Impact of Blockchain on Financial Technology Innovation in the Banking, Financial Services and Insurance (BFSI) Sector

This research paper aims to highlight the progression of the technological advancements emerging in the BFSI sector across the globe, evaluate them, and find the merits and shortcomings in this sector using literature review assisted by the prior knowledge from the renowned works published in reputed journals. The information was obtained from secondary sources, thereby helping us draw a picture of the existing state of technology in the BFSI sector and its future potential/applicability within the field. We have used advanced search criteria of two levels to comprehensively cover the existing research papers on the topic for evaluation. With the rising need for digital change, banks look up to speed up the existing plans to arrange authoritative changes driven by the new initiatives. Artificial intelligence companies in the upcoming years will thrive. Banks will make all the efforts to utilize their advances to lessen the cost, mechanize all ordinary procedures, and separate administration levels through personal information which was not accessible before

Impact of Change in Promoters’ Shareholding Pattern on the Performance of Small-Cap-Value Equity Stocks in the National Stock Exchange of India

This paper studies the impact of a change in promoter shareholding on small-cap-value stocks. NIFTY Small Cap 250 index stocks within the top 20th percentile of the book-to-market (B/M) ratio of the same universe have been considered for this study. The paper uses regression analysis for understanding the impact of independent variables on returns. The universe is further narrowed down to stocks with a positive change in promoter shareholding, which is found to be negatively related to stock returns. In addition, although the book-to-market ratio does not play any role in the prediction of returns while within this narrowed-down universe, the size effect is present. The results are discussed with reference to some relevant past research literature, and the scope for further research is also discussed

Circadian and ultradian rhythms in normal mice and in a mouse model of Huntington’s disease

Circadian rhythms in core body temperature (CBT) have been widely studied, but fewer studies have explored higher-frequency (ultradian) rhythms in detail. We analyzed CBT recordings from young and middle-aged wild-type mice as well as from the Q175 model of Huntington's disease (HD), at sufficient temporal resolution to address the question of ultradian rhythms. We used model selection methods to show that the overall circadian pattern was better fit by a square wave than a sine wave. Then, using Fourier analysis of the CBT rhythms, we identified the spectral signature of an 8-hour oscillation that occurs in the night but not the day, an observation that can be confirmed by direct inspection of the rhythms. This diurnal amplitude modulation of the 8-hour rhythm was lost with aging as well as in the HD model. Thus, the impact of aging and disease is seen here in the loss of the ability to separate rhythms into a daytime phase and a nighttime phase. These findings raise the possibility that ultradian rhythms in CBT may be a useful biomarker for the pathology within the central nervous system

Late presentation of congenital urachal sinus in a middle aged male complicated by an umbilical abscess: A case report

Urachus or the median umbilical ligament is a fibrous strand connecting umbilicus to bladder, representing embryologic remnant of cloaca and allantois. Urachal anomalies are infrequent in adult population. Moreover they have a different course in adults than pediatric age group in which they are more common, frequently involute and have a benign course. These remnants are prone to infection and development of malignancy. A proper diagnostic workup by clinical and imaging tools is required. We present a case report of a urachal sinus complicated with abscess in an adult with brief review of the literature

Cardiac TRPV1-afferent signaling promotes arrhythmogenic ventricular remodeling after myocardial infarction

Chronic sympathoexcitation is implicated in ventricular arrhythmogenesis (VAs) following myocardial infarction (MI), but the critical neural pathways involved are not well understood. Cardiac adrenergic function is partly regulated by sympathetic afferent reflexes, transduced by spinal afferent fibers expressing the transient receptor potential cation subfamily V member 1 (TRPV1) channel. The role of chronic TRPV1 afferent signaling in VAs is not known. We hypothesized that persistent TRPV1 afferent neurotransmission promotes VAs after MI. Using epicardial resiniferatoxin (RTX) to deplete cardiac TRPV1-expressing fibers, we dissected the role of this neural circuit in VAs after chronic MI in a porcine model. We examined the underlying mechanisms using molecular approaches, IHC, in vitro and in vivo cardiac electrophysiology, and simultaneous cardioneural mapping. Epicardial RTX depleted cardiac TRPV1 afferent fibers and abolished functional responses to TRPV1 agonists. Ventricular tachycardia/fibrillation (VT/VF) was readily inducible in MI subjects by programmed electrical stimulation or cesium chloride administration; however, TRPV1 afferent depletion prevented VT/VF induced by either method. Mechanistically, TRPV1 afferent depletion did not alter cardiomyocyte action potentials and calcium transients, the expression of ion channels, or calcium handling proteins. However, it attenuated fibrosis and mitigated electrical instability in the scar border zone. In vivo recordings of cardiovascular-related stellate ganglion neurons (SGNs) revealed that MI enhances SGN function and disrupts integrated neural processing. Depleting TRPV1 afferents normalized these processes. Taken together, these data indicate that, after MI, TRPV1 afferent-induced adrenergic dysfunction promotes fibrosis and adverse cardiac remodeling, and it worsens border zone electrical heterogeneity, resulting in electrically unstable ventricular myocardium. We propose targeting TRPV1-expressing afferent to reduce VT/VF following MI