A clinical study on prognostic factors in duodenal ulcer perforation

BACKGROUND: Perforation is the most common complication of peptic ulcer disease. In spite of modern progress in the management, it is still a life-threatening catastrophe. Perforation may occur in a patient with previous history of ulcer disease or it may happen without any prior symptoms. METHODS: This study comprises a retrospective analysis of all patients diagnosed of perforated duodenal ulcer disease at TVMCH, Tirunelveli India. Morbidity and mortality are associated with age of the patients, haemodynamic instability, operative delay, site of the ulcer, peritoneal contamination and quality of postoperative care AIM OF STUDY: To determine relation between postoperative morbidity and comorbid disease and preoperative riskfactors in perforated duodenal ulcers. Inclusion Criteria: All non traumatic and non malignant perforated duodenal ulcers above 12 years of age Exclusion Criteria: Perforated malignant ulcers, Traumatic perforation. MATERIALS AND METHODS: This study comprises a prospective analysis of all patients diagnosed with perforated duodenal ulcer in TVMCH, Tirunelveli. Patients with perforated malignant ulcer, traumatic perforation and gastrinoma were excluded from the study. The following data should be collected from hospital records: age, sex, previous history of ulcer disease; use of tobacco, alcohol, corticosteroid and NSAIDs; duration of symptoms suggestive of perforation; location, size of perforation and amount of peritoneal contamination. Treatment outcome was elaborated by postoperative complications, hospital stay and death. The size of ulcer was noted in diameter in millimeter. Haemodynamic instability at the time of presentation was defined as a systolic blood pressure less than 90 mmHg. A delay in treatment was defined as an interval of more than 24 hours until surgery from the suspected time of perforation. CONCLUSION: The prognostic indicators can assist in risk stratification, The use of this system can help delineate high risk patients and the identify need of early intervention and prompt treatment for better outcome

White shark optimizer with optimal deep learning based effective unmanned aerial vehicles communication and scene classification.

Unmanned aerial vehicles (UAVs) become a promising enabler for the next generation of wireless networks with the tremendous growth in electronics and communications. The application of UAV communications comprises messages relying on coverage extension for transmission networks after disasters, Internet of Things (IoT) devices, and dispatching distress messages from the device positioned within the coverage hole to the emergency centre. But there are some problems in enhancing UAV clustering and scene classification using deep learning approaches for enhancing performance. This article presents a new White Shark Optimizer with Optimal Deep Learning based Effective Unmanned Aerial Vehicles Communication and Scene Classification (WSOODL-UAVCSC) technique. UAV clustering and scene categorization present many deep learning challenges in disaster management: scene understanding complexity, data variability and abundance, visual data feature extraction, nonlinear and high-dimensional data, adaptability and generalization, real-time decision making, UAV clustering optimization, sparse and incomplete data. the need to handle complex, high-dimensional data, adapt to changing environments, and make quick, correct decisions in critical situations drives deep learning in UAV clustering and scene categorization. The purpose of the WSOODL-UAVCSC technique is to cluster the UAVs for effective communication and scene classification. The WSO algorithm is utilized for the optimization of the UAV clustering process and enables to accomplish effective communication and interaction in the network. With dynamic adjustment of the clustering, the WSO algorithm improves the performance and robustness of the UAV system. For the scene classification process, the WSOODL-UAVCSC technique involves capsule network (CapsNet) feature extraction, marine predators algorithm (MPA) based hyperparameter tuning, and echo state network (ESN) classification. A wide-ranging simulation analysis was conducted to validate the enriched performance of the WSOODL-UAVCSC approach. Extensive result analysis pointed out the enhanced performance of the WSOODL-UAVCSC method over other existing techniques. The WSOODL-UAVCSC method achieved an accuracy of 99.12%, precision of 97.45%, recall of 98.90%, and F1-score of 98.10% when compared to other existing techniques

ACE2 Deficiency Worsens Epicardial Adipose Tissue Inflammation and Cardiac Dysfunction in Response to Diet-Induced Obesity

Obesity is increasing in prevalence and is strongly associated with metabolic and cardiovascular disorders. The renin-angiotensin system (RAS) has emerged as a key pathogenic mechanism for these disorders; angiotensin (Ang)-converting enzyme 2 (ACE2) negatively regulates RAS by metabolizing Ang II into Ang 1-7. We studied the role of ACE2 in obesity-mediated cardiac dysfunction. ACE2 null (ACE2KO) and wild-type (WT) mice were fed a high-fat diet (HFD) or a control diet and studied at 6 months of age. Loss of ACE2 resulted in decreased weight gain but increased glucose intolerance, epicardial adipose tissue (EAT) inflammation, and polarization of macrophages into a proinflammatory phenotype in response to HFD. Similarly, human EAT in patients with obesity and heart failure displayed a proinflammatory macrophage phenotype. Exacerbated EAT inflammation in ACE2KO-HFD mice was associated with decreased myocardial adiponectin, decreased phosphorylation of AMPK, increased cardiac steatosis and lipotoxicity, and myocardial insulin resistance, which worsened heart function. Ang 1-7 (24 µg/kg/h) administered to ACE2KO-HFD mice resulted in ameliorated EAT inflammation and reduced cardiac steatosis and lipotoxicity, resulting in normalization of heart failure. In conclusion, ACE2 plays a novel role in heart disease associated with obesity wherein ACE2 negatively regulates obesity-induced EAT inflammation and cardiac insulin resistance

Antagonism of angiotensin 1-7 prevents the therapeutic effects of recombinant human ACE2

Activation of the angiotensin 1-7/Mas receptor (MasR) axis counteracts angiotensin II (Ang II)-mediated cardiovascular disease. Recombinant human angiotensin-converting enzyme 2 (rhACE2) generates Ang 1-7 from Ang II. We hypothesized that the therapeutic effects of rhACE2 are dependent on Ang 1-7 action. Wild type male C57BL/6 mice (10-12 weeks old) were infused with Ang II (1.5 mg/kg/d) and treated with rhACE2 (2 mg/kg/d). The Ang 1-7 antagonist, A779 (200 ng/kg/min), was administered to a parallel group of mice. rhACE2 prevented Ang II-induced hypertrophy and diastolic dysfunction while A779 prevented these beneficial effects and precipitated systolic dysfunction. rhACE2 effectively antagonized Ang II-mediated myocardial fibrosis which was dependent on the action of Ang 1-7. Myocardial oxidative stress and matrix metalloproteinase 2 activity was further increased by Ang 1-7 inhibition even in the presence of rhACE2. Activation of Akt and endothelial nitric oxide synthase (eNOS) by rhACE2 were suppressed by the antagonism of Ang 1-7 while the activation of pathological signaling pathways was maintained. Blocking Ang 1-7 action prevents the therapeutic effects of rhACE2 in the setting of elevated Ang II culminating in systolic dysfunction. These results highlight a key cardioprotective role of Ang 1-7, and increased Ang 1-7 action represents a potential therapeutic strategy for cardiovascular diseases. KEY MESSAGES: Activation of the renin-angiotensin system (RAS) plays a key pathogenic role in cardiovascular disease. ACE2, a monocarboxypeptidase, negatively regulates pathological effects of Ang II. Antagonizing Ang 1-7 prevents the therapeutic effects of recombinant human ACE2. Our results highlight a key protective role of Ang 1-7 in cardiovascular disease

Induction of apoptosis of human primary osteoclasts treated with extracts from the medicinal plant Emblica officinalis

<p>Abstract</p> <p>Background</p> <p>Osteoclasts (OCs) are involved in rheumatoid arthritis and in several pathologies associated with bone loss. Recent results support the concept that some medicinal plants and derived natural products are of great interest for developing therapeutic strategies against bone disorders, including rheumatoid arthritis and osteoporosis. In this study we determined whether extracts of <it>Emblica officinalis </it>fruits display activity of possible interest for the treatment of rheumatoid arthritis and osteoporosis by activating programmed cell death of human primary osteoclasts.</p> <p>Methods</p> <p>The effects of extracts from <it>Emblica officinalis </it>on differentiation and survival of human primary OCs cultures obtained from peripheral blood were determined by tartrate-acid resistant acid phosphatase (TRAP)-positivity and colorimetric MTT assay. The effects of <it>Emblica officinalis </it>extracts on induction of OCs apoptosis were studied using TUNEL and immunocytochemical analysis of FAS receptor expression. Finally, <it>in vitro </it>effects of <it>Emblica officinalis </it>extracts on NF-kB transcription factor activity were determined by gel shift experiments.</p> <p>Results</p> <p>Extracts of <it>Emblica officinalis </it>were able to induce programmed cell death of mature OCs, without altering, at the concentrations employed in our study, the process of osteoclastogenesis. <it>Emblica officinalis </it>increased the expression levels of Fas, a critical member of the apoptotic pathway. Gel shift experiments demonstrated that <it>Emblica officinalis </it>extracts act by interfering with NF-kB activity, a transcription factor involved in osteoclast biology. The data obtained demonstrate that <it>Emblica officinalis </it>extracts selectively compete with the binding of transcription factor NF-kB to its specific target DNA sequences. This effect might explain the observed effects of <it>Emblica officinalis </it>on the expression levels of interleukin-6, a NF-kB specific target gene.</p> <p>Conclusion</p> <p>Induction of apoptosis of osteoclasts could be an important strategy both in interfering with rheumatoid arthritis complications of the bone skeleton leading to joint destruction, and preventing and reducing osteoporosis. Accordingly, we suggest the application of <it>Emblica officinalis </it>extracts as an alternative tool for therapy applied to bone diseases.</p

Antioxidant effects of resveratrol in cardiovascular, cerebral and metabolic diseases.

Resveratrol-a natural polyphenolic compound-was first discovered in the 1940s. Although initially used for cancer therapy, it has shown beneficial effects against most cardiovascular and cerebrovascular diseases. A large part of these effects are related to its antioxidant properties. Here we review: a) the sources, the metabolism, and the bioavailability of resveratrol; b) the ability of resveratrol to modulate redox signalling and to interact with multiple molecular targets of diverse intracellular pathways; c) its protective effects against oxidative damage in cardio-cerebro-vascular districts and metabolic disorders such as diabetes; and d) the evidence for its efficacy and toxicity in humans. The overall aim of this review is to discuss the frontiers in the field of resveratrol's mechanisms, bioactivity, biology, and health-related use