To assess the efficacy and safety of using energy devices as treatment for radiation-induced hemorrhagic cystitis (RHC) and to determine the most suitable energy source, settings and techniques based on laser-tissue interaction. A search of Google Scholar, PubMed, and Web of Science databases was conducted uptil February 2024 to identify studies on use of energy devices for RHC.Additionally, ClinicalTrials.gov and the World Health Organization’s ICTRP (International Clinical Trials Registry Platform) were searched for ongoing studies. We identified 10 studies fulfilling the search criteria using modalities including Nd:YAG laser, argon plasma coagulation, 980-nm diode laser, and potassium-titanyl-phosphate (KTP) laser. Across studies (n=137), majority (n=116, 84.7%) of RHC patients achieved hematuria resolution after one treatment session, with mean/median hematuria-free intervals of 11 to 16 months. Six patients (4.4%) were unresponsive and underwent cystectomy/urinary diversion. Total adverse events occurred in patients (30/139, 21.6%), including storage symptoms, recurrent hematuria, bladder stones and urinary retention, among others. Typical laser settings involved low power (<40 W), with either a pulse duration of 2–3 seconds or 10–40 milliseconds; some used continuous wave mode. Other standard practises include selective coagulation employed in a “painting” fashion and non-contact mode (3–5 mm). The treatment endpoints were hemostasis, involution of telangiectatic vessels and formation of pale well-circumscribed mucosal ulcer. Energy devices have considerable efficacy and safety to treat RHC patients and can be considered for refractory RHC and as an adjunct after initial management. The various properties of KTP laser confers an advantage over other energy devices.

INTRODUCTION: The National Institute of Health and Care Excellence (NICE) has defined the terms, 'acute coronavirus disease 2019' (COVID-19), 'ongoing symptomatic COVID-19' and 'post-COVID-19 syndrome', with the latter two described as having persistent symptoms after the onset of COVID-19 symptoms for 4-12 weeks and >12 weeks, respectively. Persistent symptoms can either be due to the after-effects of COVID-19 or new-onset diseases after acute COVID-19. All symptoms observed beyond 4 weeks after the onset of COVID-19 need not be present at the time of onset. Previous studies on persistent post-COVID-19 symptoms have not mentioned new-onset diseases after acute COVID-19, and only a select few studies have discussed such new-onset symptoms. METHODS: Ninety-five patients who attended the post-COVID-19 clinic completed the requisite follow-up till 16 weeks after COVID-19 symptom onset. Data was recorded on a predesigned proforma. Necessary investigations were conducted to rule out any other cause of persistent symptoms. RESULTS: Fatigue (62.1%), breathlessness (50.5%) and cough (27.4%) were the most common symptoms present beyond 4 weeks after the onset of COVID-19 symptoms. Forty-nine (51.57%) patients developed post-COVID-19 syndrome - their severity of symptoms (odds ratio [OR] 17.77) and longer duration of hospital stay (OR 1.095) during acute disease were significantly associated with the development of post-COVID-19 syndrome. During follow-up, 25 patients developed new-onset symptoms, such as diabetes mellitus, hypertension and idiopathic tachycardia. CONCLUSION Patients can have persistent symptoms, new-onset symptoms and new-onset diseases after recovery from acute COVID-19.
Humans ; COVID-19/diagnosis* ; Female ; Male ; Prospective Studies ; Middle Aged ; Adult ; Fatigue/etiology* ; Post-Acute COVID-19 Syndrome ; SARS-CoV-2 ; Aged ; Cough/etiology* ; Dyspnea/etiology*

Alzheimer disease (AD) is the most common cause of dementia worldwide. Its clinical manifestations include a progressive loss of memory and other cognitive domains, as well as brain atrophy. An elevated homocysteine level (>15 µmol/L), known as hyperhomocysteinemia, is also an attributing risk factor for AD, vascular pathologies, and brain atrophy. Neuroimaging studies including T2-weighted magnetic resonance imaging scans revealed white matter hyperintensities in the periventricular and deep white matter, enlarged ventricles, widened sulci, and decreased white matter mass, which are features of aging, as well as cerebrovascular changes. This case series investigated changes in biochemical marker levels including serum homocysteine, folate, and vitamin B12, and the degree of atrophic variations in cortical-subcortical white matter in AD. The present study hypothesized that serum homocysteine levels might be used as a surrogate marker to screen for AD at an earlier stage.

Background: In recent years, medical thoracoscopy has been well established to play an important role in undiagnosed pleural effusion; however, this procedure is underutilized due to limited availability of the instruments it requires. This study analysed the outcome of single port rigid thoracoscopy in patients with undiagnosed pleural effusions. Methods: This study retrospectively analysed the outcomes of all patients with undiagnosed pleural effusion presenting to our centre between 2016 to 2020 who underwent single port rigid medical thoracoscopy as a diagnostic procedure. Results: In total, 92 patients underwent single port rigid medical thoracoscopy. The most common presenting symptom was shortness of breath. A majority of the patients had lymphocytic exudative pleural effusion. The average biopsy sample size was 18 mm, and no major complication was reported in any of the patients. Conclusion Single port rigid thoracoscopy is a safe and well-tolerated procedure that yields a biopsy of a larger size with high diagnostic yield. Moreover, the low cost of the instruments required by this procedure makes it particularly suited for use in developing countries.

Complex craniovertebral junction (CVJ) defects account for a considerable proportion of CVJ diseases. Given the heavily assimilated C1, an unfavorable C1–C2 joint orientation, an overriding C2 superior facet, a low-hanging occiput, and an abnormal vertebral artery course with a high-riding vertebral artery, placement of C1 lateral mass screws might be difficult. To address this, a novel technique for placing C1 lateral mass screws that avoid vertebral artery injury, low-hanging occiput, and overriding C2 superior facet was developed in this study. This approach enables firm fixation of C1–C2 even in difficult situations where the placement of the C1 lateral mass is challenging.

Bilateral distal anterior cerebral artery (DACA) aneurysms also called “kissing aneurysms” or “mirror aneurysm” are extremely rare, accounting for only 0.2% of all intracranial aneurysms. There have only been a few examples of mirror DACA aneurysms reported in the literature. Here, we report a rare case of mirror DACA aneurysm in a middle aged female with its successful clipping. Patient was admitted with severe headache and altered sensorium. Computed tomography (CT) head was suggestive of anterior inter-hemispheric hematoma. Digital subtraction angiography (DSA) was done which was suggestive of two distal anterior cerebral artery aneurysms located at same anatomical position. It was treated through microsurgical clipping. Mirror image DACA aneurysms are rare occurrence. All patients with ruptured DACA aneurysms should have angiography with 3D reconstruction studies. This aids in determining the aneurysm’s morphology and planning treatment accordingly.

Moderate levels of endogenous reactive oxygen species (ROS) are important for various cellular activities, but high levels lead to toxicity and are associated with various diseases. Levels of ROS are maintained as a balance between oxidants and antioxidants. Accumulating data suggest that oxidative stress is a major factor in deterioration of renal function. In this review, we highlight the possible mechanism by which oxidative stress can lead to chronic kidney disease (CKD). This review also describes therapies that counter the effect of oxidative stress in CKD patients. Numerous factors such as upregulation of genes involved in oxidative phosphorylation and ROS generation, chronic inflammation, vitamin D deficiency, and a compromised antioxidant defense mechanism system cause progressive detrimental effects on renal function that eventually lead to loss of kidney function. Patients with renal dysfunction are highly susceptible to oxidative stress, as risk factors such as diabetes, renal hypertension, dietary restrictions, hemodialysis, and old age predispose them to increased levels of ROS. Biomolecular adducts (DNA, proteins, and lipids) formed due to reaction with ROS can be used to determine oxidative stress levels. Based on the strong correlation between oxidative stress and CKD, reversal of oxidative stress is being explored as a major therapeutic option. Xanthine oxidase inhibitors, dietary antioxidants, and other agents that scavenge free radicals are gaining interest as treatment modalities in CKD patients.

Background: and Purpose Pathogenic variants in the myopalladin gene (MYPN) are known to cause mildly progressive nemaline/cap myopathy. Only nine cases have been reported in the English literature. Methods: A detailed evaluation was conducted of the clinical, muscle magnetic resonance imaging (MRI), and genetic findings of two unrelated adults with MYPN-related cap myopathy. Genetic analysis was performed using whole-exome sequencing. MRI was performed on a 1.5-T device in patient 1. Results: Two unrelated adults born to consanguineous parents, a 28-year-old male and a 23-year-old female, were diagnosed with pathogenic variants in MYPN that cause cap myopathy. Both patients presented with early-onset, insidiously progressive, and minimally disabling proximodistal weakness with mild ptosis, facial weakness, and bulbar symptoms. Patient 1 had a prominent foot drop from the onset. Both patients were followed up at age 30 years, at which point serum creatine kinase concentrations were minimally elevated. There were no cardiac symptoms; electrocardiograms and two-dimensional echocardiograms were normal in both patients. Muscle MRI revealed preferential involvement of the glutei, posterior thigh muscles, and anterior leg muscles. Whole-exome sequencing revealed significant homozygous splicesite variants in both of the probands, affecting intron 10 of MYPN: c.1973+1G>C (patient 1) and c.1974-2A>C (patient 2). Conclusions This study elaborates on two patients with homozygous MYPN pathogenic variants, presenting as slowly progressive congenital myopathy. These patients are only the tenth and eleventh cases reported in the English literature, and the first from South Asia. The clinical phenotype reiterates the mild form of nemaline rod/cap myopathy. A comprehensive literature review is presented.

Moderate levels of endogenous reactive oxygen species (ROS) are important for various cellular activities, but high levels lead to toxicity and are associated with various diseases. Levels of ROS are maintained as a balance between oxidants and antioxidants. Accumulating data suggest that oxidative stress is a major factor in deterioration of renal function. In this review, we highlight the possible mechanism by which oxidative stress can lead to chronic kidney disease (CKD). This review also describes therapies that counter the effect of oxidative stress in CKD patients. Numerous factors such as upregulation of genes involved in oxidative phosphorylation and ROS generation, chronic inflammation, vitamin D deficiency, and a compromised antioxidant defense mechanism system cause progressive detrimental effects on renal function that eventually lead to loss of kidney function. Patients with renal dysfunction are highly susceptible to oxidative stress, as risk factors such as diabetes, renal hypertension, dietary restrictions, hemodialysis, and old age predispose them to increased levels of ROS. Biomolecular adducts (DNA, proteins, and lipids) formed due to reaction with ROS can be used to determine oxidative stress levels. Based on the strong correlation between oxidative stress and CKD, reversal of oxidative stress is being explored as a major therapeutic option. Xanthine oxidase inhibitors, dietary antioxidants, and other agents that scavenge free radicals are gaining interest as treatment modalities in CKD patients.

Background: and Purpose Pathogenic variants in the myopalladin gene (MYPN) are known to cause mildly progressive nemaline/cap myopathy. Only nine cases have been reported in the English literature. Methods: A detailed evaluation was conducted of the clinical, muscle magnetic resonance imaging (MRI), and genetic findings of two unrelated adults with MYPN-related cap myopathy. Genetic analysis was performed using whole-exome sequencing. MRI was performed on a 1.5-T device in patient 1. Results: Two unrelated adults born to consanguineous parents, a 28-year-old male and a 23-year-old female, were diagnosed with pathogenic variants in MYPN that cause cap myopathy. Both patients presented with early-onset, insidiously progressive, and minimally disabling proximodistal weakness with mild ptosis, facial weakness, and bulbar symptoms. Patient 1 had a prominent foot drop from the onset. Both patients were followed up at age 30 years, at which point serum creatine kinase concentrations were minimally elevated. There were no cardiac symptoms; electrocardiograms and two-dimensional echocardiograms were normal in both patients. Muscle MRI revealed preferential involvement of the glutei, posterior thigh muscles, and anterior leg muscles. Whole-exome sequencing revealed significant homozygous splicesite variants in both of the probands, affecting intron 10 of MYPN: c.1973+1G>C (patient 1) and c.1974-2A>C (patient 2). Conclusions This study elaborates on two patients with homozygous MYPN pathogenic variants, presenting as slowly progressive congenital myopathy. These patients are only the tenth and eleventh cases reported in the English literature, and the first from South Asia. The clinical phenotype reiterates the mild form of nemaline rod/cap myopathy. A comprehensive literature review is presented.