Fahr's disease in a patient with recurrent pneumonias, parkinsonism and dementia.

Fahr's disease is a rare condition characterised by the presence of idiopathic familial bilateral basal ganglia calcifications, transmitted in an autosomal-dominant fashion. Diagnosis is based on clinical features of neuropsychiatric and somatic symptoms in conjunction with radiological findings. Our patient, a man in his early 50s, presented with pneumonia. History was significant for five admissions in the last 2 years for pneumonia and falls, with gradual cognitive and motor decline since his late 30s. Hypophonia, bradykinesia and dementia were noted on examination. CT of the brain revealed bilateral thalamic calcinosis, consistent with Fahr's syndrome. Further investigations and retrospective history taking, and similar radiological findings within first-degree and second-degree relatives with early deaths, transitioned the diagnosis from Fahr's syndrome to Fahr's disease. We present this case of Fahr's disease to emphasise the value of collaboration among multidisciplinary professionals to improve quality of care for such patients.

Pneumonia or Kaposi Sarcoma: Beneath the Dyspnea With Non-compliance of HIV.

Human herpesvirus 8 (HHV-8) or Kaposi sarcoma herpesvirus is the cause of Kaposi sarcoma (KS), the most prevalent cancer related to acquired immune deficiency syndrome. About 90% of the time, KS is accompanied by cutaneous lesions; however, systemic illness can develop without cutaneous involvement. Today's highly active antiretroviral therapy (HAART) era has seen a decrease in the prevalence of KS. In immunocompromised individuals, it may be challenging to differentiate between pneumonia and the clinical characteristics of pulmonary KS, which might make diagnosis more challenging. HAART is the first-line therapy for KS, and its usage has reduced the incidence of KS. Depending on how severe the illness is, systemic chemotherapy could be helpful. We report the case of a young man who presented with pulmonary symptoms in the presence of a pharyngeal mass and was later found to have bilateral pulmonary metastasis. Interestingly, this diagnosis was made in the absence of classic cutaneous lesions. The patient was counseled for quality of life with medication and intervention compliance, and a consultation with an oncologist was set up.

A Review of Proteins Associated With Neuroprotection and Regeneration in Alzheimer's Disease.

One of the most prevailing conditions of dementia is the illness known as Alzheimer's disease. The diagnostic signs of Alzheimer's disease progressively get worse over a long period since it is a cumulative condition. Alzheimer's disease causes modest memory loss in its initial stages, but people cannot converse or react to their surroundings in the later stages of the disease. In Alzheimer's disease, the destruction of neurons and the interconnection between them in the cortical region and the hippocampus is the beginning, after which the disease proceeds. The cerebral cortex regions are subsequently involved in thinking, linguistics, and interpersonal communication. Other parts of the brain eventually suffer harm as well. A person with Alzheimer's slowly loses the capacity to live and do daily tasks on their own over time. The illness is lethal in the end. Dementia is most commonly caused by ageing. Although dementia grows more prevalent as individuals age, this does not imply that dementia is a natural component of ageing. Up to 40% of those over 85 years who have dementia suffer from this condition. Amyloid, a beta protein that wrongly builds up and creates neurofibrillary tangles in the brain, causes Alzheimer's, a condition of protein misfolding. According to tradition, the primary cause of neuronal degeneration caused by the amyloid hypothesis is the buildup of beta-amyloid peptides. According to theory, the hazardous protein form that upsets the cell's calcium ion balance clumps amyloid fibrils, which leads to apoptotic cell death. This review article discusses the pathophysiology and biochemistry of various neuroprotective proteins to examine the potential of future anti-medications for Alzheimer's disease.

Machine learning models for non-invasive glucose measurement: towards diabetes management in smart healthcare.

Abstract: The patients of diabetes require to observe and control their glycemic profile through continuous glucose level monitoring. The blood glucose measurement is possible through invasive, minimally invasive and non-invasive methods. Invasive method is traditional method for instant glucose measurement where glucose is measured by taking blood samples from the body. However, the repeated finger pricking increases the risk of blood-related infections and trauma. Hence, the development of non-invasive real time device is essential for smart healthcare to manage glucose-insulin balance. The paper presents machine learning models for non-invasive glucose measurement. So, various machine learning algorithms including Logistic Regression, KNN, Gaussian Naive Bayes, Linear Regression, Multi-polynomial Regression, Neural Network, XGBoost, Decision Tree, Random Forest and Support Vector Machine are applied on two dataset which are PIDD (UCI repository) and iGLU dataset (iGLU device). The comparative analysis is carried out where accuracy, training time, recall, precision, f-1 score and AUC curve is measured for classification algorithms. For regression algorithms, measures like accuracy, Mean Absolute Error (MAE) and Root Mean Square Error (RMSE) are used for comparison purpose. Random forest with 84% accuracy and 68% recall, 76% precision and 72% f1-score for PIDD and Decision tree with 70% accuracy, 8% mean absolute error (MAE) and 8.5% root mean square error (RMSE) for iGLU dataset gives best results. Clark grid analysis has also been done where all the values fall under zone A which gives 100% accuracy and the device is useful for medication purpose. The proposed work has been also compared with similar methods and the proposed work has excellent results in terms of MAD, mARD, RMSE and AvgE. The device would be ideal as non-invasive solution for continuous glucose monitoring.

A Case Report on BRASH (Bradycardia, Renal Failure, Atrioventricular Blockade, Shock, and Hyperkalaemia) Syndrome: A Challenging Diagnosis.

A relatively new yet critical phenomenon of bradycardia, renal failure, atrioventricular (AV) blockade, shock, and hyperkalemia (BRASH) syndrome is hypothesized to happen in patients who take atrioventricular nodal blocking (AVNB) agents and have underlying renal insufficiency. In our case, a 67-year-old female with an extensive medical history presented to the emergency room with chief complaints of decreased appetite, nausea, vomiting, fatigue, and left-sided atypical chest pain for the past two weeks. The patient was taking losartan potassium 50 mg daily in addition to carvedilol 6.25 mg twice daily for her hypertension (HTN) and heart failure with reduced ejection fraction (HFrEF) with the addition of bumetanide 0.5 mg, which was added three weeks prior. On presentation, the patient had sinus bradycardia and hypotension along with the laboratory finding of acute kidney injury (AKI) in the setting of chronic kidney disease (CKD) and hyperkalemia. Cardiology and nephrology were consulted emergently; her clinical scenario raised suspicion of the BRASH syndrome. The patient was admitted to the intensive care unit (ICU), and all antihypertensive medications, including beta-blockers, were stopped. Intravenous (IV) fluid resuscitation and medical management of hyperkalemia were initiated, along with BiPAP for respiratory distress. She responded significantly, and her vitals remained stable. She was successfully discharged home with a cardiology and nephrology follow-up. We highlight the case to emphasize the consideration of BRASH in a patient on multiple cardiac medications who presented with deranged electrolytes and organ failure, and decompensated heart failure (HF) should not be fixed on as the principal diagnosis.

A Molecular Basis Approach of Eczema and Its Link to Depression and Related Neuropsychiatric Outcomes: A Review.

"What about my eczema do I love the most? The hurt? A scratch? The humiliation of the public? Oh, there are so many options available!" Studies have shown an association between atopic eczema (AE), a common inflammatory skin condition, and an increased risk of mental health problems. Despite this, experts are still examining the causes of the links between common mental diseases (such as depression and anxiety) and skin conditions. We collected studies that were published in the past 10 years. We searched the following databases: PubMed, PubMed Central, Science Direct, and Google Scholar. Further relevant research was assessed by examining the bibliographies of eligible studies and related ones. Two reviewers looked at the titles and abstracts of the studies to see if they were eligible, and then they read the full texts. We went through eczema and depression relationships, their etiopathogenesis, molecular basis, immune response, the role of genetic factors, and possible interactions between neurons and the immune system. Another possible contributing factor could be a change in cutaneous microbiota in eczema patients. Part of the initial connection could be explained by psychological stress, which further leads to depression in eczema patients. Healthcare professionals treating eczema patients must be aware of the comorbidity of mental problems and the potential that people with poor mental health may need social or emotional support. Patients with eczema, especially youngsters, can benefit from routine health checks since they can help identify neuropsychiatric issues like depression early and lessen the burden of both physical sickness and poor mental health. Given that AE is a condition that appears to be related to depression and anxiety, more research with larger samples is needed to determine a potential role for targeted mental health screening in people with AE, as well as the possibility of mental health modification through improved AE control (e.g., using new biologic agents).

The Impact of Tezepelumab in Uncontrolled Severe Asthma: A Systematic Review of Randomized Controlled Trials.

Asthma, a chronic illness, is characterized by inflammation and airway constriction. Uncontrolled severe asthma is related to poor quality of life and increased utilization of health resources. Conventional treatments are associated with a significant amount of adverse effects. Recent years have seen the identification of various molecular effectors and signaling pathways as interesting targets for the biological therapy of severe asthma that is resistant to current therapies. Because they only target some downstream components of the inflammatory response in asthma, leaving other components unaffected, current biologic treatments only lower the exacerbation rate by 50%. If we focus on the upstream mediators of the inflammatory response in asthma, it might have a greater effect and be more efficient. Tezepelumab is a human monoclonal IgG2 antibody that specifically binds to thymic stromal lymphopoietin (TSLP) at the level of its TSLPR (thymic stromal lymphopoietin receptor) binding site, inhibiting the interaction between human TSLP and TSLPR. It is being used to treat the cytokines on the respiratory epithelial layer known as "alarmins." It is the only biologic drug available for treating severe uncontrolled asthma, despite limitations in biomarker and phenotype. In light of recent developments, the lack of knowledge on tezepelumab prompts us to publish a comprehensive systematic review. We discovered that regardless of blood eosinophil level and fractional exhaled nitric oxide levels, tezepelumab dramatically lowers asthma exacerbation in patients with severe uncontrolled asthma when compared to placebo. Tezepelumab also lessens patients' demand for healthcare resources while improving clinical indicators of lung function, health-related quality of life, and asthma management in patients. Tezepelumab plays a role in enhancing pre-bronchodilator FEV1 and lowering blood eosinophil count and fractional exhaled nitric oxide in patients with or without chronic allergies (FeNO). There have been no reports of fatalities or severe adverse events connected to tezepelumab.