inexpensive sensors, an active Internet connection, and a mobile device that acts as the medium between the sensors and the Internet (e.g., a mobile phone or laptop). Despite the ease and convenience of remote ECG data collection and transmission, the amount of time and energy required for the related remote computational processes remains a major limitation. This short note discusses a biosignal approach that uses fewer biomedical data for screening and diagnosis that is, compared to current data collection methods, equally, if not more, efficient. Full article
Open AccessFeature PaperArticle
Do Nonalcoholic Fatty Liver Disease and Fetuin-A Play Different Roles in Symptomatic Coronary Artery Disease and Peripheral Arterial Disease?
Diseases 2018, 6(1), 17; doi:10.3390/diseases6010017 -
Abstract
Background and Aims: Nonalcoholic fatty liver disease (NAFLD) is strongly associated with both atherosclerotic cardiovascular disease (CVD) and Fetuin-A. However, the association of Fetuin-A with atherosclerosis is more controversial. We hypothesized that the pathogenic interplay of NAFLD, Fetuin-A and atherosclerosis varies based on
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Background and Aims: Nonalcoholic fatty liver disease (NAFLD) is strongly associated with both atherosclerotic cardiovascular disease (CVD) and Fetuin-A. However, the association of Fetuin-A with atherosclerosis is more controversial. We hypothesized that the pathogenic interplay of NAFLD, Fetuin-A and atherosclerosis varies based on arterial site. Accordingly, we aimed to assess NAFLD prevalence, Fetuin-A values and their relationship with symptomatic atherosclerosis occurring in different localizations: coronary artery disease (CAD) vs. peripheral arterial disease (PAD). Methods: One hundred and forty-nine consecutive patients with symptomatic atherosclerotic CVD were recruited: 45 with CAD diagnosed by coronary angiography and 104 with PAD detected by doppler-ultrasound and/or computed tomography angiography and/or angiography. NAFLD was diagnosed based on both ultrasonography and exclusion of competing etiologies. Serum Fetuin-A was measured with ELISA. Results: NAFLD was detected in 54% of the overall group, with higher rates in PAD (59%) than CAD (42%) patients. Median Fetuin-A values were 256 (111–662) μg/mL, higher in patients with CAD (378 (124−662) μg/mL) than those with PAD (236 (111−461) μg/mL). The main findings were: (1) CAD patients had higher Fetuin-A values and less frequently NAFLD than PAD patients; (2) NAFLD was positively associated with Fetuin-A values; however, this association was limited to CAD patients only; (3) Fetuin-A values were positively associated with both CAD and NAFLD. Conclusion: The pathogenic interplay of NAFLD, Fetuin-A and atherosclerosis probably varies according to the arterial site. Full article
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Open AccessReview
Diaphragmatic Palsy
Diseases 2018, 6(1), 16; doi:10.3390/diseases6010016 -
Abstract
The diaphragm is the primary muscle of respiration, and its weakness can lead to respiratory failure. Diaphragmatic palsy can be caused by various causes. Injury to the phrenic nerve during thoracic surgeries is the most common cause for diaphragmatic palsy. Depending on the
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The diaphragm is the primary muscle of respiration, and its weakness can lead to respiratory failure. Diaphragmatic palsy can be caused by various causes. Injury to the phrenic nerve during thoracic surgeries is the most common cause for diaphragmatic palsy. Depending on the cause, the symptoms of diaphragmatic palsies vary from completely asymptomatic to disabling dyspnea requiring mechanical ventilation. On pulmonary function tests, there will be a decrease in the maximum respiratory muscle power. Spirometry shows reduced lung functions and a significant drop of lung function in supine position is typical of diaphragmatic palsy. Diaphragmatic movements with respiration can be directly visualized by fluoroscopic examination. Currently, this test is being replaced by bedside thoracic ultrasound examination, looking at the diaphragmic excursion with deep breathing or sniffing. This test is found to be equally efficient, and without risks of ionizing radiation of fluoroscope. Treatment of diaphragmatic palsy depends on the cause. Surgical approach of repair of diaphragm or nonsurgical approach of noninvasive ventilation has been tried with good success. Overall prognosis of diaphragmatic palsy is good, except when it is related to neuromuscular degeneration conditions. Full article
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Open AccessArticle
Carotid Artery Calcification: A Digital Panoramic-Based Study
Diseases 2018, 6(1), 15; doi:10.3390/diseases6010015 -
Abstract
Objective: The aim of this study was to estimate the incidence of carotid artery calcification (CAC) in a sample of Lebanese population using digital panoramic radiographs. Materials and Methods: Panoramic radiographs of 500 patients (281 females and 219 males), aged between 18 and
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Objective: The aim of this study was to estimate the incidence of carotid artery calcification (CAC) in a sample of Lebanese population using digital panoramic radiographs. Materials and Methods: Panoramic radiographs of 500 patients (281 females and 219 males), aged between 18 and 88 years (mean: 47.9 years), were assessed for CAC. Data collected were analyzed statistically using IBM® SPSS® for Windows version 20.0 (SPSS, Chicago, IL, USA). Results: CAC were found in 34 cases (6.8%), among them, 23 females (8.18%) and 11 males (5.02%). Six of all the calcifications were on the right side, against six on the left side, and 22 on both sides. The mean age of patients affected with CAC was 60.9 years (ranging from 18 to 88 years). Chi-square test showed no statistical significance between gender and CAC, while Spearman correlation analysis showed positive low correlation with age (r = 0.179). Conclusion: CAC can be found on routine panoramic radiographs taken in dental clinics; dentists should automatically refer the patients in question for specialized medical evaluation. Full article
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Open AccessFeature PaperArticle
Incidence and Determinants of Health Care-Associated Blood Stream Infection at a Neonatal Intensive Care Unit in Ujjain, India: A Prospective Cohort Study
Diseases 2018, 6(1), 14; doi:10.3390/diseases6010014 -
Abstract
Very little is known about laboratory-confirmed blood stream infections (LCBIs) in neonatal intensive care units (NICUs) in resource-limited settings. The aim of this cohort study was to determine the incidence, risk factors, and causative agents of LCBIs in a level-2 NICU in India.
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Very little is known about laboratory-confirmed blood stream infections (LCBIs) in neonatal intensive care units (NICUs) in resource-limited settings. The aim of this cohort study was to determine the incidence, risk factors, and causative agents of LCBIs in a level-2 NICU in India. The diagnosis of LCBIs was established using the Centre for Disease Control, USA criteria. A predesigned questionnaire containing risk factors associated with LCBIs was filled-in. A total of 150 neonates (43% preterm) were included in the study. The overall incidence of LCBIs was 31%. The independent risk factors for LCBIs were: preterm neonates (relative risk (RR) 2.23), duration of NICU stay more than 14 days (RR 1.75), chorioamnionitis in the mother (RR 3.18), premature rupture of membrane in mothers (RR 2.32), neonate born through meconium-stained amniotic fluid (RR 2.32), malpresentation (RR 3.05), endotracheal intubation (RR 3.41), umbilical catheterization (RR 4.18), and ventilator-associated pneumonia (RR 3.17). The initiation of minimal enteral nutrition was protective from LCBIs (RR 0.22). The predominant causative organisms were gram-negative pathogens (58%). The results of the present study can be used to design and implement antibiotic stewardship policy and introduce interventions to reduce LCBIs in resource-limited settings. Full article
Open AccessArticle
p53 Gene (NY-CO-13) Levels in Patients with Chronic Myeloid Leukemia: The Role of Imatinib and Nilotinib
Diseases 2018, 6(1), 13; doi:10.3390/diseases6010013 -
Abstract
The p53 gene is also known as tumor suppressor p53. The main functions of the p53 gene are an anticancer effect and cellular genomic stability via various pathways including activation of DNA repair, induction of apoptosis, and arresting of cell growth at the
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The p53 gene is also known as tumor suppressor p53. The main functions of the p53 gene are an anticancer effect and cellular genomic stability via various pathways including activation of DNA repair, induction of apoptosis, and arresting of cell growth at the G1/S phase. Normally, the p53 gene is inactivated by mouse double minute 2 proteins (mdm2), but it is activated in chronic myeloid leukemia (CML). Tyrosine kinase inhibitors are effective chemotherapeutic agents in the management of CML. The purpose of the present study was to evaluate the differential effect of imatinib and nilotinib on p53 gene serum levels in patients with CML. A total number of 60 patients with chronic myeloid leukemia with ages ranging from 47 to 59 years were recruited from the Iraqi Hematology Center. They started with tyrosine kinase inhibitors as first-line chemotherapy. They were divided into two groups—Group A, 29 patients treated with imatinib and Group B, 31 patients treated with nilotinib—and compared with 28 healthy subjects for evaluation p53 serum levels regarding the selective effect of either imatinib or nilotinib. There were significantly (p < 0.01) high p53 gene serum levels in patients with CML (2.135 ± 1.44 ng/mL) compared to the control (0.142 ± 0.11 ng/mL). Patients with CML that were treated with either imatinib or nilotinib showed insignificant differences in most of the hematological profile (p > 0.05) whereas, p53 serum levels were high (3.22 ± 1.99 ng/mL) in nilotinib-treated patients and relatively low (1.18 ± 0.19 ng/mL) in imatinib-treated patients (p = 0.0001). Conclusions: Nilotinib is more effective than imatinib in raising p53 serum levels in patients with chronic myeloid leukemia. Full article
Open AccessFeature PaperArticle
Metabolic Syndrome and Chronic Renal Disease
Diseases 2018, 6(1), 12; doi:10.3390/diseases6010012 -
Abstract
Background: The influence of metabolic syndrome (MetS) on kidneys is related to many complications. We aimed to assess the association between MetS and chronic renal disease defined by a poor estimated glomerular filtration rate (eGFR) and/or the presence of microalbuminuria/macroalbuminuria. Methods: 149
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Background: The influence of metabolic syndrome (MetS) on kidneys is related to many complications. We aimed to assess the association between MetS and chronic renal disease defined by a poor estimated glomerular filtration rate (eGFR) and/or the presence of microalbuminuria/macroalbuminuria. Methods: 149 patients (77 males/72 females) were enrolled in the study. Chronic renal disease was defined according to KDIGO 2012 criteria based on eGFR category and classified albuminuria. MetS was studied as a dichotomous variable (0 to 5 components) including hypertension, waist circumference, low HDL-cholesterol, high triglycerides, and high glucose. Results: The association between clustering MetS and both classified eGFR and classified albuminuria (x2 = 50.3, p = 0.001 and x2 = 26.9, p = 0.003 respectively) was found to be significant. The MetS presence showed an odds 5.3-fold (1.6–17.8) higher for low eGFR and 3.2-fold (1.2–8.8) higher for albuminuria in combination with the presence of diabetes mellitus, which also increased the risk for albuminuria by 3.5-fold (1.1–11.3). Albuminuria was significantly associated with high triglycerides, hypertension, high glucose (x2 = 11.8, p = 0.003, x2 = 11.4, p = 0.003 and x2 = 9.1, p = 0.01 respectively), and it was mildly associated with a low HDL-C (x2 = 5.7, p = 0.06). A significant association between classified eGFR and both high triglycerides and hypertension (x2 = 9.7, p = 0.04 and x2 = 16.1, p = 0.003 respectively) was found. Conclusion: The clustering of MetS was significantly associated with chronic renal disease defined by both classified eGFR and albuminuria. The definition of impaired renal function by classified albuminuria was associated with more MetS components rather than the evaluation of eGFR category. MetS may contribute to the manifestation of albuminuria in patients with diabetes mellitus. Full article
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Open AccessEditorial
Acknowledgement to Reviewers of Diseases in 2017
Diseases 2018, 6(1), 11; doi:10.3390/diseases6010011 -
Abstract
Peer review is an essential part in the publication process, ensuring that Diseases maintains high quality standards for its published papers.[...] Full article
Open AccessArticle
Usefulness of a Telemedicine Program in Refractory Older Congestive Heart Failure Patients
Diseases 2018, 6(1), 10; doi:10.3390/diseases6010010 -
Abstract
Background: Home telemonitoring is a modern and effective disease management model that is able to improve medical care, quality of life, and prognosis of chronically ill patients, and to reduce expenditure. The objective of this study was to evaluate the efficacy, costs, and
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Background: Home telemonitoring is a modern and effective disease management model that is able to improve medical care, quality of life, and prognosis of chronically ill patients, and to reduce expenditure. The objective of this study was to evaluate the efficacy, costs, and patients’ and caregivers’ acceptance of our model of telemedicine in a high-risk chronic heart failure (CHF) older population. Methods: Patients with high risk/refractory CHF were included. In the case of alarm parameters’ modifications, a cardiologist decided to inform the emergency department (ED), the patient’s General Practioner, or to programme a clinical ambulatory control. Results: Forty-eight CHF patients (28 males; 58.3%), with a mean age of 80.4 ± 7.7 years, entered this clinical experience. During the 20-months follow-up, four patients dropped out from counselling (8.3%), ambulatory clinical control within-24 h was planned in 18% of patients, 11% of patients were admitted to an ED, and 18% were hospitalized. Thirteen patients (29.5%) died a cardiac death; hospital admissions for heart failure decreased during the year after the enrolment when compared to the year before (from 35 to 12 acute HF hospitalizations/year; p = 0.0001). Moreover, in these HF patients followed, accesses to an ED for an acute episode of HF decompensation reduced from 21/year to five/year (p = 0.0001). The economic expenditure, calculated for the year before and after the enrolment, reduced from 116.856 Euros to 40.065 Euros/year. Conclusions: A telemedicine surveillance in high-risk older CHF patients determines a continuous and active contact between patients/caregivers, the Heart Failure Clinic, and family physicians, permitting an early evaluation of signs and symptoms of acute decompensation. Full article
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Open AccessArticle
Rosuvastatin Improves Vaspin Serum Levels in Obese Patients with Acute Coronary Syndrome
Diseases 2018, 6(1), 9; doi:10.3390/diseases6010009 -
Abstract
Adipose tissue-derived serine protease inhibitor (vaspin), which has endocrine and local roles in atherosclerosis growth, is also synthesized by adipose tissue; it was found that vaspin was negatively correlated with blood pressure in obese patients, while vaspin levels were decreased in endothelial dysfunction.
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Adipose tissue-derived serine protease inhibitor (vaspin), which has endocrine and local roles in atherosclerosis growth, is also synthesized by adipose tissue; it was found that vaspin was negatively correlated with blood pressure in obese patients, while vaspin levels were decreased in endothelial dysfunction. The aim of the present study was to determine rosuvastatin modulation effects on serum vaspin levels in acute coronary syndrome (ACS) with class I obesity. A total number of seventy patients with acute coronary syndrome previously and currently treated with rosuvastatin was compared to 40 patients with IHD not treated by rosuvastatin as a control. Vaspin serum levels were higher in rosuvastatin-treated patients with acute coronary syndrome compared to the patients with acute coronary syndrome not treated by rosuvastatin, p < 0.01. Additionally, in the rosuvastatin-treated group, patients with STEMI showed higher vaspin serum levels compared to NSTEMI p < 0.01. Conclusion: Rosuvastatin significantly increases vaspin serum levels in acute coronary syndrome. Full article
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